ACCCN ’s

Critical Care Nursing

3e

Leanne Aitken
Andrea Marshall
Wend ' Chaboyer

Free evolve study resources at

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ELSEVIER
 ACCCN’s
Critical Care Nursing
3e
 ACCCN’s
Critical Care Nursing
3e
Leanne Aitken
RN, PhD, BHSc(Nurs)Hons, GCertMgt, GDipScMed(ClinEpi), FACCCN,
FACN, FAAN, Life Member – ACCCN
Professor of Critical Care Nursing, School of Nursing and Midwifery
and NHMRC Centre of Research Excellence in Nursing (NCREN),
Menzies Health Institute Queensland, Griffith University, Qld, Australia
Intensive Care Unit, Princess Alexandra Hospital, Qld, Australia
Professor of Nursing, School of Health Sciences,
City University London, UK

Andrea Marshall
RN, PhD, MN(Research), BN, Grad Cert Ed Studies (Higher Ed),
IC Cert, FACCCN, FACN, Life Member – ACCCN
Professor of Acute and Complex Care Nursing, School of Nursing and
Midwifery and NHMRC Centre of Research Excellence in Nursing (NCREN),
Menzies Health Institute Queensland, Griffith University, Qld, Australia
Intensive Care Unit, Gold Coast Hospital and Health Service, Qld, Australia

Wendy Chaboyer
RN, PhD, MN, BSc(Nu)Hons, Crit Care Cert, FACCCN,
Life Member – ACCCN
Professor and Director, NHMRC Centre of Research Excellence
in Nursing (NCREN), Menzies Health Institute Queensland,
Griffith University, Qld, Australia
Professor, Institute of Health and Care Sciences,
University of Gothenburg, Sweden
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National Library of Australia Cataloguing-in-Publication Data

--------------------------------------------------------------------------------------------
ACCCN’s critical care nursing / [editors] Leanne Aitken,
Andrea Marshall & Wendy Chaboyer.

3rd edition.

9780729542005 (paperback)

Intensive care nursing--Australia.

Aitken, Leanne, editor.

Marshall, Andrea, editor.
Chaboyer, Wendy, editor.

616.028
--------------------------------------------------------------------------------------------
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Content Development Specialist: Martina Vascotto
Project Manager: Devendran Kannan
Edited by Linda Littlemore
Proofread by Laura Davies
Design by Natalie Bowra
Permissions by Sarah Thomas & Anita Mercy Vethakkan
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 Contents

Foreword by Ruth M Kleinpell vi 14 Respiratory alterations and management 438

Foreword by Doug Elliott vii Sharon Wetzig, Bronagh Blackwood, Judy Currey
Preface viii 15 Ventilation and oxygenation management 470
About the Australian College of Critical Care Nurses Louise Rose, Rand Butcher
(ACCCN) x 16 Neurological assessment and monitoring 511
About the editors xii Diane Chamberlain, Leila Kuzmiuk
List of contributors xiii 17 Neurological alterations and management 546
List of reviewers xvi Diane Chamberlain, Elaine McGloin
Acknowledgements xvii 18 Support of renal function 584
Detailed contents xviii Ian Baldwin, Gavin Leslie
Abbreviations xxi
19 Nutrition assessment and therapeutic
Section 1 Scope of critical care 1 management 622
Andrea Marshall,Teresa Williams
1 Scope of critical care practice 3
20 Gastrointestinal, metabolic and liver alterations 651
Leanne Aitken,Wendy Chaboyer, Andrea Marshall
Andrea Marshall, Christopher Gordon
2 Systems and resources 19
21 Pathophysiology and management of shock 681
Denise Harris, Ged Williams
Margherita Murgo, Ruth Kleinpell
3 Quality and safety 44
Wendy Chaboyer, Karena Conroy 22 Multiple organ dysfunction syndrome 717
Melanie Greenwood, Alison Juers
4 Recovery and rehabilitation 73
Janice Rattray, Leanne Aitken Section 3 Specialty practice 737
5 Ethical issues in critical care 106
23 Emergency presentations 739
Maureen Coombs, Carol Grech
David Johnson, Julia Crilly
Section 2 Principles and practice of critical care 129 24 Trauma management 791
Catherine Bell, Kerstin Prignitz Sluys
6 Essential nursing care of the critically ill patient 131
Bernadette Grealy, Fiona Coyer 25 Resuscitation 829
7 Psychological care 164 Trudy Dwyer, Jennifer Dennett, Ian Jacobs
Leanne Aitken, Rosalind Elliott 26 Postanaesthesia recovery 857
8 Family and cultural care of the critically ill patient 193 Paula Foran, Andrea Marshall
Marion Mitchell, Denise Wilson, Robyn Aitken 27 Paediatric considerations in critical care 885
9 Cardiovascular assessment and monitoring 231 Tina Kendrick, Anne-Sylvie Ramelet
Thomas Buckley, Frances Lin 28 Pregnancy and postpartum considerations 922
10 Cardiovascular alterations and management 271 Wendy Pollock, Emma Kingwell
Robyn Gallagher, Andrea Driscoll 29 Organ donation and transplantation 966
11 Cardiac rhythm assessment and management 311 Debbie Friel
Malcolm Dennis, David Glanville Appendix A Practice standards for specialist
12 Cardiac surgery and transplantation 362 critical care nurses 986
Judy Currey, Sher Michael Graan Appendix B Normal laboratory values 989
13 Respiratory assessment and monitoring 402 Glossary of terms 994
Mona Ringdal, Janice Gullick Index 1001
Foreword
Ruth M Kleinpell

Advances in critical care treatments, procedures and laboratory analysis application and a comprehensive
technologies mandate that critical care nurses maintain glossary of terms.
current knowledge of disease states, management princi- ACCCN’s Critical Care Nursing is an outstanding resource
ples for acute and critical illness and best care principles for critical care nurses, regardless of the practice setting. In
including clinical practice guidelines. As a specialty area seeking to provide complex high intensity care, therapies
of nursing practice, critical care nursing is focused on the and interventions, critical care nurses will find that this third
care of patients who are experiencing life-threatening edition of the book reviews essential content related to
illness. Globally, critical care nurses provide care to critical care nursing knowledge and skills to provide care
ensure that critically ill patients and their families receive to acute and critically ill patients and their families.
optimal care. Critical care nursing is one of the largest specialty
This third edition of the Australian College of areas of nursing practise as, internationally, more than
Critical Care Nurses’ (ACCCN’s) Critical Care Nursing is 600,000 critical care nurses practise in high acuity, acute
a valuable resource for critical care nursing. The editors, care or critical care. It is well established that maintaining
who are acknowledged expert practitioners, educators knowledge of current practice, evidence-based care and
and researchers in critical care nursing, have organised the integrating research in clinical practice for critical care
book into topics covering essential concepts in critical patients are essential components of critical care nursing.
care. The book content addresses aspects of critical care This third edition of ACCCN’s Critical Care Nursing
nursing practice, quality and safety concepts, ethical provides a comprehensive expert resource for critical care
issues, pathophysiology and management of a variety nurses to enable them to further develop their knowledge
of critical illness states, recovery and rehabilitation after
and enhance their clinical nursing expertise.
critical illness, psychological care and family-centred care
concepts, among other topics. The chapters are written Ruth Kleinpell PhD RN FAAN FCCM
by established experts in the field of critical care and Director, Center for Clinical Research & Scholarship
provide a comprehensive overview of critical care nursing Rush University Medical Center
principles of practice. The book provides up-to-date Professor, Rush University College of Nursing
information on evidence-based practices and the chapters Nurse Practitioner, Rush Lincoln Park Urgent Care,
incorporate a variety of educational resources including Chicago, Illinois USA
website links, case studies, practice tips and appendices President, World Federation of Critical Care Nurses
addressing practice standards for critical care nursing, (http:www.wfccn.org)
 Foreword
Doug Elliott

It is a great privilege and with a sense of pride that I write with pedagogical features including summary tables,
these comments for this 3rd edition of ACCCN’s Critical illustrative figures, case studies and research vignettes to
Care Nursing. As lead editor of the previous two editions, support active and reflective learning.
publication of this revision confirms our initial thoughts The editors, all leading experts in their specialty
that there was a clear disciplinary need and reader demand fields, have assembled a strong and varied set of chapter
for an original text from this area of the world, and that authors from both clinical and academic settings, mostly
our community contained a critical mass of scholarly from Australia, but also some notable contributions from
writers able to deliver a comprehensive text on critical key international experts. The resulting collection of
care nursing. An ensuing strong and enduring collaborative 29 chapters provides a comprehensive resource for critical
relationship between the College, the Publisher and the care nurses and students seeking to maintain or develop
Editors has resulted in this robust legacy of knowledge for their knowledge and skillset in the holistic care of critically
our specialty. ill patients.
Critical care continues to be a dynamic and evolving
Doug Elliott RN, PhD, MAppSc (Nurs),
clinical specialty, and maintaining currency of knowledge
BAppSc (Nurs), ICCert
can be a challenge for nurse clinicians and students. This
Professor of Nursing
edition reflects the current evidence base for critical Faculty of Health
care nursing, tailored for practice in the Australian, University of Technology Sydney
New Zealand and Asia–Pacific region.The text continues a Past Co-Editor
strong focus of application of research findings to practice, ACCCN’s Critical Care Nursing (2007, 2012)
Preface

Critical care as a clinical specialty is over half a century old. our readers to continue to also search for the most
With every successive decade, advances in the education contemporary sources of knowledge to guide their clinical
and practices of critical care nurses have been made. Today, practice. A range of website links have been included in
critical care nurses are some of the most knowledgeable each chapter to facilitate this process.
and highly skilled nurses in the world, and ongoing This third edition is divided into three broad sections:
professional development and education are fundamental the scope of critical care nursing, core components of
elements in ensuring we deliver the highest quality care to critical care nursing and specialty aspects of critical care
our patients and their families. nursing. Inclusion of new chapters and significant revisions
This book is intended to encourage and challenge to existing chapters were based on our reflections and
nurses to further develop their critical care nursing suggestions from colleagues and reviewers as well as on
practice. Our vision for the first edition was for an original evolving and emerging practices in critical care.
text from Australasian authors, not an adaptation of texts Section 1 introduces a broad range of professional
produced in other parts of the world. issues related to practice that are relevant across critical
As international interest in our text has grown, we have care. Initial chapters provide contemporary information
expanded its content to reflect the universal core elements on the scope of practice, systems and resources and ethical
of critical care nursing practice while still retaining issues, with expanded information on quality and safety,
specific information that captures the unique elements and recovery and rehabilitation in critical care.
of contemporary critical care nursing in Australia, New Content presented in Section 2 is relevant to the
Zealand and other similar practice environments such as majority of critical care nurses, with a focus on concepts that
the United Kingdom and some parts of Europe and Asia. underpin practice such as essential physical, psychological,
This third edition of ACCCN’s Critical Care Nursing social and cultural care. Remaining chapters in this section
has 29 chapters that reflect the collective talent and present a systems approach in supporting physiological
expertise of 54 contributors – a strong mix of academics function for a critically ill individual. This edition now
and clinicians with a passion for critical care nursing – in has multiple linked chapters for some of the major
showcasing the practice of critical care nursing in Australia, physiological systems – four chapters for cardiovascular,
New Zealand, Asia and the Pacific. We also engaged three for respiratory and two for neurological. In this
contributors beyond Australasia to reflect global practices third edition we have a stronger emphasis on nutrition
and to extend the applicability of our text to a wider assessment and therapeutic management, with this topic
geographical audience. All contributors were carefully now having a dedicated chapter. Chapters on support
chosen for their current knowledge, clinical expertise and of renal function; gastrointestinal, metabolic and liver
strong professional reputations. alterations; management of shock; and multi-organ
The book has been developed primarily for use by dysfunction complete this section.
practising critical care clinicians, managers, researchers Section 3 presents specific clinical conditions such as
and graduate students undertaking a specialty critical care emergency presentations, trauma, resuscitation, paediatric
qualification. In addition, senior undergraduate students considerations, pregnancy and postpartum considerations
studying high acuity nursing subjects will find this book and organ donation, by building on the principles outlined
a valuable reference tool, although it goes beyond the in Section 2. To this section we have added a specific
learning needs of these students. The aim of the book is to chapter on postanaesthesia recovery to acknowledge the
be a comprehensive resource, as well as a portal to an array importance of this work, which might occur in some
of other important resources, for critical care nurses. The critical care areas, particularly after hours. This section
nature and timeline of book publishing dictate that the enables readers to explore some of the more complex or
information contained in this book reflects a snapshot in unique aspects of specialty critical care nursing practice.
time of our knowledge and understanding of the complex Chapters have been organised in a consistent format
world of critical care nursing. We therefore encourage to facilitate identification of relevant material. Where
 PREFACE ix

appropriate, each chapter commences with an overview of learning can be found online. It is not our intention that
the relevant anatomy and physiology and the epidemiology readers progress sequentially through the book, but rather
of the clinical states internationally and then in the Austra- explore chapters or sections that are relevant for different
lian and New Zealand setting. Nursing care of the patient, episodes of learning or practice.
delivered independently or provided collaboratively with The delivery of effective, high-quality critical care
other members of the healthcare team, is then presented. nursing practice is a challenge in contemporary health
Pedagogical features include a case study that elaborates care. We trust that this book will be a valuable resource
relevant care issues and a critique of a research publication in supporting your care of critically ill patients and their
that explores a related topic. Tables, figures and practice loved ones.
tips have been used extensively throughout each chapter
to identify areas of care that are particularly pertinent for Leanne Aitken
readers. Each chapter also has specific learning activities Andrea Marshall
and model responses to these questions to further support Wendy Chaboyer
About the
Australian College
of Critical Care Nurses (ACCCN)
The Australian College of Critical Care Nurses, with Education Advisory Panel, which advises ACCCN on all
over 2400 members, is the peak professional organisation matters relating to education specific to critical care nursing.
representing critical care nurses in Australia. Membership This panel has developed a position paper on critical care
types include standard members, international members, nursing education and written submissions on behalf of
associate members, life members, honorary members and ACCCN to national reviews of nursing education
corporate members. All individual members are eligible
Workforce Advisory Panel, which has represented
and are encouraged to participate in the activities of
ACCCN on a number of national health workforce and
the College and receive the College journal and Critical
nursing committees.The panel has also developed position
Times publication, in addition to discounts for ACCCN
statements on nurse staffing for intensive care and high-
conference registration and for ACCCN publications. Life
dependency units in Australia, and annually reviews the
and honorary memberships are awarded to individuals in
dataset design for national workforce data collection in
recognition of their outstanding contribution to ACCCN
conjunction with ANZICS
and/or to critical care nursing excellence in Australia.
ACCCN is a company limited by guarantee and has Organ and Tissue Donation and Transplantation
branches in each state of Australia, with two members from Advisory Panel, which advises the board and developed a
each state branch management committee forming the position statement on organ donation and transplantation
ACCCN National Board of Directors. Each committee as it relates to intensive care. It disseminates related
facilitates the activities of the College at a local/state level information to critical care nurses regarding the promotion
and provides local and, at times, national representation. and national reform objectives of organ and tissue donation
The ACCCN Editorial Committee and Editorial Board, in Australia
under the leadership of the editor of the Australian
Quality Advisory Panel, which provides expert
Critical Care (ACC) journal, are responsible for College
knowledge, advice and information to ACCCN on
publications including the journal Australian Critical Care
matters relevant to critical care nursing practice relating
and the digital newspaper Critical Times.
specifically to patient management
There are a number of national advisory panels
and special interest groups dedicated to providing the Paediatric Advisory Panel, which provides expert
organisation with expert opinion on issues relating to knowledge, advice and information to ACCCN on
critical care nursing. These include: matters relevant to paediatric critical care nursing in
addition to recommending content and speakers for the
Resuscitation Advisory Panel, which consists of
annual ACCCN conferences
12 members representing each branch of the ACCCN,
plus a paediatric nurse representative. It has developed a The ICU Liaison Special Interest Group, which
complete suite of contemporary advanced life support and is a collective group of ACCCN members who have an
resuscitation educational materials and offers its ACCCN interest in ICU liaison/outreach and work together to
National ALS Courses throughout Australia discuss matters relevant to this area of increasing critical
care nursing focus.
Research Advisory Panel which, in addition to providing
expert advice to ACCCN, is responsible for evaluating In addition to branch educational events and sym-
and making recommendations on research strategy and posiums, ACCCN conducts three national conferences
grant submissions to ACCCN, and for evaluating abstracts each year: ACCCN Institute of Continuing Education
submitted to the ANZICS/ACCCN Annual Scientific (ICE) and, in conjunction with our medical colleagues
Meeting on Intensive Care from The Australian and New Zealand Intensive Care
 ABOUT THE AUSTRALIAN COLLEGE OF CRITICAL CARE NURSES (ACCCN) xi

Society (ANZICS), the ANZICS/ACCCN Annual of the Coalition of National Nursing Organisations
Scientific Meeting on Intensive Care and the Australian (CoNNO). The founding Chairperson of the World
and New Zealand Paediatric and Neonatal Intensive Care Federation of Critical Care Nurses (WFCCN) continues
Conference. to represent ACCCN on the WFCCN Council, and the
ACCCN has a representative on the Australian College also has representatives on the World Federation
Resuscitation Council (ARC), and has representation at of Paediatric Intensive and Critical Care Societies, and is a
a federal government advisory level through the Nursing member of the Intensive Care Foundation.
and Midwifery Stakeholder Reference Group (NMSRG) More information can be found on the ACCCN
chaired by the Chief Nurse of Australia, and is also a member website: www.acccn.com.au.
About the editors
Leanne Aitken is Professor of Critical Care Nursing clinical practice. Her program of research also focuses on
at Griffith University and Princess Alexandra Hospital, improving nutrition delivery to acute and critically ill
Queensland, Australia, and also Professor of Nursing at City patients during hospitalisation and following discharge.
University London, United Kingdom. She has had a long Andrea has been Editor with Australian Critical Care
career in critical care nursing, including practice, education since 2003. She is an active member of the Australian
and research roles. In all her roles, Leanne has been inspired College of Critical Care Nurses and has previously held
by a sense of enquiry, pride in the value of expert nursing executive positions with the New South Wales Branch of
and a belief that improvement in practice and resultant the College as well as being a longstanding member
patient outcomes is always possible. Research interests of both the Education Advisory and Research Advisory
include developing and refining interventions to improve Panels. In 2014 her contribution to the College was
long-term recovery of critically ill and injured patients, recognised with Life Membership. She is an active reviewer
decision-making practices of critical care nurses and a range for several funding bodies including the NHMRC and
of clinical practice issues within critical care and trauma. Intensive Care Foundation and contributes to the peer
Leanne has been active in ACCCN for more than review process for over 10 international journals, many of
25 years and was made a Life Member of the College in 2006 which have an interdisciplinary focus.
after having held positions on state and national boards,
Wendy Chaboyer is Professor of Nursing at Griffith
coordinated the Advanced Life Support course in Western
University and the Director of the Centre of Research
Australia in its early years, chaired the Education Advisory
Excellence in Nursing Interventions for Hospitalised
Panel and been an Associate Editor with Australian Critical
Patients, funded by the National Health and Medical
Care. In addition, she is a peer reviewer for a number
Research Council (NHMRC) (2010–2015). Wendy has
of national and international journals and reviews grant
30 years of experience in the critical care area, as a clinician,
applications for a range of organisations within Australia
educator and researcher, and she is passionate about the
and overseas; she was the immediate past Co-Chair of
contribution nurses can make to the hospital experience
the Scientific Review Committee of the Intensive Care
for patients and their families. Her early research examined
Foundation. Leanne is an Ambassador for the World
ICU patients’ experiences and the role nurses can play
Federation of Critical Care Nurses and is the representative
to assist in their transition from ICU to the ward. She
on a number of sepsis-related working groups including
has subsequently focused on patient safety, undertaking
an international group that authored a companion paper
research into adverse events after ICU, clinical handover
to the Surviving Sepsis Campaign guidelines to summarise
and ‘transforming care at the bedside’. Three recent areas
the evidence underpinning nursing care of the septic
of work have been in relation to patient participation
patient, the revision of the Surviving Sepsis Campaign
in care, pressure injury (ulcer) prevention and surgical
guidelines and the Global Sepsis Alliance.
dressings to prevent surgical site infections.
Andrea Marshall is Professor of Acute and Complex Wendy has been active in ACCCN since her arrival
Care Nursing at Griffith University and Gold Coast in Australia in the early 1990s and was awarded Life
Health, Queensland. She has been working in critical Membership in 2006. She has been a National Board
care as a clinician, educator and researcher for more than member and member of the Queensland Branch
two decades. Andrea has a strong interdisciplinary focus Management Committee. Wendy is a past Chair of the
on research and in particular how the best evidence is Research Advisory Panel and past Chair of the Quality
translated into clinical practice to optimise outcomes Advisory Panel of the ACCCN. She played a role in the
for critically ill patients and their families. As a previous formation of the World Federation of Critical Care Nurses
NHMRC Translating Research into Practice (TRIP) and continues to support their activities. Wendy reviews
Fellow, she is strongly committed to developing and testing for a number of journals and funding bodies such as the
strategies for the effective implementation of research into NHMRC and the Australian Research Council.
 List of contributors
Leanne Aitken RN, PhD, BHSc(Nurs)Hons, GCertMgt, Diane Chamberlain RN, BNBSc, MN(Critical Care),
GDipScMed(ClinEpi), FACCCN, FACN, FAAN, MPH, PhD
Life Member – ACCCN Senior Lecturer, Flinders University, SA, Australia
Professor of Critical Care Nursing, School of Nursing National President – ACCCN
and Midwifery and NHMRC Centre of Research Maureen Coombs RN, PhD, MBE
Excellence in Nursing (NCREN), Menzies Health Professor in Clinical Nursing (Critical Care), Graduate
Institute Queensland, Griffith University, Qld, Australia School of Nursing Midwifery and Health,Victoria
Intensive Care Unit, Princess Alexandra Hospital, Qld, University of Wellington, New Zealand
Australia Capital and Coast District Health Board, Wellington,
Professor of Nursing, School of Health Sciences, New Zealand
City University London, UK
Karena Conroy BSocSci(Hons), PhD
Robyn Aitken RN, Cert Anaes/Rec, BEdSt, MEdSt, PhD Researcher, Intensive Care Co-ordination & Monitoring
Acting Chief Nursing and Midwifery Officer, Northern Unit, Agency for Clinical Innovation, NSW, Australia
Territory Department of Health, NT, Australia Honorary Associate, Faculty of Health, University of
Professorial Fellow, Charles Darwin University, NT, and Technology, Sydney, NSW, Australia
Flinders University, SA, Australia
Fiona Coyer RN, PGCEA, MSc Nursing, PhD
Ian Baldwin RN, PhD Professor of Nursing, Queensland University of
Clinical Educator Intensive Care Unit and Adjunct Technology and Metro North Hospital and Health
Professor, RMIT and Deakin University,Vic, Australia Service, Qld, Australia
Clinical Educator, Austin Health,Vic, Australia
Julia Crilly RN, MEmergN (Hons), PhD
Catherine Bell RN, MN (Crit Care) Associate Professor, Emergency Care, Griffith University,
Intensive Care Clinical Nurse Consultant – Trauma, and Gold Coast Hospital and Health Service, Qld,
Alfred Hospital,Vic, Australia Australia
Bronagh Blackwood RGN, RNT, PhD Judy Currey RN, BN, BN(Hons), CritCareCert,
Senior Lecturer, School of Medicine, Dentistry and GCertHE, GCertSc(App Stats), PhD
Biomedical Sciences, Queen’s University, Belfast, Associate Professor in Nursing, Director of Postgraduate
Northern Ireland, UK Studies, Deakin University,Vic, Australia
Tom Buckley RN, BHSc(Hons), MN (Research), Jennifer Dennett RN, MN, BAppSc (Nursing),
GCertHPol, Cert ICU, PhD CritCareCert, Dip Management, MRCNA
Coordinator Master of Nursing (Clinical Nursing & Nurse Unit Manager, Critical Care, Oncology,
Nurse Practitioner)/Senior Lecturer, Sydney Nursing Cardiology, Renal Dialysis, Central Gippsland Health
School, The University of Sydney, NSW, Australia Service,Vic, Australia
Rand Butcher RN, MClinSc (Intensive Care Nursing), Malcolm James Dennis RN, CritCareCert, BEd,
GradDipN (Nurse Education), BHlthSci (Nursing) IBHRE-CCDS
Critical Care Clinical Nurse Consultant, Northern New Technical Field Expert, Cardiac Rhythm Management
South Wales Local Health District Division, St Jude Medical,Vic, Australia
Adjunct Lecturer, School of Nursing and Midwifery, Andrea Driscoll NP, CCC, MEd, MN, PhD, FAHA,
Griffith University, Qld, Australia FCSANZ, FACNP
Wendy Chaboyer RN, PhD, MN, BSc(Nu)Hons, Crit Associate Professor, School of Nursing and Midwifery,
Care Cert, FACCCN, Life Member – ACCCN Faculty of Health, Deakin University,Vic, Australia
Professor and Director, NHMRC Centre of Research Heart Foundation Fellow
Excellence in Nursing (NCREN), Menzies Health Trudy Dwyer RN, Nurs Cert, BHScN, ICU Cert, GD
Institute Queensland, Griffith University, Qld, Australia FlexLng, MClincEd, PhD
Professor, Institute of Health and Care Sciences, Associate Professor, Central Queensland University, Qld,
University of Gothenburg, Sweden Australia
xiv LIST OF CONTRIBUTORS

Rosalind Elliott RN, PhD Ian Jacobs RN, PhD, BAppSc, DipEd, FCNA,
Lecturer, Faculty of Health, University of Technology, FANZCP, FERC, FAHA
Sydney, NSW, Australia Clinical Services Director, St John Ambulance
(Western Australia)
Paula Foran RN, PhD, Master Professional Education
Professor of Resuscitation and Pre-Hospital Care and
&Training, Grad Dip Adult Education & Training, Cert
Director, Prehospital Resuscitation & Emergency Care
Anaesthesia & Post Anaesthesia Nursing
Research Unit, Curtin University, WA, Australia
Honorary Conjoint Senior Clinical Lecturer, School of
Nursing and Midwifery, Deakin University, and South David Johnson RN, Grad Dip (Acute Care Nurs),
West Healthcare,Vic, Australia MHealth Sci Ed, A&E Cert, MCN
Director of Nursing, Caloundra Health Service, Sunshine
Deborah Friel BHSc, GC CritCare, GC ClinNr,
Coast Hospital and Health Service, Queensland Health,
GC Mmnt, GCTE
Qld, Australia
Lecturer, School of Nursing and Midwifery, Central
Queensland University, Qld, Australia Alison Juers RN, BN (Dist), MN (Crit Care)
Intensive Care Nurse Educator, Brisbane Private
Robyn Gallagher RN, MN, BA, PhD
Hospital, Qld, Australia
Professor of Nursing, Charles Perkins Centre, Sydney
Nursing School, The University of Sydney, NSW, Tina Kendrick RN, PIC Cert, BNurs (Hons), MNurs,
Australia FACCN, FACN
Clinical Nurse Consultant – Paediatrics
David Glanville RN, BNsg, GDipNsg(CritCare), MN
Newborn and Paediatric Emergency Transport Service
Nurse Educator (Critical Care), Epworth Freemasons
(NETS), NSW, Australia
Hospital,Vic, Australia
Emma Kingwell RN, RM BSc, GradCert CritCare Nsg,
Christopher J Gordon RN, BN, MExSc, PhD
PGDip (Mid), MPhil (Nsg and Mid)
Senior Lecturer, Sydney Nursing School, The University
Nurse and Midwifery Educator, King Edward Hospital
of Sydney, NSW, Australia
for Women, WA, Australia
Sher Michael Graan RN, BHS-Nursing, Post Grad Dip
Ruth Kleinpell RN, PhD, FAAN, FCCM
Crit Care, MN
Director, Center for Clinical Research and
Clinical Instructor, King Faisal Specialist Hospital and
Scholarship, Rush University Medical Center, and
Research Center (Magnet Accredited), Saudi Arabia
Professor, Rush University College of Nursing,
Bernadette Grealy RN, RM, GradCertCritCare, Chicago, IL, USA
DipAScN, BN, MN, Life Member – ACCCN
Leila Kuzmiuk RN, BN CPIT, DipAdvClinNursing,
Nursing Director, Intensive Care Services & Hyperbaric
MN, Grad Cert Hlth ServMgt
Medicine, Central Adelaide Local Health Network, SA,
Nurse Educator, Intensive Care Services, John Hunter
Australia
Hospital, New England Health, NSW, Australia
Carol Grech RN, PhD
Gavin D Leslie RN, PhD, BAppSc, Post Grad Dip
Head, School of Nursing and Midwifery, University of
(Clin Nurs) FCNA, FACCCN
South Australia, SA, Australia
Professor, Critical Care Nursing, School of Nursing,
Melanie Greenwood MN, Graduate Certificate in Midwifery & Paramedicine, Curtin University,
UniLearn & Teach, Intensive Care Cert, Neuroscience WA, Australia
Cert
Frances Lin RN, BMN, MN(Hons), PhD
Senior Lecturer, School of Health Sciences, University of
Senior Lecturer, School of Nursing and Midwifery,
Tasmania, Tas, Australia
Griffith University, Qld, Australia
Janice Gullick RN, PhD, MArt, BFA, Cardiothoracic
Andrea Marshall RN, PhD, MN(Research), BN, Grad
Cert, FACN
Cert Ed Studies (Higher Ed), IC Cert, FACCCN, FACN,
Director, Postgraduate Advanced Studies, and
Life Member – ACCCN
Coordinator, Master of Intensive Care & Emergency
Professor of Acute and Complex Care Nursing,
Nursing, Sydney Nursing School, The University of
School of Nursing and Midwifery and NHMRC
Sydney, NSW, Australia
Centre of Research Excellence in Nursing (NCREN),
Denise Harris RN, BHSc(Nurs), Menzies Health Institute Queensland, Griffith University,
GradDipHlthAdmin&InfoSys, MN(Res), ICCert Qld, Australia
Assistant Director of Clinical Services – Cardiac Services Intensive Care Unit, Gold Coast Hospital and Health
& Critical Care, Pindara Private Hospital, Qld, Australia Service, Qld, Australia
 LIST OF CONTRIBUTORS xv

Elaine McGloin Cert Crit Care Louise Rose BN, ICU Cert, Adult Ed Cert, MN, PhD
Clinical Nurse Consultant, Intensive Care Services, Royal TD Nursing Professor in Critical Care Research,
Prince Alfred Hospital, NSW, Australia Sunnybrook Health Sciences Centre
Marion Mitchell RN, Grad Cert (Higher Ed), PhD,
Associate Professor, Lawrence S. Bloomberg Faculty of
FACCN, Centaur Fellow Nursing, University of Toronto, Canada
Associate Professor Critical Care, School of Nursing and Adjunct Scientist, Institute for Clinical Evaluative Sciences
Midwifery, Menzies Health Institute Queensland, Griffith CIHR New Investigator
University, Qld, Australia Director of Research, Provincial Centre of Weaning
Princess Alexandra Hospital, Qld, Australia Excellence, Toronto East General Hospital
Adjunct Scientist, Mount Sinai Hospital, Li Ka Shing
Margherita Murgo BN, MN(Crit Care), Dip Project Mgt Institute, St Michael’s Hospital,West Park Healthcare Centre
Project Officer (Delegation and Escalation Project),
Clinical Excellence Commission, NSW, Australia Kerstin Prignitz Sluys PhD, APRN
Associate Professor, Red Cross University College,
Wendy Pollock RN, RM, GCALL, Grad Dip Crit Care Affiliated Researcher, Karolinska Institutet, Stockholm,
Nsg, Grad Dip Ed, PhD Sweden
Director, Maternal Critical Care, and Honorary Senior
Fellow, The University of Melbourne,Vic, Australia Ged Williams RN, RM, Crit Care Cert, MHA, LLM,
Honorary Research Fellow, La Trobe University,Vic, FACHSM, FACN, FAAN
Australia Nursing and Allied Health Consultant, Abu Dhabi Health
Service, United Arab Emirates
Anne-Sylvie Ramelet RN, PhD, RSCN, ICU Cert Founding President, World Federation of Critical Care
Professor of Nursing and Director, Institute of Higher Nurses
Education and Research in Healthcare, University of
Lausanne, Switzerland Teresa Williams RN, ICU Cert, BNurs, MHlthSci(Res),
GDClinEpi, PhD
Janice Rattray MN, PhD, DipN, RGN, SCM
Senior Research Fellow, Prehospital Resuscitation and
Reader in Acute and Critical Care Nursing, School of
Emergency Care, School of Nursing Midwifery and
Nursing and Health Sciences, University of Dundee,
Paramedicine, Curtin University, WA, Australia
Scotland, UK
Denise Wilson RN, PhD, FCNA(NZ)
Mona Ringdal RN, MN, PhD
Professor of Ma-ori Health, Auckland University of
Senior Lecturer, Director of Postgraduate Nursing
Technology, New Zealand
and Master Programme, Institute of Health and
Care Sciences, Sahlgrenska Academy, University of Sharon M Wetzig BN, Grad Cert Nsg (Crit Care), MEd
Gothenburg, Sweden Education Consultant, Carramar Education, Qld, Australia
List of reviewers
Jan Alderman RN, BNs, Grad Dip Anaesthetics and Renee McGill RN, MN (Education), Grad Cert Crit
Recovery Nursing, Masters/PhD candidate in Clinical Care, BSci (Nurs)
Science Simulation Lead, Lecturer in Nursing, School of Nursing,
Course Co-ordinator, Lecturer, School of Nursing, Midwifery and Indigenous Health, Faculty of Science,
University of Adelaide, SA, Australia Charles Sturt University, NSW, Australia
Sally Bristow RN, BN, Grad Dip Mid, RM, MN Gayle McKenzie RN, MEd, GradDip AdvNsg Crit Care,
Nursing Academic, University of New England, NSW, GradCert AdvNsg Clin Ed, BSocSc
Australia Lecturer in Acute Nursing, La Trobe University, Alfred
Clinical School,Vic, Australia
Elyse Coffey BNurs, GDipNur(periop), MNurs
Associate Lecturer, Deakin University,Vic, Australia Stephen McNally RN(Emergency), PhD
Clinical Nurse Specialist, Alfred Hospital,Vic, Australia Director of Academic Programs (Undergraduate),
University of Western Sydney, NSW, Australia
Rachel Cross RN, BN, GradCertEmergNurse,
MNP Claire Minton RN, MN, PhD candidate
Lecturer Practitioner, La Trobe University School of Lecturer, School of Nursing, Massey University,
Nursing and Midwifery/Emergency and Trauma Centre, New Zealand
Alfred Hospital,Vic, Australia Jonathan Mould RN, PhD
Lori Delaney RN, B Nurs, GC Ed, GDCC, MN, Lecturer, School of Nursing and Midwifery, Curtin
JBICF University, WA, Australia
Assistant Professor in Clinical Nursing, University of Holly Northam RN, RM, Masters of Crit Care Nurs,
Canberra, ACT, Australia MACN, Churchill Fellow
PhD scholar, College of Medicine, Australia National Assistant Professor in Critical Care Nursing, University
University, ACT, Australia of Canberra, ACT, Australia
Janice Elliott RN, BNsg, Grad Dip (Emerge Nursing),
Darrin Penola RN, MN (Crit Care)
Master of Nursing Science Clinical Nurse Consultant, Thoracic Medicine,
Registered Nurse, Royal Adelaide Hospital Emergency St Vincent’s Hospital, NSW, Australia
Department, SA, Australia
Clinical Title Holder, School of Nursing, University of Ron Picard RN, MHSc, CCN
Adelaide, SA, Australia Nursing Lecturer, La Trobe Rural Health School,Vic,
Australia
Beverley Ewens RN, BSc(Hons), PG Dip Critical Care,
PhD candidate Natashia Scully BA, BN GradCertTertiaryEd,
Lecturer, School of Nursing and Midwifery, Edith Cowan PostGradDipNSc, MPH, MACN
University, WA, Australia Lecturer in Nursing, University of New England, NSW,
Australia
Steven A Frost RN, ICU Cert, MPH, PhD
Lecturer, Intensive Care, Liverpool Hospital and Peita Sims RN, BAppSc (HealthProm), BNurs, Grad
University of Western Sydney, NSW, Australia Dip (Crit Care)
ICU Liaison Nurse, Epworth Healthcare,Vic, Australia
Emily Susannah Kavanagh BN, GradCert Crit Care
Donation Specialist Nurse, Tamworth Rural Referral Kerry Southerland RN, ICU cert, BAppSc (Nursing),
Hospital, NSW, Australia MClinNurs (Crit Care), GradCertTertTeach
Lecturer, School of Nursing & Midwifery, Curtin
Elizabeth Kraft RN, BN, GradDip (Anaes & Rec), MN,
University, WA, Australia
MACN
Clinical Service Coordinator, Day Surgery Unit/Surgical Jane Zeng CNE, ADNP
Admission Suite/Day Surgery Overnight, Royal Adelaide Post Graduate Subject Coordinator, University of
Hospital, SA, Australia Melbourne,Vic, Australia
Clinical Nurse Educator – ICU, Western Health,Vic,
Australia
 Acknowledgements
A project of this nature and scope requires many talented Resuscitation Council and Co-Chair of the International
and committed people to see it to completion.The decision Liaison Committee on Resuscitation.
to publish this third edition was supported enthusiastically Continued encouragement and support from the Board
by the Board of the Australian College of Critical Care and members of ACCCN, for having the belief in us as
Nurses (ACCCN) and Elsevier Australia. To our chapter editors and authors to uphold the values of the College, is
contributors for this edition, both those returning from much appreciated. We also acknowledge support from the
the previous editions and our new collaborators – thank staff at Elsevier Australia, our publishing partner. Thanks to
you for accepting our offer to write, for having the courage our Senior Content Strategist, Libby Houston, for guiding
and confidence in yourselves and us to be involved in the this major project; our Content Development Specialist,
text and for being committed in meeting writing deadlines Martina Vascotto; and to Linda Littlemore, our editor. In
while developing the depth and quality of content that Publishing Services, Devendran Kannan, thanks for your
we had planned. We also acknowledge the work of work with production. To others who produced the high
chapter contributors from our previous editions – Harriet quality figures, developed and executed the marketing plan
Adamson, Susan Bailey, Julie Benbenishty, Martin Boyle, and undertook myriad other activities, without which a
Wendy Corkhill, Sidney Cuthbertson, Suzana Dimovski, text such as this would never come to fruition, thank you.
Bruce Dowd, Ruth Endacott, Claire Fitzpatrick, Paul We acknowledge our external reviewers who devoted their
Fulbrook, Gabrielle Hanlon, Michelle Kelly, Bridie Kent, time to provide insightful suggestions in improving the text
Anne Morrison, Maria Murphy, Louise Niggemeyer, and contributed to the quality of the finished product.
Amanda Rischbieth, Wendy Swope, Paul Thurman, Jane To Doug Elliott, thank you for your original vision for
Treloggen and Vicki Wade. this text, for having the courage and commitment to make
The Editors would like to specifically acknowledge it happen and for your support, albeit from a distance, for
the contribution of Professor Ian Jacobs, who co-authored continuing the journey.
Chapter 25, Resuscitation, prior to his unexpected death. Ian Finally, and most importantly, to our respective loved
was an internationally renowned specialist in resuscitation ones – Steve; David, Abi and Hannah; and Michael –
and prehospital care and has made a sustained contribution thanks for your belief in us, and your understanding and
to teaching, research and policy in the field. One of his commitment in supporting our careers.
earliest associations with ACCCN was as convenor of the Leanne Aitken
Advanced Life Support course in Western Australia in Andrea Marshall
the early 1990s. Ian was the Chairperson of the Australian Wendy Chaboyer
Detailed contents
Foreword by Ruth M Kleinpell vi 5 Ethical issues in critical care 106
Foreword by Doug Elliott vii Introduction 106
Ethics and the law 107
Preface viii Application of ethical principles in the care
About the Australian College of Critical Care Nurses of the critically ill 111
(ACCCN) x Ethics in research 119
About the editors xii Summary 121
List of contributors xiii Section 2 Principles and practice of critical care 129
List of reviewers xvi
6 Essential nursing care of the critically
Acknowledgements xvii
ill patient 131
Abbreviations xxi Introduction 131
Personal hygiene 132
Section 1 Scope of critical care 1 Eye care 134
Oral hygiene 135
1 Scope of critical care practice 3 Patient positioning and mobilisation 137
Introduction 3 Bowel management 142
Critical care nursing 4 Urinary catheter care 144
Development of the critical care body of Care of the elderly 146
knowledge 4 Bariatric considerations 147
Critical care nursing roles 8 General principles of infection control in
Leadership in critical care nursing 9 critical care 148
Summary 11 Transport of critically ill patients: General
principles 153
2 Systems and resources 19
Summary 156
Introduction 19
Ethical allocation and utilisation of resources 20 7 Psychological care 164
Historical influences 20 Introduction 164
Economic considerations and principles 21 Anxiety 165
Budget and finance 22 Delirium 167
Critical care environment 25 Pain 174
Equipment 25 Sleep 179
Staff 27 Summary 183
Risk management 32 8 Family and cultural care of the critically
Measures of nursing workload or activity 35 ill patient 193
Management of pandemics 37 Introduction 193
Summary 38 Overview of models of care 194
Cultural care 199
3 Quality and safety 44
Religious considerations 213
Introduction 44
End-of-life issues and bereavement 216
Evidence-based nursing 45
Summary 218
Clinical practice guidelines 47
Quality and safety monitoring 48 9 Cardiovascular assessment and monitoring 231
Patient safety 55 Introduction 231
Non-technical skills 58 Related anatomy and physiology 231
Summary 63 Assessment 242
4 Recovery and rehabilitation 73 Haemodynamic monitoring 248
Introduction 73 Diagnostics 259
Summary 264
Compromise following a critical illness 74
Measuring patient outcomes following a 10 Cardiovascular alterations and management 271
critical illness 84 Introduction 271
Improving recovery following a critical illness 87 Coronary heart disease 272
Summary 95 Angina 272
 DETAILED CONTENTS xix

Heart failure 285 Weaning from mechanical ventilation 496

Selected cases 299 Summary 498
Summary 303 16 Neurological assessment and monitoring 511
11 Cardiac rhythm assessment and management 311 Introduction 511
Introduction 311 Neurological anatomy and physiology 512
The cardiac conduction system 312 Central nervous system 516
Arrhythmias and arrhythmia management 313 Peripheral nervous system 526
Cardiac pacing 333 Neurological assessment and monitoring 530
Cardioversion 350 Summary 538
Ablation 354 17 Neurological alterations and management 546
Summary 354 Introduction 546
12 Cardiac surgery and transplantation 362 Neurological dysfunction 546
Introduction 362 Neurological therapeutic management 552
Cardiac surgery 363 Central nervous system disorders 557
Intra-aortic balloon pumping 376 Summary 575
Heart transplantation 382 18 Support of renal function 584
Summary 392 Introduction 584
13 Respiratory assessment and monitoring 402 Related anatomy and physiology 585
Introduction 402 Pathophysiology and classification of
Related anatomy and physiology 403 renal failure 589
Pathophysiology 412 Acute kidney injury: Clinical and diagnostic
Assessment 414 criteria for classification 592
Respiratory monitoring 418 Management of the patient with acute
Bedside and laboratory investigations 421 kidney injury 594
Diagnostic procedures 426 Approaches to renal replacement therapy 595
Summary 429 Summary 615
14 Respiratory alterations and management 438 19 Nutrition assessment and therapeutic
Introduction 438 management 622
Incidence of respiratory alterations 439 Introduction 622
Respiratory failure 439 Metabolism 623
Pneumonia 443 Malnutrition 624
Respiratory pandemics 447 Nutritional assessment 624
Acute lung injury/acute respiratory distress Nutrition support 626
syndrome 449 Nutrition in specific clinical conditions 635
Asthma and chronic obstructive pulmonary Glycaemic control in critical illness 638
disease 451 Summary 639
Pneumothorax 453 20 Gastrointestinal, metabolic and liver
Pulmonary embolism 454 alterations 651
Lung transplantation 456 Introduction 651
Summary 461 Gastrointestinal physiology 652
15 Ventilation and oxygenation management 470 Stress-related mucosal damage 653
Introduction 470 Intra-abdominal hypertension and abdominal
Oxygen therapy 471 compartment syndrome 655
Oxygen administration devices 471 The critically ill patient with diabetes 660
Airway support 472 Liver dysfunction 663
Managing endotracheal and tracheostomy Liver transplantation 668
tubes 475 Summary 671
Mechanical ventilation 477 21 Pathophysiology and management of shock 681
Non-invasive ventilation 484 Introduction 681
Invasive mechanical ventilation 486 Pathophysiology 682
Managing the mechanically ventilated Patient assessment 684
patient 494 Hypovolaemic shock 686
xx DETAILED CONTENTS

Cardiogenic shock 689 Assessment and management in the

Sepsis and septic shock 696 postoperative period 865
Anaphylaxis 700 Assessment and management of specific
Neurogenic/spinal shock 704 postoperative complications 875
Resuscitation end points 705 Transferring care of the postoperative patient:
Summary 707 discharge to an inpatient ward 878
22 Multiple organ dysfunction syndrome 717 Summary 879
Introduction 717 27 Paediatric considerations in critical care 885
Pathophysiology 718 Introduction 885
Systemic response 719 Anatomical and physiological considerations
Endocrine response 721 in children 886
Organ dysfunction 723 Developmental considerations 891
Multiorgan dysfunction 725 Family issues and consent 892
Patient management 726 Pain and sedation 893
Summary 729 Upper airway obstruction 893
The child experiencing lower airway disease 898
Section 3 Specialty practice 737
Nursing the ventilated child 901
The child experiencing shock 902
23 Emergency presentations 739
The child experiencing acute neurological
Introduction 739
Background 740 dysfunction 904
Triage 740 Gastrointestinal and renal considerations in
Advanced clinical skills 747 children 905
Retrievals and transport of critically ill Paediatric trauma 907
patients 748 Summary 910
Multiple patient triage/disaster 749 28 Pregnancy and postpartum considerations 922
Respiratory presentations 750 Introduction 922
Chest pain presentations 753 Epidemiology of critical illness in pregnancy 923
Abdominal symptom presentations 755 Adapted physiology of pregnancy 923
Acute stroke 757 Diseases and conditions unique to pregnancy 928
Overdose and poisoning 758 Exacerbation of medical disease associated
Near-drowning 775 with pregnancy 939
Hypothermia 777 Special considerations 944
Hyperthermia and heat illness 778 Caring for pregnant women in ICU 946
Summary 779 Caring for postpartum women in ICU 951
24 Trauma management 791 Summary 954
Introduction 791 29 Organ donation and transplantation 966
Trauma systems and processes 792 Introduction 966
Common clinical presentations 795 Donation systems 967
Summary 821 Organ donation and transplant networks 967
25 Resuscitation 829 Identification of organ and tissue donors 969
Introduction 829 Organ donor care 975
Cardiac arrest 830 Donation after cardiac death 978
Resuscitation systems and processes 830 Tissue-only donor 979
Post-resuscitation phase 846 Summary 979
Special considerations 847 Appendix A Practice standards for specialist
Summary 849 critical care nurses 986
26 Postanaesthesia recovery 857 Appendix B Normal laboratory values 989
Introduction 857
Introduction to anaesthesia 858 Glossary of terms 994
Anaesthetic agents 858 Index 1001
 Abbreviations
AACN American Association of Critical-Care AVNRT atrioventricular nodal reentry tachycardia
Nurses BACCN British Association of Critical Care Nurses
ABG arterial blood gas BBB blood–brain barrier
A/C assist control ventilation BE base excess
ACCCN Australian College of Critical Care Nurses BiPAP bi-phasic positive airways pressure
ACCESS assistance, coordination, contingency, BLS basic life support
education, supervision, support BMI body mass index
ACEI angiotensin-converting enzyme inhibitor BNP B-type natriuretic peptide
ACh acetylcholine BP blood pressure
ACS acute coronary syndrome BPS Behavioural Pain Scale
ACT activated clotting time BSLTx bilateral sequential lung transplantation
ADAPT Australasian Donation Awareness Program BTF Brain Trauma Foundation
ADL activities of daily living CABG coronary artery bypass graft
AED automatic external defibrillator CAM-ICU Confusion Assessment Method for the
AF atrial fibrillation Intensive Care Unit
AFE amniotic fluid embolism CAP community acquired pneumonia
AIVR accelerated idioventricular rhythm CAUTI catheter-associated urinary tract infection
AKI acute kidney injury CAV cardiac allograph vasculopathy
ALF acute liver failure CAVH continuous arteriovenous haemofiltration
ALI acute lung injury CBF cerebral blood flow
ALS advanced life support CRRT continuous renal replacement therapy
ALT alanine amino transferase CCU coronary/cardiac care unit
AMI acute myocardial infarction CHD coronary heart disease
ANP atrial natriuretic peptide CHF chronic heart failure
ANS autonomic nervous system CI cardiac index
ANZBA Australia and New Zealand Burns CIM critical illness myopathy
Association CINM critical illness neuromyopathy
ANZICS Australian and New Zealand Intensive Care CIP critical illness polyneuropathy
Society CLAB central line-associated bacteraemia
AoCLF acute on chronic liver failure CLABSI central line associated blood stream infection
APACHE Acute Physiology And Chronic Health CMV cytomegalovirus
Evaluation (score) CNC clinical nurse consultant
APC activated protein C CNE clinical nurse educator
APH antepartum haemorrhage CNM clinical nurse manager
APRV airway pressure release ventilation CNS central nervous system
APTT activated partial thromboplastin time CO cardiac output
ARC Australian Resuscitation Council CO2 carbon dioxide
ARDS adult respiratory distress syndrome COPD chronic obstructive pulmonary disease
ARB angiotensin receptor blocker COPE Committee of Publication Ethics
ARF acute renal failure CPAP continuous positive airway pressure
aSAH aneurysmal subarachnoid haemorrhage CPB cardiopulmonary bypass
AST aspartate aminotransferase CPG clinical practice guidelines
ATN acute tubular necrosis CPOE computerised provider order entry
ATP adenosine triphosphate CPOT Critical-care Pain Observation Tool
ATP anti-tachycardia pacing CPP cerebral perfusion pressure
ATS Australasian Triage Scale CPR cardiopulmonary resuscitation
AV arteriovenous CRT cardiac resynchronisation therapy
AV atrioventricular CSF cerebral spinal fluid
AV atrioventricular node CT computerised tomography
xxii ABBREVIATIONS

CTAS Canadian Triage and Acuity Scale H+ hydrogen ion

CTG cardiotocograph H2CO3 carbonic acid
CVAD central venous access device H2RA histamine 2 receptor antagonist
CVC central venous catheter HADS Hospital Anxiety and Depression Scale
CVP central venous pressure HAI hospital-acquired infection
CVR cerebrovascular resistance Hb haemoglobin
CVVH continuous venovenous haemofiltration HCM hypertrophic cardiomyopathy
CVVHDf continuous venovenous haemodiafiltration HCO3- bicarbonate ion
CX circumflex coronary artery HD haemodialysis
CXR chest X-ray HDU high dependency unit
DCD donation after cardiac death HELLP haemolysis, elevated liver enzymes and low
DCM dilated cardiomyopathy platelets
DCS damage-control surgery HFO high flow oxygen
DIC disseminated intravascular coagulation HFOV high frequency oscillation ventilation
DKA diabetic ketoacidosis HFpEF heart failure with preserved ejection
DNA deoxyribonucleic acid fraction
DNAR do not attempt resuscitation HFrEF heart failure with reduced ejection fraction
DPL diagnostic peritoneal lavage HHS hyperosmolar hyperglycaemic state
DTS Davidson Trauma Scale Hib Haemophilus influenzae type b
DVT deep vein thrombosis HIV human immunodeficiency virus
EBN evidence-based nursing HLA human leukocyte antigen
EC extracorporeal circuit HME heat and moisture exchanger
ECG electrocardiography HR heart rate
ECMO extracorporeal membrane oxygenation HRC Health Research Council
ED emergency department HRECs Human Research Ethics Committees
EEG electroencephalogram/ HRQOL health related quality of life
electroencephalography HRS hepatorenal syndrome
EGDT early goal-directed therapy HSV herpes simplex virus
EMSB early management of severe burns IABP intra-aortic balloon pump
EN enteral nutrition IAH intra-abdominal hypertension
EPAP expiratory positive airway pressure IAP intra-abdominal pressure
EPUAP European Pressure Ulcer Advisory Panel ICC intercostal catheter
ESI emergency severity index ICD implantable cardioverter defibrillator
ET endothelin ICDSC Intensive Care Delirium Screening Checklist
ETCO2 end-tidal carbon dioxide ICH intracerebral haemorrhage
ETT endotracheal tube ICN International Council of Nurses
EVD external ventricular drain ICP intracranial pressure
EVLW extravascular lung water ICS Intensive Care Society (UK)
EVLWI extravascular lung water index ICU intensive care unit
F frequency ICU-AW intensive care unit acquired weakness
FAST focused assessment with sonography in I:E inspiratory/expiratory ratio
trauma IES Impact of Event Scale
FBC full blood count IL interleukin
FES fat embolism syndrome ILCOR International Liaison Committee on
FiO2 fraction of inspired oxygen Resuscitation
FOUR Full Outline of Unresponsiveness scale IM intramuscular
FTE full time equivalent (staff) IMA internal mammary artery
f/VT frequency/tidal volume INR international normalised ratio
GABA gamma-aminobutyric acid IPAP inspiratory positive airway pressure
GBS Guillain–Barré syndrome ITBV intrathoracic blood volume
GCS Glasgow Coma Scale ITBVI intrathoracic blood volume index
GEDV global end-diastolic volume IV intravenous
GEDVI global end-diastolic volume index IVC inferior vena cava
GFR glomerular filtration rate JVP jugular venous pressure
GTN glyceryl trinitrate kPa kilopascals
 ABBREVIATIONS xxiii

LAD left anterior descending OHCA out-of-hospital cardiac arrest

LAP left atrial pressure OPCAB off pump coronary artery bypass
LBBB left bundle branch block ORIF open reduction internal fixation
LMA laryngeal mask airway Pa arterial pressure
LOS length of stay PA alveolar pressure
LV left ventricle PAC pulmonary artery catheter
LVAD left ventricular assist device PaCO2 partial pressure of carbon dioxide in arterial
LVEDV left ventricular end-diastolic volume blood
(preload) PACU post-anaesthesia care unit
LVEF left ventricular ejection fraction PaO2 partial pressure of oxygen in arterial blood
LVF left ventricular failure PAP pulmonary artery pressure
LVSWI left ventricular stroke work index Paw airway pressure
MAP mean arterial pressure PbtO2 brain tissue oxygenation
MEDSAFE Medical Devices Safety Authority PCA patient-controlled analgesia
(New Zealand) PCI percutaneous coronary intervention
MELD model of end-stage liver disease PCP phencyclidine
MERS-CoV Middle East respiratory syndrome PCV pressure controlled ventilation
coronavirus PCWP pulmonary capillary wedge pressure
MET medical emergency team PD peritoneal dialysis
MI myocardial infarction PDH pulmonary dynamic hyperinflation
MIDCABG minimally invasive direct coronary artery PE pulmonary embolism
bypass grafting PEA pulseless electrical activity
MMSE Mini-Mental Status Examination PEEP positive end-expiratory pressure
MODS multiple organ dysfunction syndrome PELD paediatric end-stage liver disease
MRC Medical Research Council PetCO2 partial pressure of end-tidal carbon dioxide
MRI magnetic resonance imaging PGD primary graft dysfunction
MRO multi-resistant organism pH acid–alkaline logarithmic scale
MRSA methicillin-resistant Staphylococcus aureus PI pressure injury
MTS Manchester Triage Scale PiCCO pulse induced contour cardiac output
MV mechanical ventilation PICS post-intensive care syndrome
NAS Nursing Activities Score PICU paediatric intensive care unit
NEMS Nine Equivalents of nursing Manpower use Pinsp inspiratory pressure
Score PN parenteral nutrition
NETS newborn emergency transfer service PNS peripheral nervous system
NEXUS National Emergency X-radiography PPE personal protective equipment
Utilization Study PPH postpartum haemorrhage
NFkB nuclear factor kappa B PPI proton pump inhibitors
NHMRC National Health and Medical Research PR pulse rate
Council pRIFLE paediatric risk, injury, failure, loss and
NHS National Health Service (UK) end-stage kidney disease criteria
NICE National Institute for Health and Care PSG polysomnography
Excellence PSV pressure support ventilation
NIPPV non-invasive positive pressure ventilation PT prothrombin
NIPSV non-invasive pressure support ventilation PTA post-traumatic amnesia
NIV non-invasive ventilation PTCA percutaneous transluminal coronary
NO nitric oxide angioplasty
NOC Nurses’ Observation Checklist PTSD post-traumatic stress disorder
NPC nurse practice coordinator PTSS post-traumatic stress symptoms
NPUAP National Pressure Ulcer Advisory Panel PTT partial thromboplastin time
NSAID non-steroidal anti-inflammatory drug PV per vagina
NTS non-technical skills Pv venous pressure
NUM nursing unit manager PVR pulmonary vascular resistance
NUTRIC NUTritional RIsk in the Critically ill score R respiration
NYHA New York Heart Association RAAS renin–angiotensin–aldosterone system
O2 oxygen RAP right atrial pressure
xxiv ABBREVIATIONS

RBANS Repeatable Battery for the Assessment of SpO2 saturation of oxygen in peripheral tissues
Neuropsychological Status STEMI ST-elevation myocardial infarction
RBC red blood cells SV stroke volume
RCA right coronary artery SVG saphenous vein graft
RCM restrictive cardiomyopathy SvO2 saturation of oxygen in venous system
RCSQ Richards–Campbell Sleep Questionnaire SVR systemic vascular resistance
RCT randomised controlled trial SVT supraventricular tachycardia
RDC regional donor coordinator SWS slow wave sleep
REE resting energy expenditure T3 triiodothyronine
REM rapid eye movement TAD thoracic aortic dissection
RICA right internal carotid artery TBI traumatic brain injury
ROSC return of spontaneous circulation TBSA total body surface area
RR respiratory rate TEG thromboelastograph
RRS rapid response system TGA Therapeutic Goods Administration
RRT renal replacement therapy TIMI thrombolysis in myocardial infarction
RSV respiratory syncytial virus TIPS transjugular intrahepatic portosystemic
RV right ventricular shunt/stent
RVEDV right ventricular end-diastolic volume TISS Therapeutic Intervention Scoring
RVEDVI right ventricular end-diastolic volume index System
RVEF right ventricular ejection fraction TNFa tumour necrosis factor alpha
RVF right ventricular failure TOE transoesophageal echocardiography
SA sinoatrial node TSANZ Transplant Society of Australia and
SAH subarachnoid haemorrhage New Zealand
SaO2 saturation of oxygen in arterial blood TST total sleep time
SAPS Simplified Acute Physiology Score UO urine output
SARS severe acute respiratory syndrome URTI upper respiratory tract infection
SBP systolic blood pressure VAD ventricular assist device
SBT spontaneous breathing trial VAE ventilator-associated event
SCA sudden cardiac arrest VAP ventilator-associated pneumonia
SCI spinal cord injury VAS visual analogue scale
SCUF slow continuous ultrafiltration VATS video-assisted thoroscopic surgery
SE status epilepticus VCV volume controlled ventilation
SICQ Sleep in Intensive Care Questionnaire VE expired minute volume
SIMV synchronised intermittent mandatory VF ventricular fibrillation
ventilation V/Q ventilation/perfusion
SIRS systemic inflammatory response syndrome VRE vancomycin-resistant enterococci
SjO2 jugular venous oxygen saturation VT tidal volume
SLED slow low efficiency dialysis VT ventricular tachycardia
SLTx single lung transplantation VTE venous thromboembolism
SNS sympathetic nervous system WCC white cell count
SOFA sequential organ failure assessment WFCCN World Federation of Critical Care Nurses
SOMANZ Society of Obstetric Medicine of Australia WHO World Health Organization
and New Zealand WPW Wolff–Parkinson–White (syndrome)
 S e c ti o n 1

Scope of critical care

 Chapter 1

Scope of critical care practice

Leanne Aitken, Wendy Chaboyer, Andrea Marshall

KEY WORDS Learning objectives

clinical leadership After reading this chapter, you should be able to:
critical care • describe the history and development of critical care nursing practice,
nursing education and professional activities
roles of critical • discuss the influences on the development of critical care nursing as a
care nurses discipline and the professional development of individual nurses
• outline the various roles available to nurses within critical care areas or in
outreach services
• consider processes in the work and professional environment that are
influenced by local leadership styles.

Introduction
For over 50 years critical care services have been supporting the sickest of
patients and today they are available in most countries in the world.1 Although
the focus was originally at local, regional and national levels, there is now
an imperative for a strong international focus for the delivery of critical care
services. International collaborations are necessary for responding to events that
result in a sudden increased need for critical care services, such as the recent
influenza pandemic.2
There is unprecedented demand for critical care services globally. Increasing
population sizes and extended life expectancies mean that the projected
need for critical care beds will continue to increase.3 In Australia and New
Zealand, there are approximately 124,000 admissions to 141 general intensive
care units (ICUs) per year; this includes 6000 patient readmissions during
the same hospital episode.4 Patients admitted to coronary care, paediatric
or other specialty units not classified as a general ICU are not included in
these figures, so the overall clinical activity for ‘critical care’ is much higher
(e.g. there were also 10,000 paediatric admissions to PICUs).4 Importantly,
critical care treatment is a high-expense component of hospital care; one
conservative estimate of the cost exceeded A$2600 per day, with more
than two-thirds going to staff costs, one-fifth to clinical consumables and
the rest to clinical support and capital expenditure.5 In European countries
a direct cost analysis suggests the costs per ICU day range from €1168 to
€2025,6 while in developing countries such as India the cost is substantially
4 SECTION 1 SCOPE OF CRITICAL CARE

less (approximately US$200 per day)7 although this Development of critical care nursing was characterised
continues to represent a substantial cost relative to by a number of features,10 including:
the cost of living. The cost of critical care is, however, • the development of a new, comprehensive partnership
difficult to determine because there is no internationally between nursing and medical clinicians
agreed methodology, there is a wide variation in resource
consumption by patients in different settings, and there
• the collective experience of a steep learning curve for
nursing and medical staff
are different models of care.8,9
This chapter provides a context for subsequent • the courage to work in an unfamiliar setting,
caring for patients who are extremely sick – a role
chapters, outlining some key principles and concepts for that required the development of higher levels of
studying and practising nursing in a range of critical care competence and practice
areas. Development of the specialty is discussed, along
with the professional development and evolving roles of • a high demand for education specific to critical care
practice, which was initially difficult to meet owing
critical care nurses in contemporary health care.The scope
to the absence of experienced nurses in the specialty
of critical care nursing is described including advanced
practice roles and, specifically, the nurse practitioner role. • the development of technologies such as mechanical
Leadership, as it pertains to the practice and development ventilators, cardiac monitors, pacemakers,
of critical care nursing, is also reviewed. defibrillators, dialysers, intra-aortic balloon pumps
and cardiac assist devices, which prompted
development of additional knowledge and skills.
Critical care nursing There was also recognition that improving patient
Critical care as a specialty in nursing has developed over outcomes through optimal use of these technologies was
the last 30 years.10,11 Importantly, the development of the linked to nurses’ skills and staffing levels.19 The role of
specialty has occurred in concert with the development adequately educated and experienced nurses in these units
of intensive care medicine as a defined clinical specialty. was recognised as essential from an early stage,15 and led to
Critical care nursing is defined by the World Federation the development of the nursing specialty of critical care.
of Critical Care Nurses as: Although not initially accepted, nursing expertise, ability
to observe patients and appropriate nursing intensity are
Specialised nursing care of critically ill patients who have
now considered essential elements of critical care.19,20
manifest or potential disturbances of vital organ functions. As the practice of critical care nursing evolved, so
Critical care nursing means assisting, supporting and restoring did the associated areas of critical care nursing education
the patient towards health, or to ease the patient’s pain and and specialty professional organisations, of which there
to prepare them for a dignified death. The aim of critical care are at least 37 organisations across six continents.21 The
nursing is to establish a therapeutic relationship with patients combination of adequate nurse staffing, observation of the
and their relatives and to empower the individuals’ physical, patient and the expertise of nurses to consider the complete
psychological, sociological, cultural and spiritual capabilities by needs of patients and their families is essential to optimise
preventive, curative and rehabilitative interventions.12 the outcomes of critical care. As critical care continues to
Critically ill patients are those at high risk of actual or evolve, the challenge remains to combine excellence in
potential life-threatening health problems.13 Care of the nursing care with judicious use of technology to optimise
critically ill can occur in a number of different locations patient and family outcomes.
in hospitals. Critical care is generally considered a broad Research
term, incorporating subspecialty areas of emergency,
coronary care, high-dependency, cardiothoracic, paediatric The development of a body of knowledge is a key
and general intensive care units.14 characteristic of both professions22 and specialties within
professions. One criterion for a specialty identified over two
decades ago by the International Council of Nurses (ICN)23
Development of the critical is that it is based on a core body of nursing knowledge
care body of knowledge that is being continually expanded and refined by research.
Importantly, the ICN acknowledges that mechanisms are
Critical care as a specialty emerged in the 1950s and needed to support, review and disseminate research.
1960s in Australasia, North America, Europe and South Research is fundamental to the development of nursing
Africa.10,15–18 During these early stages, critical care knowledge and practice. Research is a systematic inquiry
consisted primarily of coronary care units for the care of using structured methods to understand an issue, solve a
cardiology patients, cardiothoracic units for the care problem or refine existing knowledge. Qualitative research
of postoperative patients and general intensive care units involves in-depth examination of a phenomenon of interest,
for the care of patients with respiratory compromise. typically using interviews, observation or document analysis
Later developments in renal, metabolic and neurological to build knowledge and enable depth of understanding.
management led to the principles and context of critical Qualitative data analysis is in narrative (text) form and
care that exist today. involves some form of content or thematic analysis, with
 CHAPTER 1 SCOPE OF CRITICAL CARE PRACTICE 5

findings generally reported as narrative (where words rather methods. In terms of priority, equal status may be given
than numbers describe the research findings). In contrast, to both approaches. Priority is indicated by using capital
quantitative research involves the measurement (in numeric letters for the dominant approach, followed by the symbols
form) of variables and the use of statistics to test hypotheses. + and → to indicate either concurrent or sequential data
Results of quantitative research are often reported in tables collection, for example:
and figures, identifying statistically significant findings. One • QUAL + QUANT: both approaches are given equal
particular type of quantitative research, the clinical trial status and data collection occurs concurrently.
(randomised controlled trial, or RCT), is used to test the
effect of a new nursing intervention on patient outcomes. • QUAL + quant: qualitative methods are the dominant
approach and data collection occurs concurrently.
In essence, clinical trials involve:
1 randomly allocating patients to receive either a new • QUAL ൺ quant: the qualitative study is given priority
and qualitative data collection will occur before
intervention (the experimental or intervention group)
quantitative data collection.
or an alternative or standard intervention (the control
group) Irrespective of which type of research design is used,
there are a number of common steps in the research
2 delivering the intervention or alternative treatment
process (Table 1.1), consisting of three phases: planning for
3 measuring an a priori identified patient outcome.24 the research, undertaking the research and analysing and
Statistical analyses are used to determine whether the reporting on the research findings.
new intervention is better for patients than the alternative Clinical research and the related activities of unit-
treatment. based quality improvement are integral components in
Mixed methods research has now emerged as an the practice, education and research triad.27 Partnerships
approach that integrates data from qualitative and between clinicians and academics, and the implementation
quantitative research at some stage in the research process.25 of clinical academic positions, including at the professorial
In mixed methods approaches, researchers decide on both level,28 provide the necessary infrastructure and organisation
the priority and sequence of qualitative and quantitative for sustainable clinical nursing and multidisciplinary research.

TABLE 1.1
Steps in the research process

STEP DESCRIPTION

Identify a clinical problem or issue Clinical experience and practice audits are two ways that clinical issues or problems are
identified

Review the literature A comprehensive literature review is vital to ensure that the issue or problem has not yet
been solved and that the proposed research builds on what is already known, and extends
it to fill a gap in knowledge

Develop a clear research question A precise question may follow either of two approaches:
PICO (population, intervention, comparator, outcome),
SPIDER (sample, phenomenon of interest, design, evaluation, research type)26

Write a research proposal Write a clear description of the proposed research design and sample and a plan for data
collection and analysis. Ethical considerations and the required resources (i.e. budget and
personnel) for the research are identified

Secure resources Resources such as funding for supplies and research staff, institutional support and access
to experienced researchers are needed to ensure a study can be completed. Plans for how
to access the relevant type and number of study participants are also considered

Obtain ethics approvals Approval of the proposed research by a human research ethics committee (HREC) is
required before the study can commence

Conduct the research Adequate time for recruitment of participants, data collection and analysis are crucial to
ensure that valid and relevant results are obtained

Disseminate the research findings Discussion of the results and implications for practice with clinicians within the study site
should occur as soon as possible. Distribution of a brief summary of the results is also
frequently provided to study participants. Conference presentations and journal publications
are two additional ways that research findings are disseminated and are vital to ensure that
both nursing practice and nursing knowledge continue to be developed
6 SECTION 1 SCOPE OF CRITICAL CARE

FIGURE 1.1 Example of a critical care nursing research program.

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A strong research culture is evident in critical care nursing, practice guidelines. In addition, each chapter in this text
transcending geographical, epistemological and disciplinary contains a research critique to assist nurses in developing
boundaries to focus on the core business of improving care critical appraisal skills, which will help to determine
for critically ill patients. Our collective aim is to develop whether research evidence should change practice.
a sustainable research culture that incorporates strategies
that facilitate communication, cooperation, collaboration Education
and coordination both between researchers with common Appropriate preparation of specialist critical care nurses
interests and with clinicians who seek to use research is a vital component in providing quality care to patients
findings in their practice. A sample of a guiding structure and their families.12 A central tenet within this framework
for a coherent research program that highlights the major of preparation is the formalised education of nurses to
issues affecting critical care nursing practice is illustrated in practise in critical care areas.33 Formal education – in
Figure 1.1, with identified themes and topic exemplars. conjunction with experiential learning, continuing
A number of resources are available to critical care professional development and training and reflective
nurses interested in undertaking research. For example, a clinical practice – is required to develop competence in
number of critical care nursing professional organisations critical care nursing. The knowledge, skills and attitude
provide funding for research on a competitive basis. necessary for quality critical care nursing practice have
Funding is also available to critical care nurses through been articulated in competency statements34–36 and within
other critical care organisations not specific to nursing, certification processes that recognise the knowledge and
such as the Intensive Care Foundation in Australia. expertise of critical care nurses.37
Additionally, many regions have clinical trials groups that Critical care nursing education developed in unison
hold regular meetings where potential research can be with the advent of specialist critical care units. Initially, this
discussed and research proposals refined. There is great consisted of ad hoc training developed and delivered in
value in receiving a critical review of proposed research the work setting, with nurses and medical officers learning
before the study is undertaken, as assessors’ comments help together. For example, medical staff brought expertise
to refine the research plan. in physiology, pathophysiology and interpretation of
Over the years, various groups have identified priorities electrocardiographic rhythm strips, while nurses brought
for critical care research.29,30 A review of this literature expertise in patient care and how patients behaved
identified the following research priorities: nutrition and responded to treatment.19,38 Training was, however,
support, infection control, other patient care issues, nursing fragmented and ‘fitted in’ around ward staffing needs. Post-
roles, staffing and end-of-life decision making,31 although registration critical care nursing courses were subsequently
these priorities are likely to change based on scientific developed from the early 1960s in both Australasia and the
advances and societal priorities. UK.10,15 Courses ranged in length from 6 to 12 months and
While not all nurses are expected to conduct research, it generally incorporated employment as well as specific days
is a professional responsibility to use research in practice.32 for lectures and class work. Given the specific nature of these
Chapter 3 provides a detailed description of research courses developed to meet the local needs of individual
utilisation approaches, with a description of evidence- hospitals and regions, differences in content and practice
based practice and the use of evidence-based clinical developed between hospitals, regions and countries.39–41
 CHAPTER 1 SCOPE OF CRITICAL CARE PRACTICE 7

During the 1990s the majority of these hospital-based outcomes. Recent work in Australia has been completed
courses in Australasia were discontinued as universities to develop critical care nurse education practice standards
developed postgraduate curricula to extend the knowledge that can assist in achieving consistent graduate practice
and skills gained in pre-registration undergraduate courses. outcomes and can inform professional health workforce
A similar move to the tertiary sector occurred in the UK standards.48
and much of Europe during the 1990s and the following Both the impact of post-registration education on
decade. A significant proportion of critical care nurses now practice and the most appropriate level of education that is
undertake specialty education in the tertiary sector, often required to underpin specialty practice remain controver-
in a collaborative relationship with one or more hospitals.10 sial, with no universal acceptance internationally.43,49–52
One early study of students enrolled in university-based Globally, the Declaration of Madrid, which was endorsed
critical care courses in Australia42 identified a number of by the World Federation of Critical Care Nurses, provides
burdens (workload, financial, study–work conflicts), but also a baseline for critical care nursing education (see the
a number of benefits (e.g. better job prospects, job security). website, www.wfccn.org, for the position statement).12
Internationally, there are a number of different ways A range of factors continue to influence critical care
in which critical care nurses receive education specific nursing education provision, including government policies
to their practice.43 Within Australia and New Zealand, at national and state levels, funding mechanisms and resource
most tertiary institutions currently offer postgraduate implications for organisations and individual students,
critical care nursing education at a Graduate Certificate education provider and healthcare sector partnership
or Graduate Diploma level as preparation for specialty arrangements, and tensions between workforce and pro-
practice, although this is often provided as a Master’s fessional development needs.53 Recruitment, orientation,
degree.44 In the UK, similar provisions for postgraduate training and education of critical care nurses can be viewed
critical care nursing education at multiple levels are as a continuum of learning, experience and professional
available, although some universities also offer critical care development.12 The relationships between the various
specialisation at the undergraduate level (for example, components related to practice, training and education are
City University London). Education throughout Europe illustrated in Figure 1.2, on a continuum from ‘beginner’
has undergone significant change in the past 10 years as to ‘expert’ and incorporating increasing complexities of
the framework articulated under the Bologna Process has competency. Assessing the level of competency of a critical
been implemented.45 In relation to critical care nursing, care nurse is challenging54 although ways of measuring
this has led to the expansion of programs, primarily at competency are being explored.55 All elements comprising
the postgraduate level, for specialist nursing education. the notion of competence are equally important in
Critical care nursing education in the USA maintains a promoting quality critical care nursing practice.
slightly different focus, with most postgraduate studies Practice- or skills-based continuing education sessions
being generic in nature, including a focus on advanced support clinical practice at the unit level.56 (Orientation
practice roles such as clinical nurse specialists and nurse and continuing education issues are discussed further in the
practitioners, while specialty education for critical context of staffing levels and skills mix in Chapter 2.) Many
care nurses is undertaken as continuing education.46 countries now incorporate requirements for continuing
Employment in critical care, with associated assessment professional development into their annual licensing
of clinical competence, remains an essential component of processes. Specific requirements include elements such
many university-based critical care nursing courses.44,47 The as minimum hours of required professional development
diversity of critical care programs internationally means and/or ongoing demonstration of competence against
that there is likely significant variability in programs and predefined competency standards.57,58

FIGURE 1.2 Critical care nursing practice: training and education continuum.

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8 SECTION 1 SCOPE OF CRITICAL CARE

Specialist critical care competencies In 2001 the inaugural meeting of the World Federation of
Critical care nursing involves a range of skills, classified Critical Care Nurses (WFCCN) was formed to provide
as psychomotor (or technical), cognitive or interpersonal. professional leadership at an international level.21,61 The
Performance of specific skills requires special training ACCCN is a foundation member of the WFCCN and a
and practice to enable proficiency. Clinical competence member association of the World Federation of Societies of
is a combination of skills, behaviours and knowledge, Intensive Care and Critical Care Medicine, and maintains
demonstrated by performance within a practice situation59 a representative on the councils of both these international
and specific to the context in which it is demonstrated.55 bodies. (See the ACCCN website, listed in Online resources,
A nurse who learns a skill and is assessed as performing for further details about professional activities.)
that skill within the clinical environment is deemed
competent. The Australian College of Critical Care Nurses Critical care nursing roles
developed a revised set of practice standards for specialist As critical care nursing has developed, so too has the
critical care practice which comprises 15 practice standards range of roles performed by critical care nurses. Much
grouped into four domains: professional practice, provision of this textbook describes the specialty practice and
and cordination of care, critical thinking and analysis, and roles in critical care nursing. Critical care nursing is an
collaboration and leadership34 (refer to Appendix A and to example of ‘horizontal’ specialisation within nursing with
the ACCCN website, listed in Online resources at the end of other specialties such as oncology and aged care, whereas
this chapter). These revised standards were developed over advanced practice nursing can be considered ‘vertical’
2013–2015 through a two-phase process. Focus groups specialisation within the specialty of critical care. This
were held to identify main themes that informed develop- section focuses on advanced practice roles in critical
ment of draft standards that were refined during a Delphi care. The term advanced practice may be viewed as an
process involving a national panel of critical care nurses. umbrella, describing a number of related roles including
Other competency domains and assessment tools have also nurse practitioners. The ICU liaison nurse and the ICU
been developed.55,60 Although articulated slightly differently, outreach nurse are examples of advanced practice nursing
the American Association of Critical-Care Nurses (AACN) roles. Some advanced practice nurses may also be legally
provides ‘Standards of Practice and Performance for the recognised as nurse practitioners, as some ICU liaison
Acute and Critical Care Clinical Nurse Specialist’,60 which nurses are. In this section we describe the ICU liaison
outlines six standards of practice (assessment, diagnosis, nurse role, also described as the ICU outreach nurse in
outcome identification, planning, implementation and some settings, as an example of advanced practice nursing
evaluation) and eight standards of professional performance roles. Information on nurse practitioners is then provided.
(quality of care, individual practice evaluation, education,
collegiality, ethics, collaboration, research and resource Advanced practice nursing roles
utilisation) (see Online resources). There is potentially a huge range of advanced practice
nursing roles that may be enacted in critical care. For
Professional organisations example, critical care nurses could choose to develop
Professional leadership of critical care nursing has advanced knowledge and skills in the areas of palliative
undergone considerable development in the past three care, transport/retrieval or care of the elderly patient.
decades. Within Australia, the ACCCN (formerly the Collectively, what is common is the need to develop
Confederation of Australian Critical Care Nurses) was advanced knowledge and skills in the particular area of
formed from a number of preceding state-based specialty expertise. Interestingly, it also seems that these roles may
nursing bodies (e.g. the Australian Society of Critical emerge as a means of overcoming service gaps. The ICU
Care Nurses, the Clinical Nurse Specialists Association) liaison nurse is described as an example of an advanced
that had provided professional leadership for critical practice role. The ICU liaison nurse role, which emerged
care nurses since the early 1970s. In New Zealand, the in the late 1990s in Australia, is similar to the critical care
professional interests of critical care nurses are represented outreach role developed around the same time in the UK.62
by the New Zealand Nurses Organisation, Critical Care These roles include activities such as following up patients
Nurses Section, as well as affiliation with the ACCCN.The discharged from the ICU and providing expert advice for
ACCCN has strong professional relationships with other ward patients with complex care needs, including those
national peak nursing bodies, the Australian and New experiencing clinical deterioration. Early research showed
Zealand Intensive Care Society (ANZICS), government that Australian ICU liaison nurses focused on staff education
agencies and individuals, and healthcare companies. and support, ward liaison, patient care and support and
Professional organisations representing critical care family education and support.63 A comparison of the UK
nurses were formed as early as the 1960s in the USA outreach services and the Australian liaison nurse services
with the formation of the AACN.37 Other organisations found many similarities between the two roles.62 More
have developed around the world, such as the British contemporary research showed that liaison nurse services
Association of Critical Care Nurses (BACCN), and critical operated in 27% of public Australian ICUs.64 This survey
care nursing bodies now operate in all six continents. also identified that ICU liaison nurses were involved in
 CHAPTER 1 SCOPE OF CRITICAL CARE PRACTICE 9

activities related to education, collaboration (including also emerged.68,69 As part of her review, Fry68 described
consultation), expert practice and research/quality.64 the historical developments of the nurse practitioner role
Most of the liaison nurses were classified as clinical nurse in critical care. She noted that the role was established in
consultants or clinical nurse specialists.64 In those hospitals the United States in the 1960s, in the United Kingdom in
that had the service, 55% of the liaison nurses were part of the 1980s, in Canada and New Zealand in around 2000
the rapid response team.64 A recent Argentinian study of and to some extent in Australia in 1995, although formal
the activities undertaken by ICU liaison nurses in the first recognition of the nurse practitioner role did not occur in
year of the service showed that 98% of the 387 patients Australia until somewhat later.68
they saw had been discharged from the ICU.65 The service There is a growing body of research on the nurse
was provided 24 hours per day, 7 days per week.65 Of the practitioner/advanced practice nursing roles. While a
5973 patient care activities performed during the year, comprehensive review of this work is beyond the scope
over 95% were related to patient assessment, with various of this text, several recent studies are described. One study
other activities such as patient and family education and described the activities undertaken by 30 Australian nurse
support, airway management and patient safety activities practitioners in 2008/09.70 The sample included eight
making up the other 15%.65 In terms of the 1709 staff emergency, three cardiac, two neonatal and one paediatric
education activities undertaken during the first year, 33% nurse practitioners. The five most frequent activities
were related to patient safety such as skin care, infection were: meetings and administration, coordination of care,
and falls prevention, 20% and 17% of the other educational documentation, performing procedures and history tak-
activities were related to nursing assessment and airway ing.70 A more recent Australian study conducted in 2010
management, respectively.65 A 2014 meta-analysis of the examined prescribing practices specifically.71 The sample
effect of the ICU liaison nurse on ICU readmissions of 209 nurse practitioners included 66 emergency care
showed a positive effect with a risk ratio of 0.91 (adult) and 12 paediatric/neonatal nurse practitioners. In
(95% confidence intervals 0.75–0.99).66 Thus, it appears total, 78% of the nurses reported prescribing medications.71
that the evidence base for this advanced practice nursing The five most frequent medications prescribed were: anti-
role is growing. infectives, analgesics, psychotropics and cardiovascular and
Nurse practitioners musculoskeletal drugs.71 In Taiwan, 374 of 582 invited
nurse practitioners (response rate 64%) completed a
The International Council of Nursing (ICN) defines the survey of the competencies they required and possessed.72
nurse practitioner/advanced practice roles as a ‘registered The competencies assessed included direct care, medical
nurse who has acquired the expert knowledge base, assistance, communication and coordination, practical
complex decision-making skills and clinical competencies guidance, clinical research, professional consultation,
for expanded practice, the characteristics of which are ethical decision making, leadership and reform and
shaped by the context and/or country in which she/ cultural competency.72 The scores for all required
he is credentialed to practice’.67 The ICN notes that the competencies were consistently higher than the scores for
education of nurse practitioners/advanced practice nurses actual competencies. Chang and colleagues72 noted that,
is at an advanced level and is accredited or approved, in Taiwan, the nurse practitioner role was actually more
with some form of licensure, registration, certification similar to the physician assistant role as it predominantly
or credentialing. This description of nurse practitioners/ involved medical assistance. Finally, a recent Canadian
advanced practice nurses should not be confused with study examined perceptions of team effectiveness in two
specialist critical care nurses who are credentialed. In some cardiology services using the case study methodology.73
countries, including Australia, the nurse practitioner role There were 59 participants in the study who were described
is legislated and is distinct from other advanced practice as those within nursing (n = 28), ‘interprofessionals’
roles such as clinical nurse consultants or specialists. outside of nursing (n = 19) and managers (n = 12).
The ICN67 describes the nature of practice of nurse Participants perceived the nurse practitioners improved
practitioners/advanced practice nurses as including a high team effectiveness in a number of ways including: decision
degree of autonomy and independent practice. While the making, communication, cohesion, care coordination,
ICN acknowledges country specific regulation, it suggests
problem solving and providing a focus on patients and
nurse practitioners/advanced practice nurses will be able
families.73 Thus, the various roles and opportunities for
to diagnose, prescribe medications and treatments, refer
nurse practitioners in the critical care environment appear
clients to other health professionals and admit patients
to be growing.
to hospital. Skills such as advanced health assessment and
decision making are required.There are a number of nurse
practitioner/advanced practice nursing roles in critical Leadership in critical
care. A review described three nurse practitioner roles: 1) care nursing
adult, 2) paediatric and 3) neonatal.68 The author described
aspects of the role including direct patient management, Effective leadership within critical care nursing is
assessment, diagnosis, monitoring and procedural essential at several organisational levels, including the unit
activities.68 Retrieval and trauma nurse practitioners have and hospital levels, as well as within the specialty on a
10 SECTION 1 SCOPE OF CRITICAL CARE

broader professional scale. The leadership required at any and be approachable and supportive.83,84 Effective leaders
given time and in any specific setting is a reflection of inspire their team members to take the extra step towards
the surrounding environment. Regardless of the setting, achieving the goals articulated by the leader and to feel that
effective leadership involves having and communicating a they are valued, independent, responsible and autonomous
clear vision, motivating a team to achieve a common goal, individuals within the organisation.83 Members of teams
communicating effectively with others, role modelling, with effective leaders are not satisfied with maintaining the
creating and sustaining the critical elements of a healthy status quo, but believe in the vision and goals articulated
work environment and implementing change and by the leader and are prepared to work towards achieving
innovation.74–77 Leadership at the unit and hospital levels is a higher standard of practice.
essential to ensure excellence in practice, as well as adequate Although all leaders share common characteristics,
clinical governance. In addition to the generic strategies some elements vary according to leadership style. Differ-
described above, it is essential for leaders in critical care ent styles – for example, transactional, transformational,
units and hospitals to demonstrate a patient focus, establish authoritative or laissez faire – incorporate different
and maintain standards of practice and collaborate with characteristics and activities. Having leaders with different
other members of the multidisciplinary healthcare team.74 styles ensures that there is leadership for all stages of an
Leadership is essential to achieve growth and devel- organisation’s operation or a profession’s development. A
opment in our specialty and is demonstrated through combination of leadership styles also helps to overcome
such activities as conducting research, producing publica- team member preferences and problems experienced
tions, making conference presentations, representation when a particularly visionary leader leaves. The challenges
on relevant government and healthcare councils and often associated with the departure of a leader from
committees and participation in organisations such as a healthcare organisation are generally reduced in the
the ACCCN, BACCN, AACN, European federation of clinical critical care environment, where a nursing leader
Critical Care Nursing associations (EfCCNa) and the is usually part of a multidisciplinary team, with resultant
WFCCN. As outlined earlier in this chapter, we have shared values and objectives.
seen the field of critical care grow from early ideas and
makeshift units to a well-developed and highly organised Clinical leadership
international specialty in the course of a generation. Such Effective critical care nurses demonstrate leadership
development would not have been possible without the characteristics regardless of their role or level of practice;
vision, enthusiasm and commitment of many critical care such leadership is an essential component of any effective
leaders throughout the world. team.85 Leadership in the clinical environment incorporates
Leadership styles vary and are influenced by the the general characteristics listed above, but has the added
mission and values of the organisation as well as the values challenges of working within the boundaries created by
and beliefs of individual leaders. These styles of leadership the requirements of providing safe patient care 24 hours
are described in many different ways, sometimes by using a day, 7 days a week. It is therefore essential that clinical
theoretical underpinnings such as ‘transactional’ and leaders work within an effective interdisciplinary model,
‘transformational’ and sometimes by using leadership so that all aspects of patient care and family support, as
values and characteristics. Regardless of the terminology well as the needs of all staff, are met.85 Effective clinical
in use, some common principles can be expressed. Desired
leadership of critical care is essential in achieving:
leadership characteristics include the ability to:
• articulate a personal vision and expectations • effective and safe patient care
• act as a catalyst for change • high quality, evidence-based health care
• establish and implement organisational standards • satisfied patients and family members
• model effective leadership behaviours through both • satisfied staff, with a high level of retention
change processes and stable contexts • development of staff through an effective coaching
and mentoring process.86–88
• monitor practice in relation to standards and take
corrective action when necessary Effective clinical leaders build cohesive and
adaptive work teams,82 and improve interdisciplinary
• recognise the characteristics and strengths of collaboration.89 They also promote the intellectual
individuals, and stimulate individual development and
commitment stimulation of individual staff members, which encourages
the analysis and exploration of practice that is essential for
• empower staff to act independently and evidence-based nursing.83 Clinical leadership is particularly
interdependently important in contemporary critical care environments
• inspire team members to achieve excellence.78–83 in times of dynamic change and development. We are
Personal characteristics of an effective leader, currently witnessing significant changes in the organisation
regardless of the style, include honesty, integrity, justice, and delivery of care, with the development of new roles
commitment, credibility, courage and wisdom, as well such as the nurse practitioner (see this chapter) and liaison
as the ability to develop an open, trusting environment nurse (see Chapter 3), the introduction of services such
 CHAPTER 1 SCOPE OF CRITICAL CARE PRACTICE 11

as rapid response systems, including medical emergency factors must be in a clinical setting, so the development
teams (see Chapter 3) and the extension of activities across of clinical leaders should be based in that environment.
the care continuum (see Chapter 4). Effective clinical Development programs based on mentorship, with strong
leadership ensures that: academic support, are superbly suited to developing those
• critical care personnel are aware of, and willing to that demonstrate potential for such capabilities.78,91
fulfil, their changing roles Mentorship has received significant attention in the
healthcare literature and has been specifically identified
• personnel in other areas of the hospital or outside as a strategy for clinical leadership development.92–94
the hospital recognise the benefits and limitations
Although many different definitions of mentoring exist,
of developments, are not threatened by the
common principles include a relationship between two
developments and are enthusiastic to use the new or
people with the primary purpose of one person in
refined services provided by critical care
the relationship developing new skills related to their
• patients receive optimal quality of care. career.95 A related process might also be referred to as
The need to provide educational opportunities to coaching.96,97 Mentoring programs can be either formal
develop effective clinical leadership skills is recognised.78 or informal and either internal or external to the work
Although not numerous in number or variety, programs setting. Mentorship involves a variety of activities
are beginning to be available internationally that are directed towards facilitating new learning experiences
designed to develop clinical leaders, both within the clinical for the mentee, guiding professional development and
environment and in partnership with higher education career decisions, providing emotional and psychological
institutions.77,90,91 Factors that influence leadership ability support and assisting the mentee in the socialisation
include the external and internal environment, demographic process both within and outside the work organisation
characteristics such as age, experience, understanding, to build professional networks.93,95,97 Role modelling of
stage of personal development including self-awareness occupational and professional skills and characteristics is
capability and communication skills.78,80,90 In relation to an important component of mentoring that helps develop
clinical leadership, at least some of the development of these future clinical leaders.93

Summary
This chapter has provided a context for subsequent chapters, outlining some key issues, principles and concepts for
practising and studying nursing in a range of critical care areas. Critical care nursing now encompasses a broad and ever-
expanding scope of practice. The previous focus on patients in ICU only has given way to a broader concept of caring
for an individual located in a variety of clinical locations across a continuum of critical illness.
The discipline of critical care nursing, in collaboration with multidisciplinary colleagues, continues to develop to meet
the expanding challenges of clinical practice in today’s healthcare environment. Critical care clinicians also continue their
professional development individually, focusing on clinical practice development, education and training and on quality
improvement and research activities, to facilitate quality patient and family care during a time of acute physiological
derangement and emotional turmoil. The principles of decision making and clinical leadership at all levels of practice
serve to enhance patient safety in the critical care environment.

Case study
James is a 54-year-old male who is 5 days post an Ivor Lewis oesophagectomy for cancer; his post-
operative progress to this point has followed a routine course. The ICU outreach nurse’s first contact
with this patient is a direct referral from the primary care nurse on the ward who is concerned with his
tachypnoea, tachycardia and low grade temperature. James is reviewed by the ICU outreach nurse in
regard to the following:
• physical assessment
• review of clinical course/notes and observation charts
• review of radiological and pathological investigations
• discussion of concerns with the primary care nurse.
During this assessment James is noted to have a low grade temperature (37.7° C) with two documented
episodes of elevated temperature over the last 8 hours and increasing heart rate (HR) of 115 beats/min
12 SECTION 1 SCOPE OF CRITICAL CARE

and respiratory rate (RR) of 26 breaths/min. On auscultation of the patient’s chest he was found to
have decreased air entry to both lung bases and coarse crackles in the right middle lobe. James had
dry mucous membranes, reported thirst and denied pain. He had not had a chest X-ray (CXR) in the
previous 24 hours and had a rising white cell count (WCC) on his full blood count (FBC) over the last
48 hours.
Advanced assessment skills: ICU outreach nursing requires an advanced level of nursing assessment
skills. Outreach nurses must have the ability to effectively undertake a physical assessment and integrate
these findings with other available assessment data such as radiological and pathological investigations
to rapidly build a clear picture of why the patient is clinically deteriorating. This integration of assessment
findings enables appropriate decisions around escalation of patient care to be made.
Progress: findings of this assessment were discussed with the resident medical officer and subsequently
the registrar of the treating team, with a provisional diagnosis of sepsis made. A CXR, septic screen,
increased intravenous fluids and broad spectrum intravenous antibiotics were ordered. In discussion with
the primary care nurse, observations were increased to 2nd hourly and a strict fluid balance commenced.
James was placed on the list for review by the outreach nurse during the next shift.
Subsequently, the ICU outreach nurse came into contact with James prior to this review as part of the rapid
response team (RRT) call. James had further respiratory deterioration. He had a RR of 30 breaths/min,
SpO2 of 92% on a non-rebreathing mask at 15 L/min of oxygen and was using his accessory muscles to a
moderate degree. As a member of the RRT (airway nurse) the outreach nurse discussed the indications and
possible benefits of high flow oxygen (HFO) for this patient. The outreach nurse set up and implemented
this therapy and provided bedside education for the ward nursing staff. In discussion with the nurse in
charge of the ward, a 1:1 registered nurse special for James was arranged, and a plan for management of
any deterioration was developed with the nursing and medical staff. James was also referred to the on-call
physiotherapist to ensure ongoing chest physiotherapy overnight.
James was reviewed by the outreach nurse 4 hours after the RRT call, and he appeared fatigued but was
maintaining his SpO2 at ≥95% on 30 L/min of 45% HFO. The medical staff were again contacted and, after
consultation, an arterial blood gas was taken, processed and interpreted. With further medical and nursing
team consultation James’ oxygen flow was increased to 40 L/min to assist with the work of breathing;
concurrently, the observation frequency was increased to hourly. Progress included the following:
• James was reviewed 2 hours later; his work of breathing had decreased, and he had tolerated
physiotherapy well and was clearing secretions effectively.
• James was reviewed on the next outreach nurse shift. His clinical condition continued to improve. The
outreach nurse provided education to the nursing and junior medical staff regarding the indications,
process and rationale for weaning of HFO. Discussion occurred with the nurse in charge of the ward and
1:1 nursing special was ceased for James as the primary care nurse felt he could be closely monitored
with normal staffing levels at this time.
• James was reviewed on the following shift. On clinical assessment air entry had improved, he had a
decreasing sputum load and observations were RR 20 breaths/min, HR 95 beats/min, SpO2 ≥95% on
25% HFO at 30 L/min, BP 130/90 mmHg and urine output 30–80 mL/h. The primary care nurse was
satisfied with the clinical plan for James and it was mutually agreed to remove the patient from the
outreach nurse review service.

DISCUSSION
Effective communication skills
ICU outreach nursing requires exemplary communication skills. The outreach nurse must be able to effectively
liaise with the ward nursing staff and clearly present their assessment findings and recommendations for
management to the multidisciplinary team. In this instance:
• education was provided to ward nursing staff regarding the use of HFO and associated care
• a clear plan was developed to manage any further deterioration
• in conjunction with the nurse in charge of the ward the outreach nurse assisted in facilitating a 1:1
nursing ratio for this patient to ensure close monitoring of the patient’s condition and safe staffing levels
for other patients on the ward.
 CHAPTER 1 SCOPE OF CRITICAL CARE PRACTICE 13

Leadership and corporate knowledge

Outreach nurses strive to create an inclusive culture wherein they provide the support for ward-based
nursing teams to manage deteriorating patients. Their role is not to intervene or take over the care of the
patient, but to provide appropriate support, education and potential care strategies. Achieving this goal
requires tact, diplomacy and emotional intelligence as well as knowledge of the facilities and services
available in the organisation in which they work. An understanding of the corporate/operational knowledge,
both explicit and tacit in each ward, can provide great advantage in overcoming the challenges of effectively
managing the deteriorating patient, such as staffing and ward specific protocols and practices. This
knowledge contributes to the development of effective plans to manage deteriorating patients in each of
the specific clinical settings.

CASE STUDY QUESTIONS

1 During an episode of patient deterioration urgent treatment may be required and, consequently, there
may be limited opportunity for learning by the ward nursing staff caring for the deteriorating patient.
What strategies might you use to optimise learning in this scenario?
2 As an ICU outreach nurse (or other consultant who provides support on multiple wards), you notice
that the ward-based nursing staff appear reticent to report problems or access support through the
ward hierarchy. You broach this subject with several nurses and they indicate they feel powerless and
are afraid of the senior staff in both the nursing and medical professions. How would you support the
nursing staff in this environment?

The authors thank Shannon Crouch and Amanda Vaux, CNCs Outreach, Princess Alexandra Hospital, for
developing this Case study.

RESEARCH VIGNETTE

Lakanmaa RL, Suominen T, Perttila J, Ritmala-Castren M, Vahlbert T, Leino-Kilpi H. Graduating nursing students’
basic competence in intensive and critical care nursing. J Clin Nurs 2014;23:645–53

Abstract
Aims and objectives: To describe and evaluate the basic competence of graduating nursing students in intensive
and critical care nursing.

Background: Intensive and critical care nursing is focused on severely ill patients who benefit from the attention of
skilled personnel. More intensive and critical care nurses are needed in Europe. Critical care nursing education is
general post-qualification education that builds upon initial generalist nursing education. However, in Europe, new
graduates practise in intensive care units. Empirical research on nursing students’ competence in intensive and
critical care nursing is scarce.

Design: A cross-sectional survey design.

Methods: A basic competence scale (Intensive and Critical Care Nursing Competence Scale, version 1) and a
knowledge test (Basic Knowledge Assessment Tool, version 7) were employed among graduating nursing students
(n = 139).

Results: Sixty-nine percent of the students self-rated their basic competence as good. No association between
self-assessed Intensive and Critical Care Nursing-1 and the results of the Basic Knowledge Assessment Tool-7
was found. The strongest factor explaining the students’ conception of their competence was their experience of
autonomy in nursing after graduation.

Conclusion: The students seem to trust their basic competence as they approach graduation. However, a knowledge
test or other objective method of evaluation should be used together with a competence scale based on self-
evaluation.
14 SECTION 1 SCOPE OF CRITICAL CARE

Relevance to clinical practice: In nursing education and in clinical practice, for example, during orientation
programmes, it is important not only to teach broad basic skills and knowledge of intensive and critical care nursing,
but also to develop self-evaluation skills through the use of special instruments constructed for this purpose.

Critique
This interesting study focused on Finnish nursing students’ perceptions of their competence. As described
by the authors, in Finland basic nursing education is provided by polytechnics (also described as universities of
applied sciences). There is no graduate specialty education, thus intensive and critical care nursing is taught in the
undergraduate program. Therefore, the students recruited to the study were students in the last semester of their
undergraduate education. The sample was drawn from four polytechnics, each of which was located near a university
hospital. All nurses in their final semester of education were invited to participate in a survey. A total of 139 nurses
completed it, for a response rate of 59%. The fact that four sites were sampled and the response rate was reasonably
good suggests the findings may be generalisable to other similar settings.

The survey was comprised of demographic data and two instruments, the Intensive and Critical Care Nursing
Competence Scale (ICCN-CS-1), which was developed by the Finnish authors, and the Basic Knowledge Assessment
Tool version 7 (BKAT-7), which had previously been developed in the USA. The BKAT-7 has 100 items and has been
extensively used and has been translated into several languages. In this study, it was used to test the criterion
validity of the ICCN-CS-1. That is, participants who score high on the ICCN-CS-1 knowledge base questions should
also score high on the BKAT-7 if the ICCN-CS-1 is a valid measuring instrument. The ICCN-CS-1 was developed
using a standard process of reviewing the literature, and employing a Delphi study. The ICCN-CS-1 is a 108-item
instrument comprised of two main sections, clinical competence and professional competence, both of which have
items related to knowledge, skills and attitudes/values. The reliability of the ICCN-CS-1 was good with Cronbach’s
alphas of 0.87–0.98, although the highest alpha suggests there may be more items than needed. Total scores on
the ICCN-CS-1 were calculated by adding the individual item scores together for the total instrument, for the two
sections of clinical and professional competence and also for the groupings of items within each of these sections
and for the classification as knowledge, skills and attitude/values. Then, score ranges were classified as excellent,
good, moderate or poor competence.

Participants were given 90 minutes to complete the survey. It is not clear why this amount of time was allowed or if the
timing may have affected the responses. However, the authors note they completed a pilot study, which suggested
that this time may be feasible. Returned surveys implied consent; ethics approval was gained from the relevant ethics
committees and permission to use the BKAT-7 was also obtained.

The researchers report that in terms of self-rated ‘basic’ competence (i.e. overall competence instrument score),
25% rated it as excellent, 69% rated it as good and 6% rated it as moderate. In fact, mean scores for clinical and
professional competence were similar at 3.70 (± 0.55) and 3.75 (± 0.47). When considering these same items in
relation to knowledge, skill and attitude/values, both knowledge and skills at 3.28 (± 0.62) and 3.20 (± 0.67) appeared
to be lower than attitudes/values at 4.68 (± 0.36). The researchers report there was no association between the
ICCN-CS-1 and the BKAT-7 suggesting that criterion validity of the ICCN-CS-1 was not supported. Yet, they report
the level of significance (i.e. p-value) for the correlation was 0.012, which is statistically significant. Perhaps because
the Pearson’s correlation was only 0.21, they believed that the finding was not clinically meaningful but this is
different to whether there was a statistically significant correlation (which there was based on the results presented).
In the discussion the researchers explained potential reasons for the finding that participants scored very low on the
BKAT-7 instrument.

The discussion was thoughtful and well written. The relevance to clinical practice was briefly mentioned and
suggestions for future work were woven into the discussion. Limitations of the research were also identified. Although
the paper was reasonably clear, it took time to understand the ICCN-CS-1 in terms of the sections, the subsections
and how items were also classified as knowledge, skills and attitudes/values. It also took time to understand how
the instrument was scored. Overall though, this was an interesting study undertaken by a reasonably large team of
researchers led by a nurse, who was doing this study as part of her PhD.
 CHAPTER 1 SCOPE OF CRITICAL CARE PRACTICE 15

Lear ning a c t iv it ie s
1 Consider the leaders to whom you are exposed in your work environment and identify the characteristics they
display that influence patient care. Reflect on whether these are characteristics that you possess or how you
might develop them.

2 All registered nurses are expected to demonstrate leadership in clinical practice. Reflect on what leadership
activities you undertake as part of your role. What strategies could you use to evaluate and further develop your
leadership skills?

3 A colleague who has been working in ICU for the past 3 years indicates that they are interested in moving
beyond a role in direct patient care and would like to eventually move into a clinical leadership position.
What strategies might you suggest they investigate to position them well for the future?

4 Consider the role that you have within critical care and examine the influence that research has on that role.
How might you use research to inform your practice more effectively? Are there strategies that you could
implement to influence the research that is undertaken so that it meets your needs?

5 Reflect on your practice and experience over the past year. What professional development activities have you
undertaken and what new knowledge and skills have you developed?

Online resources
American Association of Critical-Care Nurses, www.aacn.org

Annual Scientific Meeting on Intensive Care, www.intensivecareasm.com.au

ANZICS Clinical Trials Group, www.anzics.com.au/clinical-trials-group

Australia and New Zealand Intensive Care Society, www.anzics.com.au

Australian College of Critical Care Nurses, www.acccn.com.au

British Association of Critical Care Nurses, www.baccn.org.uk

Canadian Critical Care Trials Group, www.ccctg.ca/Home.aspx

College of Intensive Care Medicine (CICM), www.cicm.org.au

European Society of Intensive Care Medicine, www.esicm.org

Intensive Care Foundation (Australia and New Zealand), www.intensivecarefoundation.org.au

Intensive Care National Audit and Research Centre, www.icnarc.org

King’s College, London, www.kcl.ac.uk/schools/nursing

NHS Leadership Academy, The Healthcare Leadership Model, www.leadershipacademy.nhs.uk/discover/leadershipmodel

Royal College of Nursing (UK) Critical Care and In-Flight Nursing Forum community, www.rcn.org.uk/development/
communities/rcn_forum_communities/critical_inflight

Scottish Intensive Care Society, www.scottishintensivecare.org.uk/sics/research/index.htm

World Federation of Critical Care Nurses, http://en.wfccn.org

Further reading
Andrew S, Halcomb EJ. Mixed methods research for nursing and the health sciences. Oxford: Wiley-Blackwell; 2009.

Scholes J. Developing expertise in critical care nursing. Oxford: Blackwell Publishing; 2006.

Swanwick T, McKimm J. ABC of clinical leadership. London: BMJ Books; 2010.

16 SECTION 1 SCOPE OF CRITICAL CARE

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87 Eggenberger T. Exploring the charge nurse role: holding the frontline. J Nurs Adm 2012;42(11):502–6. Epub 2012/10/27.
88 Tregunno D, Jeffs L, Hall LM, Baker R, Doran D, Bassett SB. On the ball: leadership for patient safety and learning in critical care. J Nurs Adm
2009;39(7–8):334–9.
89 Bender M, Connelly CD, Brown C. Interdisciplinary collaboration: the role of the clinical nurse leader. J Nurs Manag 2013;21(1):165–74.
Epub 2013/01/24.
90 Dierckx de Casterle B, Willemse A, Verschueren M, Milisen K. Impact of clinical leadership development on the clinical leader, nursing team and
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92 McCloughen A, O’Brien L, Jackson D. Esteemed connection: creating a mentoring relationship for nurse leadership. Nurs Inq 2009;16(4):326–36.
93 Taylor CA, Taylor JC, Stoller JK. The influence of mentorship and role modeling on developing physician-leaders: views of aspiring and
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96 Hancock B. Developing new nursing leaders. Am J Nurs 2014;114(6):59–62. Epub 2014/05/30.
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 Chapter 2

Systems and resources

Denise Harris, Ged Williams

KEY WORDS Learning objectives

budget After reading this chapter, you should be able to:
business case • describe historical influences on the development of critical care and the
way this resource is currently viewed and used
competence
credentialling • explain the organisational arrangements and interfaces that may be
established to govern a critical care unit
critical care
• identify resources and supports that assist in the governance and
governance management of a critical care unit
pandemic
• describe considerations in planning for the physical design and
patient equipment requirements of a critical care unit
dependency
• describe the human resource requirements, supports and training
resource necessary to ensure a safe and appropriate workforce
management • explain common risks and the appropriate strategies, policies and
risk management contingencies necessary to support staff and patient safety
skill mix • discuss leadership and management principles that influence the quality,
staff efficacy and appropriateness of the critical care unit
• discuss critical care considerations in responding to the threat of a
pandemic.

Introduction
In 1966 Dr B Galbally, a hospital resuscitation officer at St Vincent’s Hospital,
Melbourne, published the first article on the planning and organisation of an
intensive care unit (ICU) in Australia.1 He identified that critically ill patients
who have a reasonable chance of recovery require life-saving treatments and
constant nursing and medical care, but that this intensity of service delivery
‘does not necessarily continue until the patient dies, and it should not continue
after the patient is considered no longer recoverable’.1
The need for prudent and rational allocation of limited financial and
human resources was as important in the 1960s as it is today. This chapter
explores the influences on the development of critical care and the way this
resource is currently viewed and used; describes various organisational, staffing
and training arrangements that need to be in place; considers the planning,
design and equipment needs of a critical care unit; covers other aspects of
20 SECTION 1 SCOPE OF CRITICAL CARE

resource management including the budget and financial particular scrutiny to justify its resource usage within a
modelling; and finishes with a description of how critical healthcare system. Therefore, not only do critical care
care staff may respond to a pandemic or other acute and managers need to be prudent, responsible and efficient
dramatic demands on resources. First, however, important guardians of this precious resource, they need to be seen as
ethical decisions in managing the resources of a critical such if they are to retain the confidence of, and legitimacy
care unit are discussed below. with, the broader community values of the day.

Practice tip Historical influences

Ethical decision making in terms of managing resources Developing larger and more sophisticated services such as
at the unit level is as critical as ethical decision making ICUs can attract media and public attention. The 1960s
at the individual patient level in terms of access to and early 1970s saw the development of the first critical
scarce critical care resources. Open and transparent care units in many parts of the developed world. If a
decision making is imperative. hospital was to be relevant, it had to have one. In fact,
what distinguished a tertiary referral teaching hospital
from other hospitals was at its fundamental conclusion,
Ethical allocation and the existence of a critical care unit.3 Over time, practical
utilisation of resources reasons for establishing critical care units have led to their
spread to most acute hospitals with more than 100 beds.
In management, as in clinical practice, careful consider- Reasons for the proliferation of critical care services
ation of the pros and cons of various decisions must be include, but are not limited to:
made on a daily basis.The interests of the individual patient,
extended family, treating team, the organisation and the • economies of scale by cohorting critically ill patients
to one area
broader community are rarely congruent, nor are they
usually consistent. Decisions surrounding the provision of • development of expertise in doctors and nurses who
critical care services are often governed by a compromise specialise in the care and treatment of critically ill
between conflicting interests and ethical theories. Two patients
main perspectives on ethical decision making, deontological • an ever-growing body of research demonstrating that
and utilitarian, are explored briefly.2 critically ill patient outcomes are better if patients are
The deontological principle suggests that a person has a cared for in a specifically equipped and staffed critical
fundamental duty to act in a certain way – for example, care unit.4
to provide full, active medical treatment to all persons. Funding for critical care services has evolved over
The rule of rescue, or the innate desire to do something – time to be somewhat separate from mainstream patient
anything – to help those in dire need, may be a corollary funding, owing to the unique requirements of critical
to the deontological principle. These two concepts, the care units. Critical care is unique because patients are
duty to act and the rule of rescue, tend to sit well with at the severe end of the disease spectrum. For instance,
many trained and skilled clinicians and the Hippocratic the funding provided for a patient admitted for chronic
Oath. In critical care there are some families and some obstructive airway disease in an ICU on a ventilator is
clinicians who, for personal and/or religious reasons, take very different from that provided for a patient with the
a strong stand and demand treatments and actions based same diagnosis, but treated in a medical ward only. Each
on a deontological view (i.e. the fundamental belief that country/jurisdictional health department tends to create
a certain action is the only one that should be considered its own unique approach to funding ICU services. For
in a given situation). instance, the Research and Development Corporation
At the other extreme is the utilitarian view, which study4 examined funding methods in many countries
suggests an action is right only if it achieves the greatest and concluded that there was no obvious example of
good for the greatest number of people.This concept tends ‘best practice’ or a dominant approach used by a majority
to sit well with pragmatic managers and policy makers. An of systems. Each approach had advantages and disad-
example of a utilitarian view might be to ration funding vantages, particularly in relation to the financial risk
allocated to heart transplantation and to utilise any saved involved in providing intensive care. Although the risk
money for prevention and awareness campaigns. A heart of underfunding intensive care may be highest in systems
disease prevention campaign lends a greater benefit to a that apply Diagnosis Related Groups (DRGs) to the
greater number in the population than does one transplant entire episode of hospital care, including intensive care,
procedure. concerns about potential underfunding were voiced in all
The appropriate provision and allocation of critical systems reviewed. Arrangements for additional funding
care services and resources tend to sit somewhere between in the form of co-payments or surcharges may reduce
these two extreme positions. This dilemma is true of the risk of underfunding. However, these approaches also
all health services, but critical care, because of its high- face the difficulty of determining the appropriate level
technology, high-cost, low-volume outputs, is under to be paid.4
 CHAPTER 2 SYSTEMS AND RESOURCES 21

Australia has established the Independent Hospital Funding based on achieving positive patient outcomes
Pricing Authority whose task it has been to harmonise the would be ideal, as it would ensure that critical care units
variations in funding processes across all states and territo- were using their resources only for those patients who
ries and to establish a common, consistent and transparent were most likely to achieve positive outcomes in terms
funding process to be agreed by all.5 But agreement on of morbidity and mortality. However, funding based only
a common funding model for intensive care services has on health outcomes does raise the risk of encouraging
been difficult. clinicians to ‘cherrypick’ only the most ‘profitable’ or
The Independent Hospital Pricing Authority deter- ‘successful’ patient groups at the expense of others. In
mined they would develop a list of ICUs that will be private (for-profit) hospitals or countries with very poor
eligible to receive an ICU adjustment based on a measure health systems, cherrypicking only those patients for
of the size of the ICU and the overall complexity of whom a successful outcome is guaranteed is likely to be
the mix of patients within each ICU, but would continue more common, whereas in the public hospitals of most
working with stakeholders and jurisdictions to explore Western countries an educated assessment is often applied
alternative patient-based mechanisms for determining the to the decision as to whether a patient should enter the
ICU adjustment for future years during 2014.6 The current critical care unit or not.
Australian National Efficient Price Determination for 2014 It is vital to note the very important role played by
used a total sample of 56,835 separations with ICU hours rural and isolated health services and, in particular, critical
and costs from establishments with eligible ICUs/PICUs. care units and outreach services in these regions. Many
The weighted mean of the hourly ICU costs taken of the contemporary activity-based funding formulas
across states was used to derive a national ICU rate of $190.7 are difficult to apply to these settings. There are disecon-
Eligible ICUs and PICUs are those belonging to hospitals omies of scale in such settings as a result of small bed
that report more than 24,000 ICU hours with more numbers, limited but highly skilled nurses and doctors
than 20% of those hours reported to involve the use of and unpredictable peaks and troughs in demand, which
mechanical ventilation.The specified hospitals with eligible make workforce planning and the management of call-in/
ICUs and/or PICUs number a total of 71 (NSW 25, Qld overtime and fatigue problems difficult for small teams
17, Vic 15, SA 5, WA 4, Tas 2, NT 2, ACT 1).7 Although to manage. The professional isolation and limited access
the Independent Hospital Pricing Authority outcome may to education, training and peer support can also create
morale problems for some members of the team. Further-
appear to be a complex compromise, it is in fact a signifi-
more, the diseconomies and isolation require empathetic
cant step forward to have a single funding model across the
funding processes to recognise the difficulties unique to
country, albeit at the strategic level. Future work by Inde-
regional and isolated critical care services. If such units are
pendent Hospital Pricing Authority and others hopes to
to remain viable and capable of delivering levels of safe
further refine the precise patient-based measures that can
and effective care equivalent to those expected in larger
align critical care activity with funding more accurately metropolitan hospitals, additional funding and support
with the ultimate ideal being that the measures will also is required to compensate for the cost and tyranny of
align with quality performance and outcomes. distance.
At the hospital level, most critical care units have
capped and finite budgets that are linked to ‘open
beds’ – that is, beds that are equipped, staffed and ready to
Economic considerations
be occupied by a patient, regardless of whether they are and principles
actually occupied.8 This is one crude yet common way
One early comprehensive study of costs found that 8% of
that hospitals can control costs emanating from the critical
patients admitted to the ICU consumed 50% of resources
care unit. The other method is to limit the number of
but had a mortality rate of 70%, while 41% of patients
trained and experienced nurses available to the specialty;
received no acute interventions and consumed only 10% of
consequently, a shortage of qualified critical care nurses resources.9 More recent studies show that, although critical
results in a shortage of critical care beds, resulting in a care services are increasingly being provided to patients
rationing of the service available. The capping of beds and who are older and with a higher severity of acute and
qualified critical care nurse positions can be convenient chronic illnesses, long-term survival outcome has improved
mechanisms to limit access and utilisation of this expensive with time, suggesting that critical care services may still be
service – critical care. cost-effective despite the changes in case-mix.10–12
Some authors provide scenarios as examples of poor
Practice tip economic decision making in critical care and argue for
less extreme variances in the types of patient ICUs choose
The capping of beds and qualified critical care nurse to treat in order to reduce the burden of cost on the
positions can be convenient mechanisms to limit health dollar.13,14 Others have suggested that if all health
access and utilisation of this expensive service – critical care provided were appropriate, rationing would not be
care. required.15 Defining what is ‘appropriate’ can be subjective,
although not always. The Research and Development
22 SECTION 1 SCOPE OF CRITICAL CARE

TABLE 2.1
Approaches to assessing treatment options

APPROACH DESCRIPTION

Benefit–risk approach The benefit of treatment and the inherent risks to the patient are assessed to inform a decision; this
approach excludes monetary costs

Benefit–cost approach Evaluate the benefit and cost of the decision to proceed; this approach incorporates cost to patient
and society

Implicit approach The medical practitioner provides the service and judges its appropriateness

Adapted from Ettelt S, Nolte E. Funding intensive care – approaches in systems using diagnosis-related groups. Cambridge: Rand
Europe, <http://www.rand.org/content/dam/rand/pubs/technical_reports/2010/RAND_ TR792.pdf>; 2010 [accessed 29.07.14],
with permission.

Corporation group4,16 suggests that there are at least benefit of critical care is associated with such factors
three approaches that can be used to assess appropriate- as survival, longevity and improved quality of life (e.g.
ness of care (Table 2.1). These include the benefit–risk, greater functioning capacity and less pain and anxiety).
benefit–cost and implicit approaches. The benefit is enhanced by sustainability: the longer the
The first two approaches are considered to be explicit benefit is maintained, the better it is.18
approaches, while the third tends to be implicit. However, Cost is separated into two components, monetary
all approaches have a subjective element. Although the (price) and non-monetary (suffering). Non-monetary
implicit approach is considered to be subjective in nature, costs include such considerations as morbidity, mortality,
the medical practitioner must contemplate benefit–risk pain and anxiety in the individual, or broader societal costs
and benefit–cost considerations but should also involve the and suffering (e.g. opportunity costs to others who might
patient/family in the contemplation and ultimate decision. have used the resources but for the current occupants, and
Similar discussions have been advocated by the Taskforce on what other health services might have been provided but
Values, Ethics and Rationing in Critical Care who suggest for the cost of this service).18
rationing is not only unavoidable but essential to ensuring Ethico-economic analyses of services such as critical
the ethical distribution of medical goods and services.17 care and expensive treatments such as organ transplanta-
What is best for the patient is not just the opinion of the tion are the new consideration of this century and are as
treating doctor and needs to be considered in much broader important to good governance as are discussions of medico-
terms such as the patient’s previous expressed wishes and legal considerations. Sound ethical principles to inform
the family’s opinion as de facto patient representatives. and guide human and material resource management and
The quality of the decision and the quality of the expected budgets ought to prevail in the management of limited
outcome require many competing considerations. health resources.2
Practice tip
Budget and finance
What is best for the patient is not just the opinion of
This section provides information on types of budget, the
the treating doctor and needs to be considered in much
budgeting process and how to analyse costs and expendi-
broader terms such as the patient’s previous expressed
tures to ensure that resources are utilised appropriately and
wishes and the family’s opinion as de facto patient
in line with the service management plan, that is the oper-
representatives.
ational and service goals of the critical care team expected
by the hospital and broader community. As noted by one
Proponents of the ‘quality’ agenda in health care
have argued for ‘best practice’ and ‘best outcomes’ in the author, ‘Nothing is so terrifying for clinicians accustomed
provision of health services, although it may be more to daily issues of life and death as to be given respons-
pragmatic to consider ‘value’ when discussing what is and ibility for the financial affairs of their hospital division!’.15
what is not an appropriate decision in critical care. The Yet, in essence, developing and managing a budget for
following equation expresses the concept ‘value’ simply: a critical care unit follows many of the same principles
as managing a family budget. Consideration of value for
Quality Benefit ⫻ Sustainability money, prioritising needs and wants and living within a
Value = = relatively fixed income is common to all. This section in
Cost Price ⫻ Suffering
no way undermines the skill and precision provided by
The quality of the outcome is a function of the benefit the accounting profession, nor will it enable clinicians to
to be achieved and the sustainability of the benefit. The usurp the role of hospital business managers. Rather, the
 CHAPTER 2 SYSTEMS AND RESOURCES 23

aim is to provide the requisite knowledge to empower variable costs that fluctuate with patient type and number
clinicians to manage the key components of budget devel- (e.g. pharmaceuticals, meals, consumable supplies such as
opment and budget setting, and to know what questions gloves and dressings, laundry).
to ask when confronted by this most daunting responsibil- Compared with personnel costs, operational costs in
ity of managing a service budget. critical care tend to be relatively small, but they can be
managed and rationed with the help of good information
Practice tip and cooperation. For example, there is a range of dressing
materials available on the market, and a simple dressing
Nothing is so terrifying for clinicians accustomed to daily that requires less expensive materials should always be
issues of life and death as to be given responsibility for used unless a more expensive product is indicated and a
the financial affairs of their hospital division! protocol exists to inform staff of this clinical need.

Types of budget Practice tip

There are essentially three types of budget that a manager
Compared with personnel costs, operational costs
must consider: personnel, operational and capital. Within
in critical care tend to be relatively small and can be
these budget types, there are two basic cost types: fixed
managed and rationed with the help of good information
and variable. Fixed costs are those essential to the service
and cooperation.
and are relatively constant, regardless of the fluctuations in
workload or throughput (e.g. nurse unit manager salary,
security, ventilators). Variable costs change with changing Fixed costs can also be turned into variable costs and
throughput (e.g. nurse agency or consumables usage), hence encourage efficient usage. For example, pressure-
especially if used in response to influx of demand and reduction mattresses, traditionally purchased as a fixed asset
resulting consumables such as linen, dressings and drugs. with variable (and unpredictable) repair and mainten-
ance costs, can now be leased on a per-day or per-week
Personnel budget basis, with no need for storage, cleaning or maintenance
Health care is a labour-intensive service, and critical care costs. Further, critical care managers can work with other
epitomises this fact with personnel costs being the most hospital managers to create ‘purchasing power’ by cooper-
expensive component of the unit’s budget. The staffing ating to standardise the range of products used to obtain a
requirement for critical care generally follows a formula of better price for a product that will benefit all users.
x nurses per open (funded) bed. This figure is expressed in Capital budget
full-time equivalents (FTEs), i.e. the equivalent of a person
working a 40-hour week if the standard full-time working Capital budget items are generally expensive and/or
week is 40 hours. This may equate to 5 × 8-hour shifts large fixed assets that are considered long-term invest-
per week or 20 × 12-hour shifts in a 6-week period. ments, such as building extensions, renovations and large
Personnel costs include productive and non-productive equipment purchases. Capital budget items tend to be
hours. Productive hours are those utilised to provide considered as assets that are depreciated over time. Most
direct work. A manager will determine the minimum or hospitals consider these items as a global asset – that is, as
optimum number of nurses to be rostered per shift and a group of investment items and activities for the hospital
then calculate the nursing hours per day, multiplied by – rather than attributing these costs to an individual unit
the hourly rate of pay and any penalties that are to be or department.
attributed to work done during the after-business-hours To request a capital budget item, a written proposal
period. Non-productive hours include sick leave, holiday is generally required describing the item, its expected
leave, education hours, maternity leave and any other paid benefits, whether it replaces an existing item’s service or
time away from the actual job that staff are employed to do. function, the cost, possible revenue and cost-mitigating
Personnel budgets tend to be fixed costs, in that the benefits.This analysis does not always have to demonstrate
majority of staff are employed permanently, based on an a profit, although the value and benefit of the service
expected or forecast demand. Prudent managers tend would need to be established.
to employ 5–10% less than the actual forecast demand Budget process
and use casual staff to ‘flex-up’ the available FTE staff
The budget includes three fundamental steps: 1) budget
establishment in periods of increasing demand, hence
preparation and approval, 2) budget analysis and reporting
contributing a small but variable component to the
and 3) budget control and action.
personnel budget.19
Operational budget Practice tip
All other non-personnel costs (except major capital The budget includes three fundamental steps: 1) budget
equipment) tend to be allocated to the operational preparation and approval, 2) budget analysis and
budget.This includes fixed costs such as minor equipment, reporting and 3) budget control and action.
maintenance contracts, utility costs (e.g. electricity) and
24 SECTION 1 SCOPE OF CRITICAL CARE

Budget preparation and approval Developing a business case

A budget plan essentially runs in parallel with a unit The most common reason for writing a business case is
or service management plan, forecasting likely activity to justify the resources and capital expenditure to gain the
and resulting financial costs. In most circumstances the support and/or approval for a change in service provision
preceding year’s activity and costs are a good benchmark and/or purchase of a significant new piece of equipment/
on which to base the next year’s budget. However, hospital technology.This section provides an overview of a business
expectations in terms of new services, greater patient case and a format for its presentation. The business case
throughput or changes to staff salary entitlements will can be an invaluable tool in the strategic decision-making
need to be factored into the new budget. process, particularly in an environment of constrained
The budget period is generally a financial year, but resources.21
developing monthly budgets (cash flowing) to coincide A business case is a management tool that is used in
with predictable variations allows for a more realistic repre- the process of meeting the overall strategic plan of an
sentation of how costs are incurred and paid throughout the organisation. Within a setting such as health care, the
financial year period. If the budget plan is well constructed, business case is required to outline clearly the clinical need
one always hopes and expects the final budget allocation and implications to be understood by leaders. Financial
(i.e. the approved budget) to be close to achievable. imperatives, such as return on investment, must also be
defined and identified.22,23 A business case is a document
Budget analysis and reporting in which all the facts relevant to the case are documented
Most critical care managers analyse their expenditure and linked cohesively. Various templates are available (see
against budget projections on a monthly basis, to identify Online resources) to assist with the layout. Key questions
variances from planned expenditure. Information should are generally the starting point for the response to a
not merely be financial: a breakdown of the monthly business case: why, what, when, where and how, with each
and year-to-date expenditures for personnel (productive question’s response adding additional information to the
and non-productive), and operational (fixed and variable) process (Table 2.2). Business cases can vary in length from
costs, should be matched against other known measurable many pages to just a couple. Most organisations will have
indicators of activity or productivity (e.g. patient bed-days, standardised headings and formats for the presentation of
patient diagnosis types/groups and staffing hours, including these documents. If the document is lengthy inclusion of
overtime and other special payments).15 an executive summary is recommended to summarise the
One common management maxim is: if it cannot be salient points of the business case (Box 2.1).
measured, then it cannot be controlled. Clinical managers
therefore need to work closely with finance managers
Practice tip
to develop consistent data measurements and reports to
inform themselves and staff about where they should A business case is a management tool that is used in
focus their efforts to achieve the approved budget target. the process of meeting the overall strategic plan of an
organisation.
Budget control and action
When signs of poor performance or financial overrun
are evident, managers cannot merely analyse the financial
BOX 2.1
reports, hoping that things will sort themselves out. Every
variance of a sizeable amount requires an explanation. Business case: Sample headings
Some will be obvious: an outbreak of community influenza Title
among staff will increase sick leave and casual staff costs for
Purpose
a period of time. Other overruns can be insidious but no
less important: overtime payments, although sometimes Background
unavoidable, can also reflect poor time management or Key issues
a culture of some staff wanting to boost their income Cost–benefit analysis
surreptitiously.19
Recommendations
An effective method of controlling the budget is to
actively engage staff in the process of managing costs. Risk assessment
Managers can explain to staff how the budget has been
developed and how their performance against budget is In summary, the business case is an important tool
progressing, and identify areas for potential improvement. that is increasingly required at all levels of an organi-
Seeking ideas from staff on how to improve efficiency and sation to clearly define a proposed service change or
productivity and giving them some responsibility for the equipment purchase. This document should include
budget performance can encourage an esprit de corps and clear goals and outcomes, a cost–benefit analysis, quality
improvements from the whole team that a single manager and safety considerations and timelines for achievement
cannot achieve alone.20 of the solution.
 CHAPTER 2 SYSTEMS AND RESOURCES 25

TABLE 2.2
Key questions in writing a business case

QUESTION EXAMPLE

Why? Consider the background to the project, and why it is needed, including PEST (political, economic, sociological,
technological) and SWOT (strengths, weaknesses, opportunities and threats) analysis

What? Clearly identify and define the project and the purpose of the business case and outline the solution. Clearly
defined goals, outcomes and measurable benefits should be documented

What if? Make a risk assessment of the current situation, including any controls currently in place to address/mitigate the
issue, and a risk assessment following the implementation of the proposed solution

When? Determine the timelines for the implementation and achievement of the project/solution

Where? Consider the context within which the project will be undertaken, if not already included in the background material

How? Determine how much money, people and equipment, for example, will be required to achieve the benefits.
A clear cost–benefit analysis should be included in response to this question

Critical care environment process. Each bed space should be a minimum of 20–25
square metres and provide for visual privacy from casual
A critical care unit is a distinct unit within a hospital that observation. At least one hand basin per single room or per
has easy access to the emergency department, operating two beds should be provided to meet minimum infection
theatre and medical imaging. It provides care to patients control guidelines.26,27 Each bed space should have piped
with a life-threatening illness or injury and concentrates medical gases (oxygen and air), suction, adequate electrical
the clinical expertise and technological and therapeu- outlets (essential and non-essential), data points and task
tic resources required. The College of Intensive Care lighting sufficient for use during the performance of
Medicine (CICM)24 and the Intensive Care Society25 bedside procedures. Further detailed descriptions are
define three levels of intensive care to support the role available in various health department documents. 26,27
delineation of a particular hospital, dependent upon
staffing expertise, facilities and support services. Critical Equipment
care facilities vary in nature and extent between hospitals
and are dependent on the operational policies of each Since the advent of critical care units, healthcare delivery
individual facility. In smaller facilities, the broad spectrum has become increasingly dependent on medical technology
of critical care may be provided in combined units to deliver that care. Equipment can be categorised into
(intensive care, high-dependency [HDU], coronary care several funding groups: capital expenditure (generally in
unit [CCU]) to improve flexibility and aid the efficient excess of A$10,000 or £5,000), equipment expenditure
use of available resources.26 While there are no national (all equipment less than A$10,000 or £5,000) and the
guidelines for defining standards of workforce and facility disposable products and devices required to support the
expectations with respect to CCUs, some state health use of equipment. This section examines how to evaluate,
services have developed their own to try and encourage procure and maintain that equipment.
consistent standards of practice across CCUs.
Initial set-up requirements
Environmental design Critical care units require baseline equipment that allows
The functional, organisational and unit designs are the unit to deliver safe and effective patient care. The list
governed by available finances, an operational brief and of specific equipment required by each individual unit
the building and design standards of the state or country will be governed by the scope of that unit’s function. For
in which the hospital is located. A critical care unit should example, a unit that provides care to patients after neuro-
have access to minimum support facilities, which include surgery will require the ability to monitor intracranial
staff station, clean utility, dirty utility, store room(s), pressure. Table 2.3 lists the basic equipment require-
education and teaching space, staff amenities, patients’ ments for a critical care unit. Information technology and
ensuites, patients’ bathroom, linen storage, disposal room, communications options and requirements are growing
pathology area and offices. Most notably, the actual bed rapidly in health and in particular in the critical care envi-
space/care area for patients needs to be well designed.26,27 ronment. The rapid pace of innovation and change in this
The design of the patient’s bed-space has received area requires managers to think carefully when setting up
considerable attention in recent years. Most governments information technology infrastructure and to be careful
have developed minimum guidelines to assist in the design not to over capitalise on technology that might not be
26 SECTION 1 SCOPE OF CRITICAL CARE

TABLE 2.3 BOX 2.2

Basic equipment requirements Example criteria for product evaluation
MONITORING THERAPEUTIC • Safety
Monitors (including central Ventilators (invasive and • Performance
station) non-invasive) • Quality
End-tidal CO2 monitoring Infusion pumps • Use
Arterial blood gas analyser Syringe drivers
( ± electrolytes) CVVHDF
purpose
Invasive monitoring EDD-f ease of
• arterial Resuscitators • Cost–benefit analysis
• central venous pressure Temporary pacemaker
include disposables
• intracranial pressure Defibrillator
• pulse-induced contour Suctioning apparatus • Cleaning
cardiac output central sterilising supply unit
pulmonary artery
infection control
Access to image intensifier
Ultrasound • Regulatory control
Access to CT/MRI Therapeutic Goods Administration

CT = computerised tomography; CVVHDF = continuous Standards

veno-venous haemodiafiltration; EDD-f = extended daily • Adaptability to future technological advancements
dialysis filtration; MRI = magnetic resonance imaging.
• Service agreements
• Training requirements
easily upgradeable when new and more efficient or more
effective substitutes come on to the market. Envisioning Adapted from:
what might be available in the future is difficult but it is Association of Operating Room Nurses. Recommended
important to consider such matters carefully to avoid very practices for product selection in perioperative practice
expensive upgrades in the future.28 Further information settings. AORN J 2004;79:678–82, with permission.
on information and communication technology can be Elliott D, Hollins B. Product evaluation: theoretical and practical
found in Chapter 3. considerations. Aust Crit Care 1995;8(2):14–9, with permission.

Practice tip
objective criteria for the evaluation of the product should
Envisioning what might be available in the future is be determined (Box 2.2). Ideally, the committee will screen
difficult but it is important to consider such matters products and medical devices before a clinical evaluation
carefully to avoid very expensive upgrades in the future. is conducted to establish its viability, thus avoiding any
unnecessary expenditure in time and money.29
The decision to purchase or lease equipment will,
Purchasing
to some extent, be governed by the purchasing strategy
The procurement of any equipment or medical device approved by the hospital or health authority. The
requires a rigorous process of selection and evaluation. advantages of leasing equipment include the capital expen-
This process should be designed to select functional, diture being defrayed over the life of the lease (usually
reliable products that are safe, cost-effective and envi- 36 months), with ongoing servicing and product upgrades
ronmentally conscious and that promote quality of care built into the lease agreement and price structure. Any
while avoiding duplication or rapid obsolescence.29 In final presentation from the product evaluation committee
most healthcare facilities, a product evaluation committee should therefore include a recommendation to purchase
exists to support this process, but if this is not the case it is or lease, based on a cost–benefit analysis of the ongoing
strongly recommended that a multidisciplinary committee expenditure required to maintain the equipment.
be set up, particularly when considering the purchase of
equipment requiring capital expenditure.30 Replacement and maintenance
The product evaluation committee should include The process for replacement of equipment is closely aligned
members who have an interest in the equipment being with the process for the purchase of new equipment. The
considered and should comprise, for example, biomedical stimulus for the process to begin, however, can be either
engineers and representatives from the central sterile the condemning of equipment by biomedical engineers or
supply unit administration, infection control, end users the planned replacement of equipment nearing the end of
and other departments that may have similar needs. Once its life cycle. In general, most capital equipment is deemed
a product evaluation committee has been established, clear, to have a life cycle of 5 years. This time frame takes into
 CHAPTER 2 SYSTEMS AND RESOURCES 27

account both the longevity of the physical equipment and nursing manager (nursing unit manager/nurse practice
its technology. coordinator/clinical nurse manager, or equivalent title) is
Ongoing maintenance of equipment is an important required for each unit to direct and guide clinical practice.
part of facilitating safety in the unit. Maintenance may The nurse manager must possess a post-registration qual-
be provided in-house by individual facility biomedical ification in critical care or in the clinical specialty of the
departments or as part of a service contract arrange- unit.24,25,32–34 A clinical nurse educator (CNE) should
ment with the vendor company. The provision of a be available in each unit. The ACCCN recommends a
maintenance/service plan should be clearly identified minimum ratio of one full-time equivalent (FTE) CNE
during the procurement phase of the equipment’s for every 50 nurses on the roster, to provide unit-based
purchase process. Although equipment maintenance is education and staff development.32 Registered nurses
not the direct responsibility of the nurses in charge of within the unit are generally nurses with formal critical
the unit, they should be aware of the scheduled main- care postgraduate qualifications and varying levels of
tenance plan for all equipment and ensure that timely critical care experience. Although no specific staffing
maintenance is undertaken. references are made for CCUs it is recommended they
Routine ongoing care of equipment is outlined in the align to the standards established in other critical care areas
product information and user manuals that accompany until such time as specific CCU staffing guidelines have
devices. This documentation clearly outlines routine care been developed in Australia.
required for cleaning, storage and maintenance. All staff In many developed economies, specialist critical care
involved in the maintenance of clinical equipment should nurse education has moved into the tertiary education
be trained and competent to carry it out. As specialist sector. Prior to this, and still in many other countries, critical
equipment is a fundamental element of critical care, care education has taken the form of hospital-based certifi-
effective resourcing includes consideration of the purchase, cates.35 Since this move, postgraduate, university-based
set-up, maintenance and replacement of equipment. programs at the graduate certificate or postgraduate
Equipment is therefore an important aspect of the budget diploma level are now available, although some hospital-
process. based courses that articulate to formal university programs
may also be accessible. Some critical care nursing organisa-
Practice tip tions have developed position statements on the provision
of critical care nursing education.36–38 Various support staff
The provision of a maintenance/service plan should be are also required to ensure the efficient functioning of the
clearly identified during the procurement phase of the department, including, but not limited to, administrative/
equipment’s purchase process. clerical staff, domestic/ward assistant staff and biomedical
engineering staff.
Staff Staffing levels
Staffing critical care units is an important human resource A staff establishment refers to the number of nurses
consideration. The focus of this section is on nursing required to provide safe, efficient, quality care to patients.
staff, although the important role that medical staff and Staffing levels are influenced by many factors, including
other ancillary health personnel provide is acknowledged. the economic, political and individual characteristics of
Nurses’ salaries consume a considerable portion of any the unit in question. Other factors, such as the population
unit budget and, owing to the constant presence of nurses served, the services provided by the hospital and by its
at the bedside, appropriate staffing plays a significant role neighbouring hospitals and the subspecialties of medical
in the quality and safety of care delivered. Nurse staffing staff working at each hospital also influence staffing.
levels influence patient outcomes both directly, through Specific issues to be considered include nurse-to-patient
the initiation of appropriate nursing care strategies, and ratios, nursing competencies and skill mix.
indirectly, by mediating and implementing the care The starting point for most units in the establishment
strategies of other members of the multidisciplinary of minimum, or base, staffing levels is the patient census
healthcare team.31 Therefore, ensuring an appropriate approach. This approach uses the number and classifica-
skill mix is an important aspect of unit management. tion (ICU, HDU or CCU) of patients within the unit to
This section considers how appropriate staffing levels are determine the number of nurses required to be rostered
determined and the factors, such as nurse-to-patient ratios on duty on any given shift. In many countries a registered
and skill mix, which influence them. nurse-to-patient ratio of 1:1 for ICU patients and 1:2 for
high-dependency unit (HDU) patients has been accepted
Staffing roles for many years.32–34 Other countries, such as the USA, have
There are a number of different nursing roles in the lower nurse staffing levels, but in those countries nursing
ICU nursing team, and various guidelines determine the staff is augmented by other types of clinical or support
requirements of these roles. Various critical care nursing staff, such as dialysis and respiratory technicians.39 The
organisations have position statements surrounding the limitations of this staffing approach are discussed later in
critical care workforce and staffing.32–34 A designated this chapter. Once the base staffing numbers per shift have
28 SECTION 1 SCOPE OF CRITICAL CARE

been established, the unit manager is required to calculate to note that nurse-to-patient ratios may be provided
the number of FTEs that are required to implement the merely as a guide to staffing levels, and implementation
roster. One FTE is equivalent to the number of hours should depend on patient acuity, local knowledge and
worked in one week by a full-time employee. expertise.
The development of the nursing establishment is Australia and New Zealand have several documents that
dependent on many factors. Historical data from previous guide nurse-to-patient ratios (Table 2.4). The WFCCN
years of patient throughput and patient acuity assist in the states that critically ill patients require one registered nurse
determination of future requirements. It is often helpful to be allocated at all times.34 The College of Intensive
for new units to contact a unit of similar size and service Care Medicine and Intensive Care Society in the United
profile to ascertain their experiences. Kingdom also identified the need for a minimum nurse-
to-patient ratio of 1:1 for intensive care patients and 1:2
Nurse-to-patient ratios for high-dependency patients.24,25
Nurse-to-patient ratios refer to the number of nursing
hours required to care for a patient with a particular set
of needs. In ICUs identified as combined units incorpo- Practice tip
rating intensive care, coronary care and high-dependency
The WFCCN states that critically ill patients require one
patients,40 different nurse-to-patient ratios are required
registered nurse to be allocated at all times.
for these often diverse groups of patients. It is important

TABLE 2.4
Documents that guide the nurse-to-patient ratios in critical care

DOCUMENT R E C O M M E N D AT I O N S

ACCCN: Position statement on • ICU patients (clinically determined) should have a 1:1 nurse-to-patient ratio
intensive care nurse staffing32 • HDU patients (clinically determined) should have a 1:2 nurse-to-patient ratio
ACCCN: Position statement on the • All intensive care patients must have a registered nurse (division 1) allocated
healthcare workers other than division 1 exclusively to their care
registered nurses in intensive care58 • High-dependency or step-down patients (in intensive care) who require a nurse-to-
patient ratio of 1:2 should have a registered nurse (division 1) allocated exclusively to
their care
• Enrolled nurses (division 2) and unlicensed assistive personnel may be allocated roles
to assist the registered nurse, but any activities that involve direct contact with the
patient must always be performed in the immediate presence of the registered nurse
(division 1)
New Zealand Nursing Organisation, • The critically ill and/or ventilated patient will require a minimum 1:1 nurse-to-patient
Critical Care Section: Philosophy and ratio
Standards for Nursing Practice in • At times, patients in the critical care unit may have higher or lower nursing acuity; the
Critical Care41 critical care nurse in charge of the shift determines any variation from the 1:1 ratio,
taking into account context, skill mix and complexity
WFCCN: Declaration of Buenos Aires, • Critically ill patients (clinically determined) require one registered nurse at all times
Position Statement on the Provision of • High-dependency patients (clinically determined) in a critical care unit require no less
Critical Care Nursing Workforce34 than one nurse for two patients at all times
College of Intensive Care Medicine • A minimum of 1:1 nursing is required for ventilated and other similarly critically ill
(CICM): Minimum Standards for patients, and nursing staff must be available to greater than a 1:1 ratio for patients
Intensive Care Units24 requiring complex management (e.g. ventricular assist device)
• The majority of nursing staff should have a post-registration qualification in intensive
care or in the specialty of the unit
• All nursing staff in the unit responsible for direct patient care should be registered
nurses
College of Intensive Care Medicine • The ratio of nursing staff to patients should be 1:2
(CICM): Recommendations on • All nursing staff in the HDU responsible for direct patient care should be registered
Standards for High-Dependency Units nurses, and the majority of all senior nurses should have a post-registration
Seeking Accreditation for Training in qualification in intensive care or high-dependency nursing
Intensive Care Medicine102 • A minimum of two registered nurses should be present in the unit at all times when a
patient is present

ACCCN = Australian College of Critical Care Nurses; WFCCN = World Federation of Critical Care Nurses.
 CHAPTER 2 SYSTEMS AND RESOURCES 29

The ACCCN,32 British Association of Critical Care Patient dependency

Nurses33 and the Critical Care Nurses Section – New
Patient dependency refers to an approach to quantify the
Zealand Nurses Organisation41,42 have outlined the appro- care needs of individual patients, so as to match these
priate nurse staffing standards for ICUs within the context needs to the nursing staff workload and skill mix.43 For
of accepted minimum national standards and evidence that many years, patient census was the commonest method for
supports best practice. The WFCCN statement identifies determining the nursing workload within an ICU. That
key principles to meet the expected standards of critical is, the number of patients dictated the number of nurses
care nursing (Table 2.5). required to care for them, based on the accepted nurse-
These recommendations serve merely to guide nurse- to-patient ratios of 1:1 for ICU patients and 1:2 for HDU
to-patient ratios, as extraneous factors such as the clinical patients. This reflects the unit-based workload, and is also
practice setting, patient acuity and the knowledge and the common funding approach for ICU bed-day costs.
expertise of available staff will influence final staffing The nursing workload at the individual patient level,
patterns that may be adapted to suit the requirements however, is also reflective of patient acuity, the complexity
of individual countries or units. In particular, patient of care required and both the physical and the psycho-
dependency scoring tools are designed to guide these logical status of the patient.43 Strict adherence to the
staffing decisions and are discussed below. patient census model leads to the inflexibility of matching

TABLE 2.5
Ten key points of intensive care nursing staffing

POINT DESCRIPTION

1 ICU patients (clinically determined) Require a standard nurse-to-patient ratio of at least 1:1

2 High-dependency patients (clinically determined) Require a standard nurse-to-patient ratio of at least 1:2

3 Clinical coordinator (team leader) There must be a designated critical-care-qualified senior nurse per shift
who is supernumerary and whose primary role is responsibility for the
logistical management of patients, staff, service provision and resource
utilisation during a shift

4 ACCESS nurses These are nurses in addition to the bedside nurses, clinical coordinator, unit
manager, educators and non-nursing support staff. They provide Assistance,
Coordination, Contingency, Education, Supervision and Support

5 Nursing manager At least one designated nursing manager (NUM/CNC/NPC/CNM or

equivalent) who is formally recognised as the unit nurse leader is required
per ICU

6 Clinical nurse educator At least one designated CNE should be available in each unit. The
recommended ratio is one FTE CNE for every 50 nurses on the ICU roster

7 Clinical nurse consultants Provide global critical care resources, education and leadership to specific
units, to hospital and area-wide services and to the tertiary education sector

8 Critical care nurses The ACCCN recommends an optimum specialty qualified critical care
nurse proportion of 75%

9 Resources These are allocated to support nursing time and costs associated with
quality assurance activities, nursing and multidisciplinary research, and
conference attendance

10 Support staff ICUs are provided with adequate administrative staff, ward assistants,
manual handling assistance/equipment, cleaning and other support staff to
ensure that such tasks are not the responsibility of nursing personnel

ACCCN = Australian College of Critical Care Nurses; CNC = clinical nurse consultant; CNE = clinical nurse educator; CNM = clinical
nurse manager; FTE = full-time equivalent; NPC = nurse practice coordinator; NUM = nursing unit manager.
Adapted from Australian College of Critical Care Nurses. ICU Staffing Position Statement (2003) on Intensive Care Nursing Staffing.
Melbourne: ACCCN, <http://www.acccn.com.au/documents/item/20>; 2003 [accessed 29.07.14], with permission.
30 SECTION 1 SCOPE OF CRITICAL CARE

nursing resources to demand. For example, some ICU this debate has been undertaken in the general ward
patients receive care that is so complex that more than setting, and still predominantly in the USA. However,
one nurse is required, and an HDU patient may require it has provided the starting point for specialty fields of
less medical care than an ICU patient, but conversely may nursing to begin to examine this issue. The use of nurses
require more than 1:2 nursing care level secondary to such other than registered nurses in the critical care setting has
factors as physical care requirements, patient confusion, been discussed as one potential solution to the current
anxiety, pain or hallucinations.43 A patient census approach critical care nursing shortage.52
therefore does not allow for the varying nursing hours Published research on skill mix has examined the
required for individual patients over a shift, nor does it substitution of one grade of staff with a lesser skilled,
allow for unpredicted peaks and troughs in activity, such trained or experienced grade of staff and has utilised
as multiple admissions or multiple discharges. adverse events as the outcome measure. A significant
There are many varied patient dependency/classi- proportion of research suggests that a rich registered nurse
fication tools available, with their prime purpose being skill mix reduces the occurrence of adverse events.48,53,54
to classify patients into groups requiring similar nursing A comprehensive review of hospital nurse staffing and
care and to attribute a numerical score that indicates the patient outcomes noted that existing research findings
amount of nursing care required. Patients may also be with regard to staffing levels and patient outcomes
classified according to the severity of their illness.The ther- should be used to better understand the effects of skill
apeutic intervention scoring system (TISS) was developed mix dilution, and justify the need for greater numbers of
to determine severity of illness, to establish nurse-to- skilled professionals at the bedside.55
patient ratios and to assess current bed utilisation.44 This While there has not been a formal examination of
system attributes a score to each procedure/interven- skill mix in the critical care setting in Australia and New
tion performed on a patient, with the premise that the Zealand, two older publications56,57 informing this debate
greater the number of procedures performed, the higher emerged from the Australian Incident Monitoring Study –
the score, the higher the severity of illness, the higher the ICU (AIMS–ICU). Of note, 81% of the reported adverse
intensity of nursing care required.43 Since its development events resulted from inappropriate numbers of nursing
in the mid-1970s, TISS has undergone multiple revisions, staff or inappropriate skill mix.56 Furthermore, nursing
but this scoring system, like the Acute Physiologic and care without expertise could be considered a potentially
Chronic Health Evaluation (APACHE)45 and Simplified harmful intrusion for the patient, as the rate of errors by
Acute Physiology Score (SAPS),46 still captures the thera- experienced critical care nurses was likely to rise during
peutic requirements of the patient. It does not, however, periods of staffing shortages, when inexperienced nurses
capture the entirety of the nursing role. Therefore, while required supervision and assistance.31,56 These important
these scoring systems may provide valuable information findings provide some insight into the issues surrounding
on the acuity of the patients within the ICU, it must be skill mix.
remembered that they are not accurate indicators of total Professional organisations have developed position
nursing workload. Other specific nursing measures have statements on the use of staff other than registered nurses in
been developed, but have not gained universal clinical the critical care environment.32,58 The British Association
acceptance or application. of Critical Care Nurses asserts that healthcare assistants
employed in a critical care setting must undertake only
Skill mix direct patient care activities for which they have received
Skill mix refers to the ratio of caregivers with varying training and for which they have been assessed competent
levels of skill, training and experience in a clinical unit. under the supervision of a registered nurse.33
In critical care, skill mix also refers to the proportion of Staffing levels and skill mix within critical care
registered nurses possessing a formal specialist critical care units should therefore be based on individual unit
qualification. The ACCCN recommends an optimum needs (e.g. unit size and location) and patient clinical
qualified critical care nurse to unqualified critical care presentations/acuity, and be guided by the best available
nurse ratio of 75%.32 In Australia and New Zealand, evidence to ensure safe, quality care for their patients
approximately 50% of the nurses employed in critical within the context of national standards, expectations
care units currently have some form of critical care and resources.
qualification.40 Rostering
Once the nursing establishment for a unit is determined
Practice tip
and skill mix considered, the rostering format is decided.
The ACCCN recommends an optimum qualified critical In times of nursing shortages, one of the factors identified
care nurse to unqualified critical care nurse ratio of 75%. as affecting the retention of staff is the ability to provide
flexibility in rostering practices. To some extent, rostering
Debate continues in an attempt to determine the practices are governed by government, hospital and
optimum skill mix required to provide safe, effective industrial policies and these should be considered when
nursing care to patients.47–51 Much of the research fuelling deciding the roster format for individual units.
 CHAPTER 2 SYSTEMS AND RESOURCES 31

The traditional shift patterns are based on 3 × 8-hour as well, generally at a fairly basic level of knowledge and
shifts per day (Figure 2.1). With the increased demand skills, which play a role in providing an introduction for a
for flexible rosters has come the introduction of novice practitioner.36 Position statements on the prepara-
additional shift lengths, most notably the 12-hour shift. tion and education of critical care nurses are available36,37,60
The implementation of a 12-hour roster requires careful that present frameworks to ensure that the curricula of
consideration of its risks and benefits, with full consul- courses provide adequate content to prepare nurses for
tation of all parties, unit staff, hospital management and this specialist nursing role.
the relevant nurses’ union. Perceived benefits of working Nursing has always been a profession that has required
a 12-hour roster include improvement in personal/social currency of knowledge and clinical skills through
life, enhanced work satisfaction and improved patient care continuing education input, because of the rapidly
continuity. Perceived risks, such as an alteration in the level changing knowledge base and innovative treatment
of sick-leave hours, decreased reaction times and reduced regimens. These changes are occurring at an increasingly
alertness during the longer shift, have not been found to rapid rate, particularly in critical care.The need for critical
be significant.59 A reported disadvantage of 12-hour shifts care nurses to maintain current, up-to-date knowledge
is the loss of the shift overlap time, which has tradition- across a broad range of clinical states has therefore
ally been used for providing in-unit educational sessions. never been more important. Specific issues related to
A consideration, therefore, for units proposing the imple- orientation and continuing education programs are briefly
mentation of a 12-hour shift pattern is to build formal discussed below.
staff education sessions into the proposal.
Orientation
Education and training The term orientation reflects a range of activities, from
During the latter half of the 20th century specialist a comprehensive unit-based program, attendance at a
critical care nursing education made the transition from hospital induction program covering the mandatory
hospital-based courses in to the tertiary education sector. educational requirements of that facility, through to famil-
Although some hospitals maintain in-house critical care iarisation with the layout of a department. The aim of
courses, these are generally designed to meet the tertiary an orientation program is the development of safe and
requirements of postgraduate education and to articulate effective practitioners.61
with higher level university programs. Unit-specific orientation should be a formal, structured
Some organisations, both private and public, continue program of assessment, demonstration of competence and
to offer a variety of short continuing education courses identification of ongoing educational needs, and should

FIGURE 2.1 Calculating staff requirements.

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32 SECTION 1 SCOPE OF CRITICAL CARE

be developed to meet the needs of all staff who are new drugs in ICUs.69 In this study 1328 patients in 113 ICUs
to the unit. Competency-based orientation is learner- worldwide were studied for 24 hours; 861 errors affecting
focused and based on the achievement of core skills that 441 patients occurred, or 74.5 parenteral drug administra-
reflect unit needs and enable new employees to function tion errors per 100 patient days. The authors concluded
in their role at the completion of the orientation period.62 that organisational factors such as error reporting systems
A number of countries have developed core competency and routine checks can reduce the risk of such errors.69
standards for specialist critical care nurses42,63,64 that may be What is more alarming is that many health practitioners
used as a framework on which to build competency-based do not acknowledge their own vulnerability to error. One
orientation programs. study asked airline flight crews (30,000) and health profes-
sionals (1033 ICU/operating room doctors and nurses, of
Practice tip whom 446 were nurses) from five different countries a
simple question, ‘Does fatigue affect your (work) perfor-
Unit-specific orientation should be a formal, structured
mance?’, with fascinating results.70 Of those responding,
program of assessment, demonstration of competence
the following replied in the affirmative to the question:
and identification of ongoing educational needs, and
pilots and flight crew, 74%; anaesthetists, 53%; surgeons,
should be developed to meet the needs of all staff who
30% (a figure for nurses’ responses to this question was not
are new to the unit.
provided in the study).The study also found that only 33%
of hospital staff thought errors were handled appropriately
Continuing education in their hospital and that over 50% of ICU staff found it
In 2003, both the Royal College of Nursing Australia and hard to discuss errors.70 Chapter 3 provides more informa-
the College of Nursing implemented systems of formally tion in this area including a description of non-technical
recognising professional development, with the awarding of skills and how training can help make critical care units
continuing education points. While professional develop- safer for patients and staff, as well as key governance and
ment has always been a requirement of continuing practice, management responsibilities in all aspects of the health
this process is becoming more formalised. On 1 July 2010 system.
the Australian Health Practitioner Regulation Agency
came into being as a national health practitioner body. Practice tip
With this, a formal requirement for continuing education
or professional development was mandated. The Nursing It is alarming that many health practitioners do not
and Midwifery Board of Australia, a subgroup of the acknowledge their own vulnerability to error.
above agency, clearly identifies the standard for continuing
professional development of nurses and midwives.65 In Managerial activities that affect quality, safety and risk
New Zealand there is an expectation that a minimum of performance have also been systematically reviewed high-
60 hours professional development and 450 hours of lighting the need to establish goals and strategy to improve
clinical practice will be undertaken over a three-year period care, setting the quality agenda, engaging in quality,
for the purposes of registration renewal.66 Conversely, North promoting a quality improvement culture, managing
American nursing associations have for many years had resisters and procurement of organisational resources
formal programs for recognising continuing education and for quality.71 In addition, such activities advocate for
awarding continuing education points. These continuing positive actions such as establishment of a Board quality
education points have often been required to support committee, with a specific item on quality at the Board
continued registration. This concept has subsequently been meeting, a quality performance measurement report and
implemented in the UK and Europe.67 a dashboard with national quality and safety benchmarks,
performance evaluation attached to quality and safety and
an infrastructure for staff–manager interactions on quality
Risk management strategies.71 Such activities are equally pertinent at the
Managing risk is a high priority in health, and critical ICU management level.
care is an important risk-laden environment in which the Governance and management of the critical care
manager needs to be on the lookout for potential error, environment require a multidisciplinary team of senior
harm and medico-legal vulnerability. The Sentinel Events clinician managers who understand both the clinical risks
Evaluation study68 has given an indication of this risk and the quality cycles of the environment as well as the
for critical care patients. It was a 24-hour observational executive requirements for financial and organisational
study of 1913 patients in 205 ICUs worldwide, which viability. An astute and careful balance between good
identified 584 errors causing harm or potential harm to clinical governance (patient care and clinician practices)
391 patients.The Sentinel Events Evaluation study authors and good corporate governance (hotel, finance, IT and
concluded there was an urgent need for development and other support services) is required to ensure sustainable
implementation of strategies for prevention and early and appropriate health care for all users. The take-home
detection of errors.68 A second study by the same team message in all this is that managers in hospitals manage
specifically targeted errors in administration of parenteral enormous risks with patients, staff and visitors but often
 CHAPTER 2 SYSTEMS AND RESOURCES 33

do not appreciate their own level of vulnerability to error

BOX 2.3
and risk. Yet claims of negligence and charges of incom-
petence can be as threatening to the manager as they are Sample headings to define a policy
to the clinician. • Policy
Negligence • Rationale
Negligence is a legal term that can be proven only in a • Procedure
court. In tort law four aspects to the charge of negligence • Statistical reports (e.g. to measure compliance with
were generally accepted: or outcome of policy)
1 The provider owed a duty of care to the recipient. • Other information
2 The provider failed to meet that duty, resulting in a • Contact person
breach of care. • References
3 The recipient sustained damages (loss) as a result. • Filing instructions
4 The breach by the provider caused the recipient to • Date of issue
suffer reasonably foreseeable damages.72 • Date for review
Since the introduction of civil liability legislation in • Signature and designation of authorising officer
most states and territories of Australia, courts use a multi-
factorial assessment of all the facts to determine the level
of liability or otherwise of the defendant. In relation to medical and nursing leadership, effective communication
and coordination and open and collaborative problem
defences, while on the surface the legislation appears
solving and conflict management. One cannot under-
to place limits on the liability of health professionals, in
estimate the value of strong, dedicated and collaborative
practice it appears to have not made much difference to
leadership from managers as the key to organisational
the outcome of whether there is a negligence action. The
success in the critical care setting. These factors are as
greatest impact has been on the quantum of damages.
pertinent now as they were when first studied over
Therefore, the result is that health professionals are held
30 years ago and remind us of the important role of
liable for negligence but the damages are reduced because
leadership in ensuring the safety of patients, visitors and
of statutory limits like thresholds and caps.73
staff alike in this complex health setting.76,77 Chapter 1
Critical to reducing liability in this area is the need
contains a discussion about leadership.
for health services and managers to have in place current
policies, procedures and supervision processes to ensure Managing injury: Staff, patient or visitor
contemporary and safe practices among its workforce. When staff members are injured, the response must be swift
and deliberate. Injury can come in many forms, involving
The role of leadership and management physical injuries or biological exposures, for example. More
Managers must also be leaders, and the need to have often, the problems are grievances, such as missing out on
good leaders and managers is as relevant to critical care an opportunity afforded to others (e.g. a promotion), feeling
as it is to any other business or clinical entity. Seminal marginalised by others or not getting a preferred roster.
research studies on organisational structures in ICUs For patients, an injury can be physical, such as a drug
across the USA in the 1980s74 and 1990s75 demonstrated error or an iatrogenic infection; however, the injury can
the important role leadership plays in patient care and also be non-physical and can affect patients, visitors and
risk management in the ICU. Using APACHE scoring, staff members, as with complaints about lack of timely
organisational efficiency and risk-adjusted survival were information, misinformation or rudeness of staff. In all
measured. High-performing ICUs demonstrated that circumstances a manager needs to intervene proactively
actual survival rates exceeded predicted survival rates.74,75 to minimise or contain the negativity or harm felt by
Further investigation and analysis of the higher- the ‘victim’. Regardless of the cause of the injury, the
performing units noted that these units had well-defined principles governing good risk management are common
protocols, a medical director to coordinate activities, to many situations and are summarised in Box 2.4.
well-educated nurses and collaboration between nurses If an incident does occur, it is always prudent to
and doctors.74,75 Clear and accessible policies and document the event as soon as possible afterwards and
procedures to guide staff practice in the ICU setting were when it is safe to do so. The clinician who discovers and
also highlighted. These policies and procedures need to follows up an incident must document the event, asking
be in written form, simple to read and in a consistent the questions that a manager, family member, police
format, evidence-based, easy to understand and easy to officer, lawyer or judge might wish to ask. The written
apply. Box 2.3 shows a possible format for clinical policies account provided soon after the event or incident by a
and protocols. person closely involved in or witness to it will form a
The latter study by Zimmerman et al75 showed similar very important testimonial in any subsequent investiga-
characteristics: they had a patient-centred culture, strong tion. Key points to document are identified in Table 2.6.
34 SECTION 1 SCOPE OF CRITICAL CARE

Contemporary wisdom in modern health agencies

BOX 2.4
advocates open disclosure: telling the truth to the patient or
Defensive principles to minimise risk after an family about why and how an adverse event has occurred.78,79
incident (patient or staff) This practice may be contrary to informed legal advice and
• Those persons encouraged to participate in may not preclude legal action against the staff or institu-
decision making are more inclined to ‘own’ the tion.80–82 However, openly informing the patient/family of
decisions made; therefore, involve them in deciding what has occurred can regain trust and respect, and may
how the issue is to be tackled and help to make the help to resolve anger and frustration. The open disclosure
expectations realistic. process can also provide learning and education on how
• Education of the person in the various aspects of such events can be prevented in the future, a right for which
the incident/activity will reduce fear and anxiety. many consumer advocates are now lobbying.83
The process of root cause analysis can also assist the
• Explain the range of possible outcomes and where the
team to explore in detail the sequence of events and
affected person is currently situated on that continuum.
system failures that precipitated an incident and help
• Provide frequent and accurate updates on the to inform future system reforms to minimise harm. An
person’s situation and what is being done to root cause analysis is a generic method of ‘drilling down’
improve that situation. to identify hospital system deficiencies that may not
• Maintain a consistent approach and as far as immediately be apparent, and that may have contributed
possible the same person should provide such to the occurrence of a ‘sentinel event’. The general char-
information/feedback. acteristics of an root cause analysis are that it:84

Adapted from Williams G. Quality management in intensive

• focuses on systems and processes, not individual
performance
care. In: Gullo A, ed. Anesthesia, pain, intensive care and
emergency medicine. Berlin: Springer-Verlag; 2003: pp. 1239–50, • includes a review of the relevant literature
with permission.
• examines the event extensively for underlying
contributing causes
Practice tip • enables procedure and system modifications.
Despite more than two decades of human error studies
If an incident does occur, it is always prudent to in health and critical care specifically, the incidence of
document the event as soon as possible afterwards error, omission and patient harm does not appear to be
and when it is safe to do so. improving at the rate hoped.68,69

TABLE 2.6
Key points when documenting an incident in a patient’s file notes

QUESTION E X P L A N AT I O N

Where did the incident occur? For example, bedside, toilet, drug room

Were there any pre-event circumstances of significance? For example, short-staffed, no written protocol

Who witnessed the event? Including staff, patient, visitors

What was done to minimise negative effects? For example, extra staff brought to assist, slip wiped up, sign
placed on front of patient chart warning of reaction/sensitivity etc

Who in authority was notified of the incident? Involving a senior, experienced manager/authority should help
expedite immediate and effective action

Who informed the victim of the event? What was the Clear, concise and non-judgemental explanations to the victim or
victim told? What was the response? representative are necessary as soon as possible, preferably from a
credible authority (manager/director)

What follow-up support, counselling and revision occurred? This is important for both victim and perpetrator; ascertain when
counselling occurred and who provided it

What review systems were commenced to limit recurrence Magistrates and coroners in particular want to know what system
of the event? changes have occurred to limit the recurrence of the event

Adapted from Williams G. Quality management in intensive care. In: Gullo A, ed. Anesthesia, pain, intensive care and emergency
medicine. Berlin: Springer-Verlag; 2003: pp. 1239–50, with permission.
 CHAPTER 2 SYSTEMS AND RESOURCES 35

Measures of nursing workload procedures, infusions and medications and cardiopulmo-

nary support. Points assigned to specific interventions
or activity ranged from 1 to 4 for a 24-hour period. A higher score
signified a greater therapeutic effort. Several revisions and
Several workload measures have been developed in variants of TISS have been developed in Europe, including
an attempt to capture the complexity and diversity of TISS-2844 and the nine equivalents of nursing manpower
critical care nursing practice (see Table 2.7 for common use score (NEMS).90
instruments).44,85,86 Some hospitals use an electronic care TISS-28 was refined to be a more user-friendly
plan with activity timings to calculate nursing time and instrument, with similar precision to measure nursing
workload. An Australian instrument, the critical care workload, staffing requirements and costing, and to differ-
patient dependency tool,87 was developed to measure entiate between ICU and HDU patients.87 This simplified
nursing costs in the ICU and is still used in some units version of 28 items is divided into basic activities
to document workload,88 although no further validation (including monitoring and medications), ventilatory
studies have been published since the original research support, cardiovascular support, renal support, neurolog-
in 1993. The most common instruments used in clinical ical support, metabolic support and specific interventions.
practice and research are variants of the TISS and the The score range is from 1 to 8 for each activity, with an
Nursing Activities Score (NAS) (see Tables 2.7 and 2.8). ICU-type patient expected to score over 40 points. It was
The TISS was initially developed to measure severity estimated that a critical care nurse was able to provide
of illness and related therapeutic activities, but has been 46 TISS-28 points per shift, with a score <10 signifying
widely used as a proxy measure of nursing workload in a ward patient, 10–19 an HDU-type patient and >20
the ICU. One of the primary uses was to aid quantitative an HDU/ICU level.44 Most studies report mean daily
comparison between patients in order to allocate resources, TISS scores from 21 (±12)91 to 36 (range 29–49).92 Such
with ongoing daily measurements giving an indication of diversity in scores reflects a range in acuity of patients.
patients’ progress.89 The original TISS had a number of TISS was not, however, developed as a predictive tool
areas for scoring, including patient care and monitoring, – rather as a record of the level of nursing intervention

TABLE 2.7
Common ICU nursing workload instruments

INSTRUMENT COMPONENTS S C O R I N G / I N T E R P R E TAT I O N

TISS 1983103 (USA) 5788/7684 nursing activities related to therapeutic Most ICU patients: 10–60 points
interventions; 0–4 points per variable Acuity: class IV (≥40 points); III (20–39); II (10–19);
I (<10)
Intensive Care Society 4 levels of care, with qualitative assessment of 0 = routine ward care
2013 (UK) organ systems 1 = ward care supported by critical care team
2 = support and monitoring of single organ
dysfunction/failure
3 = complex support and monitoring of multiple
organ dysfunction/failure
TISS-28 199644 28 in 7 categories; points vary per item (0–8) 46 points = 1:1 nursing/shift
(Europe) 23 points = HDU patient (1:2 staff-to-patient ratio)
NEMS 199786 9 categories with varied points per item (3–12): Equivalent scores to TISS-28; lack of
(Europe) basic monitoring, intravenous medication, discrimination limits use in predicting or
mechanical ventilation, supplementary ventilatory calculating workload at the individual patient level
care, single/multiple vasoactive medications,
dialysis, interventions in/outside ICU
Critical Care Patient 7 categories scored 1–4 points: (a) hygiene, 4 levels of nursing time per shift:
Dependency Tool 199687 mobility, wound care; (b) fluid therapy, intake A = ≤10 points = <8 hours
(Australia) and output, elimination; (c) drugs, nutrition; B = 11–15 points = 8 hours (1:1 ratio)
(d) respiratory care; (e) observations, monitoring, C = 16–21 points = 9–16 hours
emergency treatment; (f) mental health care, D = >22 points = >16 hours (2:1 ratio)
support; (g) admission, discharge, escort
NAS 200385 (Europe/ 23 items (5 with sub-items); varied points per item Measures calculated percentage of nursing
multinational validation) (1.3–32) (see Table 2.8 for details) time (in 24 hours) on patient-level activities;
100% = 1 nurse per shift
36 SECTION 1 SCOPE OF CRITICAL CARE

TABLE 2.8
Nursing Activities Scale

NURSING ACTIVITIES SCORE POINTS

NURSING ACTIVITIES

1 Monitoring and titration

a Hourly vital signs, regular registration and calculation of fluid balance 4.5
b Present at bedside and continuous observation or active for ≥2 h in a shift, for reasons of safety,
severity, or therapy (e.g. non-invasive mechanical ventilation, weaning procedures, restlessness,
mental disorientation, prone position, donation preparation and administration of fluids or
medication, assisting specific procedure) 12.1
c Present at bedside and active for 4 h or more in any shift for reasons of safety, severity, or therapy
(see 1b) 19.6
2 Laboratory, biomedical and microbiological investigations 4.3
3 Medication, vasoactive drugs excluded 5.6
4 Hygiene procedures
a Performing hygiene procedures such as dressing of wounds and intravascular catheters,
changing linen, washing patient, incontinence, vomiting, burns, leaking wounds, complex surgical
dressing with irrigation or special procedures (e.g. barrier nursing, cross-infection-related,
room cleaning after infections, staff hygiene) 4.1
b Performance of hygiene procedures took >2 h in any shift 16.5
c Performance of hygiene procedures took >4 h in any shift 20.0
5 Care of drains, all (except gastric tube) 1.8
6 Mobilisation and positioning, including procedures such as turning the patient, mobilisation of the
patient, moving from bed to a chair and team lifting (e.g. immobile patient, traction, prone position)
a Performing procedure(s) up to 3 times per 24 h 5.5
b Performing procedure(s) more frequently than 3 times per 24 h, or with two nurses 12.4
c Performing procedure with three or more nurses, any frequency 17.0
7 Support and care of relatives and patient, including procedures such as telephone calls, interviews,
counselling; often the support and care of either relatives or patient allows staff to continue with other
nursing activities
a Support and care of either relatives or patient requiring full dedication for about 1 h in any shift such
as to explain clinical condition, dealing with pain and distress and difficult family circumstances 4.0
b Support and care of either relatives or patient requiring full dedication for 3 h or more in any shift,
such as death, demanding circumstances (e.g. large number of relatives, language problems,
hostile relatives) 32.0
8 Administration and managerial tasks
a Performing routine tasks such as: processing of clinical data, ordering examinations, professional
exchange of information (e.g. ward rounds) 4.2
b Performing administrative and managerial tasks requiring full dedication for about 2 h in any shift
such as research activities, protocols in use, admission and discharge procedures 23.2
c Performing administrative and managerial tasks requiring full dedication for about 4 h or more of the
time in any shift such as a death and organ donation procedures, coordination with other disciplines 30.0

V E N T I L AT O RY S U P P O R T

9 Respiratory support: any form of mechanical ventilation/assisted ventilation with or without PEEP,
spontaneous breathing with or without PEEP, with or without endotracheal tube supplementary oxygen
by any method 1.4
10 Care of artificial airways: endotracheal or tracheostomy cannula 1.8
11 Treatment for improving lung function: thorax physiotherapy, incentive spirometry, inhalation therapy,
intratracheal suctioning 4.4

C A R D I O VA S C U L A R S U P P O R T

12 Vasoactive medication, disregard type and dose 1.2

13 Intravenous replacement of large fluid losses, fluid administration >83 L/m/day 2.5
14 Left atrium monitoring: pulmonary artery catheter with or without cardiac output 1.7
15 Cardiopulmonary resuscitation after arrest, in past period of 24 h 7.1
 CHAPTER 2 SYSTEMS AND RESOURCES 37

NURSING ACTIVITIES SCORE POINTS

RENAL SUPPORT

16 Haemofiltration techniques, dialysis techniques 7.7

17 Quantitative urine output measurement (e.g. by indwelling catheter) 7.0

NEUROLOGICAL SUPPORT

18 Measurement of intracranial pressure 1.6

M E TA B O L I C S U P P O R T

19 Treatment of complicated metabolic acidosis/alkalosis 1.3

20 Intravenous hyperalimentation 2.8
21 Enteral feeding through gastric tube or other gastrointestinal route 1.3

SPECIFIC INTERVENTIONS

22 Specific intervention in the ICU: endotracheal intubation, insertion of pacemaker, cardioversion, endoscopies,
emergency surgery in the previous 24 h, gastric lavage; routine interventions without direct consequences to the
clinical condition of the patient (e.g. X-ray, ECG, echo, dressings, insertion of CVC or arterial catheters) not included 2.8
23 Specific interventions outside the ICU; surgery or diagnostics procedures 1.9

T O TA L N U R S E A C T I V I T I E S S C O R E

Adapted from Miranda DR, Nap R, de Rijk A, Schaufeli W, Iapichino G, System TWGTIS. Nursing activities score. Crit Care Med
2003;31(2):374–82, with permission.

required. One study noted that patients with longer ICU development of a surge plan. Chapter 14 contains a descrip-
stays and worse quality of life outcomes did not have the tion of critical care responses to respiratory pandemics.
increase in resource consumption that would have been In earlier experience95–101 the key role that critical care
predicted, as reflected by their TISS.91 A number of direct- units have to play in an organised response to a pandemic,
care nursing activities were not captured by TISS-28 (e.g. particularly an airborne one such as influenza, has been
hygiene, activity/movement, information and emotional demonstrated, as has the reality that critical care units have
support), and a revised instrument, the nursing activities been more severely affected than other clinical areas of a
score, was developed to address those limitations.85 In this hospital. Demand for these services will, at these times,
study, the NAS explains 81% of nursing time, whereas exceed normal supply.
the earlier TISS-28 explains only 43%; thus the NAS has
become more widely used and appears simpler with only Development of a surge plan
23 measurable items.93,94 Hota et al95 describe the preparations for a surge to service
under the three headings ‘Staff ’, ‘Stuff ’ and ‘Space’. The
Management of pandemics resources required will be examined under these headings.

Planning for the impact, or potential impact, of a pandemic Staff

is required at the organisational and operational levels, as The ability to provide additional staff for a potentially
is the identification of its direct clinical implications. This expanded critical care bed base should examine the following:
section highlights the areas to be considered at the organ- • staff with critical care skills who do not currently
isational level when assessing the response of an individual work in this area
facility to such an event. • staff from other areas with critical care-based skills,
Intensive care beds and their associated resources such as recovery, anaesthetics, coronary care
(equipment and staffing) are finite resources and an organ-
isational response is required to maximise potential ICU • provision of training and education to support less
experienced staff
capacity. Lessons can be learnt from the global H1N1
pandemic in 2009. The knowledge gained from this • development of critical care nursing teams in which
experience clearly identifies the need to plan for the critical care expertise is spread across the teams
potential increased demand on critical care services.95 While to manage the patient load appropriately, i.e. in
it is beyond the scope of this chapter to cover this subject satellite units
comprehensively, the aim is to outline briefly the areas • planning for critical care staff sick leave
for further examination, touching on the concept of the • provision to redeploy pregnant staff
38 SECTION 1 SCOPE OF CRITICAL CARE

• provision of training and education for all staff to • Identify alternative clinical areas within the hospital
avoid panic and concern, for example, domestic and that may provide additional critical care beds as a
catering staff. satellite unit, such as recovery and coronary care.
Stuff • Triage access to limited ventilation and/or critical
care resources.98,101
The ability to manage supplies at times of uncertain demand
is a key element for examination, as is the knowledge and Critical care surge plan
understanding of the processes for accessing additional Templates to assist in the development of a critical
equipment such as ventilators and medications from state care surge plan are available.96 The following example
emergency stockpiles, for example: is formatted in a graduated approach and is shown as a
• Ensure supplies of appropriate personal protective percentage (%) of current unit capacity:
equipment. • pre-surge
• Develop plans/policies for the rational use of personal • minor surge: 5–10%
protective equipment. • moderate surge: 11–20%
• Ensure supplies, and access to supplies, of required • major surge: 21–50%
medications. • large scale emergency >50%
• Plan the ability to boost ventilator capacity, such as The use of such a template, which can be populated
with increased use of BiPAP or accessing the state with locally appropriate definitions and information,
emergency stockpile. can provide the basis for a comprehensive unit/facility
Space specific response to the requirement for a graduated
response to a pandemic. Planning for events such as a
This would examine and plan for strategies to functionally pandemic requires a coordinated, collaborative approach
increase the available critical care bed capacity, as follows: from all members of the healthcare team, resulting in
• Defer elective surgery. scalable, flexible plans that are underpinned by the
• Explore the ability of local private hospitals to assist normal management structure and ensure effective lines
with service provision for non-deferrable surgical cases. of communication.100

Summary
The management of all resources in the critical care unit is key to meeting the needs of the patients in a safe, ethical,
timely and cost-effective manner. Many factors influence not only the resources available but also how these resources are
allocated. Managers of critical care units are required to be knowledgeable in the design and equipping of units; human
resource management, including the make-up of the nursing workforce; and the fundamentals of the budget – how it
is determined, monitored and managed. Understanding the principles of risk management and tools such as those that
measure nursing workload help nurse managers in their planning and decision making. Having good structures and
processes in place facilitates the delivery of care during times of crisis, such as what is experienced when pandemics occur.

Case study
The Royal Hospital is a 250-bed, non-metropolitan, general teaching public hospital that is planning to
expand its intensive care unit from 7 to 10 beds. Your task as the nursing unit manager is to plan what
additional nursing resources are required to make this a functional unit once it is fully commissioned. The
hospital is geographically located close to a 300-bed private hospital and 5 kilometres from a large regional
airport that receives direct flights from Asia. This hospital also has a separate 5-bed CCU and 12-bed post
anaesthetic care unit (PACU).
Among other things you must consider certain tasks and make recommendations to the Director of Nursing
of The Royal Hospital (see the Case study question). Utilise information contained in this chapter to inform
your work and recommendations.

CASE STUDY QUESTION

1 Calculate the additional staffing numbers in FTEs that you will require to staff the increase in beds.
Determine the estimated cost of these additional staff, including a breakdown of both productive and
non-productive FTEs required.
 CHAPTER 2 SYSTEMS AND RESOURCES 39

RESEARCH VIGNETTE

Lucchini A, De Felippis C, Elli S, Schifano L, Rolla F, Pegoraro F, Funagalli R.

Nursing activities score (NAS): 5 years of experience in the intensive care units of an Italian hospital.
Intensive Crit Care Nurs 2014;30:152–158

Abstract
Objective: To retrospectively analyse the application of the Nursing Activities Score (NAS) in an intensive care
department from January 2006 to December 2011.
Method: The sample consists of 5856 patients in three intensive care units (GICU: General Intensive Care Unit,
Neuro ICU: Neurological Intensive Care Unit, CICU: Cardiothoracic Intensive Care Unit) of an Italian University
Hospital.
The NAS was calculated for each patient every 24 hours. In patients admitted to general ICU, the following scores
were also recorded along with the NAS: SAPS 2 and SAPS 3 (Simplified Acute Physiology Score), RASS (Richmond
Agitation Sedation Scale) and Braden.
Results: The mean NAS for all patients was 65.97% (standard deviation [SD] ±2.53), GICU 72.55% (SD ±16.28),
Neuro ICU 59.33% (SD ±16.54), CICU 63.51% (SD ±14.69). The average length of hospital stay (LOS) was 4.82
(SD ±8.68). The NAS was high in patients with increasing LOS (p<0.003) whilst there were no significant differences
for age groups except for children 0–10 years (p<0.002). The correlation of NAS and SAPS 2 was r=0.24 (p=0.001),
NAS and SAPS 3 was r = −0.26 (p=0.77), NAS and RASS was r = −0.23 (p=0.001), NAS and Braden was r = 0.22
(p=0.001).
Conclusions: This study described the daily use of the NAS for the determination of nursing workload and defines
the staff required.

Critique
This study was a retrospective, single centre, observational study designed to primarily examine the mean NAS score
level of admitted patients and compare that data to the nursing workforce that had actually been rostered. Secondary
objectives were to examine the differences in NAS scores and therefore nursing workloads between various units
and to determine if there was a relationship between mean NAS scores and other variables, namely level of sedation,
SAPS2, SAPS3 and risk of pressure ulcer development.
The chosen methodology was suitable and data collection and analysis were appropriate, although there are
recognised limitations of using retrospective data for research purposes. Ethics approval was gained from the
hospital ethics committee. Descriptive statistics (measures of central tendency such as mean, median and deviance
from the mean) have been used to compare the patient populations in the various units, and Spearman’s correlation,
a technique that permits analysis of ordinal level data, was used to examine the relationships between NAS and
SAPS2, SAPS3, RASS and Braden scores.
The findings of this study were that patients cared for in the GICU had a statistically significant higher median NAS
score (72.55; p<0.001) than those in the other two units; patients with an increased length of stay demonstrated a
statistically significant higher median NAS score (p<0.003). The study investigators also identified 15 diagnoses in
this patient population and the only illness that was predictive of a statistically significant higher median NAS score
was patients on extracorporeal membrane oxygenation. No relationship was found between the NAS and the other
variables examined.
The authors acknowledged the limitations of a single site study, meaning the findings may not reflect other settings.
They also identified that the sample (5856 patients) was not equally distributed across all units studied and that, while
the GICU showed a higher median NAS score than the other two units, this may have been due to this patient group
being more heterogeneous than the other two groups. Finally, as a retrospective study, the findings may not reflect
current practice.
40 SECTION 1 SCOPE OF CRITICAL CARE

Lear ning a c t iv it ie s
1 Identify the three approaches suggested by the Research and Development Corporation to economic decision
making in the ICU when assessing treatment options.
2 Identify the three fundamental steps in the budget process.
3 List the main nursing activities identified in the Nursing Activity Scale 2003.
4 List the criteria that should be included in the evaluation of a new product.
5 In preparation for writing a critical care surge plan, calculate the surge capacity required for a 10- and 25-bed
capacity ICU.

Online resources
Ettelt S, Nolte E. Funding intensive care: approaches in systems using diagnosis-related groups, www.rand.org/pubs/
technical_reports/2010/RAND_TR792.pdf
Guidance on completing a business case, Mersey Care NHS Trust, UK, www.merseycare.nhs.uk/Library/What_we_do/
Corporate_Services/Service_Development_Delivery/Document_Library/Business%20Case%20Guidance.pdf
Medical Algorithms Project website, www.medal.org/visitor/login.aspx
Tasmanian Government business case (small) template and guide, www.egovernment.tas.gov.au/__data/assets/word_
doc/0013/15520/pman-temp-open-sml-proj-bus-case.doc
University of Queensland ITS business case guide and template, www.its.uq.edu.au/docs/Business_Case.doc

Further reading
Durbin CG. Team model: advocating for the optimal method of care delivery in the intensive care unit. Crit Care Med
2006;34(3Suppl):S12–S17.
Grover A. Critical care workforce: a policy perspective. Crit Care Med 2006;34(3Suppl):S7–11.
Kirchhoff KT, Dahl N. American Association of Critical-Care Nurses’ national survey of facilities and units providing critical
care. Am J Crit Care 2006;15:13–28.
Narasimhan M, Eisen LA, Mahoney CD et al. Improving nurse–physician communication and satisfaction in the intensive
care unit with a daily goals worksheet. Am J Crit Care 2006;15(2):217–22.
Parker MM. Critical care disaster management. Crit Care Med 2006;34(3Suppl):S52–55.
Redden PH, Evans J. It takes teamwork… The role of nurses in ICU design. Crit Care Nurs Q 2014;37(1):41–52.
Robnett MK. Critical care nursing: workforce issues and potential solutions. Crit Care Med 2006;34(3Suppl):S25–31.
Valentin A, Ferdinande P. Recommendations on basic requirements for intensive care units: structural and organizational
aspects. Inten Care Med 2011;37(10):1575–1587.

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 CHAPTER 2 SYSTEMS AND RESOURCES 43

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Chapter 3

Quality and safety

Wendy Chaboyer, Karena Conroy

Learning objectives KEY WORDS

After reading this chapter, you should be able to: adverse events
• describe the contribution that evidence-based nursing can make to care bundles
critical care nursing practice
checklists
• identify the steps in developing clinical practice guidelines clinical practice
• explain the role care bundles and checklists have in promoting quality and guidelines
safety in critical care nursing practice evidence-based
• discuss rapid response systems used to respond to deteriorating patients nursing
• describe the use of information and communication technologies in failure mode and
critical care effects analysis
• identify techniques used to understand situations that place patients at health outcomes
risk of adverse events in critical care information and
• identify strategies to improve the safety culture in critical care. communication
technology
liaison nurse
Introduction measurement

Today’s critical care units are both busy and complex, where nurses, doctors and medical
other health professionals use their knowledge, skills and technology to provide emergency team
patient care. In fact, this complexity makes errors a common occurrence; one patient safety
large international study in 205 intensive care units (ICU) showed that 39 serious quality
adverse events occurred per 100 patient days.1 The Institute of Medicine in the improvement
USA defines quality of health care as ‘the degree to which health services for indi- rapid response
viduals and populations increase the likelihood of desired health outcomes and systems
are consistent with current professional knowledge’.2 Critical care nurses are well
root cause
known for their skills in patient assessment. In fact, this ongoing surveillance of
patient condition means that nurses are ideally positioned to prevent, discover and analysis
correct healthcare errors.3 Thus, nurses play a key role in improving quality and safety culture
safety in health care.This chapter provides a review of quality and safety in critical
care. First, an overview of evidence-based nursing and clinical practice guidelines
is given to provide a foundation to consider quality and safety. Next, quality and
safety monitoring are considered. Included in this section are the topics of care
bundles, checklists and information and communication technologies. Finally,
patient safety, including safety culture, rapid response systems and non-technical
skills, is described. In Chapter 2 risk management, clinical governance and the role
 CHAPTER 3 QUALITY AND SAFETY 45

of clinical leaders and managers in delivering critical care

services were addressed; this information is complementary FIGURE 3.2 Steps in the EBN process.
to what is discussed in Chapter 3.
;YHUZSH[LHJSPUPJHSX\LY`PU[VHZ[Y\J[\YLKX\LZ[PVU
Evidence-based nursing
Evidence-based nursing (EBN) is the ‘application of valid,
relevant, research-based information in nurse decision-
making.’4 Research evidence, however, is only one of 3VJH[L[OLILZ[L]PKLUJL
four considerations in making a clinical decision. Three
other considerations include: 1) knowledge of patients’
conditions (i.e. preferences and symptoms); 2) the nurses’
clinical expertise and judgment; and 3) the context in *YP[PJHSS`HWWYHPZL[OLL]PKLUJL
which the decision is taking place (i.e. setting, resources).
Figure 3.1 provides a schematic representation of EBN,
using an example of a decision about weaning a patient
from a mechanical ventilator. 0U[LNYH[L[OLL]PKLUJLPU[VWYHJ[PJL
EBN has emerged as a way to improve nursing practice
by considering the care that nurses give to patients, and
whether this care results in the best possible outcomes for
patients. It has been viewed as both an attitude and a process. ,]HS\H[LJSPUPJHSWLYMVYTHUJL
As an attitude, it is a way of approaching practice that is
critical and questioning. As a process, a number of steps in
EBN have been described. Figure 3.2 identifies these steps, comparison, outcome format, more often referred to
with more details about each step being provided below. as PICO. The population reflects the patient group or
Translate a clinical query into a clinical scenario of concern. The intervention is one
option for the particular nursing practice.The comparison
structured question is the current practice, or the second option for practice.
In situations where nurses have to make clinical decisions, Finally, the outcome is the effect that the nurse is hoping
it is important for them to carefully consider the issue to achieve, which should reflect a patient outcome.
or problem they are facing as it influences what research Another schema, SPIDER (sample, phenomenon of
evidence should be used to make decisions. Thus, the first interest, design, evaluation, research type), can be used for
step in the EBN process is translating a clinical query questions that are not about the effect of an intervention
into a well-defined, answerable, structured question. A on an outcome.5 Table 3.1 provides three examples of
well-recognised approach is the population, intervention, PICO questions relevant to critical care nursing.

FIGURE 3.1 Schematic representation of evidence-based nursing including an example of weaning from
mechanical ventilation.

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࠮^LHUPUNWYV[VJVSZ
࠮Z`Z[LTH[PJYL]PL^Z

5\YZLZ»Q\KNLTLU[ 7H[PLU[WYLMLYLUJLZ
*SPUPJHSKLJPZPVU
HUKL_WLY[PZL HUKJPYJ\TZ[HUJLZ
࠮TLJOHUPJHS]LU[PSH[PVU
࠮L_WLYPLUJL ࠮YLZWPYH[VY`OPZ[VY`HZ[OTH
^LHUPUNTL[OVK
࠮HZZLZZTLU[ZRPSSZ ࠮HU_PL[`

(]HPSHISLYLZV\YJLZ
࠮[`WLVM]LU[PSH[VY
࠮Z[HMMPUN
46 SECTION 1 SCOPE OF CRITICAL CARE

TABLE 3.1
Examples of clinical questions using the PICO format

EXAMPLE P – P O P U L AT I O N I – INTERVENTION C – C O M PA R I S O N O – OUTCOME

1 Postoperative cardiac Knee-length graduated Thigh-length graduated Prevention of deep vein

surgery patients compression stockings compression stockings thrombosis
2 Mechanically ventilated Nurse-led weaning Standard practice (doctor- Extubation
patients protocols driven)
3 Intubated patients Brushing teeth with a Normal saline mouth rinse Ventilator-associated
toothbrush and toothpaste pneumonia

Locate the best evidence intervals). The second question focuses on whether
meaningful improvements to patient care and outcome
After well-defined, answerable, structured questions have
will result if the research findings are applied in practice.
been developed, nurses can turn to reviewing the literature
It also considers how the intervention compares with
to find the answers. First, the evidence has to be located,
current practices in terms of patient care and outcomes.
which involves searching library databases. Some of the
That is, if the research is dated and clinical practice has
databases generally searched include Ovid CINAHL,
evolved, the findings of the dated research may be less
PubMed and the Cochrane Library. Articles that relate to
relevant to current practice.
the question then have to be retrieved. These articles may
The third question conveys the notion that potential
be reports about primary research (i.e. written by the person
benefits or outcomes of the intervention must be both
conducting the research), systematic reviews of existing important to the patient and able to be replicated in other
research or clinical practice guidelines that have been settings.The NHMRC6,7 identifies three types of outcome,
developed from primary research and systematic reviews. surrogate, clinical and patient-relevant, which are not
Critically appraise the evidence mutually exclusive (see Table 3.2). Surrogate outcomes
Once the various sources of evidence have been retrieved, are often used in critical care where measurement of
they are then assessed for their quality and relevance to the actual physiological change (e.g. oxygen-carrying
the clinical question. In Australia, the National Health and capacity of the blood) is replaced by a more accessible,
and equally acceptable, parameter (e.g. oxygen saturation).
Medical Research Council (NHMRC)6 has described
Clinical outcomes are those of direct relevance to clinical
strategies to assess the body of research evidence, which
practice, and patient-relevant outcomes are those likely
provide a useful framework to consider research evidence
to be articulated as significant by the patient/carer. When
for improving nursing interventions, and identify three
assessing research evidence, the type of outcome used in
questions to ask regarding potential interventions:
the research should be considered.
1 Is there a real effect? Recognising the contribution of a variety of research
2 Is the size of the effect clinically important? questions beyond intervention-type questions, the NHMRC
3 Is the evidence relevant to practice? has extended its framework for assessing research quality,
to support the development of clinical practice guidelines
This first question regarding the real effect relates
(CPG).7 This extension asks the questions:
to the strength of the research that has been conducted.
The strength of the research has three dimensions: level 1 What is the evidence base (number of studies and
of evidence, quality of the individual studies and their quality, levels of evidence)?
statistical precision (denoted by P values or confidence 2 How consistent are the study findings?

TABLE 3.2
Types of outcome

OUTCOME DEFINITION ICU EXAMPLE

Surrogate Some physical sign or measurement substituted for a clinically meaningful outcome • Oxygen saturation
• Vital capacity
Clinical Outcome defined on the basis of the problem • Ventilator days
• Hospital readmission
Patient-relevant Outcomes that are important to the patient • Functional ability
• Quality of life
 CHAPTER 3 QUALITY AND SAFETY 47

3 What is the proposed clinical impact of the evidence? improve care and may actually result in substandard
4 How generalisable is the evidence? care.11,12 In the critical care area, the Intensive Care Coor-
5 How applicable is the evidence to the context? dination and Monitoring Unit of the New South Wales
Department of Health has led the development of CPGs
Assessing research results involves an understanding of
associated with a number of common nursing interven-
the quality of evidence for a particular nursing practice.
tions that are available online including: 1) eye care; 2) oral
Integrate the evidence into practice care; 3) pressure injury prevention; 4) physical activity and
When good quality evidence for a particular practice is movement; 5) temperature measurement; 6) arterial line
identified, it is important to then consider this evidence care; 7) central venous access device care; 8) suctioning an
alongside nurses’ expertise, patient preferences and available artificial airway; 9) tracheal tube stabilisation; 10) trache-
resources. In essence, evidence may suggest that a particular ostomy care; and 11) non-invasive ventilation.12
practice achieves the best patient outcomes, but if the nurse Clinical audits are often used to establish the need to
does not have the skills needed to implement the practice, develop new CPGs and protocols at the local unit level.
the resources are not available, either the patient does not Clinical audits generally involve chart reviews, but may
want the intervention or their situation is such that the also use direct observation or surveys of practice. Clinical
intervention may not be appropriate for them, this practice audits often reveal variations in practice that are without
should not be implemented. However, in many situations adequate justification.
the practice will be applicable to the patient and nurses will
have the skills and the resources to implement the practice.
Developing, implementing and
At times, implementing this new practice may take the form evaluating clinical practice guidelines
of developing a CPG or protocol for a particular nursing A number of steps are undertaken when developing clinical
activity. CPGs are described in the next section. practice guidelines.Table 3.3 provides an overview of these
steps, which has been adapted from Miller and Kearney’s
Evaluate clinical performance work.11 Other organisations such as the NHMRC also
Once a new practice has been implemented, it is important provide detailed descriptions for various aspects of the
for nurses to assess whether it is having the desired effect. CPG development and reporting process.13,14
At the individual patient level, this often involves assessing While research, systematic review and expert opinion
the patient whereas, at the unit level, it may involve either form the foundation for CPGs, the quality of evidence must
a practice audit or research. Practice audits often involve be assessed and overall summaries of the knowledge to date
reviewing patient charts to determine both the extent to are essential. These summaries are then used to develop the
which the new practice has been implemented and related guidelines, which generally include a series of statements
patient outcomes. Research may seek to understand about the care to be provided and a rationale for this care.
similar things, but generally takes a more formal approach,
Once the guidelines are developed, a group of experts
addressing issues such as appropriate study designs, ethics
and users should assess the guidelines for accuracy,
approvals etc.
clinical utility and comprehension. International experts
developed and have subsequently revised a 23-item
Practice tip
appraisal instrument, termed the Appraisal of Guidelines
Audit and feedback can be used to support and for Research and Evaluation II (AGREE II), that assesses
reinforce practice improvements. six domains: 1) scope and purpose of the CPG (3 items);
2) stakeholder involvement in CPG development (3 items);
3) rigour of development (8 items); 4) clarity and presen-
Clinical practice guidelines tation (3 items); 5) applicability (4 items); and 6) editorial
The development and use of CPGs is one strategy to independence (2 items).15 Instruments such as AGREE II
implement EBN and improve healthcare.8,9 CPGs are can be used to assess the quality of CPG.
statements about appropriate health care for specific Based on the assessment of the CPG, revisions may
clinical circumstances that assist practitioners in their be required. Next, strategies for disseminating and imple-
day-to-day practice.9,10 They are systematically developed menting the guidelines should be developed. Importantly,
to assist clinicians, consumers and policy makers in simply publishing and circulating CPGs will have a limited
healthcare decisions and provide critical summaries of impact on clinical practice, so specific activities must be
available evidence on a particular topic.11 Other terms undertaken to promote CPG adherence.16 The following
used synonymously with CPGs include protocols and seven strategies have been shown to be moderately
algorithms. There are a number of benefits of using effective in promoting guideline adherence: 1) inter-
CPGs. They are seen to be central to quality patient care active small group sessions, 2) educational outreach visits,
because, in essence, they standardise care.11 They can guide 3) reminders, 4) computerised decision support, 5) intro-
decisions and can be used to both justify and legitimise duction of computers in practice, 6) mass media campaigns
activities and practices.12 However, limitations have also and 7) combined interventions.9,17 A Canadian study
been identified. Poorly developed guidelines may not identified the following factors as important for adherence
48 SECTION 1 SCOPE OF CRITICAL CARE

TABLE 3.3
Steps in developing clinical practice guidelines

STEP DESCRIPTION

Find the evidence After deciding on what is considered evidence, databases such as CINAHL and
PubMed must be searched to find relevant studies and expert opinions
Evaluate the evidence Relevant studies and expert opinion papers must be critically appraised for their
strengths and weaknesses. This may or may not incorporate a systematic review
Synthesise the evidence General summary statements about the state of knowledge on a particular topic
are developed
Design the guidelines Written summaries, algorithms and/or summary sheets will be developed that
include statements about appropriate healthcare practices and their rationale
Appraise the guidelines Validity, reliability, clinical applicability, flexibility and clarity are some criteria that
can be used to assess the guidelines
Disseminate and implement the guidelines Specific strategies such as seminars and patient chart reminders must be developed
to increase awareness, acceptance and implementation of the guidelines
Review and reassess the guidelines Clinical audits and research may be used to regularly evaluate the impact the
guidelines have had on patient care and outcomes

Adapted from Miller M, Kearney N. Guidelines for clinical practice: development, dissemination and implementation. Int J Nurs Stud
2004; 41:813–21, with permission.

to CPGs: characteristics of the CPG, implementation gaps between knowledge and practice. Importantly, these
process, institutional characteristics, provider intent and activities need to reflect the most recent and robust clinical
patient characteristics.16 Finally, a process for regularly evidence to improve patient care and reduce harm.Various
evaluating and updating the guidelines must be developed, activities have been used in the ICU setting to translate
which may involve quality improvement activities or research findings into improved clinical practice.21,22
clinical research. In summary, by developing, using and The most common approach used for rapid improvement
evaluating CPGs, nurses may improve patient care and in health care is the plan–do–study–act (PDSA)23 method
outcomes. Additionally, use of CPGs should ensure that where four essential steps are carried out in a continuous
nursing practice is based on the best available evidence. fashion to ensure processes are continually improved:
1 Plan – identify a goal, specify aims and objectives to
Quality and safety monitoring improve an area of clinical practice, and how that
This section discusses unit-level measures used to evaluate might be achieved (i.e. how to test the intervention).
the quality and safety of care for critically ill patients. Quality 2 Do – implement the plan of action, collect relevant
and safety in health care is commonly described in terms of information that will inform whether the intervention
Donabedian’s approach18 with three major domains: was successful and in what way, taking note of
1 structure – the way the healthcare setting and/or problems and unexpected observations that arise.
system is organised to deliver care (e.g. staffing, beds, 3 Study – evaluate the results of the intervention,
equipment) particularly its impact on practice improvement, noting
2 process – the practices involved in the delivery of care any strengths and limitations of the intervention.
(e.g. pressure ulcer prevention strategies) 4 Act – determine whether the intervention should be
3 outcomes – the results of care in terms of recovery, adopted, abandoned or adapted for further rapid cycle
restoration of function and/or survival (e.g. mortality, testing recommencing at the plan phase.
health-related quality of life). Quality monitoring includes measurement of, and
A fourth domain of culture or context has been response to, the incidence and patterns of adverse events
suggested, specifically for patient safety models, to evaluate (AEs). The rate of AEs varies greatly; retrospective studies
the context in which care is delivered.19 The contempo- from various countries have revealed that AEs occur in
rary model for healthcare improvement recognises that the 4–17% of hospitalisations.24–28 One systematic review of
resources (structure) and activities carried out (processes) eight large international studies, representing a total
must be addressed within a given context (culture) to of almost 75,000 patients, found a median incidence of
improve the quality of care (outcome). The overall aim adverse events to be 9%.29 Patients who have an ICU
of quality improvement is to provide safe, effective, stay may be at an even greater risk. In an international
patient-centred, timely, efficient and equitable health study encompassing 29 countries, serious adverse events
care.20 Quality improvement activities identify and address were shown to occur in ICUs at a rate of 39 events per
 CHAPTER 3 QUALITY AND SAFETY 49

100 patient days with those related to indwelling lines, processes.40,44 Despite this, it has been estimated that one
prescription or administration of medications, equipment potentially serious intravenous drug error occurs every
failure (e.g. infusion devices, ventilators) and airway (e.g. day in a 400-bed hospital,42 and in Australia, the rates of
unplanned extubation) the most frequently reported.1 medication incidents range from 14% to 27% of all reported
Similar categories were also reported as highly prevalent incidents, second only to falls in acute care settings.45
in a more recent study in the United Kingdom;30 however, Such errors can lead to costly additional treatments and
there was also a high rate of incidents related to patient prolonged hospital stays as well as other implications for
transfers, pressure sores and infection control issues. patients, families and healthcare providers.39 Approximately
A number of methods for reporting adverse events 5% of medication errors relate to infusion pumps. These
such as direct observation, chart audit and self or facil- pumps are used to administer high-impact medications,
itated reporting can be used; each has its strengths and such as inotropes, heparin or antineoplastics.46 Medication
limitations.31 Direct observation methods have been errors reported from a database contributed by 537
identified as being the most reliable method of detection.32 hospitals with ICUs were made during the administra-
Trained observers report more unintended events but this tion phase of medication use, and were commonly errors
method is expensive, labour intensive and vulnerable to of omission, caused by improper dose or quantity and
the Hawthorne effect.33 Both chart audits and incident incorrect administration technique.40 The leading sources
reporting only reflect what is charted or reported, but of errors that caused harm in ICUs were knowledge and
even when chart audit, incident reporting, general prac- performance deficits (57%), not following procedure or
titioner reporting and external sources such as coronial protocol (26%), communication (15%) and dispensing
review are used together, some adverse events will still be device errors (14%).40 In response to the body of evidence
missed.34,35 Voluntary or facilitated reporting, such as the pertaining to medication error, a number of strategies
Intensive Care Unit Safety Reporting System36 and the have been instituted; for example, in Australia under the
Australian Incident Monitoring Study in Intensive Care,37 auspices of the National Medicines Policy, the quality use
are routinely used surveillance methods in many countries. of medicines map is a searchable online database of related
Medication administration is the most common inter- projects to assist health practitioners and researchers plan
vention in health care, but the medication management and carry out their work, and help policy makers evaluate
process in the acute hospital setting is complex, and creates quality use of medicines activity for potential use in policy
risk for patients. As a result, medication-related events are development.
one of the most common adverse events for critically ill
patients.1 A Japanese study of adverse drug events in 459 Practice tip
patients found 99 adverse events occurred in 70 patients
(i.e. 15% of patients).38 Although the rates of medication Given the high frequency and consequences of
errors and adverse drug events vary greatly between medication errors, it is important to be cognisant of the
settings despite geographical location, they are common in potential for error and the strategies that can be used to
critical care units,32,39 with higher rates of harmful errors prevent such errors, such as limiting interruptions.
than non-ICU settings, and those errors are more likely to
be associated with requiring life-sustaining intervention, It is important to evaluate interventions that can reduce
permanent harm or death.40 the incidence and impact of adverse intravenous drug
In order to measure medication safety – either by error events, particularly in critical care settings.47,48 Evidence
or adverse event – the following definitions are typically suggests that nurses who are interrupted while adminis-
applied: tering medications may have an increased risk of making
medication errors,49 prompting calls for all healthcare
• error is a failure in clinical management, resulting in workers to make concerted efforts to reduce interruptions
potential harm to the patient
to clinical tasks.50 Other activities examining quality of
• adverse events relate to actual patient harm (injury).41 care include the analysis of incident reports that use the
Issues of measurement impact on reported error/adverse World Health Organization’s International Classification
event rates and their interpretation. The way in which for Patient Safety51 and measuring and evaluating quality
medication errors, for example, are calculated requires indicators such as the Australian Council on Healthcare
careful consideration of both the numerator (e.g. count Standards (ACHS) indicators for intensive care that include:
of any error in the medication process) and the denomi- • inability to admit a patient to the ICU due to
nator (this could be the number of patients, patient days, inadequate resources
medication days, administered doses – depending on the
aim or purpose of the measure).39 • deferral or cancellation of elective surgery due to
unavailability of an ICU bed
The true incidence of both errors and adverse events
has been found to be higher than what was reported34,35,42,43 • transfer of patients to another facility due to
and, in the absence of evidence to the contrary, this is likely unavailability of an ICU bed
to have remained unchanged. Fortunately, most healthcare • delays on discharging patients from the ICU of more
errors do not result in patient harm because of safety-net than 6 hours
50 SECTION 1 SCOPE OF CRITICAL CARE

• discharge of patients from the ICU after hours (i.e. Similar activities are evident internationally, where
between 6 p.m. and 6 a.m.) concepts of ‘safety science’ (error reduction and recovery)
have been applied to critical care practice.53,54 Examples
• recognising and responding to clinical deterioration
include the Safer Patients Initiative to implement inter-
within 72 hours of being discharged from ICU
ventions to improve delivery of care to ventilated patients55
• appropriate treatment of patients for venous and multi-faceted collaborative projects to reduce catheter-
thromboembolism prophylaxis within 24 hours of related bloodstream infections in a large number of
admission to the ICU ICUs.56,57 Process indicators of quality care have been
• ICU central line-associated bloodstream infection developed, including care related to the prevention of
rates ventilator-associated pneumonia (VAP) and central
• use of patient assessment systems (participation in venous catheter management. Table 3.4 outlines process
national databases and surveys).52 indicators with good clinical evidence and/or strong

TABLE 3.4
Evidence-based process indicators

PROCESS AIM MEASURE C A L C U L AT I O N M E T H O D

Glycaemic control Encourage Percent of blood sugars in the 6–10 mmol/L No. of glucose values within range /
normo-glycaemia range Total no. glucose tests × 100
Glycaemic control Decrease Percent of blood sugars ≤2.2 mmol/L No. of glucose values ≤2.2 mmol/L /
hypo-glycaemia Total no. glucose values collected × 100
Glycaemic control Decrease Percent of blood sugars >10 mmol/L No. of glucose values >10 mmol/L /
hyper-glycaemia Total no. glucose tests × 100
Pressure ulcer Increase full Percent of patients at risk for pressure No. of patients at risk for pressure
prevention preventative care ulcers who receive all of the following: ulcers who receive all care components /
• Daily inspection of skin for pressure ulcers Total no. patients identified at risk for
• Proper management of moisture including pressure ulcers
cleaning and moisturising skin
• Optimisation of nutrition
• Repositioning every 2 hours
• Use of pressure-relieving surfaces
Pressure ulcer Reduce incidence Pressure ulcer incidence per 100 No. of pressure ulcers developed in ICU /
prevention of pressure ulcers admissions Total no. of ICU admissions × 100
Pressure ulcer Increase pressure Percent of patients who receive the No. of patients for whom all
prevention ulcer admission following on admission to ICU: components of proper pressure ulcer
assessment • Assessment of pressure ulcer risk using admission assessment were performed
validated risk assessment tool and documented / Total no. of patients
• Skin assessment to identify existing admitted to ICU
pressure ulcers
Pressure ulcer Increase pressure Percent of patients for whom pressure ulcer No. of patients received pressure ulcer
prevention ulcer risk risk re-assessment was performed using a risk re-assessment / Total no. ICU
re-assessment validated risk assessment tool at least daily patients × 100. Exclude patients in ICU
and documented <24 hours
Central line- Decrease CLABSI CLABSI rate per 1000 central line-days No. of confirmed cases of CLABSI /
associated rate Total no. of central line-days × 1000
bloodstream
infections (CLABSI)
Ventilator-associated Decrease VAP VAP rate per 1000 ventilator days No. of confirmed cases of VAP / Total
pneumonia (VAP) rate no. of ventilator days × 1000

Adapted from:
Australian Commission on Safety and Quality in Health Care (ACSQHC). National Safety and Quality Health Service Standards.
Sydney: ACSQHC, <http://www.safetyandquality.gov.au/our-work/healthcare-associated-infection/national-hai-surveillance-initiative/
national-definition-and-calculation-of-central-line-associated-blood-stream-infection/>; 2011 [accessed 03.09.14], with permission
Institute for Healthcare Improvement, <http://www.ihi.org/resources/Pages/Measures/ EvaluationofGlycemicControl.aspx>; [accessed
03.09.14], with permission.
 CHAPTER 3 QUALITY AND SAFETY 51

recommendations provided by professional bodies, such (detailed below) these tools facilitate standardised care and
as the Institute for Healthcare Improvement (USA-based improve communication between clinicians.61
with multinational scope) and the Australian Commission
on Safety and Quality in Health Care.
Care bundles
One quality improvement approach to the optimal use of
best practice guidelines at the bedside is the development
Practice tip
of ‘care bundles’. A care bundle is a set of evidence-based
Adhering to the practices included in a ventilator care interventions or processes of care, applied to selected
bundle (where appropriate), may lead to improved patients in order to standardise and ensure appropriate
patient and service efficiency outcomes. delivery of care. A number of bundles have been developed
for critical care by the Institute for Healthcare Improve-
ment (IHI) (see Table 3.5). Studies examining the process
A range of clinical support tools has been developed
of care delivery in critical care units using the ventilator
that are used to measure compliance with these best- care bundle revealed that increased bundle compliance
practice clinical standards. Daily goals forms, for example, was associated with decreased ICU length of stay, reduced
have been used to aid communication between clinicians ventilator days and increased ICU patient throughput,62
during and after multidisciplinary ward rounds and ensure in addition to decreased rates of ventilator-associated
that all staff are aware of what care the patient should pneumonia.62–66
be receiving and what the clinical plan is.58,59 A popular Other quality improvement studies have targeted
mnemonic developed for use by ICU clinicians during similar processes of care without taking the bundled
patient assessment is ‘FASTHUG’ which stands for feeding, approach. One multicenter, cluster-randomised trial
analgesia, sedation, thromboembolism prophylaxis, head- involving 15 ICUs in Canada22 evaluated the effective-
of-bed elevation, stress ulcer prevention and glucose ness of a multifaceted quality improvement program
management.60 Along with care bundles and checklists (videoconference-based forums that included audit and

TABLE 3.5
Institute for Healthcare Improvement care bundles

BUNDLE NAME AIM BUNDLE COMPONENTS

Central line Prevent central • Hand hygiene

line-associated • Maximal barrier precautions
bacteraemia • Chlorhexidine skin antisepsis
• Optimal catheter site selection with avoidance of the femoral vein for central venous
access in adult patients
• Daily review of line necessity with prompt removal of unnecessary lines
Ventilator care Prevent • Elevating the head of the patient’s bed to 30–45°
ventilator- • Daily assessment of the patient’s readiness to extubate or wean from the ventilator
associated • Daily ‘sedation vacations’ or gradually lightening sedative use each day
pneumonia • Delivering both PUD and DVT prophylaxis
• Daily oral care with chlorhexidine
Severe Reduce mortality • Serum lactate measured
sepsis 3-hour due to severe • Blood cultures obtained prior to antibiotic administration
resuscitation sepsis • Administer broad-spectrum antibiotics
• Administer crystalloid 30 mL/kg for hypotension or lactate ≥4 mmol/L
6-hour septic Reduce mortality • Apply vasopressors (for hypotension that does not respond to initial fluid resuscitation)
shock due to severe to maintain a MAP ≥65 mmHg
sepsis • In the event of persistent arterial hypotension despite volume resuscitation (septic
shock) or initial lactate ≥4 mmol/L (36 mg/dL):
Measure CVP
Measure ScvO2
Re-measure lactate if initial lactate was elevated

CVP = central venous pressure; DVT = deep vein thrombosis; MAP = mean arterial pressure; PUD = peptic ulcer disease; ScvO2 = central
venous oxygen saturation.
Adapted from Institute for Healthcare Improvement. How-to-guide: Prevent ventilator-associated pneumonia. Cambridge, MA,
<http://www.ihi.org/knowledge/Pages/Tools/HowtoGuidePreventVAP.asp>; 2012 [accessed 03.09.14], with permission.
52 SECTION 1 SCOPE OF CRITICAL CARE

feedback, expert-led educational sessions, dissemination required when planning to incorporate checklists into
of algorithms) to improve delivery of six evidence- the clinical setting.67
based practices: 1) prevention of ventilator-associated
pneumonia via semi-recumbent positioning, 2) thrombo- Practice tip
embolism prophylaxis, 3) daily spontaneous breathing
trials, 4) prevention of central line-associated blood When developed in line with published guidelines,
stream infection (CLABSI) via use of a sterile insertion checklists may improve practice delivery by serving as
checklist, 5) early enteral feeding and 6) decubitus ulcer an aide-mémoire.
prevention via use of the Braden scale. Results showed
that adoption of the targeted practices was greater in Information and communication
intervention than control ICUs, and improvement was
greatest for CLABSI prevention and semi-recumbent
technologies
positioning. Importantly, the authors noted that the Health departments continue to develop systems and
effect of their intervention was greatest for ICUs with processes that will result in a complete electronic medical
low baseline adherence to certain practices, suggesting record. Critical care in particular is at the forefront of these
that efforts should be directed specifically to where developments, with bedside clinical information systems,
delivery of care is lacking. order-entry strategies, decision support, handheld technol-
ogies and telehealth initiatives continuing to evolve and
Checklists influence practice. This section examines the current and
Checklists have the potential to prevent omissions in future impacts that these technologies will have on patient
care by serving as reminders to healthcare providers for care and safety, and on clinician workflows and practices,
the delivery of appropriate quality care for every patient, as clinical information fully assimilates with evidence-
every time, in complex clinical environments. A checklist based practice and clinical decision support systems.
typically contains a list of action items or criteria arranged
in a systematic way, allowing the person completing it Clinical information systems
to record the presence or absence of individual items to Clinical information systems may enable improved data
ascertain that all are considered or completed.67 collection, storage, retrieval and reporting of patient-based
In critical care settings, checklists have been used to information; and facilitate unit-based outcomes research
facilitate staff training, detect errors, check compliance and quality improvement activities.75 Computerisation
with safety standards and evidence-based processes of care of monitoring and therapeutic activities for critically ill
(such as those outlined previously), increase knowledge patients began in the 1960s, and has evolved to encompass
of patient-centred goals and prompt clinicians to review all aspects of patient care such as cardiorespiratory
certain practices on morning rounds in the ICU. Reviews monitoring, mechanical ventilation, fluid and medication
of studies that have evaluated the use of checklists noted delivery, imaging and results of diagnostic testing.76,77
a number of benefits such as improved understand- Patient-based bedside clinical information systems
ing of patient therapy goals, improved compliance with offer increasingly sophisticated functionality and device
safety standards and evidence-based care and detection of interfaces,78 enabling real-time data capture, trending and
patient safety errors and omissions in care, and found they reporting76 and linkage to relational databases.79,80
were useful in preparing for a procedure and were not The introduction of intravenous ‘smart pump’
time-consuming or labour intensive.68,69 technology is one application aimed at reducing adverse
Some of these studies suggested that checklists also drug events and improving patient care by supporting
contributed to improved outcomes such as reduced evidence-based guidelines for medication management.81
length of stay, ventilator days, unit mortality;70 reduced The operator-error prevention software is based on a
CLABSI;71 and reduced mean monthly rates of device-based drug library with institution-established
ventilator-associated pneumonia.72 Another study has concentrations/dosage limits incorporated in the function
also suggested decreased infection rates (for CLABSI, of the pump. Resulting software functions include
ventilator-associated pneumonia, urinary tract infections) clinician alerts (for keystroke errors)46 and transaction
in a trauma ICU.73 However, the lack of methodologi- log data (post-incident analysis).81,82 Medication errors
cal rigour in these studies prevents inferring causal links and adverse drug events can be detected by this software.
between checklist use and improved outcomes.69 When One Australian study has revealed significant reductions in
used in isolation, checklists may not be sufficient to medication administration errors can be achieved when
improve care. One study testing the utility of checklists smart pumps are systematically implemented.83 There is
for use on the daily ward round in an ICU demonstrated evidence to suggest, however, that the features of smart
improvements in both processes and outcomes of care only pump technology are not being fully utilised by many
when clinicians were prompted by a non-care-providing hospitals that purchase them, limiting the potential for
resident physician after an aspect of care covered by the realising safety benefits such as the measurable impact on
checklist was omitted or overlooked.74 Careful consid- serious adverse drug events.84 This highlights the need for
eration of both checklist design and implementation is promotional and quality improvement activities targeting
 CHAPTER 3 QUALITY AND SAFETY 53

improved utility of the smart pump features such as impairment, fewer falls in elderly patients and reduced
increasing nurses’ use of the drug libraries.85 length of hospital stay.96 In intensive care computer-
Although the proportion of ICUs using a clinical ised alerts have been used to improve glucose control in
information system is not known, there are indications patients without the need for increased blood sampling97
that uptake is on the increase.86,87 Numerous benefits to and increase mean elevations of the head of the bed for
healthcare systems that lead to enhanced quality of care patients without contraindications for this aspect of care.98
have been reported such as improved documentation, The features that might make alerts and prompts more
legibility, evidence-based decision support, interdisciplin- effective, however, are generally unknown and require
ary communication and reduced duplication and medical further research.
errors.88 In intensive care they have reduced documen-
tation time and increased the proportion of time spent Computerised order entry and
on direct care activities.89 End-user support has been decision support
identified as an important factor in the success of clinical Computerised provider order entry (CPOE) is a system
information system implementation.90 Nurses in acute that allows orders for medications, intravenous fluids,
care settings are more accepting of new technologies diagnostic tests and procedures to be entered then rapidly
when implemented well, and dissatisfaction is likely to communicated to pharmacies. It can also be used for
result from the presence of too many barriers to successful results management, treatment orders and clinical decision
implementation.88 Barriers that have been identified support.99,100 CPOE is viewed as an important innovation
include issues related to accessibility of staff to computers in reducing medical errors, through minimising transcrib-
(e.g. too few in the clinical setting) and the system (e.g. ing errors,101 triggering alerts for adverse drug interactions
login procedures and time-out rules), accuracy and the and facilitating the adoption of evidence-based clinical
speed of operations. Other barriers identified were a lack guidelines.99,102
of: IT support, knowledge and training; experience and Implementation of CPOE and related clinical
confidence in using clinical information systems; time decision support systems have demonstrated signifi-
due to increased work demands; and consultation with cant reductions in medication errors and adverse drug
end-users.88 events,100 redundant or unnecessary order requests103–105
Accuracy of data (correctness and completeness of and improved compliance with practice guidelines.106,107
the data set) from both manual and automated inputs Decision support systems interface with hospital
to the information system requires further evaluation. databases to retrieve patient-specific and other relevant
While automated entry eliminates transcription errors clinical data and to generate recommended actions at the
from other data sources,91 the use of ‘carry-over’ data time and location of decision making.108 Importantly,
to fields that require updating by clinicians, finding the clinical decision making at the bedside can be enhanced
right sampling frequency (i.e. the rate at which a clinical by providing clinicians with a readily available tool that
information system can record and display patient data) incorporates relevant clinical information and evidence-
and human interaction such as clinician acceptance of based medicine.109 Clinician alerts (e.g. allergies or
monitor-generated data can all affect data accuracy. For interaction effects) or prompts (e.g. to check coagu-
example, if the pulmonary artery waveform is measured at lation when prescribing warfarin) can be generated.
a high frequency rate and displays large variability because A number of studies have demonstrated improved
of ‘noise’ and is not checked, erroneously high systolic delivery of patient care after the introduction of such
blood pressure readings will be recorded.75 Improvements reminders.110,111 As with clinical information system
to systems, however, have reportedly led to increased implementation, detailed planning including examina-
accuracy of data collections,88,89 suggesting that perhaps tion of clinician workflow and care delivery patterns
developments in technology and the implementation is required for successful implementation of a CPOE
strategies used have mitigated these problems. Errors can process.112,113 A number of potentially important features
also arise, however, if systems are not designed to enhance of clinical decision support systems have been identified
communication between healthcare workers and facilitate that cover communication content (e.g. provide recom-
coordination of work processes.92,93 mendations with justifications in addition to assessment),
Clinical alert functions are designed to improve clinician–system interaction (e.g. incorporate into clinical
delivery of care; however they can sometimes lack the workflow, provide at the time and location it is required
specificity required to detect clinically important events94 and request reason for not following recommendations)
and may compromise patient safety when used excessively and other general (e.g. integrate with electronic charting
in clinical settings. For example, one study demon- or CPOE) and auxiliary (e.g. provide decision support
strated 49–96% of drug safety alerts were overridden by results and feedback reports) features.108,114
clinicians.95 A systematic review revealed improvements in Additional developments involving wireless commu-
prescribing behaviours and reductions in error rates as a nication, handheld technologies and closed-loop delivery
result of computerised alerts and prompts; some studies systems may improve the efficiency, effectiveness and
reported a positive impact on clinical and organisational adoption of this innovation in clinical practice. Closed-
outcomes such as decreased prescribing-related renal loop delivery offers fully automated treatment without
54 SECTION 1 SCOPE OF CRITICAL CARE

the need for human intervention;108 it adjusts drug or

fluid delivery based on active feedback from the target Practice tip
parameter (e.g. inotropic dosages adjusted to a range While handheld devices can assist nurses in their
for mean arterial pressure). An example of a successfully practice, with a range of helpful clinical applications
implemented system includes administering protocols for now available, ensure patient confidentiality is not
weaning patients from mechanical ventilation to ventilator breached and the devices are secure.
machines.115
Handheld technologies Telehealth initiatives
Wireless applications enable clinical information access, Remote critical care management (tele-ICU) using
portability and mobility within a critical care environ- telemedicine/telehealth technologies is expanding as
ment at the point of care. Clinical uses for a personal the necessary high bandwidths for transmitting large
digital assistant (PDA), tablet computer and smartphone amounts of data and digital imagery become available
technologies continue to evolve at a rapid pace.116 between partner units or hospitals. Videoconferencing
These handheld computers use operating systems and functions enable direct visualisation and communication
pen-like styluses that enable touchscreen functional- of patients and on-site staff with the ‘virtual’ critical care
ity, handwriting recognition and synchronisation with clinician or team. Review of real-time physiological data,
other hospital-based computer systems. An increasing patient flowcharts and other documents (e.g. electro-
array of clinical applications and content is available for cardiograms, laboratory results) or images (e.g. radiographs)
downloading to these devices, including drug reference provides a comprehensive data set for patient assessment
information (e.g. Monthly Index of Medical Specialties and management.116
[MIMS]), clinical guidelines, medical calculators and This technology-enabled remote care initiative is
internet-based literature searches.117,118 of particular value for critical care units where no or
A systematic review of healthcare applications for limited on-site intensivist resources are available. Despite
smartphones revealed a total of 57 applications for various methodological limitations,128 several studies using
healthcare professionals with the majority focused on ‘before and after’ comparisons have indicated improved
disease diagnosis,21 medical calculators,8 drug reference outcomes such as decreases in severity-adjusted hospital
information,6 literature search6 and health information mortality, incidence of ICU complications, ICU length
system client applications.4 There were eleven applications of stay and ICU costs.129–131 Other studies, however, have
related to medical or nursing student education. Both not found improvement in patient outcomes as a result of
healthcare professionals and students reported disease telemedicine technology,132–134 highlighting the complex
diagnosis, drug reference and medical calculator applica- nature of these initiatives and the difficulties evaluating
tions as the most useful.119 them. More recently, a systematic review and meta-
Personal digital assistant and smartphone use has analysis of the literature found that tele-ICU coverage
been reported as a helpful nursing education tool,120–122 was associated with reduced ICU mortality and length
with nursing students reporting specific benefits of of stay but not hospital mortality or length of stay.117 The
using handheld devices such as having access to readily constantly evolving nature of technology and innovative
available data, validation of thinking processes and facil- ideas from healthcare workers can bring about novel
itation of care plan re-evaluation.121 In critical care, approaches to healthcare delivery. One study, for example,
handheld devices have been used to document clinical demonstrated improved outcomes for neurological ICU
activities, such as logging critical care procedures, which patients through the use of a robotic tele-ICU system that
was demonstrated as feasible and useful.123 They have also made rounds in response to nurse paging.131
been used to deliver point-of-care decision support to There are also characteristics of tele-ICU that are
improve antibiotic selection124 and prescribing105 and an likely to impact on both the process and outcomes of care.
interactive weaning protocol that assisted care providers Benefits are likely to be generated from the availability of
wean patients from mechanical ventilation more effi- extra resources and the ability of the tele-ICU to serve as
ciently when compared with the use of a paper-based a quality improvement trigger (e.g. checking compliance
weaning protocol.125 with evidence-based medicine) and to provide medication
The benefits of this mobile computing also create management support, software alerts and real-time patient
concerns, particularly regarding confidentiality of patient monitoring by camera.116 For these benefits to be realised,
information. Health services therefore need policies however, the technology needs to be accepted and used
for managing handheld devices, including password appropriately by ICU staff. Further studies that include
protection, data encryption, authenticated synchronisation detailed descriptions of system implementation are
and physical security.126 In particular, wireless applica- required to determine the most effective elements of this
tions require appropriate standards for data security.127 technology in critical care settings as well as their impact
As these issues are addressed, these technologies will form on care processes and outcomes.128,135
an integral component of routine clinical practice in In addition to remote patient assessment and
critical care. management, telecommunications have been used to
 CHAPTER 3 QUALITY AND SAFETY 55

deliver continuing education to rural healthcare profes- strategy has focused on understanding the safety culture
sionals for many years via audio, video and computer.136 of a unit or organisation, with subsequent activities
Distance education delivered via web-based courses aimed at improving components of this culture.
accessed over the internet is now commonplace.137 One
example of a web-based educational tool was used to Practice tip
provide information about the classification of pressure
ulcers and the differentiation between pressure ulcers and By undertaking a root cause analysis, the contributing
moisture lesions to both student and qualified nurses.138 factors to the event can be identified and strategies to
The potential use of web logs or ‘blogs’,139 online commu- mitigate future adverse events can be implemented.
nities and virtual preceptorships137 in nursing education
and intensive care practice has also been discussed.119 Safety culture
Professional development opportunities are also provided Measurement of the baseline safety culture facilitates an
online; for example, AusmedOnline contains a range action plan for improvement. Safety culture has been
of resources and learning activities that count towards defined as ‘the product of individual and group values,
continuing professional development for registration attitudes, perceptions, competencies, and patterns of
requirements. However, more work is required to deter- behaviour that determine the commitment to, and the
mine how successful these technological advances are in style and proficiency of, an organisation’s health and safety
terms of educational outcomes.139 management.’148 It is commonly referred to as ‘the way
we do things around here.’149 A systematic review found
Patient safety evidence for a relationship between safety culture and
The signing of the Declaration of Vienna in 2009140 patient outcomes at both the hospital and unit level.150
committed critical care organisations around the world, A widely used instrument to measure safety culture, the
including the World Federation of Critical Care Nurses, Safety Attitudes Questionnaire (SAQ), focuses on six
to patient safety. Patient safety is viewed as a crucial domains: teamwork climate, safety climate, job satisfaction,
component of quality.141–144 Over the years, numerous perceptions of management, working conditions and stress
definitions of patient safety have emerged in the literature. recognition.151 Interestingly, two studies in the USA152,153
The Institute Of Medicine described it as the absence of and one Australian study conducted in 10 ICUs154 showed
preventable harm to a patient during the process of health that nurses and doctors differed in their perceptions of
care,141 whereas the World Health Organization describes safety culture. The Australian study also identified some
it as the reduction of risk of unnecessary harm to an differences between bedside nurses and nursing leaders.154
acceptable level.143 Using the SAQ, a Palestinian neonatal intensive care
Three techniques used to understand patient risk unit study found wide variation in the perceptions of
are: 1) analysing reports of adverse events, 2) root the safety culture held by 164 nurses and 40 physicians
cause analyses and 3) failure mode and effect analysis. in 16 hospitals.155 Another recent European study of 378
Research on adverse events in critical care has helped to patients in 57 ICUs showed a relationship between safety
better understand patient risks and target improvement culture and fewer errors.156
activities. For example, medications, indwelling lines and
equipment failure were the three most frequent types Practice tip
of adverse events in a study of 205 intensive care units A positive safety culture is associated with better
worldwide.1 Focusing on analysing the narratives written patient outcomes.
about adverse events is viewed as an important way to
learn from errors. Root cause analysis is a structured One strategy to improve the safety culture has involved
process generally used to analyse catastrophic or sentinel identifying factors that make organisations safe, which in
events.145,146 In root cause analysis, the various situations turn allows initiatives to be developed that target areas of
that led to the event are documented and analysed in specific need. For example, five characteristics of organ-
order to identify contributing factors to the event and
isations that have been able to achieve high reliability
make recommendations for system changes to prevent
include:157
the event from occurring again. Learning from both
incident reporting and root cause analyses is based on the 1 safety viewed as a priority by leaders
premise that the information they contain is of sufficient 2 flattened hierarchy that promotes speaking up about
quality to allow accurate analysis, interpretation and concerns
detection of the root causes of problems and, even 3 regular team training
more importantly, the formulation and implementation
4 use of effective methods of communicating
of corrective actions. Failure mode and effect analysis
identifies potential failures and their effects, calculating 5 standardisation.
their risk and prioritising potential failure modes based There are a number of other resources available to
on risk.147 In addition to examining patient risk, another those interested in improving patient safety. For example,
56 SECTION 1 SCOPE OF CRITICAL CARE

WHO has published a patient safety curriculum guide 2013 systematic review of RRS found moderate evidence
to assist organisations in this endeavor.158 Leadership, for the claim that RRS were associated with reduced rates
teamwork and behaviour change strategies provide a of cardiopulmonary arrest and mortality.164 A second 2013
foundation for improvements in safety culture.159 In the systematic review concluded that much of the available
USA, the Comprehensive Unit-Based Safety Program evidence on the effects of RRS was of poor quality.165
has emerged as one specific safety intervention.160 Three The Australian Commission on Safety and Quality in
others shown to be beneficial in systematic reviews Health Care have identified eight essential elements in a
were executive or multidisciplinary wards and multi- RRS (Table 3.6).162
faceted interventions, which included a comprehensive RRS have three components.166 First, there are
unit-based safety program, and team training, which some criteria and a system for identifying and activating
included tools to improve communication. Another the rapid response team, often referred to as the afferent
American critical care quality improvement program limb.166,167 Second, there is the response, also termed
found that a nurse-led safety program that included the efferent limb.166 Finally, there is an administrative
executive walkrounds and a multidisciplinary team and quality improvement component.166 Each of these
tasked with identifying and resolving safety issues were components is briefly described.
effective.161 The three top safety issues identified related to
nursing, supplies and daily unit operations with 36–70% Afferent limb
of the issues being resolved. In summary, understanding Recognising the deteriorating patient, the afferent limb
the various dimensions of safety culture in a unit can be has focused on measuring clinical signs including vital
used as a foundation for the development and imple- signs, level of consciousness and oxygenation as well as
mentation of programs targeted at specific aspects that acting on abnormalities in these measurements.166 They
may benefit from improvements. To be successful, safety may also include concerns expressed by clinicians and
programs have to be supported by the leaders as well as families.168,169 Various scoring systems to identify ward
other members of the unit. patients with clinical deterioration have evolved as part
of the development of critical care outreach,170 including
Rapid response systems the Medical Emergency Team (MET),169 early warning
Rapid response systems (RRS) are systems that have scoring170 and patient-at-risk criteria171 (see Table 3.7).
developed to recognise and provide emergency response All systems identify abnormalities in commonly measured
to patients who experience acute deterioration.162–165 One parameters (e.g. respiratory rate, heart rate, blood pressure,

TABLE 3.6
Essential elements of a rapid response system (RRS)

DOMAIN ELEMENT DESCRIPTION

Clinical processes Measurement and Vital signs, oxygen saturation and level of consciousness should be undertaken
documentation regularly on all acute care patients
Escalation of care A protocol for the organisation’s response in dealing with abnormal physiological
measures and observations including appropriate modifications to nursing care,
increased monitoring, medical review and calling for assistance
Rapid response When severe deterioration occurs, medical emergency teams, outreach teams or
systems liaison nurses are available to respond
Clinical Structured communication protocols are used to hand over information about the
communication patient
Organisational Organisational Executive and clinical leadership support and a formal policy framework for
prerequisites supports recognition and response systems should exist
Education Education should cover clinical observation, identification of deterioration, escalation
protocols, communication strategies and skills in initiating early interventions
Evaluation, audit Ongoing monitoring and evaluation are required to track changes in outcomes over
and feedback time and to check that the RRS is operating as planned
Technological As relevant technologies are developed, they should be incorporated into service
systems and delivery, after considering evidence of their efficacy and cost as well as potential
solutions unintended consequences

Adapted from Australian Commission on Safety and Quality in Health Care: National Consensus Statement: Essential Elements for
Recognising and Responding to Clinical Deterioration. Sydney: ACSQHC; 2010, with permission.
 CHAPTER 3 QUALITY AND SAFETY 57

TABLE 3.7
Commonly used risk assessment scores

CLINICAL MEDICAL EMERGENCY TEAM M O D I F I E D E A R LY W A R N I N G

PA R A M E T E R C A L L I N G C R I T E R I A 216 PAT I E N T- AT- R I S K S C O R E 1 7 3 S C O R E 172
CALL FOR ALL CONDITIONS ANY 3 OR MORE OF THE SCORE OF ≥3 REQUIRES
LISTED BELOW FOLLOWING PRESENT REFERRAL

Airway Threatened – –
Breathing Respiratory arrest rate <5/min or Respiratory rate Respiratory rate:
>36/min 1 = 20–29 breaths/min 1 point = 15–20/min
2 = <10 or 30–39 breaths/min 2 points = <8 or 21–29/min
3 = ≥40 breaths/min 3 points = ≥30/min
Oxygen saturation:
1 = 90–94%
2 = 85–89%
3 = <85%
Cardiac Cardiac arrest pulse <40/min or Heart rate: Heart rate:
>140/min 1 = 40–49 or 100–114/min 1 = 40–50/min or 101–110/min
2 = 115–129/min 2 = <40/min or 111–129/min
3 = >130/min 3 = ≥130/min
Systolic blood pressure (SBP) SBP: SBP:
<90 mmHg 1 = 80–99 mmHg 1 = 81–100 mmHg
2 = 70–79 or ≥180 mmHg 2 = 71–80 or >200 mmHg
3 = <70 mmHg 3 = <70 mmHg
Disability Decrease in Glasgow Coma Score 1 = confused 1 = responds to voice
(neurological) >2 repeated/prolonged seizures 2 = responds to voice 2 = responds to pain
3 = responds to pain/unresponsive 3 = unconscious
Other parameters Any patient who does not fit the Temperature:
criteria above is causing clinical 1 = 35.0–35.9° or 37.5–38.4°C
concern
2 = <35° or >38.5°C
Urine output:
1 = >3 mL/kg/h
2 = <0.5 mL/kg/h
3 = nil

neurological status). Other parameters used in patient in the first 24 hours after patients had been discharged
assessment are oxygen saturation, temperature and urine from the ICU.172
output in patient-at-risk and early warning scores. The
early warning scoring/patient-at-risk systems include Efferent limb
an ordinal scoring approach used as calling criteria for The efferent limb involves the team responding to
contacting the admitting medical team, ICU staff, the clinical deterioration.166 Some teams will include physicians
critical care outreach team or the MET, depending on and nurses, known as MET or RRT, whereas others such
the severity of the patient’s clinical deterioration and the as critical care outreach teams166 and ICU liaison nurses
resources available in the local clinical environment. Yet, are nurse-led.173 Irrespective of the title of the model used,
observation charts are not always being completed and, the RRT generally assess deteriorating patients and then
when they are, sometimes the RRT is not called even initiate emergency treatments. A 2014 systematic review
when the calling criteria are met. However, an Australian of critical care transitions programs in general found they
study showed that a new observation chart incorporat- were associated with a reduced risk of ICU readmission.174
ing the modified early warning score along with training This positive association was also found when the only
significantly improved the documentation of vital signs service considered was an ICU liaison nurse.174
58 SECTION 1 SCOPE OF CRITICAL CARE

Administrative and quality skills in providing safe, high quality care, has led to the
improvement development of a number of training programs, which are
briefly described in this section.
The third component of an RRS focuses on administra-
tion and quality improvement.166 Generally, this involves Situational awareness
the collection and analysis of RRS data including the Situational awareness has been described as the cognitive,
reason for the call, the treatments administered and social and personal skills that complement technical
patient outcomes. Analysing RRS data provides managers, skills and contribute to safe and efficient task perfor-
clinicians and policy makers with guidance for future mance.178 It describes the awareness and understanding
improvements. A single site evaluation of a two-tiered of a situation and its possible outcomes.179 Situations may
RRS provides one example of how local RRS data can be be categorised on a continuum from routine and easily
collected and analysed.175 In summary, RRS have evolved managed to confusing and dangerous, requiring specific
to provide emergency care to patients whose condition skills and expertise.180 Endsley,181 whose work has been
is deteriorating, and who are not already in the critical particularly influential, describes three levels of situa-
care unit. RRS involve a mechanism to identify these tional awareness. Level 1, perception, involves gathering
patients and call for help, as well as a response team. They data about the current situation. Level 2, comprehen-
also generally involve some administrative and quality sion, reflects inter pretation and understanding the data.
improvement components to improve the service. RRT Level 3, projection, is concerned with predicting what can
rely on team members working together, which leads to happen in the future. Figure 3.3 demonstrates applica-
the next section on non-technical skills. tion of these three levels of situational awareness using
the scenario of a postoperative patient whose blood
Non-technical skills pressure has dropped. Importantly, situational awareness
is viewed as a necessary precursor for good quality
Nurses need to have current knowledge and skills in critical decision making.179
care to ensure safe, high quality care, but these technical Team situational awareness is a term applied to teams
skills are not sufficient. They also need to possess other, and reflects the notion that team members possess the
non-technical skills (NTS) to ensure patient safety. This situational awareness needed to perform their tasks in
section provides an overview of four inter-related176,177 the team.179 This team situational awareness has also been
non-technical skills: situational awareness, decision making, termed shared situational awareness.181 In the critical
communication and teamwork. Another important care environment, nurses and physicians will have some
non-technical skill, leadership, is described in Chapters 1 unique but related tasks to undertake including during
and 2. Understanding the importance of non-technical procedures such as central line insertions, intubations

FIGURE 3.3 Situational awareness example.

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 CHAPTER 3 QUALITY AND SAFETY 59

and bronchoscopies, and these tasks will require both defining a problem, generating and considering one or
complementary and shared situational awareness. The more alternatives, selecting and implementing an option
extent of team or shared situational awareness will and reviewing the outcome. Clinical decision making is a
influence the quality of decisions and subsequent team complex process and is influenced by a number of factors.
performance.179 For example, environmental factors such as the team, the
patient and resources can influence decision making as can
Practice tip situational awareness. Individual factors such as fatigue,
affective state interruption in work and distractions can
Team briefings before undertaking a complex procedure also influence decision making.185,186
can help to develop team situational awareness. Critical care nursing practice has been the focus of
many studies on decision making. One study demon-
One review identified that both individual factors strated that critical care nurses generate one or more
and interpersonal behaviours influenced situational hypotheses about a situation prior to decision making.184
awareness.177 Lapses in situational awareness can occur Other studies indicated that experienced and inexperi-
because of issues such as distractions, fatigue, time pressures enced nurses differ in their decision-making skills,185–187
and team dynamics such as assertive authority figures. and that role models or mentors are important in assisting
A number of strategies are recommended to overcome to develop decision-making skills.188 A Greek study
these lapses. They include thorough briefings about the classified ICU nurses’ decisions as urgent or non-urgent
nature and risk of a given activity, minimising distractions and as independent or dependent.189 The research-
and interruptions during critical tasks, receiving regular ers observed that 75% (962/1281) of decisions were
updates, good time management, being physically and non-urgent and 60% (220/368) were independent.189 It
mentally fit for work and speaking up when not sure of a is intuitive that good quality clinical decisions, irrespec-
goal, procedure or next step.181,182,183 tive of what they are about, will likely improve patient
care and outcomes.
Decision making
Decision making involves a judgement or choosing an Recommendations for developing
option (i.e. a course of action) to meet the needs of a given clinical decision-making skills
situation.181 In critical care, multiple, complex decisions Several strategies that can be used to help critical care
are made in rapid succession.184 Decision making entails nurses to develop their clinical decision-making abilities

TABLE 3.8
Strategies to develop clinical decision making

S T R AT E G Y DESCRIPTION

Iterative hypothesis Description of a clinical situation for which the clinician has to generate questions and develop
testing190 hypotheses; with additional questioning the clinician will develop further hypotheses. Three phases:
(Narayan and Corcoran- 1 asking questions to gather data about a patient
Perry, 2008) 2 justifying the data sought
3 interpreting the data to describe the influence of new information on decisions
Interactive model190 Schema (mental structures) used to teach new knowledge by building on previous learning.
(Narayan and Corcoran- Three components:
Perry, 2008) 1 advanced organisers – blueprint that previews the material to be learned and connects it to
previous materials
2 progressive differentiation – a general concept presented first is broken down into smaller ideas
3 integrative reconciliation – similarities and differences and relationships between concepts explored
Case study191 Description of a clinical situation with a number of cues followed by a series of questions. Three types:
(Rivett and Jones, 2008) 1 stable – presents information, then asks clinicians about it
2 dynamic – presents information, asks the clinicians about it, presents more information, asks more
questions
3 dynamic with expert feedback – combines the dynamic method with immediate expert feedback
Reflection on action190 Clinicians are asked to reflect on their actions after a particular event. This pondering focuses on
(Narayan and Corcoran- clinical judgements made, feelings surrounding the actions and the actions themselves. Reflection on
Perry, 2008) action can be undertaken as an individual or group activity and is often facilitated by an expert
Thinking aloud190 A clinical situation is provided and the clinician is asked to ‘think aloud’ or verbalise their decisions.
(Narayan and Corcoran- Thinking aloud is generally facilitated by an expert and can be undertaken individually or in groups
Perry, 2008)
60 SECTION 1 SCOPE OF CRITICAL CARE

are identified in Table 3.8.190,191 These strategies can be nurses with opportunities for social bonding, coaching
used by nurses at any level to develop their own deci- and educating and team building.196,197 A contemporary
sion-making skills or by educators in planning educational Australian study focused on the content of ICU nursing
sessions. It is important to note, however, that a review handover.198 The researchers found that while ≥95%
of interventions to improve decision making concluded of observed handovers included identifying nursing
that most studies in this area were of relatively poor care needs, vital sign observations, changes in patient
quality.192 condition and the medical management of the patient,
≤40% included a discussion of discharge or long-term
Communication plans, cross-checking and reporting on resuscitation
Communication has been described as ‘the exchange of status.198 A second study of 157 nursing shift-to-shift
information, feedback or response, ideas and feelings’.176,p 69 handovers conducted in seven ICUs in three countries
Good quality communication is viewed as a two-way (Australia, Israel and the United Kingdom)199 found
sharing of information, whereby the sender encodes handovers were more comprehensive when: 1) the
some idea into a message and transmits it to a receiver. oncoming nurse did not know the patient; 2) the patient
The receiver then decodes the message to gain an under- was expected to die during the shift; or 3) the family
standing of it. Next, the receiver becomes the sender, were present. Over 70% of nurses in Israel had cared
encoding and transmitting a subsequent message.176 There for the patient in the previous 48 hours, whereas only
are various types of communication including verbal and 29% and 20% of UK and Australian nurses had. Over
non-verbal. Non-verbal communication includes written 75% of the handover communication included the
communication and body cues or gestures. goals for care and 73% included pain management, but
Reason,193 a well-known safety researcher, suggests legal issues such as advance directives and identification
that there are three kinds of communication failure that of a health proxy were mentioned in less than 10% of
contribute to accidents. The first, system failure, occurs the handovers.
when there are either no channels of communication or A 2013 review identified three important features
the channels that exist are not working or are not used. of good quality handover including: 1) face-to-face,
The second, message failure, happens when necessary two way communication; 2) standardised templates
information is not communicated. And finally, reception or checklists that incorporate a minimum dataset; and
failure occurs when the information is misinterpreted or 3) content that includes the patient’s current diagnosis
arrives too late. and clinical situation.200 In order to improve the quality
of handovers, a group of Australians has developed an
Practice tip interactive, 3-dimensional computer simulation (virtual
world) for training intensive care nurses in shift-to-shift
Using closed loop communications, where the receiver handover.201
acknowledges the message was heard, can prevent Multidisciplinary rounds are seen to be one way
miscommunication. to promote shared situational awareness, yet seminal
research in the 1990s showed that nurses were not
Experts recommend that communication be explicit, participating in medical rounds.202 In fact, this study
efficient and closed-loop.194 By being explicit, a person is revealed communication between doctors and nurses
being clear in what they are saying. Being efficient means accounted for 2% of all activities but 37% of all errors.
that the message is conveyed using only as many words In another study published in 2006, nurses did not
as necessary. And closed-loop communication is a term believe they were allowed to talk during rounds in two
used to signify that a receiver acknowledges or responds to of four ICUs studied.203 A 2013 systematic review of
the sender of information. This response lets the initiator ICU rounds concluded that ‘rounds conducted using a
know that the message was heard. Other strategies to standardized structure and a best practice checklist by
improve communication include ensuring it is timely a multidisciplinary group of providers, with explicitly
and assertive.194 Timely communication means that the defined roles and a goal-orientated approach, had
sender is cognisant of the other activities that the receiver the strongest supporting evidence’.200, p 2025 Table 3.9
may be doing and, because of this, provides information provides more specific details of the recommendations
at a relevant time. Assertiveness involves standing up for from this review.
yourself while respecting others.
In the critical care setting two specific communication Teamwork
situations have been the focus of recent research – Teams have been described as two or more individuals
clinical handover and rounds. Handover is more than the with specialised roles and responsibilities who act inter-
transfer of patient information; it has been described as dependently to achieve some common goal,204 although
the transfer of professional responsibility and account- a systematic review noted teamwork is a broad term
ability for some or all aspects of care for a patient, or with varying definitions.205 High performing teams share
group of patients, from one care provider to another.195 an understanding of the activity they are working on;
Besides sharing patient information, handovers provide they understand the aim or mission of that activity, and
 CHAPTER 3 QUALITY AND SAFETY 61

TABLE 3.9
Recommendations for ICU rounds

BEST PRACTICE S T R E N G T H O F R E C O M M E N D AT I O N

Implement multidisciplinary rounds (including at least a medical doctor, registered Strong – definitely do it
nurse and pharmacist)
Standardise location, time and team composition Strong – definitely do it
Define explicit roles for each HCP participating on rounds Strong – definitely do it
Develop and implement structured tool (best practices checklist) Strong – definitely do it
Reduce nonessential time-wasting activities Strong – definitely do it
Minimise unnecessary interruptions Strong – definitely do it
Focus discussions on development of daily goals and document all discussed goals Strong – definitely do it
in health record
Conduct discussions at bedside to promote patient-centeredness Weak – probably do it
Conduct discussions in conference room to promote efficiency and communication Weak – probably do it
Establish open collaborative discussion environment Weak – probably do it
Ensure clear visibility between all HCP Weak – probably do it
Empower HCP to promote team-based approach to discussions Weak – probably do it
Produce visual presentation of patient information No specific recommendation

HCP = health care professional.

Adapted from Lane D, Ferri M, Lemaire J, McLaughlin K, Stelfox HT. A systematic review of evidence-informed practices for patient
care rounds in the ICU. Crit Care Med 2013;41(8):2015–29, with permission.

they know each other’s roles and expectations. They are Figure 3.4 demonstrates the content covered in the team
also trained and skilled in leadership, conflict resolution, training studies reviewed by Gordon and colleagues.206
back-up behaviour and closed-loop communication. In addition to the core non-technical skills described in
Important aspects of leadership include coordinating the this section, the review also identified training programs
team, distributing workloads equitably and monitoring focused on understanding error and systems such as the
the team’s performance. Conflict resolution often requires human/technology interface. Two well-known teamwork
clarification of roles and responsibilities, fostering useful experts noted that factors such as how the team training
debate and assertive communication. Back-up behaviour is implemented, the method of its delivery and leadership
is when one team member can step in to assist another in all influence the effectiveness of team training on both
their role, providing support to other team members. In processes and outcomes.207
essence, teamwork is dependent on each member being Figure 3.5 provides an overview of these training
able to anticipate the needs of others, adjust to others’ methods.206 Most of the team training studies reviewed
actions and the changing environment and have a shared took a multidisciplinary approach, reflecting contem-
understanding of how a task should be performed. In their porary clinical practice. Simulation has attracted a lot of
systematic review, Dietz and colleagues found standardised attention recently as a team training strategy. Simulation
protocols (such as using checklists), implementing daily allows clinicians to practise skills and reflect on their
rounds and training were the three main solutions used to performance in a simulated environment. That is, it
improve ICU teamwork.205 increases both knowledge and performance. In their 2013
systematic review, Schmidt and colleagues208 asserted that
Non-technical skills training simulation as a patient safety strategy had four purposes:
Increasing recognition of the importance of non-technical 1) education; 2) assessment; 3) research; and 4) health
skills has led to the development of a number of training system integration. It is evident that teamwork and NTS
programs. These programs recognise that, while human team training are core components of patient safety. In
error cannot be eliminated, it can be minimised, trapped summary, patient safety involves understanding the risks to
or mitigated.176 A systematic review of non-technical skills patients and developing strategies to minimise these risks.
training to enhance patient safety documented both the Safety culture and non-technical skills are two important
content of and training methods used in non-technical aspects of patient safety, with a number of strategies and
skills training.206 programs available to enhance both.
62 SECTION 1 SCOPE OF CRITICAL CARE

FIGURE 3.4 Analysis of non-technical skills training teaching methods.

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 CHAPTER 3 QUALITY AND SAFETY 63

Summary
In summary, this chapter has provided an overview of safety and quality in critical care. EBN is viewed as an important
foundation to promote quality as is the development and use of good quality clinical practice guidelines. Quality and
safety monitoring underpin understanding the risks that patients face in critical care. The use of care bundles, checklists
and information and communication technologies may improve quality of care. Improving patient safety is multifac-
eted, but often includes understanding the safety culture as well as the risks faced by patients in a particular clinical area.
Techniques such as the analysis of clinical incidents, root cause analyses and failure mode and effects analysis help in
understanding situations that place patients at risk of adverse events. One particular high-risk scenario is the deteriorating
patient, with a number of RRS now being implemented to respond to this scenario. Other initiatives to improve patient
safety include NTS training. Understanding situations that place patients at risk of harm as well as the safety culture of a
unit or organisation provides the foundation to improve safety culture.

Case study
You have just been asked to participate in a working group tasked with identifying and detailing
important content for clinical decision support within your unit’s new CPOE system. As a member of this
group you are required to contribute one key area that requires decision support – glycaemic management.
The question below asks you to plan your contribution to this working group.

CASE STUDY QUESTION

1 Use the information contained in this chapter and related learning activities to prepare a brief outline of
what needs to be incorporated into the design and functionality of the clinical decision support system.
The outline should include the following:
• aim(s) of the clinical decision support system (e.g. reduce hypoglycaemic events)
• target patient population and potential users of the system
• features that will be important to the success of this particular system
• methods for evaluating its effectiveness.
Recommended reading for this case study:
Mann EA, Salinas J: The use of computer decision support systems for the critical care environment. AACN Adv Crit
Care 2009;20(3):216–219.

RESEARCH VIGNETTE

Karra V, Papathanassoglou ED, Lemonidou C, Sourtzi P, Giannakopoulou M. Exploration and classification of

intensive care nurses’ clinical decisions: a Greek perspective. Nurs Crit Care 2014;19(2):87–97

Abstract
Aim: The recording, identification, coding and classification of clinical decisions by intensive care nurses.

Background: Clinical decision-making is an essential dimension of nursing practice as through this process nurses
make choices to meet the goals of patient care. Intensive care nurses’ decision-making has received attention
because of the complexity and urgency associated with it, however, the types of nurses’ clinical decisions have not
been described systematically.

Methods: Qualitative content analysis of daily diaries of clinical decisions recorded during nursing work by
23 purposefully selected intensive care nurses from three major hospitals of Greece. The process of data collection
and analysis continued until the point of theoretical saturation.
64 SECTION 1 SCOPE OF CRITICAL CARE

Findings: Eight categories of nursing clinical decisions emerged including decisions related to: (1) evaluation, (2)
diagnosis, (3) prevention, (4) intervention, (5) communication with patients, (6) clinical information seeking, (7) setting
of clinical priorities and (8) communication with health care professionals. Psychological assessment and support
decisions were scarce, whereas patient input in care decisions appeared to be limited. The most frequent types of
decisions were regarding intervention (29%), evaluation (25%) and clinical setting of priorities (17%), while clinical
information seeking (3%) and communication with patients’ decisions (2%) were the least frequent. Additionally,
recorded decisions were ranked in order of degree of urgency and of dependency on medical order. Non-urgent
decisions were 78% of the total and 60% of nurses’ intervention decisions were independent of medical order and
were related to basic nursing care.

Conclusions: Intensive care nurses make multiple decisions that seem to be in line with the nursing process, although
the latter is not officially implemented in Greek ICUs.

Relevance to clinical practice: The types and frequency of clinical decisions made by intensive care nurses
are related to features of ICU work environment, their professional autonomy and accountability, as well as their
perceptions of their clinical role.

Critique
This interesting study focused on identifying and classifying the decisions Greek ICU nurses made. It received
institutional approval and individual nurses consented to be part of the study. The nurses in this study were drawn
from three major hospitals and were all registered nurses. They were purposely sampled to ensure they had a range
of education and experience, but all had at least 5 years of clinical experience and 2 years of ICU experience. This
sampling technique was appropriate and resulted in a variation in participants and contexts, something that helps
ensure ‘rich data’ are collected. While qualitative research does not aim to identify generalisable findings, using three
hospitals may increase the applicability of the findings to other contexts. Nurses recorded the decisions they made
during one 8-hour shift on a ‘log sheet’ that they referred to as a ‘diary of decisions’. While the authors explained
that they considered other methods to collect the data such as the ‘think aloud’ technique, the diary of decisions
was the method favoured by participants. It is possible that there may have been missing or inaccurate information
recorded during times when the nurses were particularly busy, given writing these notes would have taken time
away from patient care and other normal work activities. Data collection occurred over eight months in late 2011
and all three shifts (day, evening and night), suggesting good sampling in terms of the times the decisions were
made and recorded. The researchers clearly explained how they undertook data analysis using content analysis.
They noted that, while they used an inductive approach to analysis, many of their emerging categories reflected
the nursing process (assess, plan, implement, evaluate). They were also able to classify the emerging categories as
urgent or non-urgent and independent or dependent. Overall, the findings were clearly and logically presented. The
tables were clear and complemented the text. The discussion of the findings was insightful and easy to understand.
Overall, this was an interesting study that may provide ideas to others for how they could investigate decision
making in their own context.

Lear ning a c t iv it ie s
1 Using each domain of quality and safety as headings (i.e. structure, process, culture, outcome), list some of the
key considerations for a quality improvement project targeting shift-to-shift nursing handover in your unit.
2 After identifying a CPG that guides nurses in providing care in your unit, assess it against the NHMRC criteria
of: 1) its evidence base; 2) consistency of the primary research findings; 3) proposed clinical impact of the
evidence; 4) generalisability of the evidence; and 5) applicability of the evidence to your unit’s context.
3 Examine the patterns of incidence for a high-frequency adverse event in your unit over the past 12 months.
What were the causes of incidents? What targeted strategies could be used to reduce the incidence of these
adverse events?
 CHAPTER 3 QUALITY AND SAFETY 65

4 Identify and provide a rationale for an aspect of care that might benefit from the use of a checklist in your unit.
Develop some specific checklist items that you think should be included.
5 Describe how technology is used in your unit to improve care delivered to patients. Using the information
outlined in the section on information and communication technologies, identify where there is potential to use
technology to improve care delivery further. Use examples specific to your unit.

Online resources
Agency for Healthcare Research and Quality, www.ahrq.gov
Australian Commission on Safety and Quality in Health Care (ACSQHC), www.safetyandquality.gov.au
Australian Council on Healthcare Standards (ACHS), www.achs.org.au
Institute for Healthcare Improvement (IHI), USA, www.ihi.org/ihi
Intensive Care Coordination and Monitoring Unit (ICCMU), New South Wales Health, http://intensivecare.hsnet.nsw.gov.au
Joint Commission (USA), www.jointcommission.org
National E-Health Transition Authority, www.nehta.gov.au/
National Health and Medical Research Council, www.nhmrc.gov.au
National Quality Forum, www.qualityforum.org
Quality Use of Medicines, www.health.gov.au/internet/main/publishing.nsf/Content/nmp-quality.htm
World Health Organization Patient Safety, www.who.int/patientsafety/en

Further reading
Ausserhofer D, Schubert M, Desmedt M, Blegen MA, De Geest S, Schwendimann R. The association of patient safety
climate and nurse-related organizational factors with selected patient outcomes: a cross-sectional survey. Int J Nurs Stud
2013;50(2):240–52.
Australian Commission on Safety and Quality in Health Care. Safety and Quality Improvement Guide Standard 9: Recognising
and responding to clinical deterioration in acute health care. Sydney: ACSQHC; 2012.
Browne M, Cook P. Inappropriate trust in technology: implications for critical care nurses. Nurs Crit Care 2011;16(2):92–8.
Craze L, McGeorge P, Holmes D, Bernardi S, Taylor P, Morris-Yates A et al. Recognising and responding to deterioration in
mental state: a scoping review. Sydney: ACSQHC; 2014.
Dubois C-A, D’Amour D, Tchouaket E, Clarke S, Rivard M, Blais R. Associations of patient safety outcomes with models of
nursing care organization at unit level in hospitals. Int J Qual Health Care 2013;25(2):110–7.
Garrouste-Orgeas M, Soufir L, Tabah A, Schwebel C, Vesin A, Adrie C et al; Outcomerea Study Group. A multifaceted
program for improving quality of care in intensive care units: IATROREF study. Crit Care Med 2012;40(2):468–76.
Groves PS. The relationship between safety culture and patient outcomes: results from pilot meta-analyses. West J Nurs
Res 2014;36(1):66–83.
Guidet B, Gonzalez-Roma V. Climate and cultural aspects in intensive care units. Crit Care 2011;15(6):312.
Nemeth CP. Improving healthcare team communication: building on lessons from aviation and aerospace. Hampshire,
England: Ashgate; 2008.
Odell M. Human factors and patient safety: changing roles in critical care. Aust Crit Care 2011;24(4):215–7.
Reason JT. The human contribution: unsafe acts, accidents and heroic recoveries. Surrey, England: Ashgate; 2008.
Rossi PJ, Edmiston CE, Jr. Patient safety in the critical care environment. Surg Clin North Am 2012;92(6):1369–86.
Runciman B, Merry A, Walton M. Safety and ethics in healthcare. Hampshire, England: Ashgate; 2007.
Thompson DN, Hoffman LA, Sereika SM, Lorenz HL, Wolf GA, Burns HK et al. A relational leadership perspective on
unit-level safety climate. J Nurs Adm 2011;41(11):479–87.
66 SECTION 1 SCOPE OF CRITICAL CARE

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 Chapter 4

Recovery and rehabilitation

Janice Rattray, Leanne Aitken

KEY WORDS Learning objectives

cognitive After reading this chapter, you should be able to:
dysfunction • discuss the physical, psychological and cognitive sequelae present for
health-related some survivors of a critical illness
quality of life • outline the common functional, psychological, cognitive and health-
intensive care related quality of life (HRQOL) instruments used to assess patient
unit-acquired outcomes after a critical illness
weakness • describe the benefits and challenges for implementing rehabilitation
post-intensive care interventions in ICU, in hospital after ICU discharge and after hospital
discharge.
syndrome
post-traumatic
stress symptoms
psychological Introduction
sequelae
Millions of people each year experience a critical illness requiring admission
to an intensive care unit (ICU). Although overall survival rates approximate
90% at hospital discharge,1 recovery for individuals is delayed often beyond
6 months postdischarge.2 Physical de-conditioning and neuromuscular
dysfunction3 as well as psychological4,5 and cognitive sequelae6 are common,
adding to the burden of illness for survivors, carers, the healthcare system and
broader society.
Although ICU clinicians have traditionally focused on survival as the
principal indicator of patient outcome and unit performance,7 physical and
psychological functioning and health-related quality of life (HRQOL) have
now emerged as legitimate patient outcomes from both practice and research
perspectives.2 With this shifting focus towards long-term health and wellbeing
has also come a reconsideration and re-conceptualisation of critical care as
only one component in the continuum of care for a critically ill patient. An
episode of critical illness is now viewed as a continuum that begins with the
onset of acute clinical deterioration, includes the ICU admission and continues
until the patient’s risk of late sequelae has returned to the baseline risk of a
similar individual who has not incurred a critical illness7 (see Figure 4.1).
Timing of this recovery trajectory is variable, and related to a number of
individual, illness and treatment factors.
74 SECTION 1 SCOPE OF CRITICAL CARE

examined patient-centred concepts such as functional status,

FIGURE 4.1 The continuum of critical illness.7 HRQOL, psychological health and cognitive function
have become more prevalent in the past 10 years.2,15 As the
7YL0*< recovery trajectory from a critical illness may be long and
0*< >HYK 7VZ[OVZWP[HS
+PZLHZLI\YKLU

incomplete, mapping this path is a complex process.

Health-related quality of life
Survivors of critical illness experience compromised
health-related quality of life for varying periods of time after
leaving ICU. Health-related quality of life covers a number
of physical, psychological, emotional and social domains
;PTL
of life and is now generally accepted as an important
)\YKLUVMJYP[PJHSPSSULZZ outcome measure. Within this chapter, we guide the reader
Adapted with permission from Angus DC, Carlet J. Surviving
to the commonly used measures but present the physical
intensive care: a report from the 2002 Brussels Roundtable. and psychological issues separately. Ongoing physical and
Intensive Care Med 2003;29(3):368–77. psychological problems tend to impact negatively on social,
environmental and economic elements in life,17 and many
Reviews of numerous observational studies confirm patients and families experience a significant economic
delayed recovery in HRQOL,8 with physical, psychologi- challenge during the recovery process. Although some
cal and cognitive symptoms prevalent: patients recover quickly and do not report ongoing issues,
others report significant and protracted compromise in
• weakness: approximately 40%3,9 their quality of life.16 It is clear that survivors of critical
• delirium: up to 74%10,11 illness have markedly lower health-related quality of life
• anxiety: up to 45%12,13 than other members in the community when matched for
age and gender. Although there is convincing evidence of
• depression: approximately 30%5 this widespread compromise, we also know that recovery
• post-traumatic stress symptoms: approximately 20%4 patterns vary for individual patients, with some recovering
• cognitive dysfunction: 36–62%.14 rapidly. Factors that have been shown to influence compon-
Recognition of the frequency, and co-occurrence, of ents of quality of life include age, lower socioeconomic
these elements of compromise has led to the develop- status, gender, severity of illness, primary diagnosis and
ment of the term ‘post-intensive care syndrome’ (PICS) length of ICU stay, although few of these factors appear to
to ‘describe new or worsening impairments in physical, affect people in a consistent manner.4,5,16
cognitive, or mental health status arising after critical illness
and persisting beyond acute care hospitalisation’ (p. 505).2 ICU-acquired weakness
While significant sequelae therefore exist for a substan- Critical illness myopathy (CIM), polyneuropathy (CIP) and
tial proportion of critical illness survivors, little evidence neuromyopathy (CINM) syndromes occur in 50–100% of
is currently available to support specific interventions for ICU survivors.18–20 ICU-acquired weakness (ICU-AW) has
improving their recovery.2,15 come into use as a term that encompasses these syndromes
In further chapters of this book psychological issues of muscle wasting and functional weakness in patients with
including sedation management and delirium monitoring a critical illness who have no other plausible aetiology.20
while in ICU (Chapter 7) and breathing trials and weaning The three syndromes above form the sub-categories of
from mechanical ventilation (Chapter 15) are discussed. ICU-AW, with CINM used when both myopathy and
Common physical and psychological sequelae associated axonal polyneuropathy are evident. Development of
with a critical illness, and how this impacts on a survivor’s ICU-AW is associated with a number of risk factors that
HRQOL, are discussed in this chapter. Common instru- occur during intensive care treatment:18,21
ments measuring physical, psychological and HRQOL are • critical illness: sepsis, systemic inflammatory response
described. Physical rehabilitation strategies, commencing syndrome (SIRS), multi-organ system failure,
with exercise and early mobility in-ICU, post-ICU and catabolic state
post-hospital services are also discussed.
• treatments: mechanical ventilation, hyperglycaemia,
glucocorticoids, sedatives, neuromuscular blocking
Compromise following a agents, immobility.
critical illness Local and systemic inflammation acts synergistic-
ally with bed rest and immobility to alter metabolic and
Examination of patient outcomes beyond survival is an structural function of muscles,22 resulting in muscle atrophy
important contemporary topic for critical care practice and contractile dysfunction, loss of flexibility, CIP, hetero-
and research.4,5,8,16 Patient outcomes after a critical illness topic ossification and entrapment neuropathy.20 Muscle
or injury were traditionally measured using a number of strength can reduce by 1–1.5% per day with a total loss
objective parameters (e.g. number of organ failure-free days, of 25–50% of body strength possible following immobil-
28-day status, or 1-year mortality). Other measures that isation.23 Patients can lose up to 2% of muscle mass per
 CHAPTER 4 RECOVERY AND REHABILITATION 75

day,24 which contributes to weakness and disability and a Diagnostic testing

prolonged recovery period. These neuromuscular dysfunc- Electrophysiological testing (nerve conduction studies,
tions are diagnosed by clinical assessment, diagnostic studies needle electromyography) may be useful to differenti-
(electrophysiology, ultrasound) or histology of muscle or ate between CIM and CIP, although this distinction is
nerve tissue. difficult and often not required in the clinical setting.18,20
The syndrome of ICU-AW manifests as prolonged Histology for CIP is primarily noted as distal axonal
weaning time, inability to mobilise and reduced functional degeneration in both sensory and motor fibres, while the
capacity. Patients with ICU-AW also experience increased characteristic findings in CIM are patchy loss of myosin
mortality.25 Some groups of ICU survivors report (thick filaments), necrosis and fast twitch fibre atrophy.20
relatively poor HRQOL due to prolonged weakness that
may persist for months and years after discharge, partic- Practice tip
ularly for those recovering from acute lung injury/adult
respiratory distress syndrome (ARDS).9 Current clinical recommendations to limit muscle
wasting include:
Clinical assessment
• minimising patient exposure to corticosteroids and
Clinical assessment includes identification of generalised
neuromuscular blocking agents
weakness following the onset of a critical illness, exclusion
of other diagnoses (e.g. Guillain–Barré syndrome) and • limiting excessive analgesia and sedation
measurement of muscle strength. Instruments are available to • moderate glycaemic control
assess both volitional and non-volitional muscle strength.26 • early mobilisation.
Manual muscle testing is commonly assessed using the
Medical Research Council (MRC) Scale,27 a 0–5 point Psychological health
ordinal scale:
Psychological responses to a critical illness and patients’
0 = no contraction memories of experiences during an ICU admission
1 = flicker or trace of muscle contraction have been explored using quantitative31–35 and/or quali-
2 = full range of active movement with gravity eliminated tative approaches.36,37 Some survivors reported increased
3 = reduced power but active movement against gravity anxiety, including transfer anxiety (discharge from ICU);38
depression;5 post-traumatic stress;4,39–41 hallucinations;42–44
4 = reduced power but active movement against gravity and continuing cognitive dysfunction.6,11,45
and resistance For some patients, recovery from a critical illness
5 = normal power against gravity and full resistance. results in short- and long-term psychological dysfunc-
For patients who are awake and cooperative, each muscle tion (e.g. anxiety, depression and post-traumatic stress
group is assessed sequentially for strength and symmetry: symptoms), which potentially result in additional health
problems, reduced HRQOL,46,47 reduction in social
• upper limb: deltoid, biceps, wrist extensors activities and functioning and failure to engage with
• lower limb: quadriceps, gluteus maximus, ankle rehabilitation programs.48 Our understanding of these
dorsiflexion. sequelae has improved over the past decade in part due to
Ordinal data are obtained in response to a subjective increased research activity and evaluations of intensive care
evaluation of muscle strength.26 In 1991 an MRC sum-score, follow-up clinics in the UK (discussed in a later section).
ranging from 0–60, was first introduced.28 Weakness is However, despite testing a variety of interventions, it is still
evident with an MRC sum score of <48 (<4 in all testable unclear how best to identify at-risk patients and initiate an
muscle groups), and re-tested after 24 hours. Weakness (<4 effective intervention in a timely way.
MRC Scale) was associated with an increased hospital
mortality.29 Inter-rater reliability following appropriate Anxiety and depression
training using the MRC has been demonstrated.30 Reported prevalence of anxiety and depression after ICU
Hand-held dynamometry and handgrip dynamome- discharge varies depending upon the questionnaire and
try can also be used to measure volitional muscle strength ‘cut-off ’ scores used, and the research design, and ranges
using a calibrated device for patients who are conscious from 7% 3 months after discharge49 to 18% 1 year after
and cooperative.The benefit of these measures is increased discharge.50 Both studies used the Hospital Anxiety and
objectivity to obtain continuous data.26 Depression Scale (HADS) with scores of ≥11 to indicate
All volitional strength measurements may be affected an anxiety or depressive problem.
by the level of awareness and cooperation of patients, as Prevalence of depression tends to be high in the
well as their motivation, although inter-rater reliability of immediate weeks after ICU discharge and Davydow and
the MRC sum score as well as hand-held dynamometry colleagues48 report significant depressive symptoms in
and handgrip dynamometry has been shown to be good 36% of medical-surgical patients 3 months after hospital
to very good.26 Further, dynamometry was demonstrated discharge. This figure reduced to 18% at 12 months.48 A
to be a reliable, rapid and simple alternative to compre- summary of studies reporting the prevalence of anxiety and
hensive manual muscle testing assessment,29 and may be a depression is provided in Table 4.1.These differences may be
surrogate measure for global strength.20 explained by differences in case mix or timing of assessment.
 76

TABLE 4.1
Summary of studies examining anxiety and depression in survivors of a critical illness

FIRST INSTRUMENT/
AUTHOR/ A C U I T Ya / I C U C U T- O F F
C O U N T RY DESIGN N/% MALES COHORT L O S D AY S AGE SCORE MAIN FINDINGS

b
Eddleston Cross-sectional 143/52% Follow-up 15/3.7 51 HADS ≥11 7% met the criteria for anxiety, and 3%
(2000)49/UK clinic 3 months depression
postdischarge Females more likely to have higher anxiety
scores

Nelson (2000)51/ Cross-sectional, 24/58% 19 months 58d/27 40 GDSc/16 Positive correlation (r = 0.30) between
UK postal survey (mean) after depression scores and days of sedation;
acute lung injury 69% of patients not depressed prior to ICU
SECTION 1 SCOPE OF CRITICAL CARE

scored >16

Scragg (2001)52/ Cross-sectional 80/52% Survival from –/– 57 HADS >8 43% scored above 8 for anxiety and 30%
UK postal survey ICU over 2 years for depression

Jones (2001)53/ Cohort 30/67% 2 and 8 weeks 17/8 57 HADS ≥11 Patients with no factual but some delusional
UK after ICU memories were more likely to be anxious
discharge and depressed at 2 weeks

Jones (2003)54/ RCT 116/61% General ICU 17/14 58 HADS >11 No statistically significant differences
UK patients – between the two groups; there was a trend
3 hospitals; to reduced depression scores for those with
8 weeks and scores >11 at 8 weeks
6 months after
discharge

Jackson (2003)55/ Prospective 34/53% Medical and 24.9/– 53.2 GDS-SF ≥6 Patients with neuropsychological
USA cohort coronary ICU; impairment were more likely to score above
6 month the threshold at 6 months (36% v 17%)
follow-up

Hopkins Prospective 66/50% ARDS; 12 month 18.1/34 46 BDI >30 9% severe levels of anxiety and 6% severe
(2004)56/USA longitudinal follow-up BAI >30 levels of depression at 12 months

Hopkins 2 year follow-up Anxiety and depression persisted up to

(2005)57/USA 2 years with 23% reporting moderate-to-
severe levels

Rattray (2005)50/ Prospective 80/64% General ICU; 17.7/4.9 54.7 HADS ≥11 Anxiety and depression significantly
UK longitudinal Hosp discharge, reduced between 6 and 12 months;
6 and 18% demonstrated probable anxiety,
12 months 11% probable depression
FIRST INSTRUMENT/
AUTHOR/ A C U I T Ya / I C U C U T- O F F
C O U N T RY DESIGN N/% MALES COHORT L O S D AY S AGE SCORE MAIN FINDINGS

Sukantarat Prospective 51/43% ICU patients ≥3 15.3/16.9 57.4 HADS: anxiety 24% had anxiety scores ≥10 at both 3 and
(2007)58/UK days; 3 and ≥10 9 months
9 months HADS: 35% had depression scores ≥8 at 3 months
depression ≥8 and 45% at 6 months

Dowdy (2009)59/ Prospective 161/55% Acute lung ≤20 = 80%/≤10 49 HADS ≥11 11% scored above threshold at 6 months
USA cohort injury; 6 months = 51%

Myhren (2009)61/ Cross-sectional 255/63% 4–6 weeks post- SAPSe 37/12 48 HADS ≥11 Mean anxiety (5.6 vs 4.2) and depression
Norway ICU discharge (4.8 vs 3.5) scores higher than general
population norms

Myhren (2010)60/ Longitudinal As above and 3 Unemployment and optimism were

Norway and 12 months predictors of anxiety scores; surgery and
optimism predicted depression

Peris (2011)62/ Cross-sectional Control: Major trauma Controle: Control: HADS ≥11 Intervention group had lower rate of anxiety
Italy using historical 86/72.1% 12 months 38.5/20.1 44.9 8.9% vs 17.4% and depression 6.5% vs
controls Intervention: Interventione: Intervention: 12.8%
123/83.7% 44.1/17.8 43.7

Wade (2012)63/UK Prospective 100/52% Level 3 patients 22/8f 57 CES-D ≥19 Probable depression 46.3%
3 months STAI ≥44 Probable anxiety 44.4%

Schandl (2013)64/ Prospective 150/41.5% General ICU 55e/1.5/6 Adverse HADS ≥8 Overall 31% had adverse psychological
Sweden 2 months psychological outcomes
outcome group 35 (23%) high anxiety scores
= 54 19 (12.6%) high depression scores
No adverse
psychological
outcome group
= 60

Kowalczyk Retrospective, 195/57.5% General ICU 14.9/not 48.1 HADS >10 64 (34.4%) scored above anxiety threshold
(2013)65 cross-sectional Variable length reported 51 (27.4%) above depression threshold
Poland of time after ICU
a
APACHE II score.
b
Hospital Anxiety and Depression Scale.
c
Geriatric Depression Scale – Short Form.
d
APACHE III score.
e
Simplified Acute Physiology Score.
f
CHAPTER 4 RECOVERY AND REHABILITATION

Median value.
BAI = Beck Anxiety Instrument; BDI = Beck Depression Instrument; CES-D = Center for Epidemiologic Studies – Depression Scale; GDS = Geriatric Depression Scale – Short Form;
ICU LOS = intensive care unit length of stay.
77
78 SECTION 1 SCOPE OF CRITICAL CARE

Patients often exhibit high levels of distress at the time thoughts, avoidance behaviours, negative alterations in
of hospital discharge and these tend to reduce during the cognitions and mood and hyper-arousal symptoms.72
first year after discharge.50,51 However, the episodic timing Individuals can re-experience a traumatic event through
of assessments may not fully capture patterns of anxiety involuntary unwanted thoughts, often in the form of
and depression, and establish whether full resolution is ‘flashbacks’ and/or ‘nightmares’. Individuals experienc-
achieved, or identify a later onset problem. For example, ing these thoughts often develop avoidant behaviours in
in patients with ARDS, levels of depression increased from the belief this action will reduce the intrusive thoughts.
16% at 1 year after discharge to 23% at 2 years.57 This may Avoidant behaviours for intensive care patients can range
reflect prolonged recovery in general for this subgroup from simply avoiding television programs about hospitals,
of patients, who tend to be among the most critically ill not talking about their ICU experience or, more seriously,
patients, with a mean ICU stay of 34 days noted. A rise non-attendance at a follow-up clinic or other hospital
in depression scores may therefore be a reflection of that out-patient appointments. The latter also compounds
prolonged physical recovery. the issue of accurate prevalence. Negative alterations in
Depression is also associated with other aspects of cognitions and mood may include continuing self-blame
recovery and, in particular, HRQOL. Depressed patients or blaming others about the cause or consequences of the
tend to rate their HRQOL as poorer than those who critical illness.72 Hyper-arousal behaviours include diffi-
are not.50,57 However, what is less clear is the direction of culties in concentrating or falling asleep. Future assessment
this relationship; it could be that patients with a poorer of post-traumatic stress in survivors of a critical illness
HRQOL tend to be depressed rather than depression should examine all four symptom areas.
leading to perceptions of poorer HRQOL. Patients As with other psychological symptoms such as anxiety
who have psychological problems prior to intensive and depression, it has been difficult to establish the pre-
care are likely to develop these after discharge. Although valence of PTSD after intensive care because of the use
assessment of pre-ICU status is difficult, in some cases this of self-report measures, different research designs, varied
infor mation can be obtained from relatives or caregivers. patient case-mix and international variations in the delivery
It is becoming increasingly clear that depression is of intensive care. These variations have resulted in over-
closely associated with post-traumatic stress symptomato- estimation of the prevalence of PTSD and post-traumatic
logy,66 and while these may be related they have distinct stress symptoms (PTSS),73 although note that patients with
differences and treatments. Patients who are depressed are significant PTSS, particularly avoidant behaviours, may be
likely to exhibit post-traumatic stress symptoms and vice less likely to participate in research studies. Patients may
versa. Diagnosis, however, can be difficult.67 have significant PTSS without developing PTSD and it is
mainly these symptoms that are assessed using the self-report
Post-traumatic stress measures. Reported prevalence of a significant post-trau-
In recent years there has been increasing interest in the matic stress reaction or PTSD ranges from 5% to 64%.63,70
development of post-traumatic stress reactions such as What is emerging from the literature is that there
post-traumatic stress disorder (PTSD) as a response to are certain non-modifiable and modifiable risk factors
critical illness,68,69 and there is increasing recognition of that predict subsequent anxiety, depression and post-
these symptoms as a problem for some intensive care traumatic stress symptoms, although not consistently. The
survivors.4,70 Individuals are required to meet a number of non-modifiable factors are those associated with individ-
criteria before a diagnosis of PTSD is considered, and in uals and include: previous psychiatric history,48 previous
2013 the American Psychiatric Association presented the stressful events,66 admission as a result of trauma,67 women
DSM-V criteria for PTSD (see Box 4.1 for these criteria). rather than men49,50,74 and younger patients more anxious
Many symptoms of post-traumatic stress that patients than older patients.50 Interestingly, individual charac-
experience in the initial days after intensive care discharge teristics such as employment and level of education also
may be considered a normal reaction, and it is important appear to predict those most at risk.5,61,64 The modifiable
that practitioners clearly separate the normal from the factors tend to be those associated with the critical illness
abnormal response.This is achieved by assessing the severity experience. Patients with a longer ICU stay,50,51 longer
and duration of symptoms, and their effect on an indi- duration, type and dose of sedation and/or neuromuscu-
vidual’s life. PTSD should not be diagnosed until at least lar blockade,63 mechanical ventilation,41,59 use of restraints
1 month after the event, and until the symptoms have been and in-ICU stress or agitation63,75 are more likely to report
present for 1 month. Symptoms commonly cause problems post-traumatic stress symptoms. Early signs of acute stress
in relation to work, social or other important activities;72 or depression are a strong predictor of ongoing problems.50
this is important to consider when developing critical care Other consequences of being in intensive care such as
follow-up services. Importantly, PTSD symptoms may be neuropsychological impairment can also predict signifi-
reactivated after some time, and being in ICU may serve as cantly higher depression scores.55
a catalyst for some patients, e.g. reliving a war event.44 What is also evident in the emerging literature is the
Signs of post-traumatic symptomatology include four effect of patients’ subjective intensive care experiences.
main symptom areas (this is a change from Diagnostic and These experiences tend to be reported as unpleasant
Statistical Manual of Mental Disorders (DSM-IV) criteria memories of being in ICU31,44,61,76,77 and are discussed later
where three symptom groups were recognised): intrusive in this chapter.
 CHAPTER 4 RECOVERY AND REHABILITATION 79

BOX 4.1

Post-traumatic stress disorder diagnostic criteria71

Criterion A: Stressor – The person was exposed to: 1 Inability to recall key features of the traumatic event
death, threatened death, actual or threatened serious (usually dissociative amnesia: not due to head
injury or actual or threatened sexual violence, as follows injury, alcohol or drugs)
(one required): 2 Persistent (and often distorted) negative beliefs and
1 Direct exposure expectations about oneself or the world (e.g. I am
2 Witnessing, in person bad, the world is completely dangerous)
3 Indirectly, by learning that a close relative or close 3 Persistent distorted blame of self or others for causing
friend was exposed to trauma. If the event involved the traumatic event or for resulting consequences
actual or threatened death, it must have been 4 Persistent negative trauma-related emotions
violent or accidental (e.g. fear, horror, anger, guilt or shame)
4 Repeated or extreme indirect exposure to aversive 5 Markedly diminished interest in (pre-traumatic)
details of the event(s) usually in the course of significant activities
professional duties. This does not include indirect 6 Feeling alienated from others (e.g. detachment or
non-professional exposure through electronic estrangement)
media, television, movies or pictures 7 Constricted affect: persistent inability to experience
Criterion B: Intrusion symptoms – The traumatic event positive emotions
is persistently re-experienced in the following way (one Criterion E: Alterations in arousal and reactivity –
required): Trauma-related alterations in arousal and reactivity
1 Recurrent, involuntary and intrusive memories that began or worsened after the traumatic event (two
2 Traumatic nightmares
required):
3 Dissociative reactions (e.g. flashbacks), which
1 Irritable or aggressive behaviour
may occur on a continuum from brief episodes to
2 Self-destructive or reckless behaviour
complete loss of consciousness
3 Hypervigilance
4 Intensive or prolonged distress after exposure
4 Exaggerated startle response
to traumatic reminders
5 Problems in concentration
5 Marked physiological reactivity after exposure to
6 Sleep disturbance
trauma-related stimuli
Criterion F: Duration
Criterion C: Avoidance – Persistent effortful avoidance
of distressing trauma-related stimuli after the event Persistence of symptoms (in Criteria B, C, D and E) for
(one required): more than 1 month
1 Trauma-related thoughts or feelings Criterion G: Functional significance
2 Trauma-related external reminders Significant symptom-related distress or functional
Criterion D: Negative alterations in cognitions and impairment (e.g. social, occupational)
mood – Negative alterations in cognitions and mood Criterion H: Exclusion
that began or worsened after the traumatic event (two Disturbance is not due to medication, substance use,
required): or other illness

Memories and perceptions These memories often seemed ‘real’ and were distressing
to patients at the time, and may be recalled in detail some
Interestingly, illness severity does not consistently predict a
months afterwards.44 Having delusional rather than factual
PTSS reaction,40,50 but such a reaction is more likely to be memories is more likely to result in distress;31,50,82 and lack
influenced by patients’ perceptions of their intensive care of memory for factual events may result in longer term
experience. This is one of the unique features of being in psychological problems,53 with the important element
intensive care: patients have limited recall for factual events being the content of the ICU memories rather than the
and often report large gaps where they remember very number of memories. Studies exploring post-traumatic
little about their critical illness. Some patients will report stress after ICU are summarised in Table 4.2.
upsetting or unpleasant factual memories such as pain,
oxygen masks on a patient’s face and difficulty breathing.78 Cognitive dysfunction
However, frequently, patients’ accounts include disturbing Cognitive impairment in survivors of critical illness has
recollections with memories of ‘odd perceptual experi- only been recognised and measured in the past decade.
ences’,79,80 ‘nightmares’ or ‘hallucinations’.31,44,78 While Although there is some variation in prevalence and severity,
not all patients experience these, those who do so tend in general more than 50% of survivors report cognitive
to report memories that are persecutory in nature,78 impairment at the time of hospital discharge and approxi-
are often associated with feelings of being elsewhere,80 mately one-quarter continue to have problems 12 months
reliving a previous life event81 or fighting for survival.80 later (Table 4.3).6,11 Cognitive problems include memory,
 80

TABLE 4.2
Summary of studies examining post-traumatic stress symptoms (PTSS) in survivors of critical care

FIRST AUTHOR/ A C U I T Ya / INSTRUMENT/

COUNTRY DESIGN N/% MALES COHORT ICU LOS AGE CUT-OFF SCORE MAIN FINDINGS
Perrins (1998)83/ Prospective 38/– General ICU; 6 weeks, 6 –/6 49 IES/– Avoidance and intrusion scores reduced
UK and 12 months post-ICU at 12 months; scores associated with
discharge patients’ recollection of ICU – those with
no recall had higher scores
Schelling Retrospective 80/51% ARDS; patients 22/31 36 PTSS >35 25% scored above cut-off score;
(1998)40/Germany cross-sectional discharged over 10-year symptoms associated with the number of
period traumatic memories of ICU
Nelson (2000)51/ Cross-sectional 24/58% 19 months (mean) after 58/27 40 7-item Significant correlation with days of
UK acute lung injury questionnaire sedation and days of neuromuscular
SECTION 1 SCOPE OF CRITICAL CARE

blockade and PTSS scores

Scragg (2001)52/ Cross-sectional 80/52% Admitted to ICU over –/– 57 IES ≥20 12% high levels of avoidance, 8% high
UK previous 2 years levels of intrusive thoughts. Younger
patients had higher IES scores
Jones (2001)53/ Cohort study 30/66% General ICU; 2 and 17/8 57 IES Patients with no factual but who reported
UK 8 weeks delusional memories had higher IES scores
at 8 weeks
Jones (2003)54/ RCT 116/61% General ICU patients – 17/14 58 IES >19 Patients who received 6-week
UK 3 hospitals; 8 weeks and rehabilitation program had lower IES
6 months after discharge scores at 8 weeks but not 6 months;
51% scored >19 at 6 months
Kress (2003)85/ RCT 32/58% Medical ICU; 11–14 Control 48 IES; structured Evaluated the effect of daily sedation
USA months after hospital 18.4/12.8; clinical interview withdrawal; patients in the intervention
discharge Intervention group reported lower IES scores (not
16.2/6.9 statistically significant); 6 patients in
the control group were diagnosed with
PTSD compared with no patients in the
intervention group
Cuthbertson Prospective 78/72% General ICU 3 months 18/5.6 58 DTS ≥27 – high 22% demonstrated high level of PTS
(2004)41/UK cohort after discharge level symptoms and 12% confirmed PTSD
≥40 PTSD
Kapfhammer Cross-sectional 46/52% ARDS; median 8 years 22.5/– 36 PTSS-10 >35 24% of patients diagnosed with PTSD;
(2004)47/Germany after treatment a further 17% had sub-threshold PTSD;
those with PTSD reported a poorer HRQOL
Rattray (2005)50/ Prospective 80/64% General ICU; hospital 17.7/4.9 55 IES ≥20 12% reported severe avoidant behaviour,
UK longitudinal discharge, 6 and 12 18% severe intrusive thoughts at
months 12 months; scores did not reduce over
12 months and were associated with
reported ICU memories and age
Sukantarat Prospective 51/43% In ICU ≥3 days; 3 and 15.3/16.9 57.4 IES: intrusion ≥21; Intrusion in 24% at 3 months and 20% at
(2007)58/UK 9 months after ICU avoidance ≥18 9 months; avoidance in 36% at 3 months
discharge and 38% at 9 months
FIRST AUTHOR/ A C U I T Ya / INSTRUMENT/
COUNTRY DESIGN N/% MALES COHORT ICU LOS AGE CUT-OFF SCORE MAIN FINDINGS
86
Wallen (2008) / Predictive 100/68% ≥24 hours ICU LOS; 13.0/2.4 63 IES-R ≥33 Mean IES-R=17.8; 13% scored higher than
Australia cohort medical/surgical ICU; cut-off score; those ≤65 years were
1 month after discharge 5.6 times more likely to report PTSS
Weinert (2008)82/ Prospective 149/52% Medical and surgical ICUs; –/– 54 PTSD PTSD prevalence at 2 months was 17%
USA 2 and 6 months 6 positive and this had reduced to 15% by 6 months;
responses across patients who reported delirious memories
3 domains had higher PTSD scores
Myhren (2009)61/ Cross-sectional 255/63% Medical/surgical ICUs SAPS 37/12 48 IES ≥35 25% above threshold
Norway and CCU; 4–6 weeks days
postdischarge
Myhren (2010)60/ Longitudinal 3 and 12 months 27% above threshold at 12 months; no
Norway differences in scores across time; high
education level, optimism trait, factual
recall, memory of pain were independent
predictors of PTSS
Peris (2011)62/ Cross-sectional Control: Major trauma Controle: Control: IES-R Intervention group had lower risk of PTSD
Italy using historical 86/72.1% 12 months 38.5/20.1 44.9 (21.1% vs 57%)
controls Intervention: Interventione: Intervention:
123/83.7% 44.1/17.8 43.7

Wade (2012)63/UK Prospective 100/52% Level 3 patients 22/8f 57 PDS ≥18 Probably PTSD 27.1%
3 months Strongest predictors were in-ICU mood,
intrusive memories, perceived illness and
psychological history
Bienvenu Prospective 186/55% Acute lung injury 23/13 IES-R item mean 35% had PTSD symptoms during the
(2013)87/USA 3, 6, 12, and 24 months score ≥1.6 2-year follow-up
Symptoms enduring
Schandl (2013)64/ Prospective 150/415% General ICU 55e/1.5/6 Adverse PTSS-10 >35 Overall 31% had adverse psychological
Sweden 2 months psychological outcomes
outcome group 21 (14%) high PTSS scores
= 54
No adverse
psychological
outcome group
= 60
a
APACHE II score.
b
Hospital Anxiety and Depression Scale.
c
Geriatric Depression Scale – Short Form.
d
APACHE III score.
e
Simplified Acute Physiology Score.
CHAPTER 4 RECOVERY AND REHABILITATION

f
Median value. ARDS = adult respiratory distress syndrome; DTS = Davidson Trauma Scale; HRQOL = health-related quality of life; ICU LOS = intensive care unit length of stay; IES
= Impact of Event Scale; PTSD = post-traumatic stress disorder; PTSS = post-traumatic stress symptoms; SAPS = Simplified Acute Physiology Score.
81
 82

TABLE 4.3
Summary of recent studies examining cognitive function after critical illness

AUTHOR/ ACUITY / ICU

C O U N T RY DESIGN N/% MALES COHORT LOS AGE INSTRUMENT MAIN FINDINGS

Adhikari Prospective 109 (71 ARDS patients APACHE II Median = 42 Memory Assessment MAC-S scores were 76 (IQR 61–93) for
200989/ cohort; variable completed (median) – 23 (IQR 35–56) Clinics Self-Rating Scale Ability and 91 (IQR 77–102) for Frequency of
Canada follow-up cognitive (IQR 15–27); (MAC-S) Occurrence; 8% and 16% of respondents
including assessment)/– ICU LOS (median) were >2 and 1.5 SD, respectively, below
6 months and 1, – 27 (IQR 16–51) USA norms
2, 3 and 4 years days
Duning Case-control 74/44 (59%) Surgical ICU SAPS – mean Mean 66.3 ± MMSE; Boston Naming Impaired neurocognitive function (compared
201090/ study of patients 39 ± 2.3; 1.3 years Test; Nuernberg to age-matched healthy controls) was
Germany patients who ICU LOS – mean Gerontopsychological PKLU[PÄLKPUTVZ[[LZ[Z"WH[PLU[Z^OV
SECTION 1 SCOPE OF CRITICAL CARE

experienced 15.2 ± 1.6 days Inventory; WMS-R; experienced hypoglycaemia experienced

™LWPZVKLVM Trailmaking Tests A and ZPNUPÄJHU[PTWHPYTLU[VM]PZ\VZWH[PHSZRPSSZ
hypoglycaemia B; Color word interference compared to those who did not experience
or not task (interference hypoglycaemia; other domains were similar
condition); Regensburg between the groups
Word Fluency Test; Rey-
Osterrieth Complex Figure
Test; Auditory verbal
learning test; Recognition
Ehlenbach Prospective Total study Older Not described Mean = 75.4 Cognitive Abilities Critical illness hospitalisation resulted in a
201091/ USA cohort population individuals (SD 6.6) Screening Instrument change in reduction in CASI by -1.5 (-3.0–
2,929; (> 65 years) with (CASI) = continuous 1.0) for the interval that included a critical
n=41 critical illness score 0 to 100 PSSULZZOVZWP[HSPZH[PVUUV[ZPNUPÄJHU[
experienced ‘Cases of dementia’ 31.1 cases of dementia per 1,000 person-
critical illness/ years (95% CI 12.9–74.6) for critically ill
23 (56%) 14.6 cases per 1,000 per years (95% CI
12.6–17.0) for never hospitalised
Girard 201014/ Prospective 126 (77 Medical ICU APACHE II Median 61 Digit Span; Trailmaking Cognitive function at 3 mths: no impairment
USA cohort completed patients – median 29 (IQR 47–71) Tests A and B; Digit – 16/76 (21%); mild/moderate impairment
cognitive (23–34) years Symbol Coding; RAVLT; – 13/76 (17%); severe impairment – 47/76
assessment)/ Rey-Osterreith Complex (62%); cognitive function at 12 months: no
40 (52%) Figure (copy test and impairment – 15/52 (29%); 18/52 (35%);
30-minute delay); Verbal 19/52 (36%);
Fluency Text, MMSE Duration of delirium was an independent
predictor of cognitive impairment 3 and
12 months after ICU
Jackson Sub-study of 180/89 (49%) Medical ICU APACHE II – 28; Digit Span; Digit Symbol *VNUP[P]LPTWHPYTLU[PKLU[PÄLKPU VMHSS
201093/ USA Awakening patients SOFA – 9 Coding; MMSE; RAVLT patients at 3 months and 71% at 12 months
and Breathing Rey-Osterreith Complex Fewer patients in the intervention group
Controlled Figure – Copy; Rey- (70% versus 91%) impaired at 3 months,
(ABC) trial Osterreith Complex similar number of patients in both groups
(RCT) with 3- Figure – Delayed Recall; impaired at 12 months
and 12-month Trailmaking Tests A and Composite cognitive scores similar in both
follow-up B; Verbal Fluency Test groups at 3 and 12 months
AUTHOR/ ACUITY / ICU
C O U N T RY DESIGN N/% MALES COHORT LOS AGE INSTRUMENT MAIN FINDINGS

Sacanella Prospective 230 (112 Medical ICU APACHE II – Mean 73 ± 5.5 MMSE 10% of patients had an MMSE score <24 at
201194/Spain cohort assessed at patients aged mean 19 ± 6.0; years 12 months
1 year)/57% ™`LHYZ ICU LOS – mean
9.4 ± 10.2
Torgersen Prospective 55/ – Mixed, primarily SAPS II – mean Mean 51 ± Cambridge At hospital discharge 18/28 (64%) patients
201195/ cohort with 3- surgical ICU 35 ± 14.0; 16.2 years Neuropsychological had cognitive impairment; at 3 months 4/35
Norway and 12-month patients ICU LOS – mean Test Automated Battery (11%) and 3/30 (10%) at 12 months continued
follow-up 10 ± 9.5 days (CANTAB) to have cognitive impairment; cognitive
impairment was not associated with any pre-
ICU or in-ICU factors tested
Jackson Pilot RCT: 21/11 (52%) Medical/surgical APACHE II TOWER: Delis-Kaplan 3 month scores:
201292/USA in-home ICU patients Control – 25.5 Tower Test: ‘normal’ TOWER: higher in intervention than controls
rehabilitation (19.5–33.0); 7 to 13 (median and IQR: 13.0 (11.5-14.0) vs 7.5
over 3 months Intervention – 23 Mini-Mental State (4.0–8.5) p<0.01
(19–27); Examination Mini-Mental State Exam: Control 26.5
ICU LOS (d) The Dysexecutive (24.8–28.5); Intervention 30.0 (29.0-30.0)
Control – 5.8 questionnaire Dysexecutive: Control 16.0 (7.8–19.2);
(4.3–7.0) Intervention 8.0 (6.0–13.5)
Intervention – 3
(2.1–7.9)
Mikkelsen Cohort study 213 (122 tested ARDS patients APACHE III – Median 49 WAIS-III: Vocabulary; Cognitive impairment present in 41/75
201296/USA (sub-study PU™KVTHPU" mean 85 (63–102) (40–58) WAIS-III: Similarities; (55%) participants at 12 months. When
of FACTT by 75 tested at WMS-III: Logical JVUZPKLYPUNHSSWHY[PJPWHU[Z[LZ[LKPU™
ARDSNet) 12 months in all Memory I; Controlled domain:
domains)/43% Oral Word Association Vocabulary – 3/98 (3%)
Test; Hayling Sentence Reasoning – 3/98 (3%)
Completion Test Memory – 12/92 (13%)
=LYIHSÅ\LUJ`¶  
Executive function – 57/100 (57%)
Lower PaO2JVUZLY]H[P]LÅ\PKTHUHNLTLU[
strategy and lower CVP were associated
with cognitive impairment at 12 months
Panharipande Cohort study 821/420 (51%) Medical/surgical APACHE II Median 61 RBANS Median RBANS cognition scores at 3 and
201311/ USA with 3- and ICU patients median 25 (51–71) years Trailmaking Test B 12 months were 79 (IQR 70–86) and 80 (IQR
12-month (19–31) 71–87) respectively; these scores were
follow-up 1.5 SD below age adjusted population mean
and were similar to scores for patients with
mild cognitive impairment
40% of patients at 3 months and 34% of
patients at 12 months had scores similar to
those for patients with moderate traumatic
brain injury
CHAPTER 4 RECOVERY AND REHABILITATION

APACHE = Acute Physiology and Chronic Health Evaluation; ARDSNet = Acute Respiratory Distress Syndrome Clinical Trials Network; FACTT = Fluid and Catheter Treatment Trial;
MMSE = Mini-Mental State Examination; RAVLT = Rey Auditory Verbal Learning Test; Rey-O = Rey-Osterrieth Complex Figure; SAPS = Simplified Acute Physiology Score;
WAIS-R = Wechsler Adult Intelligence Scale = Revised; WMS-R = Wechsler Memory Scale – Revised.
83
84 SECTION 1 SCOPE OF CRITICAL CARE

attention and executive function, which in turn includes discharge, such measurement should continue for a similar
reasoning and decision making.45 These can have significant time, for example 6–12 months. In the research setting
impact upon the daily life of not just patients but families, there is a need to extend follow-up of patients beyond
and have been linked to longer term dementia. Patients 2 years to determine the long-term morbidities associated
who have been admitted to ICU for treatment of acute with critical illness and care.2
respiratory distress appear to be more likely to experience
cognitive impairment than other critical illness survivors.6 Measures of health-related quality of
Various factors have been linked to cognitive life after a critical illness
impairment including delirium, hypoxaemia, hypoten- The range of HRQOL instruments available is large, but
sion, glucose dysregulation, use of sedatives, sepsis and can be divided into two groups: generic to all illnesses
inflammation and sleep efficiency.6,11,88 Although many of or specific to a particular disease state. One limitation of
these relationships appear inconsistent, and may be more generic instruments is that, while they can be applied to a
problematic in specific sub-groups of the critical care broad spectrum of populations, they may not be responsive
population, delirium has repeatedly been shown to be to specific disease characteristics,97 and this is problematic
highly predictive of cognitive impairment. in the usually heterogeneous critical care population. A
generic instrument that measures baseline HRQOL and
Measuring patient outcomes exhibits responsiveness in a recovering critically ill patient
with demonstrated reliability and validity has been elusive,
following a critical illness although recent review papers have identified some useful
The measurement of health outcomes after critical instruments7,16 (see Table 4.4). SF-36 is the most commonly
illness is vital – both to determine patient recovery and used and validated instrument in the literature, including
inform decisions about ongoing care. Measures related with a variety of critically ill patient groups (e.g. general
to HRQOL and physical, psychological and cognitive ICU, ARDS, trauma and septic shock). In a comparison
function are discussed. of two related instruments the 15D was considered to be
It is unclear how long patient outcomes following more sensitive to clinically important differences in health
critical illness should be measured, but given ongoing status than Euro-Qol – 5 dimensions (EQ-5D) in a critical
compromise exists for months to years post hospital care cohort.98

TABLE 4.4
Health-related quality of life (HRQOL) instruments used for patients following a critical illness

INSTRUMENT ITEMS CONCEPTS/DOMAINS

Medical outcomes study 36 Physical: functioning, role limitations, pain, general health; mental: vitality, social, role
(SF-36)100,101 limitations, mental health; health transition; variable response levels (2–5)
Euro–Qol-5 dimensions 5 Mobility, self-care, usual activities, pain/discomfort, anxiety/depression; 3 response levels;
(EQ-5D)98,102 cost-utility index
15D98,103 15 Mobility, vision, hearing, breathing, sleeping, eating, speech, elimination, usual activities,
mental function, discomfort, distress, depression, vitality and sexual activity; 5-point ordinal
scale (1 = full function; 5 = minimal/no function)
Quality of life–Italian 5 Physical activity; social life; perceived quality of life; oral communication; functional limitation;
(QOL–IT)104 varied response levels (4–7)
Assessment of Quality 15 Illness (3 items); independent living (3 items); physical senses (3 items); social relationships
of Life (AQOL)105 (3 items); psychological wellbeing (3 items); 4 response levels; enables cost-utility analysis
Quality of life–Spanish 15 Basic physiological activities (4 items); normal daily activities (8 items); emotional state
(QOL–SP)106 (3 items)
Sickness impact profile 68 Physical: somatic autonomy; mobility control; mobility range
(SIP)107 psychosocial: psychic autonomy and communication; social behaviour; emotional stability;
developed from original 136-item170
Nottingham Health 45 Experience: energy, pain, emotional reactions, sleep, social isolation, physical mobility; daily
Profile (NHP)108 life: employment, household work, relationships, home life, sex, hobbies, holidays
Perceived quality of life 11 Satisfaction with: bodily health; ability to think/remember; happiness; contact with family and
(PQOL)99 friends; contribution to the community; activities outside work; whether income meets needs;
respect from others; meaning and purpose of life; working/not working/retirement; each
scored on 0–100 scale
 CHAPTER 4 RECOVERY AND REHABILITATION 85

Measures of physical function during a critical illness episode also include agitation and
confusion/delirium39 (discussed further in Chapter 7).
following a critical illness Assessment of psychological outcomes has relied
Numerous instruments have been developed to examine mainly on self-report questionnaires administered via
the physical capacity of individuals, usually focusing either a postal survey or a structured interview format.
on functional status ranging from independent to Few studies have included clinical assessments such as the
dependent.109,110 Common instruments used with indi- Clinical Administered PTSD Scale, the ‘gold standard’
viduals after an acute or critical illness are summarised for diagnosing PTSD.125 This means, therefore, that such
in Table 4.5. Many other instruments exist for specific questionnaires are screening tools that can be used to
clinical cohorts, including Katz’s ADL index111 and the identify individuals at risk of developing a significant
instrumental activities of daily living,112 but these have not clinical problem. They are not diagnostic and this is an
been used commonly with survivors of a critical illness. important point when considering designing, imple-
Physical activity associated with cardiac or pulmonary menting and evaluating any intervention. A number
dysfunction may be assessed using perceived breathlessness of standardised questionnaires have demonstrated reli-
(dyspnoea) during exercise by the modified Borg scale,113 ability and validity in this patient group, but the use of
ranging from 0 (no dyspnoea) to 10+ (maximal). The different questionnaires makes it difficult to generalise
Borg scale is commonly used with other physical activity findings. Studies that assessed anxiety and depression
instruments, e.g. the 6-minute walk test (6MWT).114 used the HADS,31,49,50,59–61 Beck Anxiety Inventory,56
Measures of psychological function State Trait Anxiety Inventory (STAI)85 and the Beck
Depression Inventory.56,85 Post-traumatic stress has been
after a critical illness assessed using the Impact of Event Scale (IES),50,53,61,85
The psychological recovery process and trajectory Post-traumatic Stress Syndrome 10-Questions Inventory
for survivors of a critical illness remains an important (PTSS-10),40 Davidson Trauma Scale,41 the Experience
but relatively under-researched area.88 Exploration of after Treatment in Intensive Care 7 (ETIC-7) item
the impact of the intensive care experience, including scale,52 Kessler-10,126 Post-traumatic Stress Symptom
ongoing stress and distress13,79,122,123 and memories for Checklist – civilian version 5 (PCL-5)127 and Post-
the patient,76,77 has now emerged in the literature as an traumatic Stress Diagnostic Scale (PDS).128
important area of research and practice. Instruments that These instruments often include ‘cut-off ’ or
assess mood and mental wellbeing after a critical illness ‘threshold’ scores that enable screening for the presence
focus on psychological constructs, including anxiety, or severity of a disorder. For example, a score of 8–10
depression, fear and post-traumatic stress symptoms124 on either subscale of the HADS indicates the possible
(see Table 4.6). Constructs that relate to an individual presence of a disorder, while a score of 11 or above

TABLE 4.5
Common measures of physical function following a critical illness

INSTRUMENT MEASUREMENT SCORE RANGE/COMMENTS

St George’s Respiratory COPD-specific items assessing three domains: Item responses have empirical weights; higher
Questionnaire (SGRQ),121 symptoms (7 items), activity (2 multi-part scores indicate poorer health; used with patients
(SGRQ-C)120 items), impacts (5 multi-part items) with chronic lung disease, including ARDS
Six-minute walk test Walk distance, reflects functional capacity in Assesses walk function in patients with
(6MWT)114 respiratory or cardiac diseases moderate heart failure, ARDS
Barthel Index (BI)118,119 10 items of functional status (activities of daily Dependence: total = 0–4; severe = 5–12;
living [ADLs]) moderate = 13–18; slight = 19; independent = 20
Functional Independence Severity of disability in inpatient rehabilitation 18 activities of daily living in two themes: motor
Measure (FIM)117 settings (13 items), cognitive (5 items); 7-point ordinal
scales; score range 18–126 (fully dependent–
functional independence)
Timed Up and Go (TUG)116 Functional ability to stand from sitting in a chair, ≤10 seconds = normal; ≤20 seconds = good
walk 3 m at regular pace and return to sit in the mobility, independent, can go out alone;
chair 21–30 seconds = requires supervision/walk aid
Shuttle walk test (SWT)115 10-m shuttle walk with pre-recorded audio Participant keeps pace with audio sounds;
prompts to complete a shuttle turn 12 levels of speed (0.5–2.37 m/second)

ARDS = adult respiratory distress syndrome.

86 SECTION 1 SCOPE OF CRITICAL CARE

TABLE 4.6
Examples of common measures of psychological function after critical illness

INSTRUMENT MEASUREMENT SCORE RANGE

130
Impact of Event Scale (IES); 15-item; assesses levels of post-traumatic Frequency of thoughts over past 7 days;
IES-R131 distress; two subscales: intrusive thoughts, 0 = no thoughts; 5 = often; higher scores
avoidance behaviours; revised form (IES-R) indicate greater distress: scores ≥26 (combined
adds hyper-arousal subscale (7 items)131 intrusion and avoidance) are significant
Hospital Anxiety and 14-item (4-point scale); measures mood Combined score ≥11 indicates a clinical
Depression Scale (HADS)129 disorders in non-psychiatric patients; focuses disorder
on psychological rather than physical
symptoms of anxiety and depression
Center for Epidemiologic 20-item self-report scale assesses frequency Score range 0–60; higher scores reflect
Studies – Depression Scale and severity of depressive symptoms increased symptoms and severity
(CES–D)132 experienced in the previous week
Kessler 10 (K-10)133 10-item (5-point scale) self-report measure of Score range 10–50; higher scores reflect
non-specific psychological distress over the greater distress
past 4 weeks
Post-traumatic stress disorder 20-item (5-point scale) self-report assessment Score range 20–100; higher scores reflect
(PTSD) checklist (PCL)134 of symptoms of PTSD corresponding to DSM-V increased symptoms of PTSD
criteria
Post-traumatic Stress 14-item extended version of the PTSS 10 to 2 parts: Part A – Assessment of traumatic
Symptoms 14 (PTSS 14)135 cover all aspects of PTSD consistent with memories from ICU; Part B – Post-traumatic
Diagnostic and Statistical Manual of Mental stress disorder symptoms; score range 14–98
Disorders (DSM-IV) symptom categories

indicates probable presence of such a condition.129 One in an in-person format, so testing over the phone or via
limitation of these self-report measures is that while mailed questionnaires is limited. Repeated testing with
sensitivity (ability to correctly identify all patients with the same instrument on multiple occasions may lead to
the condition) can be high, specificity (ability to correctly practice effects, in other words the critical illness survivor
identify all patients without the condition) is less easy to learning how to perform better on the test; hence instru-
determine, and therefore the incidence of psychological ments with multiple versions prove beneficial in some
distress may be overstated.This makes estimation difficult circumstances. Further, some of the tests need to be admin-
and is one of the challenges in establishing the actual istered by qualified psychology or psychiatry personnel.
magnitude of psychological distress after a critical illness. Where neuropsychological testing can be carried out,
Other challenges include the recruitment of different it enables assessment of the nature, severity, prevalence
cohorts or subgroups of patients (e.g. patients with adult and incidence of cognitive impairment.136 Cross-cultural
respiratory distress syndrome56 or acute lung injury51). differences do exist in some of the domains measured in
Variations in the international provision of ICU services neuropsychological assessment so where comparison to
also mean that differences may exist in case-mix in the normative data is required for analysis and interpretation,
areas of illness severity, planned or unplanned admissions, for example in the Repeatable Battery for the Assessment
ages and reasons for admission. of Neuropsychological Status (RBANS), country-specific
data are required.137
Measures of cognitive function after a The most commonly used brief measure is the Mini
Mental Status Examination MMSE);138 however, criticisms
critical illness of insensitivity, susceptibility to ceiling effects and limited
Cognitive or neuropsychological assessment of critical capacity to differentiate between cognitive domains are
illness survivors has only become more common in often levelled at brief measures.137 In contrast, more lengthy
the past 10 years. Comprehensive and lengthy testing measures such as the RBANS,139 Trail Making Test,140 the
batteries exist, although those used in studies examining Wechsler Memory Scale – revised141 and the Wechsler
recovery after critical illness have tended to favour the Adult Intelligence Scale – revised142 provide more detail
slightly shorter testing (Table 4.7). More than 30 minutes and better differentiation of memory problems but often
is generally still required for this assessment, which may tire those being tested, particularly older people. Scales
tire some people, particularly early in their recovery phase such as the Memory Assessment Clinics Self-rating Scale
after critical illness. Neuropsychological instruments are (MAC-S)143 and Cognistat144 offer an option in between
non-invasive; however, many of them need to be used these two extremes.
 CHAPTER 4 RECOVERY AND REHABILITATION 87

TABLE 4.7
Neuropsychological instruments to assess cognitive function in patients following a critical illness

INSTRUMENT MEASUREMENT SCORE RANGE / COMMENTS

Mini-Mental State 11 items in 5 domains including orientation, Score of ˜23, or 2 points below maximum in
Examination (MMSE)138 memory, attention and concentration, delayed any domain, indicates the presence of moderate-
recall, language to-severe cognitive impairment; 5–10 minutes to
administer
Repeatable Battery Measurement of multiple areas of cognitive RBANS must be administered by a qualified
for the Assessment of functioning across 5 indices covering the psychologist; designed as a paper-and-pencil
Neuropsychological Status domains of immediate memory, visuospatial/ screening battery; has multiple versions to allow
(RBANS)139 constructional, language, attention, delayed for multiple testing without problems of practice
memory effect
Trail Making Test140 Part A requires the rapid connection of Score is obtained as the number of seconds
25 sequential numbers; Part B measures required to complete each part (the examiner
visual scanning, visuospacial sequencing and points out errors as they occur so correction time
cognitive set shifting by requiring connection of is included); this is then converted to a 10-point
25 alternate numbers and letters in ascending scale with 10 as the best possible score in each
sequence part; Total score ˜12 indicates impairment
Memory Assessment 42 items grouped into 2 scales including Ability domains include remote personal
Clinics Self-Rating Scale 21 ability items, 24 frequency of occurrence items memory; numeric recall; everyday task-oriented
(MAC-S)143 and 4 global rating items; assessment on a memory; word recall/semantic memory; spatial/
5-point Likert scale from very poor to very good topographic memory
Frequency of occurrence domains include word
and fact recall or semantic memory; attention/
concentration; everyday task-oriented memory;
general forgetfulness; facial recognition
Neurobehavioural Screening test to assess 5 domains including Available in web-based format and has been
Cognitive Status language, construction, memory, calculations translated into multiple languages, normative
Examination (NCSE)144 and reasoning data exist for adolescents and adults aged
(now known as Cognistat) 60–64, 65–74 and 75–84 years (http://www.
cognistat.com)
Wechsler Memory Scale – Measures different memory functions in adults; Performance reported as 5 index scores
Revised (WMS-R)141 7 sub-tests including spatial addition, symbol including auditory memory, visual memory,
span, design memory, general cognitive screener, visual working memory, immediate memory and
logical memory, verbal paired associates, visual delayed memory
reproducing
Wechsler Adult Intelligence Measures intelligence in adults and older 10 core sub-tests and 5 supplemental
Scale – Revised adolescents; although it is used to measure sub-tests; 4 index scores (verbal comprehension
(WAIS-R)142 intelligence rather than cognition, it is often used and working memory that combine to provide
in combination with WMS-R Verbal IQ Index; perceptual organisation and
processing speed that combine to provide
Performance IQ Index) as well as the overall full
scale IQ

Improving recovery following a while the patient remains in ICU and are directed
towards limiting the detrimental effects of intensive care
critical illness or promoting recovery as early as possible. Other inter-
ventions to improve recovery may be delivered after the
Survivors of critical illness experience multidimen- patient has left the ICU but remains in the hospital or
sional and protracted compromise over weeks to months after discharge from hospital. These later strategies are
and often extending to years. Interventions to improve often delivered in collaboration with other members of
recovery following critical illness can be delivered at the healthcare team. Although there is limited evidence
multiple time points in the critical illness continuum. of specific strategies that are effective in improving
Some of these interventions are the primary responsibility recovery, there is building evidence of the principles that
of the multidisciplinary critical care team, are delivered should underpin these strategies.15
88 SECTION 1 SCOPE OF CRITICAL CARE

Interventions delivered in ICU early mobilisation, has also been proposed,160 and although
this has not yet been confirmed in research as an effective
Interventions to improve long-term recovery that are
strategy, it has great potential and few disadvantages if
delivered in the ICU focus on strategies to minimise the
appropriate preparation is provided.
detrimental effects of critical illness and the associated care.
Implementation of ‘early’ activity for ICU patients
These interventions might focus on one aspect of care, for
relates to after clinical stabilisation is evident, and includes
example sedation minimisation or early mobilization, or
those still intubated. Factors to ensure patient safety during
might be multidimensional, for example targeting sedation
mobilisation have been identified, including confirming
minimisation, optimisation of sleep and limitation of the
that a patient has sufficient cardiovascular and respira-
use of restraints as a combined intervention. The majority tory reserve and cognitive function.161 Potential barriers
of interventions delivered within the ICU are targeted at to mobilisation during mechanical ventilation (e.g. acute
improving physical function. lung injury, vasoactive infusions) have also been examined
Interventions to minimise ICU-AW, particularly and include clinical instability, excessive staff turnover,
in relation to muscle de-conditioning from disuse (e.g. morale issues and a lack of respect among disciplines.148,158
sedation; bed-rest) have recently focused on active exercises Physiotherapy recommendations for physical de-
and mobility, including while patients are intubated and conditioning include development of ‘exercise prescrip-
ventilated.145 Multiple studies have demonstrated the safety tions’ and ‘mobilising plans’.161 Activities range from passive
and feasibility of ICU-based early mobilisation interven- stretching and range of motion exercises for limbs and
tions,146–149 although few interventions have had sufficient joints to positioning, resistive muscle training to electrical
testing yet to show improvement in patient outcomes. stimulation, aerobic training and muscle strengthening and
Interventions that have shown initial benefit in small studies ambulation.150,162 Specific mobility activities include:
include in-bed cycling using an ergometer,150 a combina-
tion of functional electrical stimulation and cycling151 or • in-bed (range of motion, roll, bridge, sitting on the
early exercise and mobilsation152 (see Table 4.8). edge of the bed)
In addition, strategies primarily directed towards • standing at the side of the bed
minimising sedation, and therefore facilitating more • standing on the tilt-table
patient movement, have demonstrated effectiveness. In a
Danish setting the use of a ‘no sedation’ strategy resulted
• transfer to and from bed to chair
in less mechanical ventilation time and a shorter stay in • marching on the spot
ICU, although it should be noted that patients in the ‘no • walking
sedation’ group did receive morphine for analgesia and • neuromuscular electrical stimulation
sedative agents such as propofol and haloperidol when
needed.155 On a similar theme, patients who received a
• bedside cycle ergometry.
combined spontaneous awakening trial and spontaneous Patient support for each activity ranges from assistance
breathing trial also spent less time ventilated and in ICU.156 with 1–2 staff through to independence under supervision.
An early multidimensional intervention that combined Inspiratory muscle training has been used for weakness
many of the above elements and was referred to by the associated with prolonged mechanical ventilation, using
acronym ABCDE has been proposed to minimise physical, resistance and threshold-training devices. While there
psychological and cognitive sequelae in ICU survivors.157 is beginning evidence that inspiratory muscle training is
This bundle of care incorporates: effective,163 this evidence is not consistent.164
A survey of practices in Australian ICUs noted that 94%
A awakening the patient daily of physiotherapists prescribed exercise frequently for both
B breathing trials (to minimise mechanical ventilation ventilated and non-ventilated patients, but practices did
duration) vary widely and no validated functional outcome measures
C coordination (of daily awakening and spontaneous were used.165 When mobilisation practices were explored
breathing trials) in point prevalence assessments in both Australia and
Germany, almost no mechanically ventilated patient was
D delirium monitoring
mobilised166,167 with activity of the mechanically ventilated
E exercise/early mobility (requires a patient to be limited to in-bed exercise or sitting on the edge of the bed.
awake, alert and cooperative). As noted earlier, a culture of patient wakefulness
Effective implementation of any of these interven- and early in-ICU activity and mobility is advocated but
tions requires a change in how critical care clinicians challenged by the status quo of work practices and health
care for their patients and this requires a cultural shift professional role delineations.158,159,168 A re-engineering
with a multidisciplinary team approach and changes in of work processes and practices to promote patient
care processes.158,159 Strong leadership in the process and activity is therefore required to ensure optimal outcomes
a culture of safety and improvement within the ICU are for survivors of a critical illness. Few reports of achieving
perceived as important factors to aid implementation of this change are available, but initial evidence suggests it is
interventions such as early mobilisation.158 Involving the possible to change practice in the local environment so
family in interventions to support recovery, including that more patients are mobilised.169
 CHAPTER 4 RECOVERY AND REHABILITATION 89

TABLE 4.8
Recent studies of in-ICU mobility

FIRST
AUTHOR/
C O U N T RY DESIGN N/AGE COHORT INTERVENTION MAIN FINDINGS

Morris 2008147/ Cohort 330/55 Acute ‘Mobility team’a > 20 Out of bed: 5 vs 11 days (p < 0.001)
USA respiratory min 3×/day ICU LOS: 5.5 vs 6.9 days (p = 0.025)
failure < 48 Hospital LOS: 11.2 vs 14.5 days (p = 0.006)
hours MV
Burtin 2009150/ Randomised 90/57 Prolonged Daily exercise; 20 mins 6MWD (hospital discharge): 196 vs 143 m
Belgium controlled trial ICU with bedside cycle (<0.05)
(expected ergometerb from day 5, Isometric quadriceps: 2.37 vs 2.03 Newton (n.s.)
12 day LOS) 5 days/week SF-36 PF: 21 vs 15 (p < 0.01)
ICU LOS: 25 vs 24 days (n.s.)
Hospital LOS: 36 vs 40 days (n.s.)
Schweickert 2-site 104/56 ICU patients Exercise and Independent function (hospital discharge): 59%
2009152/USA randomised with <72 mobilisation (PT vs 35% (p = 0.02)
controlled trial hours MV and OT)c for stable Ventilator free days: 23.5 vs 21.1 (n.s.)
and awake patients; ICU LOS: 5.9 vs 7.9 days (n.s.)
activity based on Hospital LOS: 13.5 vs 12.9 days (n.s.)
patient stability and Barthel Index (hospital discharge): 75 vs 55 (n.s.)
tolerance 1 serious adverse event in 498 therapy
sessions (desaturation <80%) and 4%
sessions discontinued due to patient
instability
Bourdin 2010153/ Cohort 20/68 ™KH`Z0*< Protocol of chair Contraindication to mobility intervention on
France ™KH`Z4= sitting, tilt-table, 230/524 (43%) patient days
walking activities; 425 mobility interventions performed, complete
33% during MV data on 275 (65%)
91 (33%) interventions during MV
Common interventions were sitting in chair
(55%), tilt-up ± arm support (33%), walking 11%
Adverse event occurred in 3% interventions
(no harm)
Needham Before/ 57/52 ™KH`Z4= Structured QI model, Reduced benzodiazepine dose (pre: 50%, post:
2010154/USA after Quality multi-disciplinary 25%, p = 0.02)
Improvement team, new PT and OT Increased number of functional mobility
(QI) project referral and sedation treatments (pre: 56%, post: 78%, p = 0.03)
reduction guidelines
Pohlman Intervention arm 49/58 <3 days Sedation interruption, Intubated participants sat at edge of bed in
2010148/USA of randomised MV with PT/OT rehabilitation 60%, stood in 33% and ambulated in 15% of
controlled trial expected protocol,d sessions sessions
further MV 25–30 minutes
Denehy 2013149/ Randomised 150/61 >5 days in Exercise rehabilitation No major adverse events
Australia controlled trial ICU in ICU, ward and 5VZPNUPÄJHU[KPɈLYLUJLZH[OVZWP[HSKPZJOHYNL
outpatients 3, 6 or 12 months in 6MWD, TUG, AQoL, SF-36
Parry 2014151/ Observational 16/63 Septic ICU FES-cycling Number of cycling sessions – 8/patient
Australia patients, >48 interventione Total cycling sessions provided 69 (73%) out of
hours MV, in 20–60 minutes daily, possible 95
ICU >4 days 5 times/week 1 minor adverse event (SPO2 86% requiring FiO2
increase)

6MWD = 6-minute walk distance; AQOL = Assessment of Quality of Life instrument; FES = Functional Electrical Stimulation;
MV = mechanical ventilation; n.s. = not significant; OT = occupational therapy; PT = physiotherapy; SF-36 = Short Form 36 Health Survey;
TUG = Timed Up and Go test.
a
Registered nurse, nursing assistant, physical therapist team; passive range of motion (ROM), turning, active resistance, sitting, transfer.
b
Passive or active cycling, 6 levels of increasing resistance; sedated patients received passive cycling at 20 cycles/minute.
c
Daily passive ROM for unresponsive; after daily interruption of sedation, assisted and independent active ROM supine, bed mobility
(transferring to upright sitting and balance) and activities of daily living (ADLs), transfer training (sit-to-stand from bed to chair), pre-gait
exercises, walking.
d
Passive ROM for unresponsive; assisted and independent active ROM supping, bed mobility (lateral rolling, transferring to upright sitting),
balance, ADLs, transfer training, walking.
e
Supine motorised cycle ergometer attached to a current-controlled stimulator, muscles were stimulated at specific stages throughout
cycling phase based on normal muscular activation patterns regulated by the bicycle software.
90 SECTION 1 SCOPE OF CRITICAL CARE

Further development and testing of potential interven- long-term exploration of the effect of the diary interven-
tions also remain to be undertaken, particularly in terms tion on patient outcomes.While there is a small amount of
of patient selection, when to commence and the duration, evidence that supports their use,177 further empirical work
intensity and frequency of the rehabilitation interventions. is necessary to ensure the patient experiences no harm
Activities may also be adopted and adapted from other on receipt of a diary. Note, however, that not all patients
established rehabilitation programs such as those for stroke may wish to be reminded of their ICU experience; this is
and chronic respiratory disease patients. Technological especially the case for patients who demonstrate avoidant
devices, such as virtual reality rehabilitation,170 may also behaviours. Two studies have reported that approximately
prove to be beneficial in this cohort with further develop- 50% of patients do not wish to know what has happened
ment and testing. to them during intensive care.50,178 Others may wish not to
be reminded of being critically ill but wish to concentrate
Interventions to improve on recovery.13 Further research that incorporates these
psychological recovery issues during assessment of post-traumatic stress symptoms
Although there is now strong empirical evidence that some will establish the effectiveness of diary use.
patients experience significant psychological dysfunctions The UK NICE guidelines179 emphasised regular
after a critical illness, it is less clear how and when to treat assessment of patient recovery including psychological
these symptoms.171 There is some evidence to support recovery. Assessment periods include during intensive care,
the minimisation of sedation, particularly with benzo- ward-based care, before discharge home or community
care and 2–3 months after ICU discharge, with the use of
diazepines, while the patient is in ICU, and strategies to
existing referral pathways and stepped care models to treat
achieve this that are relevant to each ICU context should
identified psychological dysfunctions. These services are
be implemented.67,172
usually well established and allow patients to be treated by
Evidence is emerging of the benefits of in-ICU
appropriately qualified practitioners. The role of critical
psychological care as a way of reducing anxiety, depression
care practitioners may therefore be to establish the causes
and post-traumatic stress symptoms.173 These results are
of psychological disturbances associated with critical
promising but this was a single centre study in a subgroup
illness, identifying at-risk patients through systematic
of trauma patients; therefore, further work is necessary
and standardised screening activities, closely monitoring
before considering wider implementation.
identified patients and referring to appropriate specialties
Early detection and identification of patients at risk of where appropriate, to optimise their recovery trajectory
psychological problems are important and there have been while not introducing any further harm. Once a patient
recent developments of at-risk screening tools specifically has a diagnosis of anxiety, depression or post-traumatic
for this patient population.64 From an initial 21 potential stress, treatment should follow national guidelines, for
predictors, univariate analysis identified 6 key variables example NICE guidelines for the management of adult
(pre-existing disease, parent to children < 18 years, previous patients with depression (see the NICE website, http://
psychological problems, in-ICU agitation, unemployed/ www.nice.org.uk/Guidance/CG90).
sick leave at ICU admission and appeared depressed in
ICU).64 This is an interesting development and one that Ward-based post-ICU recovery
requires further testing. For example, depression was not Follow-up services for survivors of a critical illness in
measured using a standardised tool, and the study was Australia and New Zealand have occurred sporadically
unable to capture patients’ memories of being in ICU. in individual units with interested clinician teams,180 but
Systematic follow-up services may offer appropri- there is currently no widespread systematic approach
ate assessment support during recovery for individuals to recovery and rehabilitation and the management of
identified with psychological disturbances. Intensive care physical, psychological or cognitive dysfunctions beyond
follow-up clinics where patients have the opportunity clinical stability and deterioration with ICU liaison
to discuss their intensive care experiences and receive services181,182 or medical emergency teams (MET).183
information about what had happened to them could Commencement or continuation of rehabilitation
be a useful intervention, although there are currently no activities in the general wards after discharge from ICU
empirical data to support this,13 and further research work highlights a potentially different set of challenges, partic-
is required. ularly in terms of physiotherapy resources, involvement
Diaries for patients are also thought to be important in of other medical teams and compliance to a prescribed
providing missing pieces of information that might help plan. Although some cohorts of critically ill patients (e.g.
a patient make sense of their critical illness experience. pulmonary, cardiac, stroke, brain injury) have defined
A diary approach has been adopted in a number of rehabilitation pathways,184 patients with other clinical
European ICUs;174,175 however, there has been a great deal presentations may not be routinely prescribed a rehabili-
of variation in how the diaries were compiled and viewed tation plan or be referred to a rehabilitation specialist.
by a patient, as well as how much support was offered to For patients who survive to ICU discharge, approx-
them to explain diary content.176 To this point in time the imately 3–5% will die prior to hospital discharge.185
use of such diaries tends to be atheoretical,176 with limited Some work in Europe on prognosis post-ICU discharge
 CHAPTER 4 RECOVERY AND REHABILITATION 91

using the 4-point Sabadell Score (0 = good prognosis; ICU follow-up clinics
1 = long-term poor prognosis; 2 = short-term poor Systematic follow-up for survivors of a critical illness
prognosis; 3 = expected hospital death)186 demonstrated after hospital discharge emerged in the UK in the early
that subjective intensivist assessment was able to predict 1990s, after a number of government reviews on the
the risk of patient mortality,187 and conversely those cost and effectiveness of critical care services highlighted
patients potentially suitable for rehabilitation. the need to evaluate longer term patient outcomes, in
Specific ward-based rehabilitation interventions particular quality of life,199 and recognised that patients
following ICU discharge are beginning to be investigated. had sequelae that were best understood and managed
Designing and implementing such an intervention is chal- by ICU clinicians. In 2000, the UK Department of
lenging because of the heterogeneous nature of intensive Health published a comprehensive review of critical care
care patients who have increasing complexity and ill- services. With emerging albeit limited evidence of the
defined recovery trajectories. Furthermore, these patients
benefits of an ICU follow-up clinic, the review recom-
tend to be ‘scattered’ throughout the hospital making
mended the provision of follow-up services for those
coordination of care post-ICU difficult. Some exploratory
patients expected to benefit.200 Importantly, this review
work in the UK implemented a generic rehabilitation
also recommended collection of patient recovery and
assistant to support enhanced physiotherapy and nutritional
outcome data; this has been facilitated through follow-up
rehabilitation in collaboration with ward-based staff.188,189
clinics. The review did not, however, indicate how these
Following the MRC framework for complex interven-
services should be delivered or funded. Although this
tions, the intervention focused primarily on physical
review is now quite dated, strategies have not changed
recovery from ICU discharge to 3 months. The generic
significantly over time and the emerging pattern
rehabilitation assistant was able to provide information and
in the UK has continued to be inviting patients to a
explanation of the patient’s time in intensive care, facilitate
discussions with the multidisciplinary team, assist in goal follow-up clinic.
setting and provide enhanced ward-based rehabilitation.190 The first intensive care follow-up clinics were estab-
Results from this study will be published shortly. lished in the UK in the early 1990s,201 driven by a few
The benefits of physical exercise training for patients interested and committed intensive care clinicians. A
with COPD was affirmed in a recent review, with recom- recent UK survey indicated that approximately 27% of
mendations focused on maintenance of health behaviour UK ICUs offered a follow-up service.202 Although there
change,191 and these guidelines could be applied to some are few reports of clinics operating outside the UK,
cohorts of critically ill survivors. Identification of the occasional clinics do exist.203 Different clinic models
most effective level of intervention, however, remains have evolved as nurse-led, doctor-led or a combination
elusive. One Australian study of acute medical patients of multidisciplinary team members with more than half
(not after critical illness) noted that individually tailored in the UK nurse-led. Many clinics restrict patients invited
physical exercise (20–30 minutes twice daily, 5 days to return to those with an ICU length of stay of at least
per week) in hospital was not sufficient to influence 3 or 4 days. This decision is often based upon resources
functional activity at discharge.192 Further research is rather than evidence, as patients who have a shorter stay
therefore required to test specific interventions during may also have subsequent physical and psychological
the post-ICU hospital period aimed at improving the problems.196
recovery trajectory and health outcomes for patients with Common practice is to invite patients to attend a
limited physical function. As noted with in-ICU rehabil- first clinic appointment approximately 2–3 months after
itation, the optimal duration, intensity and frequency of discharge from intensive care or hospital, although timing
interventions is not yet clear. has to be flexible given the length of hospital stay for
some patients. For many, one appointment is sufficient,204
Recovery after hospital discharge but others have continuing problems and may need to
Of patients who survive their critical illness to hospital return on a number of occasions. Some clinics routinely
discharge, 5% will die within 12 months, and their risk of offer return appointments up to 1 year after discharge,
death is 2.9 times higher than for the general population.1 determined on an individual patient basis. Attendance
Functional recovery can be delayed in some individuals can be problematic; only 70–90% in some studies.180,196
for 6–12 months8,16,193,194 or longer.195 In a Norwegian Non-attendance can occur because a patient has no
study, only half of 194 patients had returned to work or identified problems (shorter ICU length of stay, less ill)
study 1 year after surviving their critical illness.194 or, more importantly, because of individual limitations
There is, however, only limited research and mixed (limited mobility, living a distance away from the clinic
study findings identifying specific interventions during or significant post-traumatic stress symptoms including
the post-hospital period that may improve a patient’s avoidant behaviours).205
recovery trajectory and health outcomes. Most work While these services developed in a relatively ad hoc
has involved practice evaluations or studies of outpatient manner, tended to be underfunded and used a variety of
‘ICU follow-up’ clinics,54,196,197 while there is some work models in their delivery, the purposes for such a service are
exploring home-based programs.198 similar (see Box 4.2).
92 SECTION 1 SCOPE OF CRITICAL CARE

rehabilitation staff, however, need to ensure that issues are

BOX 4.2
not ‘problematising’ for aspects of recovery that are not of
Purpose of an intensive care follow-up service concern to the patient.
• Review and assess patient progress Content of an assessment tool structures the clinic
visit and identifies any patient problems. These assess-
• Facilitate early identification of problems and refer
to appropriate specialties where necessary
ments can include the use of standardised questionnaires
of HRQOL, physical function, psychological status and
• Coordinate care cognitive function and other free-text responses that
• Support a rehabilitation program incorporate patient comments and other issues. Use of
• Discuss the intensive care experience and offer standardised questionnaires is, however, inconsistent,201,202
patient the opportunity to comment on care which limits evaluation and comparisons of clinic
• Offer patient the opportunity to visit the ICU outcomes. Common examples of questionnaires were
• Provide a forum for relatives to ask questions
previously listed in Tables 4.4, 4.5, 4.6 and 4.7. The issue
of respondent burden must be considered and question-
• Use information to inform delivery of intensive care
naire fatigue recognised. This can be managed in part by
asking patients to bring completed questionnaires with
Clinic activities them to the clinic appointment. Administration, scoring
Patient progress is reviewed for identification of sub- and interpretation of questionnaires must also be managed
sequent problems and timely referral to appropriate in accordance with instrument guidelines.
services for further treatment. A major advantage of Referral to appropriate specialists using a systematic
follow-up clinics is the increased understanding of patient approach and timely response times are necessary, as other
recovery, as a range of physical and psychological assess- healthcare professionals will not usually be present when
ments can be conducted (see an example in Table 4.9). patients attend the clinic. Delays in treatment following
Content of assessment is informed by the understand- identification of significant post-traumatic symptom-
ing and knowledge of the problems patients commonly atology can result in PTSD that is enduring and lasts for
face during their recovery period. Critical care and several years.47 Implementing defined referral criteria and

TABLE 4.9
Sample clinic assessment tool

SUBJECT AREA R AT I O N A L E

General health Assessed on a linear analogue or forced choice response to elicit a patient’s
subjective account of how they view their general health and how it has changed
since critical illness
Medications Review of medications commenced during the critical illness and continued
postdischarge, with advice provided to the patient’s general practitioner196
Movement and mobility, household Assess mobility problems, often due to continuing fatigue and weakness, but also
management and joints perhaps joint problems;207 identify impact on daily activities179
Breathing and tracheostomy Breathlessness is common after critical illness and there are a number of potential
difficulties post-tracheostomy; these can be identified and the patient referred to the
appropriate specialist
Sleep and eating Sleep and concentration disturbances are common, and muscle loss and weakness
are important contributors to delayed recovery179
Urology/reproduction, skin and senses Patients may have sexual problems206 and skin and nail problems
Recreation, work and lifestyle change Patients may experience difficulties reintegrating into society and in particular
returning to work
Memory, concentration, decision making This will provide an indication of ongoing cognitive problems that may influence
ongoing recovery6
Intensive care experience Patients rarely remember factual events of their time in ICU, but their memories are
often of unpleasant and disturbing events;78 offering an opportunity to discuss actual
events and sometimes distressing memories can be beneficial204
Quality of life The ultimate aim of treatment and care is to return a patient to an acceptable and
optimal quality of life; it is important to gauge how patients perceive their life quality,
and may identify areas for practice improvement
 CHAPTER 4 RECOVERY AND REHABILITATION 93

pathways can, however, be challenging particularly when Clinic attendance by relatives varies196 and may be related
a clinic is nurse-led.196 While identification of referrals to them having no identified problems or unanswered
during a follow-up clinic reflects a potential unmet need questions about the patient’s recovery, or being unable
for these patients, one survey reported that 51% of clinics to attend because of work commitments. Some relatives,
had no formal referral mechanisms.201 This referral activity however, may not attend because of also adopting avoidant
also reflects an additional function of the clinic in coordi- strategies if they are experiencing post-traumatic stress
nating patient care after hospital discharge. symptomatology,212 depression213 or other health problems.
Coordination of care for these patients with complex
needs often includes multiple outpatient appointments Clinic evaluation
and investigations at a time when they are least able to Given the development of follow-up clinics and the nature
cope with this complexity. An additional patient benefit of implementation, formal evaluation is difficult and this is
of returning to a follow-up clinic is in supporting them to reflected in the paucity of empirical evidence. Anecdotally,
negotiate their way through this complex care, coordinate nurses who deliver these clinics consider them beneficial
outpatient appointments and to have someone whom and patients seem to value them. Intuitively, it is a good
they know help them understand and interpret the entire idea for intensive care practitioners who have unique
critical illness and recovery experience.196 The follow-up insights into patient experiences to follow their patients
clinic can also be a vehicle for supporting and evaluating after discharge. Three approaches to follow-up clinic
a rehabilitation program.54 Rehabilitation in the form evaluation are evident: a service evaluation,180 a qualitative
of a 6-week supported self-help manual with weekly study204 and a pragmatic, randomised controlled trial;196
telephone calls and completion of a diary demonstrated each provides different insights.
an improvement in physical recovery at 8 weeks and Twenty-five interviews were performed to evaluate
6 months after intensive care discharge. one service, with a number of important themes evident:
As noted earlier, a unique element of a patient’s patients valued easy access to the clinic, being well-
intensive care experience is their limited recall of factual treated by staff and not having to wait long to be seen.
events but a common experience of ‘nightmares’ and Some patients attended because they simply received the
‘hallucinations’ that can be distressing both at the time appointment, while others identified the need to have
and during recovery. The benefits of having an oppor- questions answered, and wanted to discuss their distressing
tunity to discuss their experiences with intensive care dreams and hallucinations.180 While there was an insightful
staff should not be underestimated, and as such effective account of the development and initial evaluation, no
communication skills are vital for those delivering ICU demonstrable patient benefits were evident.
clinic services.208 Patients value being able to speak to Four main themes emerged from another study of
‘experts’ about their experience, being given information 34 patients: continuity of care; receiving information;
about what happened to them in ICU and also receiving importance of expert reassurance; and giving feedback to
reassurances about the length of time that recovery will intensive care staff.204 Continuity of care enabled reassur-
take and that their distressing memories are common. ance to patients that their progress was being monitored
Clinics also offer patients the opportunity to comment and any problems dealt with if referral to other specialties
on their care both during and after intensive care.180,204 was needed. Opinions varied about the number of clinic
This is important not just for the patient but to inform appointments and this reflects individual perceptions and
care delivery. For ICUs that complete patient diaries, needs. Receiving information was invaluable because
the follow-up clinic is often the place where these are of the poor memory for factual events. General infor-
introduced and discussed with the patient.177,209,210 mation about what had happened to them in ICU was
Offering the patient an opportunity to visit the ICU also important for gauging the length of time needed for
is possible during the follow-up clinic appointment. As recovery. Patients also found specific information about
noted earlier, the lack of factual memory of intensive care tracheostomy scars and other specific areas beneficial.
often leaves patients with gaps that may be distressing. While much of this information could be delivered by
Visiting the ICU may therefore be beneficial for some non-ICU staff, it was noted patients and relatives were
patients, particularly when they report odd perceptual specifically reassured by experts familiar with their ICU
experiences, and enable them to make sense of some of experiences.204 Being informed that other patients had
these experiences. However, care should be taken, as some similar experiences, particularly with problems sleeping or
patients may find this experience distressing and appropri- the nightmares and hallucinations, was also comforting to
ate explanation and support is essential. patients. Clinics also offered the patient the opportunity
A follow-up clinic also provides an important forum to give feedback to ICU staff, and allowed patients and
for relatives. Relatives may have different needs to a patient, relatives to thank staff for the care received.
and it is common to encourage relatives to attend with the The PRaCTICaL study randomised eligible patients
patient. Relatives may not only have short- and long-term to a control group of usual care (in-hospital review by a
consequences for their emotional wellbeing and physical liaison nurse) or intervention group (a physical rehabilita-
health,211 but also be faced with supporting a patient tion handbook and a nurse-led intensive care follow-up
who has unrealistic expectations about their recovery. clinic 2–3 months after discharge and 6 months later).196
94 SECTION 1 SCOPE OF CRITICAL CARE

Referral pathways were developed with ‘fast-track’ access considered. Telephone contact in the initial weeks after
to psychiatric or psychological services. There were no discharge can offer some reassurance to patients and also
demonstrated differences between groups for the prim- identify early problems. Patients could then be referred to
ary (HRQOL: SF-36) or secondary outcome measures other specialties, have their outpatient appointments coor-
(anxiety and depression: HADS; post-traumatic stress: dinated or be invited to return to a follow-up clinic if they
Davidson Trauma Scale). There were also no differences experience identified difficulties. Home visits could also
between patients who had a short intensive care stay and be an option for those who are physically or practically
those with longer stays.196 unable to return to a clinic or for those with avoidant
Despite the lack of evidence to support any improve- behaviours.
ment in outcome, there is little doubt that patients value
intensive care follow-up.214 There are a number of reasons Other considerations
for the lack of empirical evidence. Our contemporary It is important to consider that while interventions may
understanding of patient recovery is evolving constantly. not always benefit patients, it also has to be demonstrated
The clinics tend to see all patients at the same time in that they cause no harm and, therefore, initiating a new
the recovery process and this may not be appropriate, and service has governance issues. There are also knowledge
perhaps the timing of the clinic is either too late or too and skill-set development issues. Intensive care nurses tend
early for some patients. It may be that studies have been not to have training in managing patients on an outpatient
based on an outdated intervention that did not recognise basis and new skills have to be learned. They may also not
other challenges such as the effects of delirium or cognitive have knowledge and experience in managing many of the
compromise. Sample sizes tend to be relatively small and patient problems evident at follow-up, in particular the
often fail to identify what can be small subgroups of psychological and cognitive issues. Other considerations
patients who might benefit from a specific intervention. include accommodation, documentation, communica-
Other models that incorporate a more person-centred tion with other healthcare professionals and evaluation
approach and allow more flexibility should therefore be processes. Table 4.10 provides an example of how these

TABLE 4.10
Examples of considerations in setting up a nurse-led follow-up service

C O N S I D E R AT I O N ACTION

Staff preparation and training • Attend at least one established clinic

• Arrange to access educational preparation in relation to psychiatric problems
• Discussion and frequent contact with relevant healthcare practitioner, e.g. consultant
psychiatrist, psychologist
• Observe or ‘shadow’ a community psychiatric nurse
Accommodation • Arrange outpatient accommodation with an area close to but separate from the ICU
In-hospital follow-up • Introduce patients to the presence of the follow-up clinic prior to hospital discharge
• Identify how best to communicate with the patient after discharge, i.e. telephone
consultation, home visit or clinic appointment
Timing of clinic and number of • Initial appointment 2–3 months after ICU discharge
appointments • Further appointments determined by patient need or request
• All patients can contact the follow-up nurse without formal appointments
Structure of clinic • Patient’s case notes reviewed prior to the clinic appointment and discussed between nurse
and intensivist
• General assessment questionnaire forms the basis of the discussion between the nurse
and patient
• Standardised measures include for example Short-Form 36, Hospital Anxiety and
Depression Scale and Intensive Care Experience Questionnaire and the Mini-Mental State
Examination
• Consider offering patients a visit to the ICU but ensure they are ready for this, e.g. if they
do not ‘trigger’ referral on the Hospital Anxiety and Depression Scale
Documentation • General assessment questionnaire will form the basis of the record of appointment; the
nurse records any additional information on this form
Referral criteria • Develop and negotiate clear referral criteria for the relevant specialties, in collaboration with
intensivists, other medical specialties and allied health professionals
Letter to general practitioner • A letter summarising the appointment and any recommendations is sent to the patient’s GP
 CHAPTER 4 RECOVERY AND REHABILITATION 95

issues were addressed when setting up a follow-up service received a graded, individualised endurance and strength
in a Scottish teaching hospital, an evolving service that training intervention at home that incorporated a printed
developed from the PRaCTICaL study.196 A more flexible manual, three home visits and four follow-up phone calls
approach is used with different options discussed with the over 8 weeks post hospital discharge.198 No difference in
patient regarding delivery, with a telephone consultation, physical function on the SF-36 or 6-minute walk test was
home visit and/or clinic appointment. reported. More recently, Denehy and colleagues provided
150 patients with an exercise program that commenced
Home-based care
in ICU and continued through their ward stay and first
Although there are home-based programs to manage 8 weeks post hospital discharge; patients attended outpatients
ongoing care for some clinical cohorts (e.g. patients with clinics for exercise twice a week for 60 minutes in this
heart failure), no specific follow-up programs currently post-hospital phase.149 No difference in physical function
exist to support survivors of a critical illness. Initial studies was identified. One home-based study has been conducted
in this setting are also yet to identify an optimal interven-
in the USA where 21 patients received a multi-component
tion to improve recovery. A small number of studies have
intervention incorporating physical, functional and
been undertaken where various interventions lasting from
6 to 12 weeks after hospital discharge have been examined; cognitive training.92 Despite the small patient numbers,
inconsistent results have been identified. improved physical and cognitive functions were identified
Two studies have been conducted in the UK. In the in patients who received the intervention.
first patients were provided with a self-help manual that Further research is therefore required to determine
included instructions for exercise; they also received two what elements of interventions are effective, and at what
phone calls in the 6-week period.215 In this group of 126 time-points these interventions should be delivered;
patients improvement in physical function as measured on a number of these are currently underway.216,217 With
the SF-36 instrument was reported. In contrast, a self-help further study, future continuity of care and follow-up
manual was used by Cuthbertson and colleagues over a services after hospital discharge should enable the devel-
3-month period after hospital discharge and no difference opment of a series of seamless services that start recovery
in either physical function or mental health on the SF-36 and rehabilitation activities for a patient while in ICU, are
was reported by the 192 participants.196 In Australia two carried through to hospital discharge and continue into
studies have also been undertaken. In the first, 195 patients the community setting.

Summary
In summary we now have increasing evidence of the significant burden of health issues faced by critical illness survivors.
We know many face a prolonged and difficult recovery period that will include physical and psychological problems and
that these affect not just the patient themselves but family members and other carers. Patients’ lives may be significantly
altered after critical illness, placing a social and economic burden on the patient and family but also on the healthcare
system. Quality of life is often viewed as diminished and we now need to look to focusing on two main areas by identifying
a) effective interventions that will reduce these burdens and improve overall life quality and b) the patients most likely to
benefit from these interventions. Currently health systems are not organised in such a way as to recognise these problems
and, therefore, care after ICU discharge tends to be ad hoc and does not follow a recognised rehabilitation pathway. We
perhaps need to look at and learn from other long-term conditions and to adopt approaches that recognise the concept of
survivorship after critical illness218 and develop the appropriate systems and processes that will improve life after critical care.

Case study
Mr Smith was a 70-year-old man admitted to ICU with community-acquired pneumonia. He required
14 days of mechanical ventilation and was sedated through much of this time. Mr Smith’s wife and
extended family visited him each day while he was in the ICU; on some days he didn’t appear to recognise
his family members immediately, although as they spoke to him he would become more oriented and
recognise them. Mr Smith was then discharged to the high dependency unit for 3 days and then to a
medical ward for a further 10 days. An ICU liaison nurse saw him three times prior to discharge from the
ward where he initially had some confusion, could not remember what had happened to him and was
suffering from hallucinations. He was sent an out-patient appointment to attend the nurse-led ICU follow-
up clinic around 3 months after hospital discharge.
96 SECTION 1 SCOPE OF CRITICAL CARE

Mr Smith and his wife both attended the clinic. He seemed to be progressing well physically although he
struggled a bit at times, but had returned to his usual activities of walking to the corner shop each day as
well as starting to do a little weeding in his garden, which he cherished. Despite this aspect of recovery,
Mr Smith found it was really upsetting him that he had continuing memory loss. He complained he had
to write everything down or he would forget appointments. His wife also commented he still had vivid
dreams about being in intensive care and these seemed to upset him. He almost did not attend the clinic
appointment. He was a bit irritable with his family and at times was short-tempered. Mr Smith had visited
his general physician and described these problems, but was told it was quite common to experience these
problems after a lengthy hospitalisation and time in the ICU.

CASE STUDY QUESTION

1 How and when should Mr Smith have been screened or assessed specifically for psychological
symptoms?

RESEARCH VIGNETTE

Corner EJ, Soni N, Handy JM, Brett SJ. Construct validity of the Chelsea critical care physical assessment tool:
an observational study of recovery from critical illness. Crit Care 2014;18(2):R55

Abstract
Introduction: Intensive care unit-acquired weakness (ICU-AW) is common in survivors of critical illness, resulting in
global weakness and functional deficit. Although ICU-AW is well described subjectively in the literature, the value of
objective measures has yet to be established. This project aimed to evaluate the construct validity of the Chelsea
Critical Care Physical Assessment tool (CPAx) by analyzing the association between CPAx scores and hospital-
discharge location, as a measure of functional outcome.

Methods: The CPAx was integrated into practice as a service-improvement initiative in an 11-bed intensive care unit
(ICU). For patients admitted for more than 48 hours, between 10 May 2010 and 13 November 2013, the last CPAx
score within 24 hours of step down from the ICU or death was recorded (n=499). At hospital discharge, patients were
separated into seven categories, based on continued rehabilitation and care needs. Descriptive statistics were used
to explore the association between ICU discharge CPAx score and hospital-discharge location.

Results: Of the 499 patients, 171 (34.3%) returned home with no ongoing rehabilitation or care input; 131 (26.2%)
required community support; 28 (5.6%) went to inpatient rehabilitation for <6 weeks; and 25 (5.0%) went to inpatient
rehabilitation for >6 weeks; 27 (5.4%) required nursing home level of care; 80 (16.0%) died in the ICU, and 37 (7.4%)
died in hospital. A significant difference was found in the median CPAx score between groups (P<0.0001). Four
patients (0.8%) scored full marks (50) on the CPAx, all of whom went home with no ongoing needs; 16 patients (3.2%)
scored 0 on the CPAx, all of whom died within 24 hours. A 0.8% ceiling effect and a 3.2% floor effect of the CPAx is
found in the ICU. Compliance with completion of the CPAx stabilised at 78% of all ICU admissions.

Conclusion: The CPAx score at ICU discharge has displayed construct validity by crudely discriminating between
groups with different functional needs at hospital discharge. The CPAx has a limited floor and ceiling effect in survivors
of critical illness. A significant proportion of patients had a requirement for post-discharge care and rehabilitation.

Critique
This study is the second by this group of authors examining the development of a physical assessment instrument –
the Chelsea Critical Care Physical Assessment tool (CPAx). Content and construct validity, internal consistency and
inter-rater reliability were demonstrated initially in a small pilot study.219 In this second study the authors have explored
construct validity in a larger cohort by examining the association between CPAx scores on ICU discharge and hospital
discharge location and support. In addition, they have examined usability of the CPAx and floor and ceiling effects as
well as future care needs for survivors of critical illness.
 CHAPTER 4 RECOVERY AND REHABILITATION 97

Ten components of physical function are assessed using the CPAx, including respiratory function, cough, moving
within the bed, dynamic sitting, standing balance, sit to stand, transferring bed to chair, stepping and grip strength.
Each of these components is assessed on a 6-point scale from 0 (complete dependence) to 5 (independence). The
instrument is designed to be used by physiotherapists during their routine treatment of critically ill patients, with
only the grip strength assessment representing assessment that is not routinely undertaken. Hospital discharge
location/support incorporated five survival categories including home with no rehabilitation needs, home with
community support, short inpatient rehabilitation (<6 weeks), long inpatient rehabilitation (>6 weeks) or nursing
home care. In addition, two non-survival categories were incorporated: non-survival in ICU and non-survival in
hospital.

Good separation of CPAx scores was identified between most of the seven discharge groups, with gradual reduction
of scores from the category requiring no rehabilitation support to those who died in ICU. The only discharge location
that was not distinct in terms of CPAx scores was the non-survival in hospital group, possibly reflecting the many
different reasons patients die while they are in hospital wards.

Further, few patients scored the extreme scores of 0/50 (complete dependence) or 50/50 (complete independence)
suggesting few problems with floor or ceiling effects, in other words a large grouping of patients at the minimum
or maximum score due to insufficient spectrum of the function being measured. All 16 (3%) of the patients who
scored 0 died within 24 hours of this score, and all four (1%) of the patients who scored 50 were discharged home
without requiring support.

A number of limitations of this study should be considered. The CPAx is designed, and has only been tested, when
used by physiotherapists. It is not known if the reliability and validity would remain consistent when used by other
members of the healthcare team, particularly nurses; therefore this limits generalisability to ICUs that have limited
or no physiotherapy service. Despite this, the fact that scoring using the CPAx requires only 2 minutes in addition to
routine assessment should be seen as a strength as this improves feasibility of completion.

The average length of stay for patients included in this study was 6 days (median). In addition, patients had a relatively
low APACHE II score16 for this length of stay and no information has been provided regarding the proportion of
patients who received mechanical ventilation. These characteristics should be taken into account when considering
if the cohort examined in this study reflects the usual cohort in each individual ICU. In the study centre (Chelsea
and Westminster Hospital, London, UK) only 1524 patients were admitted to ICU over 3.5 years, representing
approximately 435 patients per year – this is low throughput for an 11-bed ICU and raises the question of whether
there is something unique about the population that is not reflected in the general demographic description. Some
post hoc analysis had limited power, but this was clearly noted by the authors.

Despite these limitations, good construct validity has been demonstrated suggesting that, with further testing, final
CPAx scores before discharge from ICU might be appropriate to use to plan discharge support both prior to leaving
ICU and throughout the patient’s ward stay.

When considering the applicability of these results to each individual setting, generalisability is further affected by
individual patient characteristics, for example age, desire for rehabilitation and level of family support as well as local
facilities such as rehabilitation services. In this particular cohort 34% of patients required no further support after
hospital discharge, 26% required ongoing community healthcare support, 11% required inpatient rehabilitation and
5% were discharged to a nursing home. Recognising that more than 40% of critical illness survivors require ongoing
support is important to inform planning for future services.

The CPAx is consistent with the Function Status Score for the ICU (FSS-ICU) first described by Zanni and
colleagues,220 which incorporates multiple different components such as rolling, sitting, standing and walking that
are each scored on a multi-level scale. In contrast, the ICU Mobility Scale221 considers these components in
one continuous domain, with patients receiving a score that represents their maximum ability; this instrument
has undergone initial reliability testing only at this stage. Although all of these scales are in an early phase of their
development, the potential to measure progress and identify patients who require assistance with physical function
is an important step forward in our planning to provide appropriate support across the critical care continuum.
98 SECTION 1 SCOPE OF CRITICAL CARE

Lear ning a c t iv it ie s
1 Patients transferred from ICU to the ward may have complex care needs. In your hospital, if a follow-up service
was planned, how do you think this should be developed?
2 Review the evidence for psychological assessment and management of patients after a critical illness and
intensive care admission.
3 What are the educational implications for staff in relation to supporting the physical and psychological problems
patients experience after ICU?

Online resources
I-CAN UK (Intensive Care After Care Network), www.i-canuk.co.uk/default.aspx
ICU Steps, www.icusteps.com
Patient-reported Outcome and Quality of Life Instruments Database (PROQOLID), www.proqolid.org
Patient-Centered Outcomes Research Institute, www.pcori.org
PTSD NICE Guidelines, www.nice.org.uk/CG26

Further reading
National Institute for Health and Clinical Excellence. Rehabilitation after critical illness. NICE clinical guideline 83. 2009
March: 1–91, <http://www.nice.org.uk/CG83>; 2009 [accessed 03.02.15].

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2008;94(3):220-9.
166 Nydahl P, Ruhl AP, Bartoszek G, Dubb R, Filipovic S, Flohr HJ, et al. Early mobilization of mechanically ventilated patients: a 1-day
point-prevalence study in Germany. Crit Care Med 2014;42(5):1178-86.
167 Berney SC, Harrold M, Webb SA, Seppelt I, Patman S, Thomas PJ, et al. Intensive care unit mobility practices in Australia and New Zealand:
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168 Bailey PP, Miller RR, 3rd, Clemmer TP. Culture of early mobility in mechanically ventilated patients. Crit Care Med 2009;37(10 Suppl):S429-35.
169 Drolet A, DeJuilio P, Harkless S, Henricks S, Kamin E, Leddy EA, et al. Move to improve: the feasibility of using an early mobility protocol to
increase ambulation in the intensive and intermediate care settings. Phys Ther 2013;93(2):197-207.
170 Van de Meent H, Baken BC, Van Opstal S, Hogendoorn P. Critical illness VR rehabilitation device (X-VR-D): evaluation of the potential use for
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171 Mehlhorn J, Freytag A, Schmidt K, Brunkhorst FM, Graf J, Troitzsch U, et al. Rehabilitation interventions for postintensive care syndrome: a
systematic review. Crit Care Med 2014;42(5):1263-71.
172 Wade D, Hardy R, Howell D, Mythen M. Identifying clinical and acute psychological risk factors for PTSD after critical care: a systematic
review. Minerva Anestesiol 2013;79(8):944-63.
173 Perris A, Bonizzoli M, Iozzelli D, Migliaccio M, Zagli G, Bacchereti A, et al. Early intra-intensive care unit psychological intervention promotes
recovery from post traumatic stress disorders, anxiety and depression symptoms in critically ill patients. Crit Care 2011;15:R41.
174 Backman CG, Walther SM. Use of a personal diary written on the ICU during critical illness. Intensive Care Med 2001;27(2):426-9.
175 Bergbom I, Svensson C, Berggren E, Kamsula M. Patients’ and relatives’ opinions and feelings about diaries kept by nurses in an intensive
care unit: pilot study. Intensive Crit Care Nurs 1999;15(4):185-91.
176 Aitken LM, Rattray J, Hull A, Kenardy JA, Le Brocque R, Ullman AJ. The use of diaries in psychological recovery from intensive care. Crit Care
2013;17(6):253.
177 Jones C, Backman CG, Capuzzo M, Egerod I, Flaatten H, Granja C, et al. Intensive care diaries reduce new onset post traumatic stress
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178 Rattray J, Crocker C, Jones M, Connaghan J. Patients’ perception of and emotional outcome after intensive care: results from a multicentre
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179 National Institute for Health and Clinical Excellence. Rehabilitation after critical illness. NICE clinical guideline 83, <http://www.nice.org.uk/
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180 Cutler L, Brightmore K, Colqhoun V, Dunstan J, Gay M. Developing and evaluating critical care follow-up. Nurs Crit Care 2003;8:116-25.
181 Eliott SJ, Ernest D, Doric AG, Page KN, Worrall-Carter LJ, Thalib L, et al. The impact of an ICU liaison nurse service on patient outcomes.
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182 Williams TA, Leslie G, Finn J, Brearley L, Asthifa M, Hay B, et al. Clinical effectiveness of a critical care nursing outreach service in facilitating
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183 Hillman K, Chen J, Cretikos M, Bellomo R, Brown D, Doig G, et al. Introduction of the medical emergency team (MET) system: a cluster-
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184 Morris PE, Herridge MS. Early intensive care unit mobility: future directions. Crit Care Clin 2007;23(1):97-110.
185 Moran JL, Bristow P, Solomon PJ, George C, Hart GK. Mortality and length-of-stay outcomes, 1993–2003, in the binational Australian and
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186 Fernandez R, Baigorri F, Navarro G, Artigas A. A modified McCabe score for stratification of patients after intensive care unit discharge: the
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187 Fernandez R, Serrano JM, Umaran I, Abizanda R, Carrillo A, Lopez-Pueyo MJ, et al. Ward mortality after ICU discharge: a multicenter
validation of the Sabadell score. Intensive Care Med 2010;36(7):1196-201.
188 Salisbury LG, Merriweather JL, Walsh TS. Rehabilitation after critical illness: could a ward-based generic rehabilitation assistant promote
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189 Salisbury LG, Merriweather JL, Walsh TS. The development and feasibility of a ward-based physiotherapy and nutritional rehabilitation
package for people experiencing critical illness. Clin Rehabil 2010;24(6):489-500.
190 Ramsay P, Salisbury LG, Merriweather JL, Huby G, Rattray JE, Hull AM, et al. A rehabilitation intervention to promote physical recovery
following intensive care: a detailed description of construct development, rationale and content together with proposed taxonomy to capture
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191 Langer D, Hendriks E, Burtin C, Probst V, van der Schans C, Paterson W, et al. A clinical practice guideline for physiotherapists treating
patients with chronic obstructive pulmonary disease based on a systematic review of available evidence. Clin Rehabil 2009;23(5):445-62.
192 de Morton NA, Keating JL, Berlowitz DJ, Jackson B, Lim WK. Additional exercise does not change hospital or patient outcomes in older
medical patients: a controlled clinical trial. Aust J Physiotherapy 2007;53(2):105-11.
193 Adamson H, Elliott D. Quality of life after a critical illness: a review of general ICU studies 1998-2005. Aust Crit Care 2005;18:50-60.
194 Myhren H, Ekeberg O, Stokland O. Health-related quality of life and return to work after critical illness in general intensive care unit patients:
a 1-year follow-up study. Crit Care Med 2010;38(7):1554-61.
195 Cuthbertson BH, Roughton S, Jenkinson D, Maclennan G, Vale L. Quality of life in the five years after intensive care: a cohort study. Crit Care
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196 Cuthbertson BH, Rattray J, Campbell MK, Gager M, Roughton S, Smith A, et al. The PRaCTICaL study of nurse led, intensive care follow-up
programmes for improving long term outcomes from critical illness: a pragmatic randomised controlled trial. BMJ 2009;339:b3723.
197 McWilliams DJ, Atkinson D, Carter A, Foex BA, Benington S, Conway DH. Feasibility and impact of a structured, exercise-based rehabilitation
programme for intensive care survivors. Physiotherapy Theory and Practice 2009;25(8):566-71.
198 Elliott D, McKinley S, Alison J, Aitken LM, King M, Leslie GD, et al. Health-related quality of life and physical recovery after a critical illness: a
multi-centre randomised controlled trial of a home-based physical rehabilitation program. Crit Care 2011;15(3):R142.
199 UK NHS Audit Commission. Critical to Success. The place of efficient and effective critical care services within the acute hospital. London:
Audit Commission; 1999.
200 UK Department of Health. Comprehensive critical care: a review of adult critical care services. London: HMSO, 2000.
201 Griffiths JA, Barber VS, Cuthbertson BH, Young JD. A national survey of intensive care follow-up clinics. Anaesthesia 2006;61(10):950-5.
202 Connolly B, Douiri A, Steier J, Moxham J, Denehy L, Hart N. A UK survey of rehabilitation following critical illness: implementation of NICE
Clinical Guidance 83 (CG83) following hospital discharge. BMJ Open 2014;4(5):e004963.
203 Modrykamien AM. The ICU follow-up clinic: a new paradigm for intensivists. Respir Care 2012;57(5):764-72.
204 Prinjha S, Field K, Rowan K. What patients think about ICU follow-up services: a qualitative study. Crit Care 2009;13(2):R46.
205 Cutler L. From ward-based critical care to educational curriculum 1: a literature review. Intensive Crit Care Nurs 2002;18:162-70.
206 Griffiths J, Gager M, Alder N, Fawcett D, Waldmann C, Quinlan J. A self-report-based study of the incidence and associations of sexual
dysfunction in survivors of intensive care treatment. Intensive Care Med 2006;32(3):445-51.
207 Griffiths RD, Jones C. Seven lessons from 20 years of follow-up of intensive care unit survivors. Curr Opin Crit Care 2007;13(5):508-13.
208 Hazzard A, Harris W, Howell D. Taking care: practice and philosophy of communication in a critical care follow-up clinic. Intensive Crit Care
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209 Akerman E, Granberg-Axell A, Ersson A, Fridlund B, Bergbom I. Use and practice of patient diaries in Swedish intensive care units: a national
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 CHAPTER 4 RECOVERY AND REHABILITATION 105

210 Egerod I, Storli SL, Akerman E. Intensive care patient diaries in Scandinavia: a comparative study of emergence and evolution. Nurs Inq
2011;18(3):235-46.
211 Paul F, Rattray J. Short- and long-term impact of critical illness on relatives: literature review. J Adv Nurs 2008;62(3):276-92.
212 Paul F, Hendry C, Cabrelli L. Meeting patient and relatives’ information needs upon transfer from an intensive care unit: the development and
evaluation of an information booklet. J Clin Nurs 2004;13(3):396-405.
213 Choi J, Sherwood PR, Schulz R, Ren D, Donahoe MP, Given B, et al. Patterns of depressive symptoms in caregivers of mechanically
ventilated critically ill adults from intensive care unit admission to 2 months postintensive care unit discharge: a pilot study. Crit Care Med
2012;40(5):1546-53.
214 Williams TA, Leslie GD. Beyond the walls: a review of ICU clinics and their impact on patient outcomes after leaving hospital. Aust Crit Care
2008;21(1):6-17.
215 Jones C, Skirrow P, Griffiths RD, Humphris GH, Ingleby S, Eddleston J, et al. Rehabilitation after critical illness: a randomized, controlled trial.
Crit Care Med 2003;31(10):2456-61.
216 Batterham AM, Bonner S, Wright J, Howell SJ, Hugill K, Danjoux G. Effect of supervised aerobic exercise rehabilitation on physical fitness and
quality-of-life in survivors of critical illness: an exploratory minimized controlled trial (PIX study). Br J Anaesth 2014;113(1):130-7.
217 O’Neill B, McDowell K, Bradley J, Blackwood B, Mullan B, Lavery G, et al. Effectiveness of a programme of exercise on physical function in
survivors of critical illness following discharge from the ICU: study protocol for a randomised controlled trial (REVIVE). Trials 2014;15(1):146.
218 Iwashyna TJ. Survivorship will be the defining challenge of critical care in the 21st century. Ann Intern Med 2010;153(3):204-5.
219 Corner EJ, Wood H, Englebretsen C, Thomas A, Grant RL, Nikoletou D, et al. The Chelsea critical care physical assessment tool (CPAx):
validation of an innovative new tool to measure physical morbidity in the general adult critical care population; an observational proof-of-
concept pilot study. Physiotherapy 2013;99(1):33-41.
220 Zanni JM, Korupolu R, Fan E, Pradhan P, Janjua K, Palmer JB, et al. Rehabilitation therapy and outcomes in acute respiratory failure: an
observational pilot project. J Crit Care 2010;25(2):254-62.
221 Hodgson C, Needham D, Haines K, Bailey M, Ward A, Harrold M, et al. Feasibility and inter-rater reliability of the ICU Mobility Scale. Heart
Lung 2014;43(1):19-24.
Chapter 5

Ethical issues in critical care

Maureen Coombs, Carol Grech

Learning objectives KEY WORDS

After reading this chapter, you should be able to: autonomy

• appreciate the diversity and complexities of ethical issues involved in beneficence
critical care practice
confidentiality
• understand key ethical and legal principles in health care and how to consent
apply them in everyday practice as a critical care nurse
euthanasia
• identify and access additional resource material that may inform and
support ethical professional conduct in critical care futility
Human Research
• discuss ethical decision making involved in withdrawing and withholding
of treatment, brain death and the organ donation decision-making Ethics Committee
process justice
• describe the ethical conduct of human research, in particular issues of non-maleficence
patient risk, protection and privacy, and how to apply ethical principles patient rights
within research practice.
privacy
quality of life

Introduction
Nursing work, regardless of the context, will always involve an ethical dimension:
it is therefore essential that nurses are guided by ethical principles. This is well-
recognised by the International Council of Nurses (ICN) who in 1953 adopted a
Code of Ethics for Nurses,1 which ICN continue to refine.This code informs the
ethical standards and guidelines developed by nursing authorities across the world.
As a result, nurses are expected to provide compassionate and ethically coherent
care, meet professional standards as stated by their regulatory authority and act in
accordance with relevant codes of ethics at all times (see Box 5.1).
So why is ethics so important? Critical care nurses regularly encounter
clinical situations that require them to employ ethical reasoning. However,
the application of such reasoning that informs clinical decision making can
be challenging and demanding. The vulnerability of patients in critical care
settings, the distress experienced by their families, issues related to the adequacy
of informed consent, quandaries that arise from life-sustaining technologies,
potential conflict related to withdrawal of life support, equitable allocation of
resources and many other challenges encountered in caring require nurses to
utilise rational and logical reasoning to determine the right course of action(s)
in the face of conflicting choices.
 CHAPTER 5 ETHICAL ISSUES IN CRITICAL CARE 107

BOX 5.1

Codes of ethics from selected countries

Australia: Nursing and Midwifery Board of Australia Ireland: Irish Nursing Board Draft Code of Professional
Code of Ethics for Nurses (2008), http://www. Conduct and Ethics for Registered Nurses and
nursingmidwiferyboard.gov.au/Codes-Guidelines- Registered Midwives for consultation (2013), http://
Statements/Codes-Guidelines.aspx www.nursingboard.ie/en/professional_practice.aspx
and Japan: Japanese Nursing Association The Code of
Nursing and Midwifery Board of Australia Code of Ethics for Nurses (2003), http://www.nurse.or.jp/jna/
Professional Conduct for Nurses (2008), http://www. english/activities/pdf/ethics2003.pdf
nursingmidwiferyboard.gov.au/Codes-Guidelines- Malaysia: Nursing Board Malaysia Code of
Statements/Codes-Guidelines.aspx Professional Conduct for Nurses (1998), http://nursing.
Canada: Canadian Nurses Association – Code of Ethics moh.gov.my/uploads/PDdownloads/nursing_board_
for Registered Nurses (2008), http://www.cna-aiic.ca/en/ malaysia-code_of_professional_conduct_1998.pdf
on-the-issues/best-nursing/nursing-ethics New Zealand: Nursing Council of New Zealand Code
European Union: European Federation of Nursing of Conduct for Nurses (2013), http://www.nzno.org.
Regulators – The Code of Ethics and Conduct for nz/Portals/0/publications/Code%20of%20Ethics,%20
European Nursing (2007), http://nej.sagepub.com/ (2010,%202013).pdf
content/15/6/821.full.pdf United Kingdom: Nursing and Midwifery Council
Hong Kong: The Nursing Council of Hong Kong Code of (NMC) The Code: Standards of conduct, performance
Professional Conduct and Code of Ethics for Nurses in and ethics for nurses and midwives (2008), http://
Hong Kong (2002), http://www.nchk.org.hk/en/code_of_ www.nmc-uk.org/Publications/Standards/The-code/
conduct_and_practice/code_of_professional_conduct_ Introduction
and_code_of_ethics_for_nurses_in_hong_kong/index.html
United States of America: American Nurses
India: Indian Nursing Council Code of Ethics & Professional Association Code of Ethics for Nurses with
Conduct, http://www.indiannursingcouncil.org Interpretive Statements (2001) [Note: Code was
International Council of Nurses (ICN): Code of Ethics updated June 2014], http://www.nursingworld.
for Nurses (revised 2012), http://www.icn.ch/images/ org/MainMenuCategories/EthicsStandards/
stories/documents/about/icncode_english.pdf CodeofEthicsforNurses

Working in contemporary health care, where health Ethics and the law
technology is constantly evolving and life expectancy is
increasing, requires increasingly complex decisions to be When debates about clinical situations occur in critical
made about patient and health resource management. care, these inevitably involve focused consideration on what
Difficult situations now arise where no consensus has the legal and ethical issues are. Although ethics are often
developed about the ethical decision making or where all made evident through the laws of society, the principles and
the alternatives in a given situation have specific short- frameworks of ethics, as they are used in society, can be very
comings.These types of situations are referred to as ‘ethical different. Understanding the distinction between ethics and
dilemmas’. Dilemmas are different from problems, because the law becomes increasingly important as clinical situations
problems have potential solutions.2 It is in this world that encountered become more complicated.
critical care nurses often find themselves. This chapter
therefore seeks to provide a resource to understand some Distinction between ethics, morality
of the current ethical issues across the continuum of critical and values
care services. The chapter has three sections. The first
section outlines the broad principles that underpin ethical Ethics is concerned with the many clinical situations that
decision making. There is exploration about the distinc- invite reflection and raise questions about health profes-
tion between ethics, morality and values and of key ethical sionals’ inherent values informing decision making, as
concepts. In linking ethics with the law, legal positions that distinct from specific diagnostic or technical questions.
inform health care are also described. The second part of Ethics involves the study of rational processes to inform
the chapter explores the application of ethical principles a course of action in response to a particular situation
in critical care, with particular emphasis on withholding where conflicting options exist.3 Morality, however, can be
and withdrawing of treatment and the decision-making understood as the norms widely shared by a community
principles that inform this.The third section of the chapter or among a professional group about what is ‘right’ or
explores key ethical issues that arise from clinical research ‘wrong’ about human conduct, the widely held views then
in the context of critical care. forming stable social consensus.4 Values are the beliefs and
108 SECTION 1 SCOPE OF CRITICAL CARE

attitudes that individuals hold about what is important possible, for example by attempting to discover what the
and therefore influence individual actions and decision patient’s preferences and decisions would have been in
making.5 It is important that critical care nurses be aware the circumstances.
of, and reflect on, their personal and professional ethical,
moral and value positioning to understand how they will Practice tip
approach ethical decision making in clinical practice.
Where personal ethics can be described as a personal A competent person has a right to make an informed
set of moral values that an individual chooses to live by, choice about his or her treatment. When giving
professional ethics refer to agreed standards and behaviours information about care options to a patient, keep
expected of members of a particular professional group.6 the discussion accurate and factual. Do not direct or
The value statements developed to underpin nursing influence the patient’s decision making. Respect the
and medical practice were originally informed by the right of the person to make self-determining decisions.
moral traditions of Western civilisations with the resultant
standards intended to guide and justify professional Beneficence and non-maleficence
conduct. Interest in ethical practice in the healthcare area The principle of beneficence (i.e. to do good) requires
has now developed to such an extent that bioethics has that actions are undertaken to promote the wellbeing of
emerged as a subject area concerned with moral issues another person. This incorporates the actions of doing no
raised by biological science developments and health care. harm and maximising possible benefits while minimising
Although this section has clearly delineated the possible harm (non-maleficence).9 In healthcare practice,
differences in definitions of ethics and morality, these treatment is focused on ‘doing no harm’. However, there
concepts are sometimes used interchangeably when may be times where, to ‘maximise benefits’ for health
professional organisations articulate codes of professional outcomes, it may be ethically justifiable to expose the
conduct, for example in the Australian Code of professional patient to a ‘higher risk of harm’. For example, consider
conduct for nurses.7 a clinical situation in the coronary care unit (CCU).
Ethical principles A patient requires a central venous catheter (CVC) to
Key ethical principles often used to explore healthcare optimise fluid and drug therapy, but this intervention is
ethics include autonomy, beneficence, non-maleficence, not without its own inherent risks (e.g. infection, pneumo-
justice, veracity and fidelity.4 While these are important thorax on insertion). To minimise possible harm to the
in understanding the ethical dimensions of care, there are patient, evidence-based protocols are therefore developed
other ethical concepts important to understanding health to ensure safe insertion of a CVC and subsequent care.
care including integrity, best interests, informed consent Justice
and advance directives. All are applicable to critical care
practice. These are explored individually in the following Justice may be defined as fair, equitable and appropriate
paragraphs or incorporated as part of the discussion of treatment in light of what is due or owed to an individual.
clinical issues, such as treatment withdrawal. The fair, equitable and appropriate distribution of health
care, as determined by justified rules or ‘norms’, is termed
Autonomy distributive justice.4 There are well-regarded theories of
An autonomous person is an individual who is capable justice in health care including egalitarian theories that
of deliberation, self-determination and action without propose people be provided with an equal distribution
the influence of external coercion. To respect autonomy of particular goods or services. However, it is recognised
is to give weight to, and respect, the autonomous person’s that justice does not always require equal sharing of
considered opinions and choices and to not obstruct all possible social benefits. In situations where there is
their actions unless these are detrimental to themselves or insufficient resource to be equally distributed, guidelines
others. To show lack of respect for an autonomous agent (e.g. intensive care unit [ICU] admission policies) may
or to withhold information necessary for that person to be developed in order to ensure treatment is as fair and
make a considered judgement when there are no reasons equitable as possible.
to do so, is to reject that person’s judgement. To deny a Conditions of scarcity and competition for resources
competent individual their autonomy is to treat that lead to the main problems associated with fair and equitable
person paternalistically. All individuals, including critical allocation of resources (distributive justice). For example,
care patients, should be treated as autonomous agents a shortage of intensive care beds may result in critically ill
and be able to self-determine, unless otherwise indicated. patients having to ‘compete’ for access to the ICU. There
However, individuals with diminished autonomy, for is considerable debate about ICU admission criteria that
example an unconscious person, are entitled to protection varies across institutions, jurisdictional boundaries and
and, depending on the risk of harm and likely benefit of countries with differing health funding structures. Such
protecting them, paternalism may be considered justifi- resource limitations can impact on distributive justice if
able.4,8 In such cases, healthcare professionals should act decisions about access are influenced by economic factors
to respect the autonomy of the individual as much as as distinct from clinical need.10
 CHAPTER 5 ETHICAL ISSUES IN CRITICAL CARE 109

Veracity and fidelity Ethics and the law

The principle of veracity is concerned with telling the Although distinct, ethics and the law overlap in many
truth and is based on respect for persons and the concept important ways. Moral rightness or wrongness may be
of autonomy. To provide the opportunity for patients, or quite distinct from legal rightness or wrongness and, while
those authorised by law to act on their behalf, to make ethical decision making will always require consideration
informed decisions about treatment options they must of the law, there may be conflict about the morality of the
be provided with full and honest disclosure so that they law. Ethically based nursing practice, such as confidenti-
can weigh up the risks and benefits of treatments.3 It ality, respect for human rights and consent, are also legal
is also important to note that the principle of veracity requirements for health practice.6,13
can be violated through omission of important infor- The law enforces rules that are desirable for social
mation – deliberately withholding information or using good in every country. The terms ‘legislation’ and ‘law’
medical jargon or language that may camouflage or are used to refer generically to statutes, regulation and
mislead the patient or their legal guardian. Critical care other legal instruments that may be the forms of law
environments are highly complex, as are the technolo- used in a particular country. A general distinction can be
gies and procedures patients are exposed to. Patients and made between civil law jurisdictions (e.g. in counties like
their families can easily feel overwhelmed by the critical France, Germany, Spain), which codify laws and in which
care environment and by the choices that they may be the law is almost entirely based on legislative enactments
faced with during critical illness.11 Ensuring patients and and considered binding for all, and common law systems
families are informed and fully involved in the decision (e.g. in England, the USA, Australia and New Zealand
making is pivotal. Nurses and medical staff need to be (NZ)), where the law continually evolves in addition to
vigilant in ensuring they convey information to patients being amended by laws passed by parliament.3 In some
and their families using language that can be readily countries, religion informs law such as Sharia or Islamic
understood and ensuring support services are drawn on law that specifically influences the legal code in some
(e.g. social workers, religious and spiritual advisors) to Muslim countries.
provide additional help to augment understanding so Laws related to health care are often created on the
that patients or their legal guardian can make informed basis of what is considered morally right and of benefit to
choices about care. members of society. Statute law, i.e. written law set down
by a legislature (e.g. parliament), has particular relevance
Practice tip to ethics in the critical care context. An example of how a
statute law in one jurisdiction might be applied in practice
If you know a person’s treatment is not working for pertaining to, for example, consent for life-sustaining
them, you must help get their voice heard. This means measures is the Consent to Medical Treatment and Palliative
having the courage to raise the matter with a more Care Act 1995 (SA).14 This Act at s17 (2) states that: ‘in
senior nurse or the doctor in a way that will be heard the absence of an express direction by the patient or the
and considered in a timely way. patient’s representative to the contrary, [the doctor is]
under no duty to use, or to continue to use, life sustaining
Fidelity refers to the concepts of keeping promises measures’.14
and honouring contracts and commitments12 and is based In some countries such as Australia, each state and
upon the fundamental nursing virtue of caring. This territory has many different Acts pertaining to healthcare
principle encompasses qualities including loyalty, fairness, practices, and this can be confusing when practitioners
providing compassionate care to patients, advocacy and work across jurisdictional borders. This is less problematic
being responsible and accountable for the standard of in some countries, such as New Zealand, where health
nursing practice provided. Acts are applicable across the whole country. Therefore,
The principles of veracity and fidelity underpin the when sourcing laws relevant to health care in specific
practice of every nurse. These values relate to professional countries, it is important to use validated sources such as
ethics and the expectation that nurses are honest in all government websites.
professional interactions, and demonstrate compliance Privacy and confidentiality
with the professional codes of conduct, practice standards
and regulatory reporting requirements. Although not an ethical principle as such, privacy
and confidentiality are fundamental human entitle-
ments recognised in all major international treaties and
Practice tip
agreements on human rights. Nearly every country in
Communicate with patients honestly and respectfully. the world acknowledges privacy as a fundamental human
If you tell a patient that you will be back in 10 minutes, right in their constitution, either explicitly or implicitly.
mean it. However, if you know that you are busy and The right to privacy has been involved in new areas of
unlikely to meet that timeline, explain this to the patient debate given technology’s increasing erosion of privacy, for
instead of making false assurances. example via video surveillance cameras, the internet and
use of social media. Recently drafted constitutions now
110 SECTION 1 SCOPE OF CRITICAL CARE

include specific rights to access and control one’s personal concept, has received little exploration in the literature to
information, with a growing trend towards comprehensive date22 although some resources exist23 to inform practice.
privacy and data protection legislation around the world. Professional codes of conduct should incorporate an
Currently, over 40 countries and jurisdictions have, or understanding of patients’ rights and acknowledge that
are in the process of enacting, such laws.15 Countries are nurses accept the rights of individuals to make informed
adopting these laws to ensure compatibility with inter- choices about their treatment and care. Box 5.2 provides
national standards developed by the European Union, the some useful tips to ensure that the needs of diverse popu-
Council of Europe and the Organization for Economic lations in critical care may be met.
Cooperation and Development.
In New Zealand, privacy legislation is described in the BOX 5.2
Privacy Act 199316 and in Australia in the Commonwealth
Privacy Act 1988.17 In addition, each state and territory Needs of diverse population groups in critical care
in Australia has additional jurisdictional regulatory To cater for the needs of diverse population groups in
guidelines that apply to privacy matters and disclosure critical care it is important to:
of health information.18 Increasingly, government depart- • organise and use qualified interpreters and cultural
ments and hospitals also have dedicated policies on the advisors when required
use of social media.
• create care environments that facilitate optimal
patient and family control of decisions
Practice tip
• work collaboratively with other healthcare workers
Details about a patient’s personal circumstance, in a culturally sensitive and competent manner to
condition and medical treatment must always be ensure optimal outcomes
kept private and confidential. Do not discuss patients • identify and address bias, prejudice and
in inappropriate environments (e.g. in corridors and discrimination in healthcare service delivery
elevators where others could overhear). Do not take
• integrate measures of patient satisfaction into
handover sheets or papers that have recorded patient
improvement programs.
details outside the unit where they could be found by
unauthorised personnel or members of the public; and
never discuss patients, colleagues or work-related Consent
matters on social media.
Any procedure that involves intentional contact by a
healthcare practitioner with the body of a patient is
Patients’ rights considered an invasion of the patient’s bodily integrity
Patients’ rights arise from human rights law that univer- and requires patient consent. A healthcare practitioner
sally recognises that everyone is born free and with equal must not assume that a patient provides a valid consent
rights irrespective of nationality, place of residence, gender, purely on the basis that the individual has been admitted
ethnic origin, race or religion.19 Statements with a focus on to a hospital.24 All healthcare staff (nurses, doctors, allied
patients’ rights relate to the particular moral interests that a health professionals) are expected to give information on
person might have in a healthcare context and any particular management, care and alternative options to the patient to
protection required when a person assumes the role of a enable informed consent and decision making to occur.25
patient.6 Institutional-based charters (position statements), The responsibility for obtaining consent for medical
such as those in hospitals, are helpful in developing a shared treatment rests with the medical practitioner and generally
understanding amongst patients/consumers, families and may not be delegated to a nurse.24
carers of the rights of people receiving health care and of Patients have the right, as autonomous individuals, to
the entitlements and special interests to be respected. Such discuss any concerns or raise questions at any time with
charters also emphasise to healthcare professionals that rela- staff. Hospitals should provide detailed patient admission
tionships with patients are constrained ethically and bound information, including information regarding ‘patients’
by certain associated duties.6 The World Federation of rights and responsibilities’ and a broad explanation of the
Critical Care Nurses has recognised the importance of this consent process within that institution. In many countries
and developed a Position Statement on the rights of the there is no distinction between the obligation to obtain
critically ill patient (see the World Federation of Critical valid consent from the patient and the overall duty of care
Care Nurses website, http://wfccn.org). that a practitioner has in providing treatment to a patient.
To further protect patients’ rights, attention should Obtaining consent is part of the overall duty of care.14
be paid to cultural differences in the provision of health In order to provide safe care where patients are able
care and to ensure cultural safety of both patients and the to make choices with informed consent, clear systems
healthcare team. Clinical situations are culturally safe when and processes are required. Critical care nurses need to
patients and their families feel that cultural and spiritual be aware of relevant professional, organisational and
needs are acknowledged and that those needs are met unit-based policies and understand their individual
without prejudice.20,21 Cultural competency, as a health obligations and responsibilities in this area. While the
 CHAPTER 5 ETHICAL ISSUES IN CRITICAL CARE 111

treating medical officer is legally regarded as the person

BOX 5.3
who informs the patient about associated risks,26 it is
incumbent on all critical care nurses to be aware of the Criteria for consent
potential risks in critical care and ensure that informed Consent is considered VALID if:
consent is gained cognisant of these. Due to the nature of
• informed (the patient must understand the broad
critical illness, direct informed consent is often difficult
nature and effects of the proposed intervention and
in critical care and surrogate consent may be the only the material risks it entails)
option in emergency situations. Consent issues in critical
care may be concerned with healthcare treatment or, as • voluntarily given
discussed later, participation in human research and the • it encompasses the act to be performed
use and disclosure of personal health information.27 • given by a person legally competent to do so.

Practice tip
able to weigh that information up (i.e. consider the effects
Make sure that informed consent is consistently of having or not having the treatment). Many jurisdic-
applied in every healthcare encounter. As such, tions around the world have legislation that addresses
consent is required for turning a patient and making situations where adults lack the capacity to give consent.
them comfortable, for making sure that the patient In emergencies, healthcare treatment may be provided
understands the procedure that they are undergoing or without the consent of a person. However, consent should
that they understand what is involved in the research be obtained for all procedures that involve ‘doing’ to a
study that they have recently enrolled in. If a patient patient (e.g. administering an injection). Consent should
does not understand, stop and ensure appropriate never be implied irrespective of the situation of the person
information is given by the person whose responsibility or the place of care, e.g. critically ill in ICU.25 In many
it is before continuing your intervention further. countries, if patients perceive that informed consent was
not obtained, a civil court case can be actioned on the
Consent to treatment grounds of battery (deliberate touching without their
consent) or negligence (receiving insufficient information
A competent individual has the right to decline or accept
about risk). Doctors and nurses therefore need to make
healthcare treatment. This right is enshrined in common
clear what they are proposing to do to a patient and why
law in Australia (with some variation across state or territory
they need to do it, with a ‘reasonable’ amount of informa-
jurisdictions) and in the Code of Health and Disability
tion about any risks involved.32
Consumers’ Rights in New Zealand (1996).28 With the intro-
If a person is assessed as not having capacity, consent
duction of human rights Acts (for example in the United
must be sought from someone who has lawful authority to
Kingdom [UK])29 there is global awareness of the individual
consent on his or her behalf. If the courts have appointed a
rights of patients in health care and of patients being actively
person to be guardian for an individual, then the guardian
encouraged to participate in treatment decisions.
can provide consent on behalf of that individual. However,
Informed consent provides assurance that patients
even for legally appointed guardians, consent cannot be
and others are neither deceived nor coerced in decision
given for certain procedures and the consent of a guard-
making; this recognises the person’s autonomy. Consent
ianship statutory authority may be required. Some states
procedures should minimise the potential for deception
have legislated to allow this authority to be delegated to a
and coercion and should be designed to give patients
‘person responsible’ or ‘statutory health authority’ without
control over the amount of information received and the
prior formal appointment. This person would usually be
opportunity to rescind consent already given.30 However,
a spouse, next-of-kin or unpaid carer of the individual.
clinical information can be complex and confusing for
As with formally appointed guardians, the powers of a
patients and obtaining informed consent can be prob-
‘person responsible’ are limited by statute.27
lematic. Improved communication skills for doctors and
nurses go some way toward resolving this problem. Shared
decision making in clinical care can best be achieved by Application of ethical principles
framing the relevant information in a comprehensible way
to the patient, while understanding that some patients
in the care of the critically ill
may not wish to make such choices themselves, preferring Any health professional working with critically ill patients
to have decisions made by clinicians.31 Box 5.3 lists key knows that critical care is complex and the number of
criteria that describe valid consent. decisions about clinical interventions that should, or
Patients must have the mental capacity and be competent should not, be offered to those who are critically ill
in order to give informed consent in healthcare decisions. are ever increasing. Given this, it becomes even more
To be competent, an individual must be able to comprehend important that clinical questions raised about medical
and retain information, must not be impervious to reason and nursing care be underpinned by consideration of the
or incapable of judgement after reflection and must be ethical dimensions of that care.33
112 SECTION 1 SCOPE OF CRITICAL CARE

Alongside the increasing number of technological Withdrawing and withholding

developments in critical care, critical care nursing has
also evolved in scope and practice. Critical care nurses treatment
are more autonomous in their role, using more developed The incidence of withholding and withdrawal of life
assessment and diagnostic skills and more advanced respi- support from critically ill patients has increased to the
ratory, cardiac and renal patient interventions. With such extent that these practices now precede the majority of
increased autonomy comes increased responsibility,34 deaths in intensive care40 with evidence that the majority
and this increases the potential for ambiguity in the role of clinicians in the USA41–43 and Europe44,45 have been
and conflict with others in the interdisciplinary team. involved in the withholding or withdrawal of treatments
To minimise such risks it is important that critical care for critically ill patients. Although there is a legal and
nurses understand the fundamental ethical principles moral presumption in favour of preserving life, avoiding
that apply to, and underpin, their clinical practice. This death should not always be the pre-eminent goal.46 The
is not always an easy task. As demonstrated in findings withholding or withdrawal of life support is considered
from a Portuguese study,35 ethical issues pervade many ethically acceptable and clinically desirable if it reduces
aspects of day-to-day care including: patient privacy issues unnecessary patient suffering in those whose prognosis is
(confidentiality); patient and family interaction (right considered hopeless (i.e. ‘futile’). Patients’ preferences, as
to self-determination); teamwork relationships and role evidenced through advanced care planning conversations,
responsibilities (equity, paternalism); end-of-life decision documented current advance directives or accounts from
making (respecting autonomy); and healthcare access proxy decision makers, should be used to inform decision
(equality, distributive justice). making in this area. Treatments that may be withdrawn
When faced with operating in such a difficult envi- (removed) or withheld (not commenced) in critical care
ronment, nurses in clinical practice feel vulnerable when may include the provision of ventilator support, inotropic
managing such a range of ethical responsibilities.36 support, haemodialysis, blood transfusions and antibiotics.
The ongoing challenge of navigating practice while The assumption is that, after the withholding or withdrawal
upholding professional values, responsibilities and duties of such treatments, the patient will most probably die from
can lead nurses to experience moral distress resulting in their underlying disease.47 This is an area of health care
increased levels of emotional distress, withdrawal from receiving increased attention of late. In Australia, work is
patient care, decreased job satisfaction and, ultimately, underway to develop a consensus statement with the aim of
increased attrition in nursing.37 However, proactively setting out expected standards of care and agreed practice
addressing ethical issues at a clinical team level through for recognising and responding to people in need of end-of-
dedicated case reviews, support systems and processes, life care in acute hospitals,48 including in situations where
including clinical supervision, debriefing, case conferences treatments are withheld or withdrawn for the critically ill.
and mortality and morbidity meetings, can help in main- In the United Kingdom, care pathways have been used with
taining ethical awareness in healthcare organisations. some success,49 although this remains a contentious area.
There are marked differences in the foregoing of
End-of-life decision making life-sustaining treatments between countries and even
With technological advances in health care, it is now more within states.What may be adopted legally and ethically in
possible than ever before to restore, sustain and prolong life one country may not be acceptable in another. For example,
with the use of technology and associated therapies includ- a recent publication highlights current challenges experi-
ing mechanical ventilation, extracorporeal oxygenation, enced by clinicians in Japan where, despite clear support
intra-aortic balloon counter pulsation and haemodialysis. from end-of-life guidelines, the practice of treatment
Each new medication or treatment on the market seems to withdrawal is limited.50 Further, complexities in care arise
promise added benefits to patients with improved outcomes due to the differing views held internationally on whether
and fewer side effects. However, in many cases managing withdrawal and withholding treatment is ethically the
the critically ill patient is more concerned with provision of same.51 In Australasia, when active treatment is withdrawn
supportive therapies, rather than curative ones.38 or withheld, the same legal and ethical principles apply.
A common ethical dilemma experienced by doctors The Australian and New Zealand Intensive Care Society
and nurses in critical care concerns the opposing (ANZICS) and College of Intensive Care Medicine of
decision-making positions of ‘maintaining life at all costs’ Australia and New Zealand (CICM) recommend that,
and ‘relieving suffering associated with the prolongation of when treatment withdrawal or withholding has been
life’. However, there are critically ill patients who receive discussed and agreed with the family, an ‘alternative care
life-sustaining therapies for prolonged periods with a plan’ with a focus on dignity and patient comfort be imple-
limited evidence-base about survival rates or longer term mented. It is suggested that such discussions be recorded
quality of life indicators. These are complex, emotive and in the patient notes including the basis for the decision,
much debated areas requiring decision making around the those involved in the discussions and the specifics of treat-
withdrawal and withholding of life support treatments and ment(s) being withheld or withdrawn.52
substantial deliberation with the patient, their family and all Although doctors and nurses appear clear in their
clinical teams involved.39 support for treatment withdrawal in cases of futility,
 CHAPTER 5 ETHICAL ISSUES IN CRITICAL CARE 113

the public at large hold different perceptions about this Once a decision to limit or withdraw treatment has
aspect of care. This is demonstrated in results from the been agreed, a plan is made as to how this will occur,
Ethicatt study53 where questionnaires on end-of-life which treatments will be withdrawn/withheld, when and
decision making were administered to 1899 doctors, by whom. It is at this stage that critical care nurses play an
nurses, patients and family members across intensive important role in managing end-of-life care.59 Concepts
care units in six European countries. The results demon- of caring for the dying patient in a critical care unit are
strated that less than 10% of doctors and nurses wanted no different to those in a hospital ward or hospice. The
their life prolonged by all available means, compared to principles of care encompass privacy, dignity, relief of pain,
40% of patients and 32% of families. When asked where provision of comfort and support for patient and relatives.
they would prefer to be cared for if they had a terminal Recognising and being respectful of the religious, spiritual
illness with a short time to live, more doctors and nurses and cultural needs of the patient and family are also
preferred care at home or in a hospice and more patients important. Care given at this time continues beyond the
and families preferred care in intensive care. Differences moment of the patient’s death with particular attention
in responses were based on the respondent’s country.53 placed on how the death of the person is pronounced,
A similar spread of views across healthcare staff and the how the family is notified of this death and the immediate
general public was demonstrated when consulted about bereavement support offered to the family, including
physician-assisted suicide in the USA.54 It is therefore discussions about possible autopsy. Compassionate care to
interesting that North American observational studies the family at this time is essential.
demonstrate healthcare staff consult families more often
than European healthcare staff53,55 with some seriously ill Decision-making principles
patients indicating a willingness to participate in end-of- Despite significant advances in critical care medicine,
life decisions, while others did not.56 approximately 20% of patients admitted to intensive care
It is clear that having in-depth knowledge of the units do not survive.60 The majority of patients who die
critical care environment and of futile treatments in critical care do so after planned withdrawal of life-
influences clinicians’ views on the practice of treatment prolonging therapies, as opposed to dying after unexpected
withdrawal or limitation. Cultural, religious, philosophi- and unsuccessful cardiopulmonary resuscitation.61 In order
cal and professional attitudes also influence views held in for care and treatment to be oriented away from active
this area. In a UK study57 reviewing the use of treatment intervention to palliation requires communication to occur
withdrawal guidelines, staff reported concern over the with the patient (if able), with the patient’s family and with
legal, moral, ethical and professional accountability issues the health team. Communication can be a complicated
involved in this area.The study demonstrated that medical process especially when difficult and challenging informa-
decisions to withdraw treatment were inconsistent within tion is required to be exchanged within a short timeframe,
medical teams and in similar patients. With such a range as sometimes happens at end of life in critical care.
of factors influencing decision making about withdrawal Lack of communication or misunderstood communi-
and withholding of treatment, it is not surprising that cation about end-of-life issues can lead to decisions being
gaining consensus on complex clinical situations, such as made that do not respect patient autonomy and that are
withdrawal of treatment, can be difficult. In cases where not made in the patient’s best interests. This can result in
there is uncertainty about the efficacy or appropriate- patients receiving burdensome and expensive treatments
ness of a life-sustaining treatment, it may be considered that they may not want. Such communication issues may
preferable to commence treatment, with an option to result from the lack of professional guidance for end-of-
withdraw treatment after broad consultation has occurred. life practices or from fear of litigation.62 With the profiled
However, managing such situations can be challenging role that family members hold as key decision makers in
as conflicts can occur about when and how to withdraw critical care, complex family dynamics cause a further
life-sustaining treatment;10 this is an area that critical challenge when working with relatives as surrogate
care nurses can actively contribute to in supporting the decision makers or patient advocates. Collectively, these
processes of decision making at end of life.45 factors can lead to misunderstandings and confusion about
Although it is essential that all members of the critical what the patient wants, what the family wish for and what
care team contribute to such discussions, legal respon- critical care staff feel is achievable.
sibility and accountability for the decision lies with the End-of-life decision making can be difficult leading to
senior treating doctor. Where conflict arises with family inconsistencies in the initiation of end-of-life care and the
members, especially if a family member has medical power withdrawal of life-supporting treatment.39 A further area
of attorney (or equivalent), the doctor must take this into that contributes to conflict between medical and nursing
consideration and respect the rights of any patient legal staff during end-of-life decisions is the impact of different
representative. It is unlikely that withdrawal of treatment professional ethical decision-making frameworks. While
will occur until a consensus decision is reached. This is the values of patients’ rights, justice and quality of life are
a different situation to that of a person who is legally central to medicine’s ethical framework, empirical work
declared brain dead52 where different ethical challenges demonstrates that nursing staff focus on patient dignity,
are posed58 (see Brain death section). comfort and respect for patients’ wishes that are central
114 SECTION 1 SCOPE OF CRITICAL CARE

FIGURE 5.1 Factors influencing decision-making processes in healthcare ethics.

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to nurses’ ethical framework.63 In enacting these values, The best interest principle relies on decision makers
nurses provide important support to patients and families holding an understanding of, and knowing the views held
enabling them to become involved in end-of-life decisions by, the person in question (e.g. critically ill patient) and of
ensuring that decisions match with stated care preferences, articulating those views relevant to decisions being made.
expectations, values and circumstances64 (see Figure 5.1). The best interest principle poses particular challenges
including how assumptions are made about what quality
Quality of life of life means for individuals and how a person’s views can
Despite the importance placed on quality of life in influ- change over time and not be communicated to significant
encing clinical decision making in critical care, there others. As a case example, Mary witnessed her mother’s
is no single agreed definition of what quality of life is. death several years ago on a ventilator after an acute exa-
Debate about quality of life is often engaged with when cerbation of chronic obstructive respiratory disease. After
justifying the continuation or discontinuation of life- this, Mary said to her family that she would never want to
sustaining treatment in critical care.6 Definitions of quality be ventilated. However, after a sudden collapse following
of life focus on subjective components related to the
a perforated duodenal ulcer, Mary required emergency
notions of desires and wellbeing (e.g. personal satisfac-
surgery and, due to unexpected intraoperative bleeding,
tion or happiness) and objective components related to
required postoperative ventilation until she was stabilised.
the meeting of personal needs (work, income, housing,
leisure factors) with both aspects needing consideration Although Mary’s doctors and family were aware of her
when making quality-of-life assessments.10 When making views, they made the decision for short-term ventilation
decisions about medical treatments based on quality-of-life as it was seen to be in her best interests. Ethical justifica-
arguments, it is important therefore that consideration is tion of medical decisions using the best interest principle
given to the personal preferences and wellbeing of the therefore requires a relevant and current understanding of
individual together with review of the person’s indepen- what quality of life means to that particular person.65
dent health and welfare status. Patient advocacy
Best interests Patient advocacy has, at its heart, a focus on patient rights,
Best interest is a guiding principle for making decisions values and interests and seeks to promote autonomy
in, and about, health care. It is defined as acting in a way when patients are unable or incapable of participating in
that optimally promotes good for the individual and is making decisions about their health care. Internationally,
referred to when one person makes a decision on behalf there are many recognised titles for individuals acting in
of another, as when a doctor makes a decision to cease the role of patient advocate. ‘Medical or healthcare agent’,
life-sustaining treatment for a particular patient. The best ‘medical power of attorney’ and ‘enduring guardian’ are
interest principle is often invoked in situations where terms and roles related to the concept of patient advocacy.
the patient may be assessed as incompetent and therefore With regards to health care, a patient advocate is usually
unable to participate in the decision-making process. someone chosen by an individual (e.g. a partner, child, good
 CHAPTER 5 ETHICAL ISSUES IN CRITICAL CARE 115

friend over 18 years of age) to make medical decisions on clinical experiences, experiential knowledge gained from
behalf of that person, should a situation arise where that colleagues and reported empirical data to conclude that
person lacks decisional capacity. Most patient advocates treatments are futile.71 There is no international definition
are known to, and appointed by, the person or are repre- of futility although some country-specific and profession-
sentatives of recognised bodies (e.g. guardianship boards, specific guidance exists to inform care.14 It is generally
Office of the Public Advocate) appointed into the role to agreed that healthcare practitioners should help the sick
safeguard vulnerable persons who lack capacity to make and that treatments should be offered, if of benefit to the
decisions. Each country has legislation in place to protect patient. Futile interventions are seen to cause pain and
the patient, patient advocate and healthcare team and such discomfort at end of life, give false hope to patients and
legal provision should be consulted to fully understand the family, delay palliative care and expend limited medical
conditions and safeguards in place. resources. However, determining which interventions
are beneficial to patients can be difficult, especially as the
Substituted judgement views of patients, families and clinicians may differ. While
If a person does not have the mental capacity to make the ethical requirement to respect patient autonomy
medical decisions, a surrogate decision maker should be entitles a patient to choose or reject the medically
identified. Substituted judgement is where an appro- acceptable treatment options, it does not entitle patients to
priate surrogate attempts to determine what the patient receive whatever treatments they would want. Clinicians
would have wanted in his/her present circumstances66 by are only required to offer treatments consistent with
utilising the values and preferences of the patient. In order professional standards and that give benefit to the patient.
to do this, the proxy decision maker needs an in-depth With respect to the law governing withholding and with-
knowledge of the patient’s values. Making a substituted drawing treatment in such circumstances, although there
judgement is a relatively informal process, in the sense that have been few cases in Australia and New Zealand where
the patient has not formally appointed the proxy decision these decisions have been litigated, the courts have been
maker. Rather, the role of proxy tends to be assumed on the consistent in concluding that there is no duty to provide
basis of an existing relationship between proxy and patient, life-sustaining treatment that is futile.72
for example, next of kin or family member. However, this
informal arrangement means that making an accurate Advance directives
substituted judgement can be difficult and that the proxy For individuals wanting to document preferences about
might not be the most appropriate person for this role.67 their future health care should situations arise where
they are no longer competent to make decisions, antici-
Medical futility patory direction or advance directive forms are able to
Treatment with no apparent benefit to the patient is be completed. With the increasing availability of medical
generally considered futile. In this it is acknowledged that technology, use of advance directives has improved.73,74
the physiological decay of the body due to old age and/or Advance directives inform health professionals how
illness exceeds the body’s response to medical treatments.68 medical decisions are to be made and who is to make
Futility is a concept in widespread use in healthcare ethics them, should the person be no longer able to make
and poses clinical challenges and debate at an international those decisions for themselves. An advance directive, also
level.69 Futility is often used by critical care doctors and known as a living will, a personal directive or an advance
nurses as a rationale for why medical treatments, including care directive, sets out instructions from a competent
life-saving or sustaining treatments, are considered not individual specifying what actions should be taken for
to be in the patient’s best interest. At times, the concept their health in the event that they are no longer able to
of futility may be used inappropriately and unethically, make decisions due to illness or incapacity.The five wishes
for example if the argument of ‘futility’ is used to coerce advance directive created by ‘Aging with Dignity’, a
relatives into agreeing to stop treatment of a patient.70 It is non-profit organisation in the USA, is one example of an
therefore important that a clear working understanding of advance directive.75 There are also national frameworks for
‘futility’ is held by healthcare practitioners. advanced care directives76 and specialty specific exemplars,
Treatment is considered futile if the medical therapy will e.g. the Western Australian Cancer and Palliative Care
never enable the person to achieve a state beyond permanent Network Advance Health Directive.77
unconsciousness or if, even with the treatment, it is unlikely Some people are hesitant to document their end-of-life
that the person will ever be discharged alive from intensive care plan so there is legal provision for the appointment of
care.66 Futility can be used to describe situations where the a person holding enduring power of attorney for matters
predicted success of the treatment is unlikely (physiological of health.55 The enduring power of attorney can make
futility) or where the benefit of recovery is outweighed by healthcare decisions on their behalf should the person
the burden of survival (e.g. the person survives but with loose capacity (for example, become unconscious).
potential of physical or mental incapacity).4
Physiological futility is being referred to when practi- Do not resuscitate considerations
tioners discuss ‘useless treatments’ in patient management. Cardiopulmonary resuscitation (CPR) remains the only
In such situations, clinicians usually reflect on their past intervention that patients explicitly state that they do or
116 SECTION 1 SCOPE OF CRITICAL CARE

do not want.78 If patients have acute, reversible illness professional and legal debate on this matter. Oregon was
conditions, they should have the right to CPR. However, the first state in the USA to legalise physician-assisted
discussions may occur regarding the withholding of CPR suicide when it passed the Death with Dignity Act in 1997.80
in patients with irreversible or terminal illnesses.This is an The Death with Dignity Act outlines a rigorous process for
important point to consider as every patient will have CPR, assisted dying with strict criteria requiring details pertaining
unless documented otherwise. The decision to withhold to: the patient’s request; the patient’s suffering; information
CPR may be termed a ‘do not resuscitate’ (DNR), ‘do provided to the patient; the presence of reasonable alterna-
not attempt resuscitation’ (DNAR) or ‘not for resuscita- tives; consultation with another physician; and the applied
tion’ (NFR) order. While such ‘orders’ reflect a decision method of ending life. Under the Death with Dignity Act,
against any resuscitation treatment, there are other types physicians may not administer the medication; patients
of resuscitation orders seen written in patient notes that must ingest it independently.
use limited treatment, including ‘for defibrillation only’ or Since 2002 euthanasia and physician-assisted suicide
‘for one round of ALS only’. These can be confusing for in the Netherlands are not punishable if the attending
staff and families who may perceive such orders to be half- physician acts in accordance with criteria of due care.
hearted attempts at resuscitation or, indeed, that no care These criteria are similar to the Oregon areas outlined
is meant to be given.78 As each patient case is considered above. In reporting on a review of 158 reported euthanasia
on its own merit, it is important that any medical orders and physician-assisted suicide cases from the Nether-
or directives are clearly documented in the patient’s notes lands, Buiting et al81 identified that medical care including
or on the appropriate forms so that misinterpretations do medication (89%), radio- or chemotherapy (21%) and
not occur. It is important that clear discussion and broad palliative care options (46%) had been administered with
consultation across the clinical team(s) and patient/family continued unbearable suffering leading to the request for
occurs. A management plan that incorporates assessment physician-assisted suicide. This is clearly a contentious
of patient and family understanding, disclosure of the area and so, to guide current practice in Australasia, when
patient’s situation, discussion and consensus gaining with requests for euthanasia are made, it would be appropri-
the patient and family may be particularly useful.79 ate to explore alternative treatment options to support
symptom relief and develop an agreed future treatment
Euthanasia plan. Assistance from other specialist teams and profes-
Euthanasia continues to be the subject of ongoing inter- sionals, for example palliative care, a counsellor or other
national debate. Generally understood as the termination qualified professional, may also be useful.79
of a person’s life in order to relieve suffering, in most cases
euthanasia is carried out because it is requested by the Brain death
person. Although the concept of euthanasia is supported in Death can occur in the critical care setting due to
some areas, it remains illegal in Australia and New Zealand. unexpected cardiac arrest, expected death after a planned
With confusion occurring about the difference between treatment withdrawal or treatment withholding, and as a
treatment withdrawal and euthanasia, the primary distinc- result of the diagnosis of brain death. Brain death occurs
tion between the two relates to the issue of ‘intent’. If in the setting of a severe brain injury associated with
the primary intention of the intervention (e.g. a lethal marked elevation of intracranial pressure. To ascertain
injection) is to cause death, this is regarded as euthanasia. that brain death has occurred requires that the patient be
If the primary intention of the intervention is to reduce in an unresponsive coma and demonstrate no brainstem
pain and suffering, this may not be regarded as euthanasia reflexes or respiratory centre functioning. Clear clinical
but this may still be tested legally in a court of law. It is or neuroimaging evidence of acute brain pathology (e.g.
this complexity that causes the vigorous ‘for’ and ‘against’ traumatic brain injury, intracranial haemorrhage, hypoxic
debates about euthanasia. Those opposing euthanasia encephalopathy) consistent with the irreversible loss of
do so in the belief of the sanctity of life and that life is neurological function is also required.82 However, cases
God-given and that effective symptom control should be have been reported where brainstem death has occurred
able to keep individuals comfortable. Other opponents without injury or death of the cerebral hemispheres, for
raise the concern that, if euthanasia were made legal, the example in patients with severe Guillain–Barré syndrome
laws regulating it could be abused and this would lead or isolated brainstem injury.83
to euthanasia being used with people not expressing a Defining brain death is a complex area with different
wish to die. Those in support of euthanasia argue that international interpretations of death in this context. In
a civilised society should support a person’s autonomy and Australia and New Zealand, the standard definition of
self-determinism and that people should die in dignity and brain death is cell death within the brain stem and cerebral
without pain. If people are not able to terminate their own hemispheres. This contrasts with the UK where brainstem
life, others should be allowed to help them to do so. death (even in the presence of cerebral blood flow) is the
Several countries have considered the physician’s role in standard. In the USA, according to the Uniform Deter-
euthanasia (termed physician-assisted suicide) including the mination of Death Act, brain death occurs when a person
USA and the Netherlands. Many other countries, including permanently stops breathing, the heart stops beating and
the UK, New Zealand and Australia, have ongoing public, ‘all functions of the entire brain, including the brain stem’
 CHAPTER 5 ETHICAL ISSUES IN CRITICAL CARE 117

cease. Yet determining brain death is a complex process Organ donation

that requires a series of tests to ensure the correct diagnosis
The retrieval of organs and tissues after death has important
is made. With that in mind, the American Academy of
legal and ethical perspectives that need to be considered.
Neurology issued guidelines in 201084 to remove some
As a result, there is legislative guidance in Australia and
of the uncertainty and variability amongst doctors in their
New Zealand for the removal of organs and tissues after
procedures. Periodically, there are news reports about death for the purpose of transplantation. Human tissue
patients in long-term coma who regain consciousness, or Acts in both counties prohibit trading in human organs
reports of conflict about the management of people in or tissue and there are guidelines to support practice in
a persistent vegetative state. However, brain death should this area,89 together with specific resources that are useful
not be confused with persistent vegetative state, where for critical care clinicians (see Table 5.1). Although organ
limited brain activity remains. and tissue donation are spoken about together in clinical
The international variation in brain death definition practice, it is often organ donation that provokes the
and procedures was highlighted in a survey of 89 greatest ethical debate and discussion, and this is now
countries undertaken a decade ago.85 Results from this explored in more depth here.
study demonstrated that practice guidelines for brain
death in adults were present in 88% of countries surveyed Nurses’ attitudes to, and knowledge
with legal standards on organ transplantation present in of, organ donation
69% of countries. All guidelines agreed on the presence
Even where there are dedicated nurses who coordinate
of irreversible coma, absent motor response and absent
tissue and organ donation, nurses who work in critical
brainstem reflexes to determine brain death. Although
care areas should still be able to raise and discuss donation
there was broad agreement on the role of apnoea testing
matters with patients, families and the wider clinical
(59% of the surveyed countries), differences across the
team. In order to competently manage this, nurses need
guidelines were noted with regard to the length of
to have well-developed communication and interper-
time of observation and the professional credentials for
sonal skills75 and an understanding of the ethical and
the physicians examining for brain death. ANZICS
legal frameworks within which donation occurs. Organ
recommends that testing for brain death be undertaken
donation can challenge the personal ethical and belief
independently by two medical practitioners with specific systems for some nurses. This situation can be further
experience and qualifications pertinent to this area. It is
recommended that the two sets of tests be performed
separately, using the same procedures and assessments. Table 5.1
Although it is recognised that brain death will have Organ donation resources
occurred sometime before the brain stem testing, the
time of death of that patient is recorded as the time of RESOURCE DESCRIPTION

completion of the second set of tests.82 Organ and Tissue Donation These guidelines outline
Certification of brain death, while a distinct diagnosis by Living Donors: Guidelines ethical practice for health
with an associated set of diagnostic testing procedures, is for Ethical Practice for Health professionals involved in
often associated in clinical practice with organ donation Professionals 200778 living organ and tissue
as this allows for retrieval of well-perfused organs from donation and provide
patients who have already been certified dead (‘beating- guidance on how these
principles can be put into
heart donors’). There is also increasing international
practice
recognition of the role of donation after cardiac death
(DCD) where organs are retrieved after the circulation Organ and Tissue These guidelines outline
has ceased and the person has died.86 DCD has not gained Donation After Death, for ethical principles for health
Transplantation: Guidelines professionals involved in
the level of support within the healthcare community
for Ethical Practice for Health donation after death and
as brain death donation,87 and this may be because of
Professionals51 provide guidance on how
ethical concerns that are different to those encountered in
these principles can be put
brain death organ donation. Key issues reported in DCD into practice
include concerns about whether appropriate efforts are
Making a Decision This booklet aims to help
undertaken to save patients, whether irreversibility exists
about Organ and Tissue people think through some
and difficulties associated with the decision to remove
Donation after Death; ethical issues and make
mechanical or organ-perfusion support.88 this booklet is derived informed decisions about
While the diagnosis of brain death and cardiac from Organ and Tissue organ and tissue donation
death for any patient must be unequivocal, it is partic- Donation after Death, for after death.
ularly important when organs are being retrieved that Transplantation: Guidelines
the diagnosis of death is a systematic, comprehensive and for Ethical Practice for Health
transparent process so that it is fully understood by the Professionals78
family and the healthcare team as the absolute diagnosis.89
118 SECTION 1 SCOPE OF CRITICAL CARE

complicated by the general public misunderstanding Supporting the family of the person who is brain dead
the concept of brain death and easily confusing brain is stressful.97 There is often concern from critical care
death with profound coma or massive brain damage.90 nurses that discussing organ donation may further increase
More worryingly, this confusion can even reside within the distress of the grieving family. However, consenting
families of deceased patients involved in organ donation. to organ donation has been shown to neither hinder nor
An Australian study reported that 20% of bereaved prolong the grief process of bereaved families.98 Empirical
families of brain dead patients remained concerned about work demonstrates that nurses possessing higher knowledge
whether their family member had actually been dead at about organ donation hold more positive attitudes towards
the time of withdrawal of the ventilator.91 It is under- organ donation99 and are more likely to discuss organ
standable why this confusion can occur as researchers donation with families.89 The role of healthcare staff in
have described the contradictions associated with caring raising awareness and education about organ donation
for brain dead patients, in particular the ambiguity of is important as donation rates continue to be low,100
caring for a pink and warm brain dead body, a body with only half of those who support organ donation
that is exhibiting traditionally accepted signs of life.92,93 actually consenting to donate.96 In 2009, the Australian
In another study of experienced intensive care nurses, Organ and Tissue Authority (AOTA)101 was established
almost half the participants did not regard brain death as with the mandate to significantly improve organ and
a state of death.94 Participants who were non-accepting tissue donation and transplantation. This national reform
or ambivalent towards brain death did not perceive that program was based on the world’s best practice approach
the medico-legal construct of brain death was congruent using learning from leading country performers, e.g.
with their ‘personal foundational death notions’.94 It is Spain, France, Belgium, Austria and the USA. Awareness
therefore important that critical care nurses possess a and engagement with the general public, healthcare sector,
thorough understanding of brain death and are supported non-government sectors and donor families was seen as
to reflect on their personal understanding of death, paramount to improve donor rates.89,101 This raises a debate
including the concept of brain death. about the mechanism of consent, with many European
Such ambiguity for staff and families surrounding countries using ‘opt-out’ consent processes, as opposed to
brain death can be illustrated by nursing and medical staff ‘opt-in’ processes. Equally important is adequate training
continuing to talk to a patient who is brain dead while of health professionals to sympathetically and sensitively
providing direct care.This can cause confusion for relatives approach the grieving family with full knowledge of the
who have already been informed that the patient is brain donation process.89
dead with no possibility of recovery or being able to
comprehend/hear. Alternatively, staff and family members The role of the critical care nurse in
may be comforted by staff talking to their family member: ethical decision making
they may perhaps be demonstrating a respectful attitude
towards that person and who that person was. It is clear that With the most frequently occurring and most stressful
there is no right and wrong here, rather that such situations ethical issues for nurses being protecting patients,
reinforce the need for all staff to be sensitive to how their autonomy and informed consent to treatment, staffing
actions may be perceived and be clear with families as to patterns, advanced care planning and surrogate decision
what is informing such actions. Another area to consider is making,102 ethical issues challenge nurses on a daily basis.
the language used by healthcare staff with families. Deper- As the bedside role allows nurses to have an intimate
sonalising terms such as ‘cadaver’ and ‘harvesting’ may be understanding of the patient/family and their views on
inadvertently used during organ donation and, although direction of care and treatments being delivered, nurses
these may serve to psychologically protect staff, they can are well-placed to support patient autonomy and help the
also act as a barrier to effective communication and under- patient/family make choices congruent with their values
standing with grieving families.95 What is important here and wishes.103 This view is reflected in the Australian Code
is that doctors and nurses have a heightened awareness as of Ethics for Nurses: specifically, that nurses should ensure
to the emotional distress that families may be under at this patients are appropriately informed to make choices about
time, and to ensure that communication with families is their treatment and to maintain optimal self-determination
timely, clear and compassionate. (Value statement 2.3).7 Practice is made more challeng-
Critical care nurses are therefore in a strong position ing when further ethical conflicts for doctors and nurses
to foster a positive attitude and understanding of organ result from organisational ethical issues, e.g. allocation of
donation through provision of education and support to funding and resources, and administration support – or
families of such patients. It is important that families have lack of it.104 In such times, it is important that person-
time to consider organ and tissue donation only after the centred care becomes the focus of care delivery with
subject of the patient’s death has been discussed. If organ patients and their families being the lead advocates in care
donation is to be raised, it may be useful to note that the and, where this is not possible, advocacy being collaborative
majority of donor families would make the decision to rather than any one professional taking a paternalistic role.
donate, if in that situation again.96 See Chapter 29 for In situations where complex ethical dilemmas are faced,
further details. access to a clinical ethicist or a clinical ethics committee105
 CHAPTER 5 ETHICAL ISSUES IN CRITICAL CARE 119

may help in bringing together those involved and offer an

BOX 5.4
ethical review to mediate the problem.
Many aspects of critical care nursing hold moral and Information requirements for participant consent in
ethical challenges. Ethical issues in practice range from medical research
the ‘big’ subjects, such as assisted dying or treatment (or Consent to medical research documentation should
non-treatment) based on religious beliefs, through to the include the following:23
‘everyday’ ethical challenges of nursing practice,106 such as
• A statement that the study involves research
the use of chemical versus physical restraints for patients.
It is important that critical care nurses understand such • An explanation of the purposes of the research
dimensions of their work and have considered the personal • The expected duration of the subject’s participation
and professional positions from which they operate. • A description of the procedures to be followed
• Identification of any procedures that are experimental
Ethics in research • A description of any reasonably foreseeable risks or
When it comes to conducting research, ethical codes of discomforts to the subject
conduct and ensuring all criteria for valid consent are met • A description of any benefits to the subject or to
are requirements for all those conducting human research. others that may reasonably be expected from the
There are various ethical guidelines for the conduct of research
research, for example the Declaration of Helsinki is • A disclosure of appropriate alternative procedures
regarded as an authoritative source.107 In the UK, the or courses of treatment, if any, that might be
General Medical Council provides clear overall modern advantageous to the subject
guidance in the form of its Good Medical Practice • A statement describing the extent, if any, to which
Statement.108 Other organisations, such as the Medical confidentiality of records identifying the subject will
Protection Society in the UK, are often consulted by be maintained
British doctors regarding issues relating to ethics.With this
guidance developed at a national level to inform research • For research involving more than minimal risk,
ethics, there is also guidance for local research and ethics an explanation as to whether any compensation,
boards to ensure that research ethics are attended to at and an explanation as to whether any medical
the institutional level. There is usually country-specific treatments are available, if injury occurs and, if so,
guidance to inform the expected composition of these what they consist of, or where further information
local research and ethics bodies.9,109 may be obtained
Healthcare research in Australia is performed in • An explanation of whom to contact for answers to
accordance with guidelines issued by the National Health pertinent questions about the research and research
and Medical Research Council (NHMRC), while in New subjects’ rights, and whom to contact in the event
Zealand the guidelines are issued by the Health Research of a research-related injury to the subject
Council (HRC). Both councils have statutory authority, • A statement that participation is voluntary, refusal to
and health service and university human research ethics participate will involve no penalty or loss of benefits
committees (HRECs) (Australia) and both health and to which the subject is otherwise entitled, and the
disability ethics committees (HDECs) and institutional subject may discontinue participation at any time
ethics committees (IECs) (NZ) are required to consider without penalty or loss of benefits, to which the
research proposals in accordance with the relevant recom- subject is otherwise entitled
mended processes and procedures outlined by these
Research Councils (see Online resources at the end of the
Chapter for a list of relevant resources provided by the ethical requirements for consent in medical research.27
NHMRC and HRC). When research studies are being considered in critical care
areas, surrogate consent may be applicable.110
Application of ethical principles Other important and relevant ethical principles for
When considering human clinical research in the context consideration in human research are beneficence and
of critical care, the concept of respect for persons is linked non-maleficence. Beneficence in the research context is
to the ethical principle of autonomy.9 In human research, expressed by the researcher’s responsibility to minimise
respect for persons demands that participants receive the risk of harm or discomfort to research participants.9
adequate information and choose to participate volun- Research protocols should be designed to ensure that
tarily in the research without coercion. Similar criteria as respect for dignity and wellbeing takes precedence over
for consent to treatment should be applied by researchers any expected knowledge benefits from the research.
seeking to recruit participants into their study. Although With regard to justice in research, this requires that within
there may be some variation between organisations and a population there is a fair distribution of ‘benefits and
jurisdictions, Box 5.4 provides the type of information burdens’ for research participation. In using this concept
that potential participants should be provided with to meet it is the scientific objective, as opposed to membership of
120 SECTION 1 SCOPE OF CRITICAL CARE

either a privileged or vulnerable population, that should her consent is a problematic issue that most critical care
determine the participants for a study, and the sample researchers and HRECs have to attend to.9,111 Paramount
population should be selected to most equitably share the in these considerations is the careful weighing of potential
risks and benefits of the research. risks and benefits by a competent individual. However,
When recruiting research participants it is important analysis of these risks and benefits by a surrogate on behalf
to ensure that any initial approach is made appropriately. of an incompetent individual poses a range of ethical diffi-
When the study involves recruitment of hospital inpatients, culties. Most national and international guidelines concur
this approach should be made by someone directly that such research is justified as long as safeguards are in
involved in their care, with the aim of seeking permission place. Both the National Statement9 and the Operational
to then be approached by the investigators specifically Standards112 outline categories of vulnerable persons and
about the research. If the study involves recruitment of the relevant ethical considerations that apply to these
individuals from the community, this can be done by groups. The governing bodies recommend careful con-
public display (e.g. flyers, published advertisements) that sideration of these highly vulnerable groups. Of note,
provides the contact details of the researcher. Control for the New Zealand Operational Standards112 recognise
involvement in the research is then with the participant to that research on unconscious patients is appropriate, but
make contact with the researcher. While these processes emphasise the need for communication with the family
may be interpreted as putting an extra barrier to recruit- or other legal representatives wherever possible. These
ment, the principles of respect and autonomy for persons Standards do note that in emergency situations consul-
are upheld as the potential for coercive recruitment is tation with the family/legal representatives may not be
reduced. Another guiding value in ethical research is that possible, but that the ‘health care practitioner must always
of integrity. This requires that the researcher be committed act in the best interests of the consumer.’112
to the search for knowledge and to the principles of ethical
research, conduct and results dissemination.9 Clinical trials
Clinical trials are a specific type of research study that
Human research ethics committees explores whether a medical treatment or device is safe and
HRECs play a central role in the ethical supervision of effective for humans. As these trials use people/patients
research involving humans. Individual research institutes/ as subjects in the study, these studies must follow strict
centres, universities, regional/local health authorities and scientific standards that are set within each country. The
hospitals will have an HREC (or equivalent body) and Therapeutic Goods Administration (TGA) in Australia
articulate requirements for research to be conducted in has adopted the Note for Guidance on Good Clinical
their institution. The HREC will review proposals for Practice to replace the Guidelines for Good Clinical Research
research involving humans to ensure that the research Practice,113 but at the same time note there is some overlap
is soundly designed, and conducted according to high with The National Statement, which prevails. The TGA
ethical standards such as those articulated in Australia in has published an annotated version for the Australian
the National Statement on Ethical Conduct in Human Research regulatory context. The Note for Guidance on Good Clinical
2007 (known as the National Statement).9 Individual Practice113 is an internationally accepted standard for the
HRECs have protocols for submission of ethics applica- designing, conducting, recording and reporting of clinical
tions, compliance, monitoring and complaints handling trials.
processes. Importantly, no research study involving The Australian government, through the NHMRC,
humans can be commenced until ethical clearance has has funded and established the Australian Clinical Trial
been formally given by the relevant HREC(s). Registry (ACTR) at the NHMRC Trials Centre in
The role of an HREC should not be confused with Sydney, which complies with these requirements. Clinical
another form of clinical ethics committee that has been trials can be registered online. For trials commencing
established in some hospitals and health services to provide recruitment after 1 July 2005, registration must occur
closed forums for clinicians to raise ethical and legal prior to subject recruitment, as there are important impli-
concerns associated with particular clinical treatments or cations for future research publication in journals. In
decisions.These are advisory committees that can also take parallel, as more national trial registries emerge, the World
into account patients’ and or their families’ wishes when Health Organization (WHO) is developing an approval
this raises complex decision making with clinicians. In process to assess trial register compliance. The WHO
addition to providing clinicians with advice on particular International Clinical Trial Registry Platform (ICTRP)114
cases these committees may also assist with the devel- is a global project to facilitate access to information
opment of organisational policies on patient care and about controlled trials and their results. The Clinical
facilitate staff and patient education about ethical issues. Trials Search Portal provides access to a central database
Research involving unconscious containing the trial registration data sets provided by the
registries listed. It also provides links to the full original
persons records.To facilitate the unique identification of trials, the
The question of whether it is justifiable to include an Search Portal bridges (groups together) multiple records
unconscious patient in a research project without his or about the same trial.114
 CHAPTER 5 ETHICAL ISSUES IN CRITICAL CARE 121

Ethics in publication • conception and design, or data collection or analysis/

One of the key ways in which research findings are dissem- interpretation of data
inated is through publication in peer-reviewed journals. • drafting the article, or revising it critically for
Many international high quality journals, including important intellectual content
Australian Critical Care, support the implementation of the
Committee of Publication Ethics (COPE) Code of Conduct
• final approval of the version to be published.116
and Best Practice Guidelines115 for journal editors and Authors must also ensure that all those who have
publishers. These guidelines recognise the important roles contributed to the work are recognised and acknowledged.
of editors, editorial boards and publishers in promoting Acquisition of research funding or general supervision of a
and supporting ethical practices in reporting research. research group is not considered sufficient for authorship.
Therefore, journal editors are increasingly requiring that Intellectual honesty should be paramount and used to
researchers demonstrate evidence of their ethics review inform publication ethics and to prevent misconduct.116
process before a manuscript/study is considered for publi- Furthermore, under best practice guidelines, journals
cation. should ensure processes whereby researchers are obliged
In Australia the NHMRC Australian Code for the to disclose any potential competing interests before a
Responsible Conduct of Research (2007)116 provides guidance manuscript is published and ensure all published reports
on the minimum requirements for authorship of research. and reviews of research papers have been peer reviewed
Authorship is defined as substantial participation, where by suitably qualified persons and, where needed, publish
all the following conditions are met: corrections, clarifications, retractions and apologies.115

Summary
Effectively dealing with ethical issues in any healthcare setting is complex and at times contentious. This is even more
so in the critical care environment, where the patient cohort is predominantly vulnerable and lacking capacity and
competence regarding autonomous decision making. Hence, critical care nurses need to be familiar with guiding ethical
principles in the care of the critically ill and with the ethical considerations relating to the conduct of clinical human
research. While a broad knowledge of these principles is a requirement for all health professionals as critical care nurses
are often involved in these discussions and debates, they need to be particularly well informed in order to actively parti-
cipate in ethical decision making. They must also be cognisant of the dynamic nature of the world we inhabit where
rapidly changing communication media (e.g. the use of social media) and digital health technologies will create new and
emerging ethical conundrums and legal challenges associated with privacy and confidentiality.
Critical care nurses have a unique position, being with the patient around the clock, often side-by-side with their
relatives. Responsibilities include acting as patient advocate, frequently with a counselling and listening role at the bedside
with patients and relatives. With medical officers having specific legal responsibilities surrounding consent and end-of-
life decision making, a multidisciplinary approach is therefore important and indeed prudent to ensure all pertinent
ethical matters are considered appropriately and according to guiding ethical principles.

Case study
This study reports on a high profile case from the UK. The case was a noteworthy ethico-legal dilemma
and vividly illustrates key ethical principles that inform clinical reasoning in the face of a challenging event.
Firstly, the case is presented and then the ethical issues arising from this case are explored. Finally, learning
activities are included in the form of questions to stimulate thinking and help reflection on ethical areas of
practice.
On 17 September 2007 Kerrie Wooltorton, a 26-year-old woman, drank 350 mL of ethylene glycol (antifreeze)
and called an ambulance. She took with her a letter written by her and dated 14 September 2007, stating
that she knew the consequences of her actions and wanted no life-saving treatment but had come to
hospital so that she could be made comfortable as she did not want to die alone. The letter stated:
To whom this may concern, if I come into hospital regarding taking an overdose or any attempt of my
life, I would like for NO lifesaving treatment to be given. I would appreciate if you could continue to
give medicines to help relieve my discomfort, painkillers, oxygen etc. I would hope these wishes will be
carried out without loads of questioning.
122 SECTION 1 SCOPE OF CRITICAL CARE

Please be assured that I am 100% aware of the consequences of this and the probable outcome of
drinking anti-freeze, e.g. death in 95–99% of cases and if I survive then kidney failure, I understand and
accept them and will take 100% responsibility for this decision.
I am aware that you may think that because I call the ambulance I therefore want treatment. THIS IS NOT
THE CASE! I do however want to be comfortable as nobody wants to die alone and scared and without
going into details there are loads of reasons I do not want to die at home which I realise that you will not
understand and I apologise for this.
Please understand that I definitely don’t want any form of Ventilation, resuscitation or dialysis, these are
my wishes, please respect and carry them out.
Yours sincerely
Kerrie Wooltorton117
After admission, Kerrie Wooltorton was questioned by doctors on several occasions and over that period
of time she continued to refuse medical treatment. Kerrie was known to hospital services and had taken
overdoses on previous occasions and received treatment. Consultation was carried out with the full clinical
team and the medical director and legal advice was taken. Kerrie Wooltorton was assessed as having
mental capacity and therefore had the right to refuse treatment.
Kerrie Wooltorton died on 19 September 2007, from ethylene glycol toxicity.

CASE STUDY QUESTIONS

1 What legal and ethical issues were raised by this case?
2 How can capacity be assessed?
3 Does a person’s autonomy have limits?
4 Ethically, is there a difference between a competent person making a well-thought-through request as
opposed to an irrational one?

RESEARCH VIGNETTE

Bloomer MJ, Morphet J, O’Connor M, Lee S, Griffiths D. Nursing care of the family before and
after a death in the ICU – an exploratory pilot study. Aust Crit Care 2013;26(1):23–8

Abstract
This qualitative descriptive study was undertaken in two metropolitan ICUs utilising focus groups to describe the ways in
which ICU nurses care for the families of dying patients during and after the death. Participants shared their perspectives
on how they care for families and their concerns about care, and detailed the strategies they use to provide timely and
person-centred family care. Participants identified that their ICU training was inadequate in equipping them to address
the complex care needs of families leading up to and following patient deaths, and they relied on peer mentoring
and role-modelling to improve their care. Organisational constraints, practices and pressures impacting on the nurse
made ‘ideal’ family care difficult. They also identified that a lack of access to pastoral care and social work after hours
contributed to their concerns about family care. Participants reported that they valued the time nurses spent with
families, and the importance of ensuring families spent time with the patient, before and after death.

Critique
Introduction and aims: This qualitative descriptive study explores how nurses facilitate ‘a good death’ for families
of dying patients in intensive care. The paper reports on the preparedness of nurses to provide this care and on the
organisational factors that impact on care delivered. At the beginning of the paper, the context of the study is well
presented. Reference is made to the body of international work exploring how decisions are made with families
during end-of-life care in the ICU and identifies that our understanding is less developed about nursing challenges
when caring for dying patients. This then sets the scene for the aims of this work, one of which provides the focus
 CHAPTER 5 ETHICAL ISSUES IN CRITICAL CARE 123

for the title of this exploratory pilot study. The study reads as if the original intention of the research team was to
undertake a small study. The intention may have been that this would lead to a larger study (hence pilot) in an area
considered poorly explored in the research literature, hence the need for ‘exploration’. An alternative title for this
paper could have been: ‘a qualitative exploratory study’.

Methods: As a qualitative study, no hypotheses are put forward for testing and no research question is used.
However, several study aims are used that align with the preceding literature and subsequent study design and
findings. The particular qualitative approach employed (e.g. phenomenology) is not acknowledged; this may be due
to the applied nature of this clinical research. Ethical approval and funding support particulars are supplied, details of
the sample and setting are provided and the recruitment strategy is well detailed. Specifics about the open questions
used in the focus groups (for example, was a template used?) and the use of ‘body language and participation’ field
notes would have been useful. Although there is good detail about the inductive method of data analysis, the rationale
for content analysis is not clear. However, such lack of detail can easily result from choices made by authors to meet
word limits set for published papers.

Results and discussion: In describing findings of the study, details are provided about the number and duration
of focus groups but the overall sample size is not given. It may be that the authors considered this and chose not
to report on specific data in what is, potentially, a sensitive area. Four themes develop from the data incorporating
aspects of the nursing role (e.g. presence), constraints on the nursing role (e.g. time and place) and preparedness of
nurses (e.g. culture). The themes are well-supported by data extracts. The discussion section of the paper explores all
salient points raised by the data, using recent references to support assertions made. However, there is less evidence
of data saturation to support discussion about poor educational preparation and lack of organisational support.

Conclusion: The paper concludes with a clear exploration of study limitations together with recommendations for
future work in the area. This study, undertaken by an interdisciplinary team and published in a peer-reviewed, clinical
journal, contributes to our knowledge about the role of nurses during end of life in intensive care.

Lear ning a c t iv it ie s
1 Consider the issues of mental capacity raised by the Case study. How are assessments about someone’s
mental capacity made in your clinical area? What legal, professional and organisational processes and guidance
are in place to assist this? What actions would you take if your assessment of a patient’s mental capacity were
not reflective of others in your team?
2 If a similar case to Kerrie Wooltorton’s presented to your hospital, how would it be managed – similarly or
differently? Why? What were the key issues from a legal perspective that might have prevented the medical
team in this case being seen as aiding and abetting her suicide?
3 In your practice, are there decisions made by adult patients with capacity that challenge you in thinking there
are limits to someone’s autonomy? What are those circumstances and how are these managed in practice?
4 What would you do if a competent patient made a request about their treatment that you considered irrational?

Online resources
AUSTRALIA
Australian Organ and Tissue Authority (AOTA), www.donatelife.gov.au
Australian state and territory privacy law, www.oaic.gov.au/privacy/other-privacy-jurisdictions/state-and-territory-privacy-law
Human research ethics committees and the therapeutic goods legislation, Department of Health and Aged Care, Canberra,
2001, www.tga.gov.au/pdf/access-hrec.pdf
National Health and Medical Research Council (NHMRC), An ethical framework for integrating palliative care principles into
the management of advanced chronic or terminal conditions, www.nhmrc.gov.au/_files_nhmrc/publications/attachments/
rec31_ethical_framework_palliative_care_terminal_110908.pdf
124 SECTION 1 SCOPE OF CRITICAL CARE

National Health and Medical Research Council (NHMRC), Challenging ethical issues in contemporary research on human
beings, 2007, current, www.nhmrc.gov.au/_files_nhmrc/publications/attachments/e73.pdf
National Health and Medical Research Council (NHMRC), Ethical considerations relating to healthcare resources allocation
decisions, 1993, current, www.nhmrc.gov.au/_files_nhmrc/publications/attachments/e24.pdf
National Health and Medical Research Council (NHMRC), Health ethics, research integrity, www.nhmrc.gov.au/health-ethics/
research-integrity
National Health and Medical Research Council (NHMRC), National Statement on Ethical Conduct in Human Research 2007,
updated 2014, www.nhmrc.gov.au/guidelines/publications/e72
National Health and Medical Research Council (NHMRC), Revision of the Joint NHMRC/AVCC Statement and Guidelines on
Research Practice 2007, www.nhmrc.gov.au/_files_nhmrc/publications/attachments/r39.pdf
National Health and Medical Research Council (NHMRC), Values and ethics: Guidelines for ethical conduct in Aboriginal and
Torres Strait Islander health research, 2003 and current, www.nhmrc.gov.au/_files_nhmrc/publications/attachments/e52.pdf

NEW ZEALAND
Health Act 1956 (NZ), www.legislation.govt.nz/act/public/1956/0065/latest/DLM305840.html
Health Research Council of New Zealand (HRCNZ), Ethics overview, www.hrc.govt.nz/ethics-and-regulatory/nz-ethics-
overview and www.hrc.govt.nz/ethics-and-regulatory
Health Research Council of New Zealand (HRCNZ), Guidelines for researchers on health research involving Maori, revised 2010,
www.hrc.govt.nz/news-and-publications/publications/guidelines-researchers-health-research-involving-m%C4%81ori
National Ethics Advisory Committee NZ, http://neac.health.govt.nz/home
New Zealand multi-region ethics committees, http://ethics.health.govt.nz/about-committees/archived-minutes-and-reports-
pre-2012/multi-region-committee
New Zealand Privacy Commissioner website, www.privacy.org.nz
Public Health and Disability Act 2000 (NZ), Amended as NZ Public Health and Disability Amendment Bill 2010, www.parliament.
nz/en-nz/pb/legislation/bills/digests/49PLLawBD17731/new-zealand-public-health-and-disability-amendment-bill

OTHERS
Council for International Organisations of Medical Sciences (CIOMS), International guidelines for biomedical research involving
human subjects, 1993, revised in August 2002; International guidelines for epidemiological research, 1991, www.cioms.ch
International Committee of Medical Journal Editors (ICMJE) Recommendations (The Uniform Requirements), www.icmje.org
Medical Research Council of Canada (MRC), National Science and Engineering Research Council of Canada (NSERC) and
the Social Science and Humanities Research Council of Canada (SSHRC), Tri-Council Policy Statement: Ethical conduct for
research involving humans, Ottawa, MRC, NSERC & SSHRC, 1998, www.ncehr-cnerh.org/english/code_2
NHS Organ Donation Register Wall of Life, www.walloflife.org.uk
US Department of Health and Human Services and Other Federal Agencies Common Rule, www.hhs.gov/ohrp/human
subjects/commonrule
World Health Organization, Operational guidelines for ethics committees that review biomedical research, 2000, www.who.
int/tdr/publications/training-guideline-publications/operational-guidelines-ethics-biomedical-research/en
World Medical Association, Declaration of Helsinki, updated 2013, www.wma.net/en/30publications/10policies/b3

Further reading
Benatar S. Reflections and recommendations on research ethics in developing countries. Soc Sci Med 2002;54(7):1131–41.
DeAngelis CD, Drazen JM, Frizelle FA, Haug C, Hoey J, Horton R et al. Clinical trial registration: a statement from the
International Committee of Medical Journal Editors. JAMA 2004;292:1363–4.
Emmanuel EJ, Wendler D, Killen J, Grady C. What makes clinical research in developing countries ethical? The benchmarks
of ethical research. J Infect Dis 2004;189:930–7.
Hurley C. A model to support the ethical elements of decisions made by advanced level practitioners. Nurs Crit Care
2011;16:53–4.
Kim Y-S, Kang SW, Ahn JA. Moral sensitivity relating to the application of the code of ethics. Nurs Ethics 2013;20(4):470–8.
 CHAPTER 5 ETHICAL ISSUES IN CRITICAL CARE 125

Laabs CA. (2012). Confidence and knowledge regarding ethics among advanced practice nurses. Nurs Educ Perspectives
2012;33(1):10–4.
Lavery JV, Grady C, Wahl ER, Emanuel EJ. Ethical issues in international biomedical research: a casebook. Oxford: Oxford
University Press; 2007.
McGowan CM. Legal issues. Legal aspects of end-of-life care. Crit Care Nurs 2011;31(5):64–9.
Organ Donation Taskforce Implementation Programme. Working together to save lives: The Organ Donation Taskforce
Implementation Programme’s Final Report, 2011. London: Department of Health. Available from http://www.nhsbt.nhs.uk/
to2020/resources/TheOrganDonationTaskforcImplementationProgrammesFinalReport2011.pdf.
Settle PD. Nurse activism in the newborn intensive care unit: actions in response to an ethical dilemma. Nurs Ethics
2014;21(2):198–209.
Woods M. Beyond moral distress: preserving the ethical integrity of nurses. Nurs Ethics 2014;21:127–8.

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 Section 2

Principles and practice

of critical care
Thispageintentionallyleftblank
 Chapter 6

Essential nursing care of the

critically ill patient
Bernadette Grealy, Fiona Coyer

KEY WORDS Learning objectives

bowel After reading this chapter, you should be able to:
management • identify risks posed to critically ill patients relating to inadequate physical
eye care care and hygiene
infection control • describe best practice in the provision of physical care and hygiene
intra-hospital • understand the key elements of safe transfer of critically ill patients within
transport the hospital setting
oral care • understand the principles of infection-control risk identification and
patient positioning management for critically ill patients.
and mobility
personal hygiene
pressure injury
Introduction
urinary catheter This chapter is about essential nursing care. Because it is often referred to as
care basic nursing, nurses may not always perceive it as deserving of priority. Yet,
how well patients are cared for has a direct effect on their sense of wellbeing
and their recovery. ‘Interventional patient hygiene’ is a systematic, evidence-
based approach to nursing actions designed to improve patient outcomes using
a framework of hygiene, catheter care, skin care, mobility and oral care.1 This
chapter focuses on the physical care, infection control, preventative therapies
and transport of critically ill patients. The first two areas are closely linked:
poor-quality physical care increases the risk of infection. The final areas are
essential features of critical care nursing.
Comfort is a paramount concern in intensive care. The two key areas of
care – reducing risk and providing quality care – are closely related and served
by a series of principles (see Table 6.1). The implementation of evidence-based
essential nursing care is a key strategy to reduce avoidable errors and improve
patient outcomes.1,2 Thus, good risk management is an important component
of quality care; if patients are assessed thoroughly and on a continuing basis,
problems may be detected and treated early, preventing the development of
unnecessary complications.These principles underpin this chapter. Additionally,
it is important always to treat the patient as a person. Although this chapter
focuses on the physical dimension of nursing care, patients’ psychosocial care
should not be ignored (see Chapters 7 and 8). Further, while this chapter
describes essential nursing care, care bundles, which encompass a number of
these activities, are described in Chapter 3.
132 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 6.1
Assessment of personal hygiene
Principles of practice Assessment of critical care patients’ personal hygiene
should be undertaken on two levels: first, determining
REDUCING RISKS TO PROVISION OF QUALITY what patients are able and want to do for themselves and,
PAT I E N T S CARE second, the nurse’s assessment of what is required. As with
• Recognition of the • Development of all aspects of care, the patient has the right to refuse personal
specific needs of knowledge and skills for hygiene measures. Many critical care patients are unable to
critically ill patients, practice participate in decision making, and in these cases it falls to
particularly those who are • Evidence-based practice the nurse at the bedside to determine what level of care
unconscious, sedated or • Optimal use of protocol- is necessary.4 Washing patients provides opportunities for
immobile driven therapy the nurse to assess the patient’s skin and tissue. Often this
• Recognition of specific • Competent, efficient and enables the nurse to: pick up vital clues about the patient’s
complications that safe practice health status; identify tissue damage that requires treatment;
may require special • Selection and application
and identify dressings or wounds that require attention.4
observation or treatment of appropriate nursing
There are a number of areas to consider when assessing
• Vigilant monitoring and interventions
the skin (see Table 6.2). Excessive moisture on the patient’s
early recognition of signs • Monitoring the
of deterioration consequences of nursing
skin from sweat can be problematic, particularly in skinfolds.
• Selection, implementation interventions
Perspiration is a normal insensible loss, and is invisible. Body
and evaluation of specific • Review and evaluation of sweat is usually related to temperature and is observed on
preventive measures nursing practices all skin surfaces, especially the forehead, axillae and groins.
• Management of • Continuity of care Emotional sweating is stress-related and is observed on the
potentially detrimental • Effective critical care palms of the hands, soles of the feet, forehead and axillae.
environmental factors team functioning
that may affect the
Essential hygiene care
patient A daily bed-bath with intermittent washes of the face and
hands is standard care; however, patients who are sweating,
incontinent, bleeding or with leaking wounds should be
washed and their linen changed as often as necessary. Wet,
creased sheets may contribute to changes in the support
Practice tip surface microclimate and cause pressure on dependent
Make sure patients know your name when you are areas, increasing the risk of pressure injury development.5
caring for them; introducing yourself is professionally For many critically ill patients, being moved is painful
appropriate and reassuring to patients. and it may be appropriate to give prophylactic pain relief
before commencing a bed-bath.
Personal hygiene including bed-baths should be timed
Personal hygiene to avoid disruption to patients’ sleep.4 When several nurses
are required to move the patient, it makes sense to consult
It is important to provide the critically ill patient with with colleagues to coordinate their availability. Planning
effective personal hygiene as poor hygiene may increase ahead with respect to events such as medical rounds, chest
the risk of bacterial colonisation and subsequent infection.3 X-ray requirements and family visits helps avoid unnecessary
Daily bed-baths are usually provided for most critically ill delays in completing personal hygiene and interruptions
patients, although their effectiveness at reducing bacterial that affect the dignity of the patient. Privacy for the patient
colonisation is questionable.3 However, bed-baths provide during personal hygiene should be of paramount concern.
an opportunity to achieve other clinical goals such as skin The length of time taken to wash a patient and the
examination, comfort and stimulating circulation. Personal environmental temperature are factors that affect cooling.
hygiene is closely related to an individual’s esteem and Water on exposed skin causes rapid heat loss through
sense of wellbeing. It may also influence family members’ conduction, convection and radiation, and for many
perception of the quality of care the patient is receiving years tepid sponging was used in critical care as a method
and the confidence they have in the staff ’s ability to care of cooling pyrexic patients. Vasoconstriction increases
for their loved one. the patient’s perception of cold and the possibility of
Consideration of the patient’s specific condition may shivering,6 which can affect the patient’s cardiovascular
influence when and how personal hygiene is performed. stability. When shivering occurs, vulnerable patients, with
For example, the patient may have to be moved slowly low energy reserves, can rapidly use energy to keep warm.
when changing bed linen because of their cardiovascular The higher oxygen consumption associated with shivering
instability, or they may require a blanket while bathing may be particularly significant in elderly patients.6
if they are hypothermic. Finally, providing essential care A range of cleansing solutions is available for washing.
should be timed to promote optimal rest. Although soap is effective in facilitating the removal of
 CHAPTER 6 ESSENTIAL NURSING CARE OF THE CRITICALLY ILL PATIENT 133

TABLE 6.2
Skin and tissue assessment

FA C T O R O B S E R VAT I O N S

Colour of the skin • Jaundice, erythema, pallor, cyanosis

Condition of the skin • Skin turgor (elasticity): evidence of oedema (taut skin), dehydration (dryness, tenting of the skin),
age-related or steroid-related damage (thin, papery, easily torn skin), skin tears
• Presence of: rash, cellulitis, irritation, bruising, swelling
Tissue perfusion • Hypoperfusion: capillary refill time, cool extremities, pulse strength and volume, blanching of the skin
• Hyperaemia: very warm, red areas of skin
• Thrombus formation: warm, red, swollen areas (especially calves)
Moisture • Excessive sweating
• Skin damage caused by moisture, especially in skinfolds: under the breasts, in the groin, between
the buttocks
Wounds, drains, • Evidence of inflammation, infection, pressure damage, skin excoriation caused by leaking exudates,
cannulae, catheters correct positioning of drains, need to redress wounds

bacteria, it can cause dryness of the skin. Use of a pH Skin tears

appropriate skin cleanser is recommended.5 The patient’s Dependent patients who require total care are at greatest
skin should be dried thoroughly to protect the skin from risk of skin tears. Injuries result from routine activities
excess moisture and water-based emollients applied to such as dressing, positioning and transferring.9 The
maintain skin hydration.5 Baby care products are often used, elderly, those with fragile skin (particularly those with a
although these may be the least effective due to their low history of previous skin tears), those who require the use
oil content.7 Specific topical treatments may be required of devices to assist lifting, those who are cognitively or
for patients with skin diseases such as dermatitis. Disposable sensorially impaired and those who have skin problems
cloths should be used for washing, as linen flannels have such as oedema, purpura or ecchymosis are at greatest
been shown to harbour bacteria. Complete disposable wash risk. Most skin tears occur on the arms and the back of
kits are available with potential advantages of being effective the hands. The International Skin Tear Advisory Panel
for patients’ skin cleaning without requiring rinsing and (ISTAP) classification system9 uses three categories to
therefore drying the skin, and being disposable may reduce describe skin tears: skin tears without tissue loss; skin
potential for infection and certainly reduces linen costs.3 tears with partial tissue (flap) loss; and skin tears with
Personal hygiene involves washing the patient’s hair as complete tissue (flap) loss.
necessary, shaving the patient, management of cerumen in Skin tears can be prevented by careful handling of
ears and care of finger and toe nails.While normal shampoo patients to reduce skin friction and shear during repo-
can be used, hair caps and washing products are available sitioning and transfers. Padded bed rails, pillows and
that are easier to use for bedridden patients. Male facial hair blankets can be used to protect and support arms and
should be managed as per the patient’s normal routine, such legs. Paper-type or non-adherent dressings should be
as maintaining a beard or shaving. Ears should be gently used on frail skin, and should be removed gently and
inspected for debris or injury. If assessed as appropriate, wax slowly. Wraps or nets can be used instead of surgical tape
softening drops may be needed for 3–5 days if cerumen is to secure dressings and drains in place. Application of a
present and causing the patient difficulties with their hear- moisturising lotion to dry skin helps to keep it adequately
ing.8 Maintaining clean nails is another aspect of personal hydrated. Treatment of skin tears9 is outlined in Table
hygiene. Care should be taken if nails require trimming, 6.3. The focus of nursing care should be on careful
especially if the patient has brittle nails or is diabetic. cleansing and protection of the skin tear to prevent
further damage and documentation of interventions and
Practice tip healing progress.
Although personal grooming is not vital from a health
perspective, it is a factor in how we see ourselves and Practice tip
how others identify with us. With the many changes that Monitor any bruising regularly, as these areas may be at
come with illness and therapies applied in critical care, risk of developing skin tears.
it is important to keep the patient’s ‘look’ as normal as
possible – simple things such as styling hair or trimming
beards – if not for the patients themselves, who might
be unaware, then for their families.
134 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 6.3
Treatment of skin tears

FA C T O R INTERVENTIONS

Cleansing • Gently clean skin with saline or non-toxic wound cleaner

• Allow to dry or pat dry carefully
Skin flap • Approximate the skin tear flap/tissue, if present, as closely as possible
Dressing • Provide appropriate topical wound care, such as a moist wound dressing
• Remove any product with an adhesive backing with utmost care to avoid further trauma
• Secure non-adherent dressing with a gauze or tubular non-adhesive wrap
• Change dressings according to the manufacturer’s recommendations
Documentation • Record details of skin tear, describe or photograph wound, record details of dressings and
implementation of measures to reduce the risk of further occurrences

Eye care there is potential to unintentionally damage one of the eyes

with one of these devices during position changes.13
The eyes are one of the most sensitive parts of the human
body. If their eyes are not properly cared for, critical care Eye assessment
patients may experience unnecessary discomfort. Simple Eye assessment should be undertaken at least every
bedside procedures such as turning on lights at night or 12 hours, even for conscious patients who are able to blink
assessing pupil reactions can be uncomfortable. There are spontaneously. The risk of corneal abrasion or iatrogenic
a number of physiological processes that protect the eye. trauma is greatest when patients are unable to close their
For example, the eye is protected from dryness by frequent eyes spontaneously,14 so these patients are at greatest
lubrication facilitated by blinking. Antimicrobial substances risk of injury. The second at-risk group is those patients
in tears help prevent infection, and the tear ducts provide receiving positive pressure ventilation, who may develop
drainage. When the eye is unable to close properly, the conjunctival oedema (chemosis), sometimes referred to as
‘ventilator eye’.11 Third, patients who are exposed to high
tear film evaporates more quickly.10 If any of these defense
flows of air/oxygen, such as that with continuous positive
mechanisms are compromised the eyes are at greater risk.
airway pressure (CPAP) systems, may be vulnerable to its
There is considerable risk to patients’ eyes while they are
drying effects. Finally, all patients are at risk of eye inflam-
in the ICU.11 The blink response may be slowed or absent mation and infection. Serious infections with bacteria
in some patients, such as individuals receiving sedatives and such as pseudomonas can progress rapidly, resulting in
muscle relaxants, or those with Guillain–Barré syndrome.12 blindness if not treated promptly.
A number of complications can result, such as keratopathy, The general principles of eye assessment are shown in
corneal ulceration and viral or bacterial conjunctivitis.11 Table 6.4, including a full examination of the eye’s external
Corneal abrasions may occur within 48 hours of ICU structure, colour and response. Various assessment tools
admission13 and in up to 40–60% of critically ill patients.11 have been developed for this purpose.11 Thorough eye
When the eyes are exposed they are at greater risk of assessment should assess appearance (which may provide
injury and infection, and conjunctival oedema can lead indications of disease or trauma) and physical and neuro-
to sub-conjunctival haemorrhage.11 For the intensive care logical functions. If there is concern about any aspect of a
patient, who often has multiple intravenous lines, nasogas- patient’s eyes, a referral for assessment should be made to
tric tubes, ventilation tubes and their various connections, an ophthalmologist.

TABLE 6.4
Assessment of the eyes

EXTERNAL STRUCTURE COLOUR REACTION

• Is it bulging or misshapen? • Is the sclera its normal off-white • Is the blink reflex present?
• Is the pupil circular? colour or is there evidence of jaundice • Do both pupils react to light with
• What size are the pupils? or haemorrhage? equal speed?
• Are both pupils the same size? • Does it look red and inflamed? • Is there a composite reaction to light
• Is the pupil clear? in the opposite eye?
• Is there any visible trauma?
• Is it weeping?
• Does it look dry or moist?
 CHAPTER 6 ESSENTIAL NURSING CARE OF THE CRITICALLY ILL PATIENT 135

Essential eye care Conjunctival oedema (chemosis)

The goals of eye care are to provide comfort and protect Conjunctival oedema (chemosis) is a common problem
the eyes from injury and infection. Eye care and the admin- associated with positive pressure ventilation, positive
istration of artificial tears should be provided as required, end-expiratory pressure (PEEP) above 5 cmH2O and
if the patient complains of sore or dry eyes or if there is prone positioning.11 Although the oedema itself usually
visible evidence of encrustation. If a patient is receiving resolves without treatment when ventilation is discontin-
high-flow oxygen therapy via a mask, they may benefit ued, it may be advisable to seek an ophthalmic opinion if
from regular 4-hourly administration of artificial tears to there is concern. The literature is inconclusive concerning
lubricate the eyes,11,14 although this may be unnecessary the best method of treatment for conjunctival oedema, but
while they are sleeping. evidence supports the use of artificial tear ointment and
The Intensive Care Collaborative project team offer maintaining eye closure as effective measures to reduce
an evidence-based eye care guideline for critically ill corneal abrasions.11
patients, which makes a number of practice recommen- Severe oedema often results in the patient’s inability
dations relating to the assessment and management of to maintain eye closure. Under such circumstances, the
ophthalmologic complications in the critically ill.15 These majority opinion is that eye closure may be maintained
recommendations are outlined in Table 6.5. Further by applying a wide piece of adhesive tape horizontally to
recommendations relate to regular monitoring, reporting the upper part of the eyelid.10,11 This usually anchors the
and timely referral of ophthalmologic complications. lid in the closed position, while allowing the eyelid to be
For at-risk patients, the general consensus is that opened for pupil assessment and access for eye care. It is not
eye care should be performed using a sterile technique, necessary to change the tape at each pupil assessment using
cleansing the eye from the inside to the outside usually this method. However, the use of tape may be inappropri-
with saline and gauze; however, eye care regimens have ate for patients whose skin is very friable. Furthermore, if
not been rigorously researched.11 Cotton wool is not the eyelid becomes sore and inflamed, taping should be
recommended because of the presence of particulates discontinued and an alternative method employed to close
that may cause corneal abrasions. Eye-drops should be the eyes, e.g. gel eye pads.10,11 When it is not possible to
administered gently, inserting the drop in the uppermost close the eyes, artificial tear ointment has been shown
part of the opened eye and as close to the eye as possible to reduce the incidence of corneal abrasion.15
without touching it. Sometimes eye-drops can sting, so it If it is difficult to maintain eye closure by taping
is advisable to warn the patient of this possibility. Regular the upper part of the eyelid, the entire eye can also be
scheduled eye care with an ocular lubricant plus eye covered with polyethylene film, which has been shown to
closure with tape or wrap is used to reduce the potential reduce the incidence of corneal abrasion.17 This should be
for corneal abrasions or subsequent corneal ulceration changed 4-hourly with eye care and assessment. Commer-
or infection in patients who are either paralysed or cially available eye-closing tape products are also available
heavily sedated.16,17 along with gel eye dressings, which may be used instead
of polyethylene film.18,19 Current evidence indicates that
Practice tip polyethylene film is the superior and most cost-effective
product for maintaining the ocular surface.11,19
Another source of irritant to the eyes can be the
constant air flow from air-conditioning vents or fans, so Oral hygiene
check that your patient at risk is not positioned directly
in line with these vents or poorly-positioned fans. Poor oral hygiene is unpleasant, causing halitosis and
discomfort. Although mouth care is one of the most

TABLE 6.5
Eyecare in the critically ill

Assessment Patients must be assessed for risk factors for iatrogenic eye complications
Daily assessment of the ability of the patient to maintain eyelid closure
Weekly assessment of iatrogenic eye complication (at the microepithelial level) using instillation or fluorescein
or a cobalt blue pen torch
Management Eyelid closure should be maintained either passively or mechanically
All patients who cannot achieve eyelid closure should receive 2-hourly eye care
Eye care should be cleaning with saline-soaked gauze and administration of an eye-specific lubricant

Adapted from Marshall A, Elliott R, Rolls K, Schacht S, Boyle M. Eye care in the critically ill: clinical practice guideline. Aust Crit Care
2008;21(2);97–109, with permission.
136 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

basic nursing activities, in some cases lack of oral hygiene 2- to 12-hourly.22 If the mouth is unhealthy, it may be
can lead to serious complications or increase their risk, necessary to provide oral hygiene as often as hourly.
such as ventilator-associated pneumonia in the ventilated The basic method for oral care is to use a soft toothbrush
patient.20 Attendance to oral hygiene including the and toothpaste (even for intubated patients), as this will
removal of dental plaque that harbours pathogens is an assist with gum care as well as cleaning teeth.23 Toothpaste
important component of nursing care.21 Using a well- loosens debris24 and fluoride helps to prevent dental caries.28
developed oral protocol can improve the oral health of However, if it is not rinsed away properly, toothpaste dries
ICU patients. However, the practice of mouth care is not the oral mucosa. Using mouth swabs only for oral hygiene
always evidence based,22,23 although evidence supports is ineffective, and toothbrushes perform substantially better
having a standardised oral care protocol to improve oral than foam swabs in removing plaque.28,29 Mouth rinses have
hygiene.24 Factors associated with poor quality of oral care not conclusively shown benefit;29 however, they may be
include lack of education, insufficient time, non-prioritising comfortable for the patient to use. Tooth brushing every
of oral care and the perception that it is unpleasant.25 8 hours was recommended in a study as being an adjunct
Saliva produces protective enzymes, but absence of to other ventilator-associated pneumonia prevention
mastication, for example due to the presence of an endo- practices30 while use of chlorhexidine tooth brushing was
tracheal tube (ETT) or deep sedation, leads to a reduction found to be of benefit in another study.31
in saliva production. An ETT can cause pressure areas in Although it is an effective saliva stimulant, practices such
the mouth (which may be exacerbated if the patient is as the use of lemon and glycerine are outdated, as glycerine
oedematous) and may thus need to be relocated regularly causes reflex exhaustion of the saliva process, resulting in
to a different position in the patient’s mouth. a dryer mouth.29 Lemon juice is to be avoided, as it can
decalcify enamel.29 Commercial mouthwashes moisten
Oral assessment and soften the mucosa and help to loosen debris, which
Mouth care should be reviewed regularly based on a can be washed away.21 They must be used with caution
thorough assessment of the oral cavity.24 Oral assessment in patients with oral problems, due to their potential to
tools have been designed specifically for intubated cause irritation and hypersensitivity.26 In addition to tooth
patients.26 Essentially, a healthy mouth is characterised by brushing, regular sips of fluid or mouth washing with
several factors,27 as identified in Box 6.1, and all of these water is recommended. A recent report identified thirst
areas should be assessed as a basis for good oral care. as one of the three most prevalent, intensive and distress-
ing symptoms critically ill patients suffer.32 If the patient
BOX 6.1 is able to suck and swallow, small pieces of ice are very
refreshing. Patients with clean mouths, who are febrile
Characteristics of a healthy mouth and/or receiving antibiotics, should also have their mouths
• Pink, moist oral mucosa and gums. Absence of moistened often with water to prevent drying, coating and
coating, redness, ulceration or bleeding subsequent discomfort. Immunosuppressed patients or
• Pink, moist tongue. No coating, cracking, blisters or those on high-dose antibiotics may also require antifungal
areas of redness treatment to treat oral thrush.
There are many oral hygiene products and solutions
• Clean teeth/dentures; free of debris, plaque and
available to suit the needs of all patients.21 Commercial
dental caries
mouthwashes should be used as a comfort measure to
• Well-fitting dentures supplement toothbrushing.33 A range of other products is
• Adequate salivation available to treat oral problems, for example benzydamine
• Smooth and moist lips. No cracking, bleeding or hydrochloride (anti-inflammatory), aqueous lignocaine
ulceration (anaesthetic) and nystatin (antifungal). For patients
• No difficulties eating or swallowing (uncommon in intubated for more than 24 hours, rates of nosocomial
ICU) pneumonia may be reduced by using twice-daily chlor-
hexidine gluconate mouthwashes,31,34 which also prevent
plaque accumulation. This has the disadvantage of an
Essential oral care unpleasant taste and can discolour teeth.27 For patients
Oral care aims to ensure healthy oral mucosa, prevent with crusty build-up on their teeth, a single application
halitosis, maintain a clean and moist oral cavity, prevent of warm dilute solution of sodium bicarbonate powder
pressure sores from devices such as ETTs, prevent trauma with a toothbrush is effective in removing debris and
caused by grinding of teeth or biting of the tongue and causes mucus to become less sticky, although its use has
reduce bacterial activity that leads to local and systemic not been definitively tested.33 However, it can cause super-
infection.20 Oral care for an un-intubated conscious patient ficial burns and its use should be followed immediately by
with a healthy mouth generally involves daily observation a thorough water rinse of the mouth to return the oral pH
of the mucosa and twice-daily tooth brushing with a non- to normal. Hydrogen peroxide has an antiplaque effect but,
irritant fluoride toothpaste.22 In general, for unconscious if incorrectly diluted, it can cause pain and burns to the
patients oral care should be performed 2-hourly, although oral mucosa and a predisposition to candida colonisation.35
the evidence is inconclusive and frequency ranges from It is not pleasant tasting and is sometimes rejected by
 CHAPTER 6 ESSENTIAL NURSING CARE OF THE CRITICALLY ILL PATIENT 137

patients although it is the substance that impregnates some • to prevent pressure injuries, also known as pressure
of the foam sticks available for oral care.28 As a preventive ulcers
measure, to reduce the incidence of fungal colonisation,
natural yoghurt may be used. Normal oral hygiene is • to ensure the limbs are supported appropriately and
to maintain flexible joints
followed by coating the mouth and tongue with yoghurt.
While evidence suggests that probiotics are safe complete • to facilitate patient activity to minimise muscle atrophy
consideration of the risk–benefit ratio before administra- • to implement early mobilisation as the patient’s
tion to the critically ill patient is recommended.36 condition allows.
Plastic water ampoules (10 mL) can be used to drip There is growing evidence that early mobilisation is an
water into the mouth for convenient administration to important aim for critically ill patients42–45 and an essential
patients unable to easily open their mouths or swallow. A goal of nursing care is to support the patient in main-
Yankauer suction catheter facilitates rinsing of toothpaste taining or attaining a normal level of physical function
from the mouth, and a bite-guard device may be used for mobility. As with many other aspects of care for the
temporarily to prevent patients from inadvertently biting critically ill, this is best achieved through multidisciplinary
on the toothbrush or their tongue. They should not be team members working together. Here, physiotherapists
used long term due to the risk of pressure sores. Lanolin and occupational therapists have a lead role in assessing
may be applied to help maintain integrity of the lips. patients and planning programs of care and activity to
facilitate attaining the goals of normal physical function,
Practice tip while nurses contribute by ensuring the programs of care
are delivered when other personnel are not available.
If the patient objects to the taste of the chlorhexidine
gluconate mouthwash, consider a follow-up rinse of water.
Practice tip

Practice tip Movement of the lower legs, ankles and feet can be
achieved in conjunction with a gentle massage or
Performing oral hygiene with toothbrush and toothpaste application of moisturiser. Family members may wish
in an intubated patient and ensuring the mouth is rinsed to undertake this, giving them an opportunity to provide
well may be assisted by the use of a dental sucker, the patient with care and touch.
which is flexible. This disposable device attached to
a continuous suction system can be positioned in the Assessment of body positioning
mouth to aid in the continual removal of fluids while
A risk assessment should be undertaken and those patients
brushing and rinsing is performed. The dental sucker
at highest risk of complications related to their position
can also be used for continuous oral suction in patients
are those who are unable to move for long periods, for
with excessive saliva.
whatever reason.46 For example, unstable patients whose
status is compromised when they are moved, patients
Patient positioning and who are in critical care for a long time, elderly and frail
or malnourished patients and patients who are unable to
mobilisation move themselves (e.g. due to sedation, trauma, surgery or
obesity) are all at risk. Numerous significant risk factors
Positioning patients correctly is important for their
exist, for example age, length of intensive care stay, use
comfort and the reduction of complications associated
of adrenaline and/or noradrenaline infusions; patients
with pressure areas5,37 and joint immobility. Lying in bed
with restricted movement; patients with comorbidities
for long periods can be a painful experience.38 Research-
such as cardiovascular disease and diabetes and unstable
ers39–41 describe neuromyopathy from critical illness and
patients.47 However, even previously fit patients who
disuse atrophy from prolonged immobility contribut-
experience a critical illness can develop severe limitations
ing to intensive care acquired weakness. This weakness
in their mobility. The common short- and long-term
may contribute to prolonged ventilation and intensive
complications of immobility are pressure injuries, venous
care length of stay as well as delayed return to physical
thromboembolism and pulmonary dysfunction, each
normality.42–45 Cardiovascular stability, respiratory function
of which carries a significant comorbidity.46 Regular
and cerebral or spinal function are all factors that influence
musculoskeletal assessment should be made, focusing on
the positioning of patients in critical care areas. Modern
the patient’s major muscles and joints and the degree of
beds and pressure-relieving devices have helped consider-
mobility. Table 6.6 offers a simple guide to assessment,
ably to enhance the care of critically ill patients.
which includes visual and physical assessment of all
The primary goals of essential nursing care for patient
limbs and joints. Provided there are no contraindications,
positioning are:
function should be stimulated by regular passive then
• to position the patient comfortably active movements of all limbs and joints to maintain both
• to enhance therapeutic benefits flexibility and comfort.
138 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 6.6 Practice tip

Musculoskeletal assessment
When planning to reposition the patient, ensure that
MUSCLES AND JOINTS MOBILITY there are enough staff to give the patient a feeling of
• Power/strength • Degree of independence security during the procedure and that all the patient’s
• Range of movement • Need for assistance devices (e.g. IV lines) are managed. Check that all
• Symmetry • Adherence/compliance devices are placed to accommodate the repositioning
• Tenderness and pain with physiotherapy/ before you begin to move the patient.
• Inflammation, swelling, mobility regimen
wasting • Need for planned rest
Active and passive exercises
periods
• Use of splints or collar Spontaneous physical activity decreases by as much as 50%
in hospitalised patients54 and physical activity is essential to
healthy functioning and beneficial for the cardiovascular
system.44 Inactivity, age and the inflammatory process that
Positioning and mobilising patients occurs during critical illness combine to progress muscle
Positioning the patient to achieve maximum comfort, breakdown and loss of physical function in older hospi-
therapeutic benefit and pressure area relief and talised patients with muscle mass reduction, which occurs
employing active and passive exercises to maintain as early as several hours from the onset of immobility.54
muscle and joint integrity and progress to regaining Active exercises are those that can be performed by the
mobility are important nursing activities. Provided there patient with no, or minimal, assistance. Passive exercises are
are no specific contraindications, the immobile patient performed when patients are either too weak or incapable
should be positioned with the head raised by 30° or of active exercise. Exercises can be employed to help the
more, as research has demonstrated that it improves recovering patient develop power and regain function, to
mortality48 and helps reduce ventilator-associated assist in venous return and maintain the normal sensation
pneumonia.49 When combined with thromboembolic of movement.54 They should be performed at least
prophylaxis, gastric ulcer prophylaxis and daily sedation daily. Passive exercises put the main joints through their
assessment, ventilator-associated pneumonia may range of movement, which helps reduce joint stiffness
be reduced by around 45%.49 Good body position- and maintain muscle integrity, preventing contractures.
ing and alignment helps prevent muscle contracture, Shoulders, hands, hips and ankles are particularly at risk of
pressure injuries and unnecessary pain or discomfort for stiffness and muscle contracture.54 It is important, however,
the patient.50,51 to ensure that joints and muscles are not overstretched,
Mobilisation for the critically ill patient can be as this is painful for patients and can cause permanent
described as a graduated increase in range of activity injury. Splints may be used when the patient is resting, to
from positioning, passive movement, sitting upright maintain joints in a neutral position.54 The physiothera-
in bed, sitting in a chair to actually ambulating.50,52 pist’s advice should be sought regarding the correct range
Stiller52 describes a range of safety factors that need to of movement and the frequency of passive exercises.This is
be considered prior to mobilising the critically ill patient, particularly important for burn-injured patients. Concern
which fall into two groups: those specific to the patient has been expressed about the effects of limb movements
and their physical and physiological condition and those on head-injured patients; however, two dated yet seminal
extrinsic to the patient such as the environment, staffing studies detected no significant cardiovascular or neuro-
and patient devices attached. Creating an individualised logical changes during passive exercises in neurosurgical
mobility plan that can be adapted according to patient patients,55 and found no detrimental effects on cerebral
assessment and general health progress will optimise early perfusion or intracranial pressure (ICP), whether ICP was
movement and mobilisation.52,53 raised or not.56
Changing body position
Practice tip
Mobility is defined as the ability to change and control
From the perspective of patient comfort, even small body position.57 The complications of immobilisation in
readjustments in positioning may be advantageous, critically ill patients are well documented, and include
and often can be made without much effort by the pressure injury, venous thromboembolism and pulmonary
nurse or disturbance to the resting patient. Most dysfunction such as atelectasis, retained secretions,
electric beds provide for adjustments to the backrest pneumonia and aspiration.45 The routine standard for
angle, knee bend and bed tilt, and adjustments can be immobilised patients in ICU is 2-hourly body repo-
easily made. In addition to comfort, these adjustments sitioning, although this does not always happen,46 and
will aid in pressure changes between re-positioning of the optimal interval for turning critically ill patients is
the patient. unknown.58 In addition to providing pressure relief, it
is recommended that the patient’s position be changed
 CHAPTER 6 ESSENTIAL NURSING CARE OF THE CRITICALLY ILL PATIENT 139

often to ensure comfort, relaxation and rest; to inflate Pressure area care
both lungs, improve oxygenation58 and help mobilise The term ‘pressure injury’ rather than ‘pressure ulcer’ is
airway secretions; to orient the patient to the surround- now used in Australasia. Terms that have been used to
ings and for a change of view; and to improve circulation describe pressure injuries are numerous and include bed
to limbs through movement.42 The frequency of body sore and decubitus ulcer. This new term recognises the
repositioning should be determined according to the general consensus that the majority of pressure injuries
patient’s pressure injury risk (preferably using one of are preventable adverse events.5 The prevalence of pressure
the assessment tools described below), clinical stability injuries in an ICU ranges from 5% to 50%47 and the risk
and comfort. of developing a pressure injury is cumulative: 5% risk after
Good body alignment helps prevent pressure points, 5 days; 30% risk after 10 days; and 50% risk after 20 days
contractures and unnecessary pain or discomfort for the in the ICU.60 Pressure injury risk for critically ill patients
patient.50 Here, careful consideration should be given to can be attributed to their immobility, lack of sensory
factors (outlined in Table 6.7) such as haemodynamic and protective mechanisms, suboptimal tissue perfusion and
cardiopulmonary responses of the patient,59 the timing and environmental factors that cause pressure and friction.5,47
method of positioning patients and whether there are any The commonest locations for pressure injuries are the
restrictions on movement. It is important to fully consider sacrum, the heels and the head.5 Significant risk factors
the individual needs of patients: they may have a history include the age of the patient, the number of days
of back or neck problems, and the selective use of soft or since admission, malnutrition47 and delays in the use of
firm pillows and mattresses may be relevant. Pillows can pressure-relieving mattresses.60
optimise the patient’s position so that the shoulders and Pressure risk assessment tools can help nurses identify
at-risk patients.5,37 However, it is unusual for a patient in
chest are squared, and may reduce the work of breathing
critical care to be assessed as low-risk. There are several
for patients with chronic airways disease.42 Some pres-
pressure injury risk assessment tools available such as the
sure-relieving mattresses have an adjustable pressure Braden score57 and the revised Jackson/Cubbin pressure
control, which can be changed according to pressure risk calculator61 (Table 6.8) that was designed specifically
relief assessment and patient comfort.5 When patients are for use in ICU and provides an awareness of the many
positioned lying on one side, consideration should be factors that need to be considered and monitored prior to
given to their feeling of security; for example, ensuring and during procedures for pressure injury prevention. Risk
that they are well supported by pillows and the bed rails are assessment should be undertaken as soon as possible after
raised. Provided cerebral perfusion pressure is maintained the patient’s admission and within 8 hours of admission.5
above 50 mmHg, even severely head-injured patients can A comprehensive head-to-toe skin assessment for pressure
be moved safely;56 however, it is important to maintain should be scheduled at least daily and include a review
the neck in alignment to promote venous drainage (see of pressure-relieving devices for effectiveness or require-
Chapter 17) and, for those with spinal injuries, log-rolling ment for change. Skin should be inspected at each episode
may be required (see Chapter 17). of patient repositioning. Skin assessment should include

TABLE 6.7
Factors to consider when positioning patients

FA C T O R S COMMENTS

Haemodynamic and • Placing patients in the left lateral position can cause a (usually harmless) fall in oxygenation for a
cardiopulmonary responses few minutes
Timing • Position the patient to avoid clashes with treatment/investigations such as chest physiotherapy
or chest X-ray
• Consider the need for the patient to rest
Method • The need to use lifting devices
• The availability of staff to perform a safe manoeuvre
• The placement of pillows to support limbs, to facilitate both comfort and respiratory efficiency
• Use of bed adjustments to create ‘chair’ positions to prepare patients to sit out of bed
Restrictions on positioning • The need for spinal alignment
• Cerebral injury
• Haemodynamic instability
• Respiratory compromise
• Access to devices for therapies
• Body size
140 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Intensive care patients are at risk of pressure injuries and

TABLE 6.8 injury from a number of devices in everyday use, such as
Components of the revised Jackson/Cubbin pressure endotracheal tubes and blood pressure cuffs (see Table 6.9).
area risk calculator61 Close attention to detail with frequent observation of the
RISK ASSESSMENT
patient, the patient’s position and the presence and location
C AT E G O R I E S SCORING of equipment is required to prevent skin damage.62 It is
important to remove aids such as compression stockings
• Age • Score range = 12–48
• Weight/tissue viability • One point is deducted for
and cervical collars to assess the skin. Vulnerable patients,
• Past medical history each of the following:
such as those with poor tissue perfusion, anaemia, oedema,
affecting condition o The patient has spent diaphoresis and poor sensory perception,37 can develop
• General skin condition time in surgery/scan in pressure injuries relatively quickly, and pressure injuries
• Mental status the past 48 hours caused by equipment are entirely avoidable.
• Mobility o The patient has received All pressure points and any pressure injuries should
• Haemodynamics blood products be monitored closely. The key areas of monitoring are
• Respiration o The patient is identified in Table 6.10, and it is important to use stan-
• Oxygen requirements hypothermic dardised methods to objectively assess pressure injuries
• Nutrition • A lower score indicates and their response to therapy. If a patient develops one
• Incontinence higher risk pressure injury, there is a good chance he/she could
• Hygiene • A score of <29 indicates develop another. Nursing intervention includes the
high risk placing of patients in positions that avoid pressure on the
affected area(s), employing measures such as good fluid
management to improve tissue perfusion, reducing the
testing for blanching response and checking for areas of
risk of infection and promoting tissue granulation with
oedema, induration, redness or localised heat.37
the use of appropriate dressings.
Pressure injury prevention practices include alter-
The International NPUAP–EPUAP Pressure Ulcer
nating the use of pressure-relief mattresses, low-pressure
Classification System37 grades pressure injuries as follows:
mattresses and air-flow mattresses.37,60 For bariatric
patients (usually those heavier than 150 kg), specialist beds • Stage I: Non-blanchable redness of intact skin
and mattresses are required. • Stage II: Partial thickness skin loss or blister

TABLE 6.9
Risk of pressure injuries from commonly used equipment

R I S K FA C T O R COMMENTS

Endotracheal tubes (ETTs) The ETT should be repositioned from one corner of the mouth to the other on a daily basis to
prevent pressure on the same area of oral mucosa and lips. Care should also be taken when
positioning and tying ETT tapes: friction burns may be caused if they are not secure; pressure
sores may be caused if they are too tight (particularly above the ears and in the nape of the neck).
Moist tapes exacerbate problems and harbour bacteria
Oxygen saturation probes Repositioning of oxygen saturation probes 1–2-hourly prevents pressure on potentially poorly
perfused skin. If using ear probes, these must be positioned on the lobe of the ear and not on the
cartilage, as this area is very vulnerable to pressure and heat injury
Blood pressure cuffs Non-invasive blood pressure cuffs should be regularly reattached and repositioned. If left in
position without reattachment for long periods of time they can cause friction and pressure
damage to skin. Care should be taken to ensure that tubing is not caught under the patient,
especially after repositioning
Urinary catheters, central The patient should be checked often to ensure that invasive lines are not trapped under the
lines and wound drainage patient. In addition to causing skin injury, they may function ineffectively
Bed rails Limbs should not press against bed rails; pillows should be used if the patient’s position or size
makes this likely
Oxygen masks Use correct-size mask and hydrocolloid protective dressing on the bridge of the nose to assist with
prevention of pressure from non-invasive or continuous positive airway pressure masks, especially
when these are in constant or frequent use
Splints, traction and cervical Devices such as leg/foot splints, traction and cervical collars can all cause direct pressure when
collars in constant use and friction injury if they are not fitted properly. ICU patients often have rapid body
mass loss (especially muscle) following admission, so daily assessment is required
 CHAPTER 6 ESSENTIAL NURSING CARE OF THE CRITICALLY ILL PATIENT 141

• Stage III: Full thickness skin loss (fat visible) helps to relieve pressure areas and can significantly improve
oxygenation.64,65 Continuous lateral rotation therapy may
• Stage IV: Full thickness tissue loss (muscle/bone
reduce the prevalence of ventilator-associated pneumonia
visible)
in patients requiring long-term ventilation.66 Appropriate
• Unstageable pressure injury: depth unknown evaluation of the benefits and suitability of the patient for
• Suspected deep tissue injury: depth unknown Continuous lateral rotation therapy should be undertaken
Further, the NPUAP differentiates skin injuries from by the team and the therapy implemented according to
mucosal injuries. Mucosal pressure injuries are defined as local protocols.64 In implementing this therapy, the goal
injuries found on mucous membranes with a history of a is to achieve continuous rotation through the maximum
medical device in use at the location of the injury. These angle that the patient tolerates for 18 hours per day.67
injuries cannot be staged.63
The use of standardised tools to both assess pressure risk
Venous thromboembolism (VTE)
and stage pressure injuries is vital to effective continuity of prophylaxis
care. Treatment of pressure injuries is complex and based Deep vein thrombosis (DVT) and pulmonary embolism
on individual patient factors; however, the main issues (PE) are separate conditions collectively referred to as
include: venous thromboembolism (VTE).68,69 DVT is a blood
• protecting tissue from further damage with pressure clot in a major vein of the lower body, i.e. leg, thigh or
re-distribution techniques pelvis, which causes disruption to venous blood flow
and is often first noticed by pain and swelling of the leg.
• preventing infection either localised or systemic by The blood clot forms due to poor venous flow, endo-
closely observing the injury for signs of infection
thelial injury to the vein or increased blood clotting that
such as friable, oedematous, pale or dusky tissue
may be caused by trauma, venous stasis or coagulation
• aiding wound healing such as use of negative pressure disorders.70 Pulmonary emboli occur when a part of a
wound therapy for deep injuries or foam and alginate thrombosis moves through the circulation and lodges in
dressings to control heavy exudate.5,37 the pulmonary circulation. VTE is a major risk factor for
hospitalised patients in general and critically ill patients
Practice tip in particular, due to blood vessel damage, coagulation
It is worthwhile knowing the key features of the beds disorders and limited mobility leading to venous stasis.69
and mattresses commonly used in your area so that you Further, around 50% of patients with DVT will also suffer
can use them effectively to match patient requirements a pulmonary embolism, which can be fatal causing around
for bed functions, bed type (e.g. bariatric suitability) and 10% of hospital deaths in Australia.69,71 Patients with
pressure prevention (e.g. high-, medium- or low-risk VTE may also develop post-thrombotic syndrome where
mattress systems). tissue injury occurs leading to pain, paraesthesia, pruritus,
oedema, venous dilatation and venous ulcers.68,70
It is important to consider the individual patient
Rotational therapy (age, body mass index) and their history (previous
Continuous lateral rotation therapy or kinetic bed therapy VTE, coagulation disorders) along with their current
is an intervention in which the patient is rotated continu- condition whether it be surgical or medical and features of
ally, on a specialised bed, through a set number of degrees; it their treatment (immobilisation) when determining risks

TABLE 6.10
Monitoring pressure injuries (PIs)

FA C T O R ACTIONS

Size • Objectively assess length, width and depth

Stage/grading • Use a standardised measure to grade the injury (e.g. International NPUAP & EPUAP Pressure Ulcer
Classification System)
Documentation • Note the absence/presence/location of PIs on admission and discharge
• Keep a record of nursing interventions and treatments used to treat PIs
Treatment • Monitor response to therapy by assessing the size and stage/grade of the PI on a daily basis
Observing other sites • Dependent areas of the body are susceptible: sacrum, heels, back of the head, hips, shoulders,
elbows, knees
• Areas of the body where equipment is causing pressure are susceptible: nose, ears, corners of the
mouth, fingertips
• Areas of the body where tissue perfusion is poor are susceptible: extremities
142 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

for VTE.72–74 Both the risk assessment and the patient’s Bowel management
current condition will determine the most appropri-
ate VTE prophylaxis strategy.73 Prophylaxis consists of a Although bowel care is an essential aspect of critical care
combination of pharmacological and mechanical inter- nursing care, there is limited research on the topic specific
ventions that may be used together or separately according to this cohort of patients. Good bowel care promotes
to the degree of risk for VTE and/or contraindications patient comfort and reduces the risks of further associated
to particular therapies. The use of combined therapies problems such as nausea, vomiting and abdominal/pelvic
is supported by recent reviews and guidelines.70,73 The discomfort. Maintaining good bowel care in the critically ill
National Health and Medical Research Council Clinical patient can have changing foci from promoting defecation
practice guideline for the prevention of venous thromboembolism to containing diarrhoea, as throughout the critical illness
(deep vein thrombosis and pulmonary embolism) in patients gut function is influenced by changing therapies, medi-
admitted to Australian hospitals69 provides a comprehensive cations, nutrition, hydration and mobility of the patient.
guide to risks and management relating to VTE for critical Enteral feeding is often cited in the literature as a cause
care in Australia. of diarrhoea,78 but poor gastric fluid intake causes consti-
Low-molecular-weight heparin or unfractionated pation, and improved gut motility decreases the risk of
heparin is the most common pharmacological therapy aspiration and subsequent pneumonia. Additional to the
prescribed, while other medications will be prescribed need to manage faecal incontinence, the two spectrums
for patients according to individual factors.69,74 Special of constipation and diarrhoea are particular challenges for
consideration of an appropriate regimen for pharmaco- nurses to provide patient-specific, effective management in
logical prophylaxis will need to be given to patients with a sensitive and dignified way for their critically ill patient.
renal and hepatic impairment.74 Heparin-induced throm- Causes of constipation in critically ill patients
bocytopenia (HIT) may develop in some patients75 so, as range from shock and reduced gut motility to changes
with all heparin therapy, close monitoring of the patient’s in nutrition and lack of mobility. The consequences
platelet count and assessing for signs of bleeding such as of constipation are not well defined but can include
bruising or haematuria will form part of the nurse’s role in increased abdominal distension and resulting impedance
managing VTE prophylaxis. of lung function, inability to establish adequate enteral
In principle, it is advised that graduated compres- nutrition and increased acquired bacterial infections.79
sion stockings are used for all general, cardiac, thoracic The prevention of constipation is particularly important
and vascular surgical patients until full mobility is for patients with high cervical spinal injuries, as if left
achieved irrespective of pharmacological prophylaxis.69,73 untreated it may cause potentially fatal autonomic dys-
Mechanical prophylaxis is provided through a range of reflexia.79 de Azevedo et al80 discussed the need to determine
graduated compression stockings and various pneumatic whether constipation is a marker of severity and poor
venous pump or sequential compression devices.76,77 It is prognosis in critically ill patients or if it is a dysfunction
important to make sure that the relevant devices are fitted contributing to a worsening clinical condition. However,
correctly and monitored closely. Comparisons between the need for effective prevention and management of
a number of pneumatic pumps have been published75–77 constipation in critically ill patients is clear.
with all displaying relative effectiveness. The availability of Bowel care can be one of the most distressing aspects
battery-operated sequential compression devices can assist of nursing care, from a patient’s perspective. Often patients
with the continuous application of the therapy during find bowel care to be awkward and embarrassing, and the
patient transports away from their bedside, such as to the routines that individuals may have developed, especially
imaging department for radiological procedures.77 the elderly, to sustain effective bowel function in their
Along with pharmacological and mechanical venous daily lives are then interrupted by their illness, and their
thromboembolism prophylaxis, maintaining patients’ loss of control over their body for this function can be
hydration and implementing early mobilisation are key particularly distressing. Sensitive nursing care that respects
components of care in preventing VTE.69,72 Rauen et the dignity of the patient is paramount.
al68 describe the most common reasons cited for lack
of proper VTE prophylaxis as being lack of knowledge Bowel assessment
among healthcare providers and underestimation of the Initial bowel assessment should be undertaken to determine
risk of VTE along with overestimation of the potential the patient’s usual bowel habits, as a daily bowel action is
risk of bleeding from prophylaxis. Given the risks of VTE not common for most of the population. In general, older
for critically ill patients, it is clearly important that nurses patients are more susceptible to constipation.
contribute to lowering risks for their patients by knowing Gut function should be assessed at the start of
the range of risk factors for their patients, along with the each nursing shift78 (see Box 6.2). Several authors have
appropriate pharmacological prophylaxis that may be developed bowel care protocols for intensive care patients
prescribed. It is also important to know how to appropri- and studies suggest that use of a protocol improves bowel
ately implement and manage the mechanical prophylactic care in critically ill patients.81,82 Rectal examination should
devices and, most importantly, facilitate the early mobili- be undertaken if the patient has not had their bowels
sation of the patient. open for 3 consecutive days.81 If the bowels have not been
 CHAPTER 6 ESSENTIAL NURSING CARE OF THE CRITICALLY ILL PATIENT 143

of laxative agents. Where bowel care is concerned, it is

BOX 6.2
always appropriate to first explain to patients what is to
Assessment of gut function be done, and to gain their consent if they are conscious.
• Observation of nasogastric aspirate volume Constant reassurance is important so that patients feel safe
and secure in the knowledge that their privacy will be
• Visual inspection and palpation of abdomen, noting
maintained to the greatest degree possible.
any tenderness, pain or distension
Peristaltic movement of the gut is stimulated by exer-
• Recording the frequency, nature and quantity of cise. Although difficult in the intensive care setting, many
bowel actions patients are awake, and even those who require sedation
• The presence or absence of bowels sounds should be sedated with the minimal amount necessary for
their safety, as this will enable some degree of movement.
Promoting patient mobility, especially voluntary move-
opened during this period, action should be taken.81 For ment, is helpful as it will improve gut motility.
some patients in whom defecation is problematic, it may
be appropriate to objectively assess the quality of faecal Diet and fluids
stools using a tool such as the Bristol stool form scale, Diet and fluids are two important considerations in
which uses a 7-point grading system to assess stool consis- maintaining normal bowel function. Ensuring the appro-
tency (see Table 6.11).83 Establishing the cause of faecal priate administration of fluid and an adequate dietary
incontinence is important as this will direct the treatment fibre intake81 helps to prevent constipation. Although
and management plan. Faecal incontinence may occur enteral feeding increases faecal bulk and provides gastric
in conditions such as neurological and spinal conditions, fluid, which helps to maintain gut motility, Bishop
intestinal diseases such as Crohn’s, cognitive impairment et al85 found a higher rate of enteral nutrition was
such as dementia or be the result of anal sphincter or rectal strongly associated with a looser type of stool. Chapter
injury or dysfunction, medications or intestinal impaction 19 contains an in-depth discussion on the principles of
and overflow.84 enteral feeding.

Practice tip Drugs

The use of sedatives is often an ascribed cause of consti-
When undertaking bowel assessment you should also pation in critically ill patients. This is not due to their
consider the patient’s normal diet and any laxatives direct effect, but due to the subsequent immobility
routinely taken, as this information may influence any of patients when sedatives are used. Opiates, which are
bowel regimen developed for the patient. often used to control pain, slow propulsive gut contrac-
tion. In a small cohort study, Sawh et al86 reported the
Essential bowel care successful resumption of target enteral feeding after
Nursing care is based on managing privacy and embar- treating opioid-induced constipation with subcutaneous
rassment, increasing exercise where possible, ensuring methylnaltrexone. The main drugs that cause constipation
adequate fibre and fluid in the diet, reducing unnecessary in critical care settings are analgesics, anaesthetic agents,
anticonvulsants, diuretics and calcium channel blockers.
use of drugs that cause constipation and appropriate use
Although it is difficult to avoid giving these drugs, their
judicious use in tandem with other preventive measures
TABLE 6.11 will help avoid constipation. Anti-emetic and pro-kinetic
Bristol stool form scale agents can also be used in critical care patients and Bishop
et al85 found the administration of ondansetron was a
GRADE DESCRIPTION significant predictor of defecation on that day in their
0 No bowel movement critical care patient cohort.
1 Separate hard lumps; like nuts; hard to pass Constipation
2 Sausage-shaped but lumpy From practice we know that constipation is a common
3 Like a sausage but with cracks on the surface issue for critically ill patients, but reported incidence
4 Like a sausage or snake but smooth and soft varies enormously from 5–83%.87 Variations in incidence
5 Soft blobs with clear-cut edges; easily passed
may be attributed to the lack of a consistent definition for
constipation. Constipation is described as fewer than three
6 Fluffy pieces with ragged edges; a mushy stool
bowel movements per week, incomplete evacuation, hard
7 Watery; no solid pieces; entirely liquid or difficult to pass stools or the requirement of manual
faecal removal, according to the American Gastroentero-
Adapted from Riegler G, Esposito I. Bristol scale stool form.
A still valid help in medical practice and clinical research.
logical Association.88
Tech Coloproctol 2001;5(3):163–4, with permission. Non-pharmacological methods to reduce constipa-
tion include exercise or moving, increasing fluid intake
144 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

and adding dietary fibre.78 These means should be

implemented routinely before the need to use laxatives Practice tip
arises. There are many types of laxatives available, which
Monitoring the security and position of a faecal
can be given to prevent or treat constipation. Bulk-
management system is necessary for effective func-
forming agents work by increasing faecal size; stimulants,
tioning of the system as well as the prevention of
such as senna, increase peristalsis; and osmotic agents
pressure-related injury and potential rectal bleeding.
draw fluid into the gut. Faecal impaction should
be treated with enemas, not stimulant laxatives. In
general, existing protocols advise that treatment of Urinary catheter care
constipation should commence with senna administra-
tion and, if ineffective after 2–3 days, lactulose should Urinary catheters are inserted into many critically ill
be commenced.81 patients. Catheter-associated urinary tract infections
(CAUTI) are a common cause of infection in this group,
Diarrhoea and are associated with increased mortality and length of
Diarrhoea can be a major problem for intensive care stay in the ICU.96 Monitoring the incidence of CAUTI is
patients, and in severe cases may lead to electrolyte a requirement in many jurisdictions. In principle, urinary
imbalances, dehydration, malnutrition (see also Chapter catheters should be inserted only when deemed clinically
19) and skin breakdown. Furthermore, it can be very necessary, and they should be removed as soon as they are
distressing for the patient, who may also suffer from no longer required clinically. Alternatives to urinary cath-
abdominal distension, nausea and cramp-like pain. Inves- eterisation should be considered; however, most critically
tigations should be implemented to determine the cause ill patients require accurate monitoring of their urinary
of the diarrhoea and the patient should be managed with output and fluid balance, and a catheter is required for this
appropriate precautions to prevent cross-contamination reason.97 CAUTI are primarily caused by contamination
if the cause is infectious. If laxatives are being given from the healthcare worker or from the patient’s own flora
they should be stopped, and a stool specimen should be during catheter insertion or management of the urinary
obtained for microbiological examination. Anti-motility drainage system or via reflux of contaminated urine.98,99
drugs may be used, except with bloody diarrhoea or While routine screening for urinary tract infection is not
proven infection with E. coli.81 Appropriate re-hydration required,98 critical care nurses should be mindful of the
should be implemented. If patients are being fed enterally risk factors for CAUTI such as prolonged catheterisation,
there may be a reduction in episodes of diarrhoea if older patients, impaired immunity and any breaches in
fibre-enriched feed is used.78 good practices related to the insertion and maintenance
Faecal containment devices should be used in severe of urinary catheters and drainage.98 The consequences of
cases of diarrhoea in conjunction with all other measures poor urinary catheter care and management are not only
to support the patient’s comfort.89 The patient should be distressing to the patient but detrimental to their health.
assessed for suitability for using the incontinence system
as per the manufacturer’s guidelines as there are signifi- Urinary catheterisation assessment
cant contraindications for use of some systems. Broadly, The rationale for urinary catheter insertion outlined in
indications for use of a faecal containment device are Table 6.12 should be carefully considered. Once it is
persistent diarrhoea, diagnosis of C. difficile infection, established that a urinary catheter is necessary, the type
peri-anal wound or skin breakdown in the presence of of catheter should be determined. While the primary
incontinence, plus the patient must have anal sphincter purpose of urinary catheters is management of urine
tone to enable securement of the device balloon.90,91 drainage, the choice of catheter type may be influenced by
There are many conditions and factors that may prevent the concurrent need for urinary temperature monitoring.
a patient being suitable for these devices such as allergy The smallest size catheter possible is used to reduce
to the materials in the product and including the risk of urethral damage98 although narrow-bore tubes flex easily,
autonomic dysreflexia in spinal cord injury patients, but which can be problematic in male catheterisation where
mostly they relate to rectal and anal conditions.90,91 It is the urethra rounds the prostate gland. Larger-diameter
imperative that both medical and nursing consultation catheters may be required to drain haematuria and clots.
occurs, along with patient consent before use of such The routine use of antibiotic-impregnated catheters or
devices as the potential for complications ranges from silver alloy catheters is not currently recommended.98
discomfort and failure of the device through to infection
and rectal and bowel injuries. Significant rectal haem- Urinary catheterisation essential care
orrhage associated with the use of faecal management Catheter insertion and maintenance should be according
devices has been described in case reports92–95 as well to facility policies and undertaken by people appropriately
as the development of recto-urethral and ano-vaginal trained in the procedures.98,99 Aseptic techniques should
fistulas.93,95 An appropriate bowel therapy regimen and be adhered to during catheter insertion, and hand hygiene
close monitoring of these systems should be imple- should be performed before and after and gloves used during
mented to optimise functioning and reduce risk. any manipulation of the catheter or drainage system.98
 CHAPTER 6 ESSENTIAL NURSING CARE OF THE CRITICALLY ILL PATIENT 145

TABLE 6.12
Urinary catheter quick reference

COMPONENT OF CARE C O N S I D E R AT I O N S

Rationale for insertion and/or Acute urinary retention or bladder obstruction

continuing use Need for accurate measurement of urinary output in critically ill patients
Perioperative use for selected surgical procedures
Re-evaluate continuing use daily Assist in healing of open sacral or perineal wounds in incontinent patients
against rationale and remove Patient requiring prolonged immobilisation, e.g. spinal injury
catheter as soon as possible Patient admitted with chronic indwelling catheter
when no longer required Exceptional circumstances such as to improve end-of-life care
Insertion Follow documented facility policy on urinary catheter insertion
Staff performing procedure follow policy and are trained in technique
Use principles of aseptic non- Use sterile equipment, including sterile drape
touch technique Use aseptic technique when inserting catheter and connecting to sterile drainage system
Clean meatus with sterile normal saline before catheter insertion
Use appropriate sterile, single use lubricant or anaesthetic gel
Secure catheter after insertion to prevent movement and urethral traction
Document insertion information in patient record
Maintenance Maintain aseptic continuously closed system drainage
Perform hand hygiene and use non-sterile gloves prior to any manipulation of the drainage system
Consider each shift: Position drainage bag to prevent backflow or contact with floor
࠮ How long has the catheter Empty drainage bag frequently to maintain urine flow and prevent reflux and empty before
been in situ? patient transport
࠮ Is the catheter still required? Use separate urine collection container for each patient, avoiding contact between drainage
࠮ Are there any indications of bag and container. This collection container should be discarded if single use or cleaned and
infection or complications? sterilised if reusable
࠮ Is the drainage system being Change drainage bags only according to manufacturers’ guidelines or patients clinical need,
managed appropriately? without clamping as it is unnecessary
Daily meatal hygiene via routine hygiene
Avoid use of bladder irrigation, instillation or washouts as routine measures to prevent catheter-
associated infections
Document all related assessment and procedures for the catheter and drainage system

Adapted from NHMRC Australian guidelines for the prevention and control of infection in healthcare, <http://www.nhmrc.gov.au>;
2010 [accessed 06.14].

The urine drainage system should be sterile and Cleansing with antiseptic solution is not recommended
continuously closed with an outlet designed to avoid and can lead to multi-resistant organism infection.
contamination. It should have a sample port for taking Urinary catheters should be changed according to
urine samples. Where appropriate, patients should be clinical need and with regard to the manufacturer’s
given a choice of system suited to their needs: for example, guidelines, and the closed drainage system should be
a shorter drainage tube with a leg-bag may be more broken only for limited, clearly defined clinical reasons.
comfortable for a patient who is mobile. All procedures Bladder washout or irrigation should be avoided and only
involving the catheter and drainage system should be performed for a specific clinical reason, such as intermit-
documented in the clinical notes, including size and type tent irrigation for clots or debris. If obstruction is likely, a
of catheter, balloon size and the date of insertion. If an closed continuous irrigation system may be utilised.
anticipated date of removal is also documented at the time Critically ill patients should be provided with appro-
of insertion and subsequent assessments, it may trigger priate information about their catheters and drainage
staff to remove the catheter as soon as possible. system, according to their needs and ability to understand.
The drainage system should be simple to operate with
Catheter maintenance one hand and easy to position, and the tap should have an
The ongoing need for a urinary catheter should be open–close device. Contamination of the outlet must be
assessed on a daily basis. The introduction of criteria that avoided during emptying. An aseptic technique and sterile
enable registered nurses to remove catheters without equipment must be used when taking a urine sample via
a medical review may result in a reduction in catheter- the sample port. The sample port should be cleaned with
related infections. Routine hygiene at appropriate intervals an alcohol wipe for 30 seconds before and after sampling.
for patient comfort is adequate for urethral meatal care.98 Urine samples should be taken on clinical need and must
146 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

be refrigerated if more than 1 hour is expected to elapse result of anorexia of ageing, 102,103 and, after 65 years of
before the specimen reaches the laboratory. age, a person may have less body fat and lower weight as a
The whole drainage system should be maintained consequence of reduced food intake. Other consequences
with patient comfort in mind, and care should be taken to include impaired muscle function and decreased bone
ensure that the patient is not lying on the drainage tube, mass, which will impair mobility and lead to increased
which can cause pressure sores and blockage. Furthermore, falls. The decrease in bone mass is also age-related and the
the catheter itself should be positioned and then secured decline begins in the 40s, so in the elderly this is quite
so that it is not pulling on the urethra or kinked. The significant.101 Mobility problems are exacerbated by both
drainage bag should be kept below the level of the bladder loss of muscle mass and function and degenerative joint
at all times to maintain an unobstructed flow of urine,98 disease.101 Loss of muscle mass and then muscle activity
and it should be emptied into a disinfected or single-use reduces metabolic function and subsequently causes loss
container. The drainage bag should be changed according of body heat, so care should be taken to ensure the older
to the manufacturer’s instructions, which is usually in the patient is well covered at all times with additional light-
range of 5–7 days. In addition, it should be replaced if it is weight warming devices available to be used as required.
leaking, if there has been a break in the closed system or Skin, the biggest organ, is often the most visible sign of
whenever the catheter is changed. age in the older patient.The epidermis atrophies especially
in exposed areas of the body, and once over 65 years,
Practice tip blistered skin takes longer to repair than in a young adult.
From fragile to easily bruised skin or moist skin folds in
Using a catheter support device or bandage on the leg
those who are overweight, careful hygiene care is required
to secure the urinary catheter is recommended. This
and consideration should be given to the use of specific
lessens tension and irritation from catheter movement,
products for these patients.
patient comfort is improved, and it also promotes
effective drainage and, in restless patients, may prevent
Practice tip
accidental catheter removal as well.
Pay extra attention to the positioning of devices when
used in elderly patients and check them more frequently
Care of the elderly than normal, as the patient may not have full sensation
Older and elderly patients are being admitted to the in the affected area or the physical ability to adjust the
intensive care unit in greater numbers as this section of device themselves, or the confidence to tell you that
the population continues to grow.100 There are no absolute the device is causing pressure or discomfort. Examples
definitions of elderly, but the United Nations describes may be non-invasive blood pressure cuffs that are left
60 plus years as older, while many developed countries on too long or sequential compression device leggings
use 65 plus years as older. Some groupings of chrono- that have slipped.
logical age may have an older person between 65 and 75,
elderly person between 75 and 85 and very elderly over Persistent abdominal discomfort and pain should be
85 years. However, ageing is more than chronological age, triggers for considering bowel obstruction in the elderly,
especially related to health, where biological and psycho- as with age the colon is hypotonic resulting in slower
logical ageing may be more of a factor. In an Australian stool transit and subsequent increased hardening of the
and New Zealand cohort, those over 80 years were more stool from dehydration.101 Faecal incontinence in the
often admitted to the ICU with cardiac and gastro- elderly can be as a result of loss of anal sphincter tone
intestinal conditions than patients in younger age groups, and, therefore, planning for toileting is a practical way of
although rates of admissions for sepsis were comparable managing continence and eliminating the distress caused
between the elderly and young groups.100 by this problem. Symptoms of urinary tract infection such
There are a multitude of physiological changes that as dysuria and frequency are less likely to be as obvious
result from ageing and critical care nurses should be aware in the elderly as the young, as the capacity of the bladder
of these differences so that therapies and care can be decreases with age and especially if the patient suffers from
titrated and adjusted accordingly.101 stress incontinence already.101 As with other functions,
Common causes of anemia in the elderly are iron ageing blunts the immune system response, which results
deficiency and the presence of chronic disease or inflam- in increased susceptibility of the elderly to infection. This,
mation followed by chronic kidney dysfunction. The along with the additional deterioration in skin integrity
presence of anemia not only adversely affects outcomes and likely increased exposure to antibiotics over time,
from illness, but adds to the elderly patient’s difficul- means that this group of patients may be at greater risk of
ties with mobility and managing daily activities. When hospital-acquired infections and multi-resistant organisms.
critically ill, this may contribute to the elderly patient’s Consideration should be given to a suitable environ-
fatigue, so careful consideration should always be given ment for the elderly, such as increased sound proofing, more
to planning activities such as hygiene and mobilisation. comfortable and supportive chairs and cutlery and utensils
Some elderly patients are quite fragile, this being the that are easy to grip to enable more comfortable meals.
 CHAPTER 6 ESSENTIAL NURSING CARE OF THE CRITICALLY ILL PATIENT 147

Above all, nurses should adjust some of their behaviours important is maintaining the patients’ dignity and feelings
with the older person, such as speaking clearly, listening of safety and minimising their self-consciousness during
carefully without interruption, anticipating frequent repositioning, irrespective of the method required. Lifts
personal care needs and allowing time to enable mobil- and hoists and other equipment that are designed for
isation without haste, all of which may help to facilitate heavier people should be used.110,111 A well-thought-out
feelings of independence and control of their circum- strategy by an interdisciplinary group can work through
stances for these patients. the local issues within a hospital or unit and produce a
bariatric kit, containing a range of equipment appropriate
Bariatric considerations to the needs of the bariatric patients in various settings
including the ICU.111
Obesity continues to be a major health issue around the A major concern in the ICU is the positioning of the
world.While many bariatric patients will present to hospital morbidly obese patient with respect to airway management
with various health issues, obesity has its own physiological and oxygenation. Boyce et al found no differences in the
impact to be considered, such as impaired chest expansion difficulty of airway management when patients were
and respiration from a large abdomen or insulin resistance in the 30° reverse Trendelenburg (head up, feet down),
related to altered glucose metabolism.104,105 Close glucose supine-horizontal or 30° back-up position.112 However,
monitoring regimens should be implemented and appro- when patients were positioned in the reverse Trendelen-
priately calculated dosages for medications prescribed. burg position, their oxygen saturation dropped the least
Adapted techniques to enhance patient assessment may and took the shortest time to recover. While the reverse
be required, such as auscultating over the left lateral chest Trendelenberg position should decrease pressure on the
wall to hear heart sounds while the patient is positioned diaphragm and therefore decrease intrathoracic pressure, a
towards their left side or using a thigh or regular blood likely outcome of using this position is the patient slipping
pressure cuff on the patient’s forearm.104 down the bed and then having to be re-positioned, so
Studies have found that persons who are obese contend frequent tilt adjustments may assist with limiting this
with a negative bias within a social context,106 but this same consequence. Ask patients about techniques that work
negative bias from health professionals including nurses for them at home when re-positioning and mobilising.
may then interfere with their ability to obtain quality As with all patients, bariatric patients are vulnerable to
health care.107,108 According to Susan Bejciy-Spring, the fears and anxieties resulting from their illness; however,
key to providing quality, patient-centred, sensitive care to additional concerns for their physical safety may be expe-
the bariatric patient is R-E-S-P-E-C-T: rapport, environ- rienced, such as during re-positioning, if the activity is not
ment/equipment, safety, privacy, encouragement, caring/ arranged competently and with sensitivity. Care should be
compassion and tact.108 Simple things such as an appro- given to monitoring the obese patient, especially those
priately sized gown and suitable bed linen that provide post bariatric surgery with prolonged immobility, for
the patient with adequate covering are often not well- pressure-induced rhabdomyolysis.113
organised for this patient group, unless the nurse takes the As obese persons often have venous stasis disease,VTE
time to arrange specific supplies if they are not routinely prophylaxis in bariatric patients is vital especially for those
available. patients having bariatric surgery. Routine prophylaxis is
Sedation in the bariatric patient needs to be carefully recommended with weight-adjusted dosing of medica-
managed to avoid the resultant risk of respiratory failure tions.70,105 Combining pharmacological and mechanical
and need for ventilation. Reducing narcotic usage through prophylaxis is recommended for this high-risk group. The
use of combinations of other analgesia along with sedatives application of leggings or sleeves for sequential compres-
will also reduce the risk of respiratory failure.109 Bispectral sion devices or pneumatic venous pumps can often be
index monitoring can be used to assist in the titration of easier than applying graduated compression stockings in
sedations during procedures where levels of sedation that any patient when they are supine in bed. Care must be
eliminate awareness and recall are necessary.109 taken with measuring the limb to obtain the correct size
The use of arterial monitoring rather than non- legging or stocking. Careful monitoring of the limb for
invasive blood pressure measurements for patients receiving signs of skin deterioration from moisture or of pressure
titrated vasoactive infusions should be considered, because from an ill-fitting legging, sleeve or stocking must be
of the difficulty in obtaining accurate readings if the cuff undertaken diligently in the bariatric patient.70 The
is not sized or positioned correctly. Use specific bariatric insertion of a removable inferior vena cava (IVC) filter
equipment and techniques to move patients safely for as a component of pulmonary embolism prophylaxis for
both the patient and the staff involved. It is important to patients undergoing bariatric surgery may occur in some
be aware of the weight capacities of various facilities, such institutions,105 especially patients with BMI >50 kg/m2,
as lifts and equipment, which may be required in the care or with prior history of thromboembolism. The post-
of the bariatric patient. operative management of the bariatric patient will include
Overweight patients can be challenging in any setting, nutrition to support tissue repair. The use of post pyloric
and it is important to consider the health and safety of enteral nutrition may be of benefit in reducing the risk of
the staff involved in lifting and moving patients. Equally aspiration in the bariatric patient, as these patients often
148 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

experience postoperative vomiting and nausea.109 For BOX 6.3

critically ill patients who are obese, nutritional goals are
similar to those of other patients but may include weight Infection-control guidelines for the prevention of
reduction while preserving lean muscle.114 Unless there transmission of infectious diseases in the healthcare
is a particular rationale for the use of a urinary catheter setting99
for the patient, plans should be in place for assisting the • Healthcare-associated infections are those acquired
bariatric patient with toileting, as many obese patients in care establishments (‘nosocomial’ infections)
have stress incontinence. and infections that occur as a result of healthcare
interventions (‘iatrogenic’ infections). The infection
General principles of infection may manifest after people leave the healthcare
establishment.
control in critical care • A healthcare establishment is any facility that
Effective infection control is vital in the critical care setting delivers healthcare services.
to prevent further health risks to critically ill patients already • Healthcare workers (HCWs) are all people delivering
compromised by their disease or trauma (Box 6.3). And a healthcare services, including students, trainees
vital factor of infection control is effective hand hygiene. and mortuary attendants, who have contact with
Critically ill patients often require multiple invasive devices patients or with blood and body substances.
and therapies to manage their illness and these increase the • Standard precautions are standard operating
potential risk to the patient of infection. While using ther- procedures that apply to the care and treatment of all
apeutic medical devices is often vital to the management patients, regardless of their perceived infection risk.
of the patient, they are not without risk. Ventilator- They are work practices required to achieve a basic
associated pneumonia (VAP), catheter-associated urinary level of infection control and are recommended for
tract infections (CAUTIs) and central line-associated the treatment and care of all patients.
bacteraemia (CLAB) are all aligned with invasive device • Transmission-based precautions are required
use and form a significant source of healthcare-acquired when standard precautions may not be sufficient
infections (HAIs) within critical care.99 Critical care staff to prevent the transmission of infectious agents
themselves need to protect against contracting infections (e.g. in tuberculosis, measles, Creutzfeldt–Jakob
while providing care for their patients. disease). These precautions are tailored to the
When patients are admitted to critical care it is specific infectious agent concerned and may
impossible to identify whether or not they are newly include measures to prevent airborne, droplet or
colonised with bacteria, or are carrying an infection, contact transmission, and healthcare-associated
without further investigation. Standard Precautions are transmission agents (see Table 6.13).
applied in the management of all patients regardless of the
• Transmission-based precautions are recommended
reason for their admission. Standard Precautions include:
for patients known or suspected to be infected
hand hygiene, respiratory hygiene and cough etiquette;
or colonised with disease agents that cause
the use of appropriate personal protective equipment;
infections in healthcare settings and that may not
safe handling of sharps, waste and used linen; appropriate
be contained by standard precautions alone.
cleaning and environmental controls; appropriate re-
processing of reusable equipment; and the use of aseptic
Adapted from NHMRC Australian guidelines for the prevention
non-touch techniques during procedures.99 and control of infection in healthcare, <http://www.nhmrc.gov.
With the advent of influenza outbreaks, there has been au>; 2010 [accessed 06.14].
an emphasis on respiratory hygiene and cough etiquette,
which effectively means covering the mouth with a
tissue when coughing or sneezing and then immediately protocols for shared equipment, placement of patients
disposing of the tissue into waste bins, followed by effective in single rooms (or cohorted if appropriate) and specific
hand hygiene.99 Further Transmission-based Precautions air filtration or circulation and environmental cleaning
are implemented as required in response to suspicion protocols.99
(while awaiting confirmation from tests) or diagnosis of There are three types of Transmission-based Precau-
a condition in which Standard Precautions may not be tions recommended to counteract the various infectious
sufficient to control the transmission of microorganisms.99 agents: Contact Precautions, Droplet Precautions and
Transmission-based Precautions appropriately applied to Airborne Precautions99 (see Table 6.13). These types of
specific microorganisms disrupt their method of trans- precautions are applied with refinement to the use of
mission to other patients, visitors and healthcare workers. personal protective equipment, room requirements and
Transmission-based Precautions include continuation recommendations for visitors specific to the mode of
of Standard Precautions, the use of personal protective transmission of the organism. Critical care nurses should
equipment specific to the risk of transmission, individual be knowledgeable about both local and national guidelines
patient equipment where possible and specific cleaning and protocols for infection control in order to provide safe
 CHAPTER 6 ESSENTIAL NURSING CARE OF THE CRITICALLY ILL PATIENT 149

the healthcare setting (see Box 6.3).99 All health services

TABLE 6.13 should apply designated guidelines and operate within
Transmission-based precautions and infectious clearly defined infection-control procedures, which
conditions are based on Standard Precautions. Although formerly
TRANSMISSION- EXAMPLES OF
referred to as ‘Universal Precautions’ and ‘Additional
BASED PRECAUTIONS INFECTIOUS CONDITIONS Precautions’, the recent guidelines on infection control
from the National Health and Medical Research Council
Contact MROs : MRSA, MRGN, VRE,
uses the terms ‘Standard Precautions’ and ‘Transmissions-
ESBL, CRE
Gastrointestinal pathogens:
based Precautions’, respectively, to clearly describe these
C. difficile, norovirus
levels of precautions.99 Critical care nurses should refer to
Highly contagious skin
their specific hospital infection-control policies regarding
infections details of procedures that must be followed.
Droplet Influenza Control
RSV
Once an organism has been identified, the goal is to
Meningococcal
limit its spread. Although patients may be colonised with
Airborne Pulmonary TB bacteria, they may not be infected. Colonisation refers to
Chickenpox (varicella), the presence of microorganisms in any amount, whereas
measles (rubella) infection means that pathological tissue injury or disease
SARS, MERS has occurred due to the invasion and multiplication of
CRE = carbapenem resistant Enterobacteriaceae; the microorganism.119 Typically, surveillance measures
ESBL = extended-spectrum beta-lactamase-producing identify many patients who are colonised with MRSA or
(Enterobacteriaceae); MERS = Middle East respiratory VRE and, although they themselves are not infected, it is
syndrome coronovirus; MRGN = ; MRO = multi-resistant important to stop the spread of bacteria to patients more
organism; MRSA = methicillin-resistant Staphylococcus vulnerable and thus more susceptible to opportunistic
aureus; RSV = pertussis; SARS = severe acute respiratory infection, by implementing Transmission-based Precau-
syndrome; TB = tuberculosis; VRE = vancomycin-resistant
enterococcus.
tions.120 Several measures demonstrated to be effective
in managing multi-resistant bacterial infections in ICUs
Adapted from NHMRC Australian guidelines for the prevention are summarised in Box 6.4. Due to the vulnerable nature
and control of infection in healthcare, <http://www.nhmrc.gov. of critically ill patients, specific issues are described in
au>; 2010 [accessed 06.14], with permission. more detail including: hand hygiene, personal protective
equipment (PPE), MROs, HAIs,VAP and CLAB.
care to all their patients. Breaks to the consistent appli-
cation of Standard Precautions and, when implemented, BOX 6.4
Transmission-based Precautions put patients at risk, Preventative measures to reduce the spread of
especially those who are critically ill. MRO infection
Although good hand hygiene is the single most effective
tool in infection control,115,116 the key components of • Identifying the infected patient – infection control
notification in patient’s record
effective infection control are surveillance, prevention and
control, which are described in more detail. • Hand washing with antiseptic solution before and
after contact with the patient
Surveillance • Contact precautions using gloves and gowns during
ICU patients may be colonised or infected with a multi- direct patient contact
resistant organism (MRO) prior to admission,117 so routine • Separation of stethoscopes, sphygmomanometers
screening should be undertaken to detect the presence of and thermometers for individual use
bacteria. Ideally, all critically ill patients will be screened
for multi-resistant Staphylococcus aureus (MRSA) and • Separation of other articles and equipment for
vancomycin-resistant Enterococcus (VRE) on admission.117 exclusive use of the patient
Regular surveillance to identify rates of nosocomial • Daily surface cleaning and disinfection
infection, with feedback to critical care staff, helps to
improve compliance with infection control guidelines.99 Adapted from:
In the 1980s, a landmark study established that hospital- NHMRC. Australian guidelines for the prevention and control
acquired infection may be reduced by around a third if of infection in healthcare, <http://www.nhmrc.gov.au>; 2010
[accessed 06.14], with permission.
surveillance and prevention programs are implemented.118 Haley RW, Culver DH, White JW, Morgan WM, Emori TG, Munn
Prevention VP et al. The efficacy of infection surveillance and control
programs in preventing nosocomial infections in US hospitals.
The Australian Government Department of Health and Am J Epidemiol 1985;121(2):182–205, with permission.
Ageing provides guidelines for infection control within
150 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Practice tip Practice tip

When using open tracheal suctioning techniques, it is Compliance with local protocols for surveillance,
most important to ensure that the ventilator connection isolation and use of PPE for MROs and infectious
is not contaminated during the procedure while dis- conditions is vital to the management of all patients,
connected from the tracheal tube. and the safety of personnel and visitors in critical
care units.
Hand hygiene
At the core of Standard Precautions is effective hand Personal protective equipment (PPE)
hygiene. Good hand hygiene is a simple yet effective PPE may include any and all of the following: plastic aprons,
technique that reduces the spread of bacteria. It is the gowns (single use or sterile), gloves (single use or sterile),
most effective and least expensive method of preventing masks ranging from surgical to particulate filter N95 mask
healthcare-associated or nosocomial infection.115 However, or P2 respirators and eye protection such as goggles or
hand hygiene compliance is poor,99,115 but can be face shields that also protect mucous membranes of the
improved significantly if regular education programs, mouth and nose.99 Specific sequences have been outlined
feedback and reminders are employed.99,116 For example, for putting on and taking off PPE that minimise the risk
the five moments for hand hygiene (see Box 6.5) created of contamination.99
by the World Health Organization (WHO) in 2009115 can Epidemic outbreaks of severe acute respiratory
be adopted for local implementation, such as by Hand syndrome (SARS) coronavirus occurred in Canada,
Hygiene Australia.116 Evidence has led to the current China, Hong Kong, Singapore and Vietnam122 in 2003
recommendation of using an alcohol-based hand rub and cases were reported in over 25 countries.123 SARS
for hand hygiene unless the hands are soiled.115,116,121 The was transmitted between patients, healthcare workers
use of alcohol hand rubs is associated with higher rates and hospital visitors, and large within-hospital outbreaks
of hand hygiene compliance and effectiveness although were associated with aerosol-generating procedures such
effectiveness is dependent on technique.115,116,121 as bronchoscopy, endotracheal intubation and the use of
aerosol therapy,123 which are commonplace in critical
BOX 6.5 care areas. In Hong Kong, more than 20% of cases
were healthcare workers.124 Because of the high level of
WHO ‘5 moments’ of hand hygiene
morbidity and mortality associated with SARS,125 the risk
Hand hygiene is performed: to healthcare staff is considerable and, during the Hong
• before touching a patient Kong SARS outbreak, healthcare workers wore full head
• before commencing a procedure covers with a visor.126
Previous research has demonstrated relatively low rates
• after a procedure or exposure to body fluids
of compliance with standard precautions, ranging from
• after touching a patient 16% to 44%.127 The SARS outbreaks emphasised the
• after touching a patient’s environment need for effective infection-control procedures, especially
plus for airborne pathogens. With airborne pathogens such as
pulmonary TB or the Middle East respiratory syndrome
• after the removal of gloves.
coronavirus (MERS-CoV),128,129 Airborne Precautions129
using properly fitted N95 masks (face mask with 95%
Adapted from Grayson L, Russo P, Ryan K. Hand hygiene.
or greater filter efficiency), gowns and gloves are imple-
Australia manual. Australian Commission for Safety and Quality
in Healthcare 2009, <http://www.hha.org.au/>; [accessed 11.10], mented to reduce the spread of the organism, plus the
with permission. use of airborne infection isolation rooms or negative air
pressure rooms with room exhaust via high-efficiency
particulate air (HEPA) filtration and strict control of
family visiting.129 Additional measures may include the use
Practice tip
of high-efficiency bacterial filters to filter patients’ expired
Good hand hygiene is vital before and after all air, closed suction systems and ventilator scavenging
interventions with patients. There are large numbers systems.126
of objects in a single ward or unit, such as computer MERS-CoV was first reported in 2012 in Saudi Arabia
keyboards and door handles, which are touched by and, up to 2014, there were nearly 700 cases in countries
many people within a day. Movement of contaminants near to the KSA and from travelers returning home from
from inanimate objects to patients and the reverse the area. 129 The severity of respiratory infection symptoms
is possible if adherence to good hand hygiene is varies, but as of 2014 the mortality is around 30% for
not upheld. Remember the five moments of hand confirmed MERS-CoV infections.129
hygiene. The influenza H1N1 pandemic alerted everyone to the
need for vigilance in infection control.The use of Droplet
 CHAPTER 6 ESSENTIAL NURSING CARE OF THE CRITICALLY ILL PATIENT 151

Precautions is the main feature of infection control for Medical devices or therapies may expose patients to
influenza, along with early testing.130 The influenza the potential risk of acquiring an HAI.This risk may occur
outbreak also drew attention to the need for vaccinations. during the insertion procedure or subsequent maintenance
Influenza vaccines are developed as the influenza A virus care of the medical device, unless appropriate techniques
changes. All healthcare workers and especially those in are used. The use of an aseptic technique during insertion
critical care should be knowledgeable of the vaccinations of a device is a feature of infection control, asepsis being the
that may be available to them through their employers elimination of pathogens. Aseptic non-touch technique
and those that are recommended by local jurisdictions. A is a format for guiding practice in the application.133,134
variation of the avian influenza A (H7N9) virus was first Standard aseptic non-touch technique involves standard
reported in China in 2013.131 hand hygiene, a general aseptic field and non-sterile or
sterile gloves and is used for minor procedures that are
Practice tip simple and of short duration, that is, less than 20 minutes.
Examples of procedures include simple wound dressings
Reminder: hand hygiene is performed before putting and intravenous cannulation or urinary catheterisation
on PPE and after removing PPE. Hand hygiene is also by proficient practitioners. Surgical aseptic non-touch
performed after removal of gloves. technique is used for complex or lengthy procedures such
as insertion of a central venous catheter and involves the
Multi-resistant organisms use of full barrier precautions (sterile gown and gloves,
MROs, or multi-drug-resistant organisms, is a collective face mask), extensive drapes and critical aseptic field.99
term for a number of infections from multi-resistant Box 6.6 provides some basic points to guide management
organisms. While the early diagnosis of an MRO of the use of medical devices in critical care.
and immediate implementation of organism-specific The commonest HAIs occur at surgical sites, the
Transmission-based Precautions is key to management, urinary tract, lower respiratory tract and bloodstream. For
it is true that MRSA and extended-spectrum beta- the critically ill patient intravascular cannulas including
lactamase-producing Enterobacteriaceae (ESBL-E) have central venous catheters, urinary catheters, enteral or
reached epidemic proportions. Multiple strains of MRSA nasogastric tubes and artificial airways and ventilation are
have been identified, and in many studies ICUs have the some of the healthcare devices associated with risk. See
highest incidence.120 In the past decade VRE has become a the section on urinary catheters for information regarding
serious health issue and, more recently, carbapenem-resistant catheter-associated urinary tract infections.
Enterobacteriaceae (CRE).132 Other multi-resistant organisms
include multi-drug resistant Pseudomonas aeruginosa and
Ventilator-associated pneumonia
Acinetobacter spp.119 As with MRSA, transmission of these Ventilator-associated pneumonia (VAP) is common
other MROs is associated with contact. in intensive care and usually occurs within 48 hours of
There are a number of methods for reducing the initiating ventilation.135 Changing entire team practices
spread of MROs (see Box 6.4), although not all methods
may be effective and, if the organism is not identified, its BOX 6.6
spread will continue unseen. Another key component of
Invasive device management
management of MROs is surveillance, such as the routine
screening for MRSA and VRE of all patients on admission • Does the patient need the invasive device for
to critical care areas and on a regular basis thereafter. Once effective management of their condition?
diagnosed, it is common practice to use single rooms for • Is the chosen device the most suitable for the
patients with MROs to reduce cross-infection. Growing individual patient, e.g. size and type of device?
antimicrobial resistance can be reduced with effective • Are the healthcare professional/s trained to safely
infection prevention and control and prescribing anti- insert and manage the device?
biotics only when needed.
• Use the appropriate aseptic procedure for device
Healthcare-acquired infections (HAI) insertion.
Nosocomial, or hospital- or healthcare-acquired, infection • Follow management protocols to minimise the risk
(HAI) is a major problem in critical care that may of infection while the device is in situ.
affect up to 20% of patients, with a mortality of around • Monitor the patient for signs and symptoms of
30%.117 Critically ill patients are 5–10 times more likely infection.
to become infected than hospital ward patients.119 • Review the need for the device in the management
Multi-drug-resistant bacteria are a worldwide problem; of the patient daily and remove as early as possible.
their acquisition by patients can lead to infection with the
same bacteria, and multiple antibiotic therapy encourages Adapted from: NHMRC. Australian guidelines for the prevention
the proliferation of resistant organisms.119 The introduc- and control of infection in healthcare, <http://www.nhmrc.gov.
tion of antibiotic stewardship assists in focusing on the au>; 2010 [accessed 06.14], with permission.
optimal use of antibiotics.99
152 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

and behaviours is critical to successful reduction of VAP an inconsistent reduction in ICU mortality, and there
within an intensive care unit.136,137 A number of strategies remains concern about the promotion of antimicrobial
that are effective in helping to prevent infection135 are resistance with its prolonged use.138 Related information
identified in Table 6.14, and two of the simplest and most on respiratory failure,VAP and ventilation can be found in
effective are raising the head of the bed and frequent oral Chapters 14 and 15.
hygiene.31 Effective analgesia and minimising sedation
plus avoidance of muscle-relaxant medications along with Central line-associated bacteraemia
early mobilisation are some of the other strategies that (CLAB)
may contribute to the reduction of VAP. Using a heat and The use of central lines is common in critical care areas.
moisture exchanger (HME) limits the need to change Catheter-related sepsis is defined by the International
ventilator circuits, while maintaining a closed ventilator Sepsis Forum as at least one peripheral positive blood
circuit and the use of closed suction systems for endo- culture plus at least one of the following: a positive
tracheal suction assist with prevention strategies. catheter tip culture, a positive hub or exit-site culture or a
Selective digestive decontamination has been studied positive paired central and peripheral blood culture where
extensively. In theory, the use of antimicrobial agents the central culture is positive ≥2 hours earlier than the
to reduce gut flora in intubated intensive care patients peripheral culture or has 5 times the growth.139 CLAB
reduces the risk of pneumonia due to micro aspiration is one of the most important and severe infections that
(see Chapter 19). Although most studies have demon- can occur in ICU. Renal failure may significantly increase
strated a reduction in the incidence of VAP, there has been the risk of infection.140 Berenholtz et al demonstrated that
implementing quality improvement measures to ensure
adherence to evidence-based infection control guidelines
TABLE 6.14 results in a significant reduction of catheter-related blood-
Strategies to prevent VAP stream infection.141
MEASURE INTERVENTIONS
Southworth et al142 noted that, after implementing
strategies to reduce CLAB, staff engagement in constant
Infection control • Hand hygiene vigilance is required to maintain success. The use of anti-
measures • Active surveillance biotic-impregnated catheters has been shown to reduce
• Appropriate PPE when managing
bacteraemia143 and, although it is common practice in
ventilation-related devices, e.g.
many critical care units to routinely change intravenous
ETT, ventilator circuits, tracheal
administration sets, with antiseptic-coated catheters they
suctioning
can be used safely for up to 7 days.144 Currently available
Gastrointestinal • 2-hourly oral hygiene evidence supports the use of maximal barriers (head cap,
tract • Stress ulcer prophylaxis face mask, sterile body gown, sterile gloves and full-size
• Avoid gastric over-distention
body drape) during routine insertion of central venous
• Enteral nutrition
catheters along with antiseptic solutions to prepare the skin,
Patient position • Semi-recumbent with head raised and catheter insertion by appropriately trained personnel.99
to >30° Chapter 3 contains information on central line care
• Rotational bed therapy bundles and checklists. Although chlorhexidine solutions
Artificial airway • Respiratory airway care are recommended, their effectiveness depends upon the
• Avoid unplanned extubations strength of the solution. In Australia decontamination of
• Secure tracheal airway cuff the insertion site is with 0.5% chlorhexidine gluconate
• Inline or intermittent subglottic in 70% isopropyl alcohol.99 Nurses are responsible for the
secretion removal maintenance of central venous catheters once inserted,
Mechanical • Maintenance of ventilation including care of the insertion site dressing and infusion
ventilation equipment, heat and moisture line management. The types of dressing commonly used
exchangers, safe removal of are transparent semi-permeable and, more recently, chlor-
condensate from circuits hexidine gluconate gel dressings.99,145 Transparent dressings
• Minimisation of ventilation time are advantageous because they allow direct observation of
• Daily interruption to sedation and/ the entry site of the catheter. Dressings should be replaced
or assessment for readiness to wean whenever their seal is broken or every 7 days.99 Catheter
therapy and/or extubate hubs are another site of colonisation for microorgan-
• Non-invasive mechanical ventilation isms such as Staphylococcus epidermidis, and effective hand
hygiene combined with non-touch aseptic techniques
ETT = endotracheal tube; PPE = personal protective
equipment; VAP = ventilator associated pneumonia. when accessing the catheter hub should be implemented.
Adapted from NHMRC. Australian guidelines for the prevention
Intravenous administration sets containing blood products
and control of infection in healthcare, <http://www.nhmrc.gov. or lipids or parenteral nutrition infusions are changed
au>; 2010 [accessed 06.14], with permission. when the infusion completes or daily, while others are
changed according to local protocols. Infusions such as
 CHAPTER 6 ESSENTIAL NURSING CARE OF THE CRITICALLY ILL PATIENT 153

propofol or nitroglycerine may have additional manufac- The primary focus of assessment should be on patient
turer guidelines regarding administration set changes.99 safety and the prevention of adverse events. A transport
After removal of the catheter, and once homeostasis ‘event’ can be any event that has an adverse impact and can
has been established, the site should be covered with be patient-, staff- or equipment-related.152,155 The patient
an occlusive dressing, which should be left in place for may be adversely affected during transport, ranging
48 hours to minimise the risk of infection. The catheter from anxiety or pain to respiratory or cardiovascular
should be examined after removal and any damage compromise.152 Staff may have difficulty with managing
reported. It may be hospital or unit policy to send the the patient’s needs during transport and equipment-
catheter tip for culture and sensitivity; however, a recent related problems during transport of critically ill patients
single-centre study has shown that colonisation is heaviest are a major consideration along with device dislodge-
at the intravascular proximal segment compared to the ment.154,155 Risk–benefit assessment is helpful to identify
distal tip of the catheter.146 patients with a high risk of complications.151 For example,
the potential risk of moving a severely head-injured
Practice tip patient with unstable intracranial pressure may outweigh
the potential benefit of a CT scan. Parmentier-Decrucq et
Unless contraindicated in a specific patient, a central al153 ‘found sedation of the patient before transport, PEEP
venous catheter dressing should be changed whenever >6 cmH2O and the need for fluid infusion for transport,
there is evidence of fluid accumulation or loss of the to be risk factors for any adverse event during intra-
dressing’s occlusive seal. hospital transport’. Meticulous planning for all aspects
of the transport, based on a thorough assessment of
Transport of critically ill the patient’s anticipated needs, is the key to safe intra-
hospital transport.147,151 Consideration of specific patient
patients: General principles needs such as the availability of lifting devices for transfer-
ring bariatric patients from bed to CT table or appropriate
The transport of a critically ill patient may occur for
warming devices for the use of elderly patients during
several reasons, such as from an accident site, categorised
lengthy interventional radiological procedures need to be
as pre-hospital transport, or to move a patient to another
communicated to the procedural areas prior to transport
facility for treatment, which is known as inter-hospital
commencing so that no delays occur. A comprehensive
transport, or within a hospital from one department to
outline of information addressing key components of
another, this being intra-hospital transport.147 This section
intra-hospital transport of critically ill patients should be
will focus on intra-hospital transport, while inter-hospital
available to personnel at every hospital.147,149
transport is described in Chapter 23. A large proportion
Safe transport requires accurate assessment and stabil-
of intra-hospital transports occur from the emergency
isation of the patient before transport.147 Key elements150
department148 to the critical care unit. Another significant
are identified in Box 6.7. Securing vascular accesses
group is the deteriorating patient within a hospital ward
should be a primary concern, while some consideration
who requires emergency transfer to the ICU. Patients
may be given to having two intravenous accesses in situ.
within the ICU may require transport to imaging depart-
All equipment should be checked for functionality prior
ments for scans or operating theatres for procedures or to transport and, while it is vital to ensure that sufficient
cardiac cathlab for angiography.
Guidelines for the transport of critically ill patients are
available in many countries including Australia and New BOX 6.7
Zealand147,149 with the principles applying to intra-hospital Key elements of safe transfer
and other transport.147,150 Specific guidelines may need to • Experienced staff
be observed for certain groups of patients, for example
those with head injury. A careful assessment of risk versus • Appropriate equipment
benefit should be undertaken before making a decision • Full assessment and investigation
to transport a patient.150,151 To reduce the risk of adverse • Extensive monitoring
events during transport, various diagnostic tests or surgical • Careful stabilisation of patient
procedures should be evaluated in terms of their potential
• Reassessment
to be undertaken in the critical care unit.149
• Continuing care during transfer
Considerations • Direct handover
Fanara et al152 outlined a diversity of adverse events during • Documentation and audit
intra-hospital transport. In one study 16.8% of intra-
hospital transport adverse events were considered Adapted from Wallace PGM, Ridley SA. ABC of intensive care:
serious.153 Recognition of the risk of adverse events transport of critically ill patients. Br Med J 1999;319(7206):
during intra-hospital transports has long been a concern 368–71, with permission.
in critical care and remains so today.154,155
154 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

equipment is taken to maintain the patient, unnecessary e.g. intra-aortic balloon pump. Team members should be
equipment complicates the logistics of managing the aware of their specific roles and ensure excellent commu-
transport smoothly. Specifically constructed transport nication throughout the transport procedure.
beds or attachments such as equipment tables designed to
support equipment safely during transfer are useful.147,151 Practice tip
The period of transport should ideally be as short as
possible, although safety should not be sacrificed for speed. Staff involved in patient transports should be
Pre-planning the route of transport and good dialogue knowledgeable of the most efficient route to take as
between department staff can help to maximise the well as the facilities at their destination such as power
efficiency of transport and reduce unnecessary delays.149 and gas supplies.
At all times, the team must be confident that all safety Equipment used during patient transport must be
considerations have been made. Flabouris et al156 noted robust, lightweight and battery-powered,151 and must
both ‘haste’ and ‘pressure to proceed’ with transport as adhere to relevant national manufacturing and safety
contributing factors in adverse events. standards. Equipment-related complications occur in
around a third of transports.154 All equipment must
Practice tip be adequately secured during transport, and must be
Transport preparation should include: 1) establishing available continuously to the operator.147 Oxygen
the need and purpose of transport; 2) time duration
requirements should be calculated in advance (or it
relating to the route to be taken, length of procedure
should be established that piped oxygen is available at the
and return journey; 3) necessary equipment; 4) patient
destination department) to ensure an adequate supply,
preparation; 5) appropriately skilled and numbers of
both for the journey and for the duration of the investi-
staff; 6) supplies required to continue therapies during
gation/procedure. Standard equipment for inter-hospital
transport event; and 7) consideration of emergency and
transport is identified in Table 6.15147 and, while some
contingency plans.
items may be unnecessary for all intra-hospital transport,
this table provides a useful checklist so that all necessary
equipment is taken. Additional specialist equipment may
Essential nursing care during be required for certain patients, such as spare trache-
transport ostomy tubes in case of accidental extubation.
Essential care during transport involves three components:
Practice tip
the patient, the personnel and the equipment and
monitoring. Importantly, the patient and their family To ensure safe equipment preparation, especially
should be given an explanation of why the transport is during emergency transport events, have two nurses
necessary, how long the procedure is expected to take and perform independent checks against a transport
that the transport process includes a team accompany- checklist that includes battery life and gas cylinder
ing the patient to continue monitoring and provide any data for equipment in your unit as a standard transport
required treatment. preparation practice.
Nursing responsibilities during transport of the patient
include all aspects of patient and therapy monitoring, Before transport, all equipment should be prepared
comfort and maintaining appropriate documentation. and checked, including the function of visible and audible
Continuous or frequent monitoring of the patient’s vital alarms. All non-essential therapy should be discontinued
signs and physiological parameters and equipment alarms temporarily during the transport, such as enteral nutrition.
and parameters should be undertaken throughout the Where possible, therapies should be simplified, such as
transport event, and all equipment should be checked exchanging chest drainage systems for one-way valves, or
regularly to ensure correct functioning. Gas reserves of disconnecting completed infusion administration sets from
oxygen cylinders and battery time of all devices require intravenous lines. The patient’s physical safety should be
pre-transport calculation before being used and vigilant maintained and care should be taken to ensure that bed rails
attention during transport. Patient safety is paramount are used and the patient’s limbs are secure and not likely to
and close attention to detail is required. Throughout be injured by equipment. All vital monitoring and therapy
the transport, patients should be reassured regarding equipment should be transferred to portable equipment,
their condition and the progress of the purpose of the and the patient should be stabilised before being moved.
transport. Some transport equipment ventilators may not provide
The level of experience and specialty of personnel identical parameters or functioning to a ventilator the
involved in the transport of critically ill patients are patient is already using, so time must be taken to adjust the
factors influencing safe transport.147,149 Staff should be transport ventilator to effective ventilation for the patient.
trained in the various aspects of patient transport,147,154 If the patient is being transported for magnetic resonance
including competent management and troubleshooting imaging (MRI), it is important to ensure that all equipment
of all equipment required for particular patient needs, is compatible.
 CHAPTER 6 ESSENTIAL NURSING CARE OF THE CRITICALLY ILL PATIENT 155

TABLE 6.15
Standard equipment for intra-hospital transport

R E S P I R AT O RY S U P P O R T C I R C U L AT O RY S U P P O R T PHARMACOLOGICAL
EQUIPMENT EQUIPMENT OTHER EQUIPMENT AGENTS

• Airway management • Monitor/defibrillator/ • Nasogastric tube and bag • Checked and clearly
equipment, including external pacer combined • Dressings, antiseptic labelled drugs: standard
intubation set, range of unit lotions, bandages, tape, resuscitation drugs and
endotracheal tubes and • Non-invasive blood • Torch those specific to the
laryngeal mask airways, pressure device • Thermal insulation and patient’s condition
hand ventilation set with • IV cannula, IV fluids, temperature monitor
PEEP valve and emergency pressure infusion set, • PPE for transport team
surgical airway set infusion pumps
• Oxygen, masks, nebuliser • Arterial cannulae and
• Pulse oximeter and arterial monitoring device
capnography • Syringes and needles,
• Sufficient oxygen supply sharps disposal container
• Suction equipment • Pericardiocentesis
• Portable ventilator with equipment
disconnect and high-
pressure alarms
• Pleural drainage equipment

IV = intravenous; PPE = personal protective equipment.

Adapted from College of Intensive Care Medicine Australia and New Zealand (CICM). Guidelines for transport of critically ill patients,
<http://www.cicm.org.au>; 2013 [accessed 06.14], with permission.

Practice tip TABLE 6.16

Monitoring during transport
If ceasing nutrition during patient transport, make sure
that the patient is not at risk of hypoglycaemia from C L I N I C A L PAT I E N T EQUIPMENT
concurrent insulin therapy. MONITORING MONITORING

• Circulation • Pulse oximeter, and

The need for monitoring relates to both the patient • Respiration capnography
and equipment, and is identified in Table 6.16.147 Some • Oxygenation • Breathing system alarms
monitoring should be continuous, such as cardiac, oxygen • Neurological • Electrocardiograph
saturation, capnography if the patient is intubated and • Pain score • Physiological pressures
arterial, pulmonary artery and intracranial monitoring if • Patient comfort • Other clinically indicated
the respective devices are in situ. Intermittent monitoring equipment
of central venous pressure (CVP), non-invasive blood • Audible and visual
pressure and respiratory rate should be undertaken as equipment alarms
indicated by the patient’s condition.147
Adapted from College of Intensive Care Medicine Australia
A complete record should be kept of all details of the
and New Zealand (CICM). Guidelines for transport of critically
patient’s condition, personnel involved, clinical events, ill patients, <http://www.cicm.org.au>; 2013 [accessed 06.14],
observations and therapy given during transport.The trans- with permission.
porting team should hand over directly to the receiving
team providing continuing care for the patient151,154 or
should remain during the intervention/procedure to
manage the patient’s care.
156 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Summary
In the management of critically ill patients there is always an initial focus on assessing and treating the patient’s most
life-threatening and immediate problems. Early attention should then be given to the implementation of preventative
therapies such as VTE prophylaxis and pressure injury prevention, along with a thorough assessment of physical care
needs and a subsequent plan of management. Recovery for patients to normal functioning after a critical illness is
dependent upon a multitude of factors and is a dynamic process over time; however, much of the essential nursing care
given to critically ill patients assists in both reducing deficits associated with their episode of illness and reducing the time
taken to achieve normal functioning.
Good personal hygiene is at the heart of essential nursing care, and many other aspects of essential care (e.g. eye care
and oral care) are closely related. Personal hygiene is often attended to when patients are repositioned, and whenever they
are moved the nurse has an opportunity to assess patients, particularly their dependent pressure areas. Bowel and urinary
catheter care are vital but often neglected areas of care. When patients are critically ill, the development of preventable
complications such as constipation and urinary tract infection may have significant consequences for them. All critically
ill patients are at risk of infection, and essential nursing care requires effective application of surveillance, prevention and
control measures that should be applied equally to all patients. This principle is embedded in the recommended use of
standard precautions.
Critically ill patients are often transferred to other departments for further investigation or specific interventions.
All transports pose a potential risk to patients, particularly if they are unstable. Essential nursing care of patients during
transfer is based on thorough assessment and preparation in an attempt to anticipate their every need so that adverse
events do not occur. This chapter has provided a comprehensive overview of the general but essential nursing care of
critically ill patients. It offers a guideline for nurses that is relevant for most patients, most of the time. As with all other
aspects of nursing practice, nursing care and intervention should be based on a thorough assessment of each individual
patient and tailored to their needs and preferences.

Case study
Mrs C is a 70-year-old female living in a supported residential care home. She presented to the emergency
department with abdominal pain, fevers and general malaise. Mrs C was febrile with mild tachycardia and
her blood pressure was slightly lower than her normal reading. Initial investigations revealed a urinary tract
infection and pyelonephritis. Her white cell count was 47 and IV antibiotics were initiated and she was
admitted to a medical ward. Mrs C has diabetes controlled with oral hypoglycaemics and hypertension
managed with medication.
Mrs C is a widow with one daughter who lives interstate. Mrs C moved to the residential home 5 years
ago because of her increasing inability to cope with daily living in her own home, exacerbated by long-
term depression and increasing obesity. Mrs C lives a relatively solitary life, having become increasingly
withdrawn from interactions with other residents, and has almost become bed bound due to limited mobility.
She presented to hospital with a stage 2 pressure injury on her sacrum and oedema of her lower limbs.
The day after being admitted to the medical ward, Mrs C was in increasing abdominal discomfort and
was found to have midline suprapubic abdominal wall distension. An ultrasound showed a suprapubic
abdominal wall collection. Reviewed by a surgeon, and on suspicion of necrotising fasciitis, it was
determined that debridement needed to be undertaken urgently. A CVC and arterial catheter had been
inserted in preparation for theatre to provide vascular access for an aramine infusion and to monitor
Mrs C’s decreasing blood pressure.
After a 7-hour operation involving plastic, urology and general surgeons performing a laparotomy, pelvic
exploration and extensive surgical debridement through to abdominal rectus, Mrs C was transferred to
the intensive care unit. Preparatory handover from the anaesthetic team prior to Mrs C’s transfer from the
operating theatre enabled her to be placed directly onto a suitable pressure relief mattress system bed in
the ICU. She arrived in the ICU intubated and ventilated, still under the effects of the anaesthetic and with a
noradrenaline infusion sustaining a mean arterial pressure of 70 mmHg. She had an indwelling catheter with
temperature sensor in situ displaying a temperature of 39°C but, despite intraoperative fluids of 7 units of
packed red cells and 2 units of fresh frozen plasma, had minimal urine output. Her limbs were oedematous
with knee-high leggings in situ for sequential compression therapy and a bolus of intravenous albumin was
administered. Mrs C’s abdominal wound extended down to the perineum and was packed but not closed.
 CHAPTER 6 ESSENTIAL NURSING CARE OF THE CRITICALLY ILL PATIENT 157

Over the following days Mrs C’s management was focused on the treatment of sepsis, management of an
extensive open wound and prevention of further infection and prevention of other complications related to
invasive devices, ventilation, reduced mobility and poor skin condition. Ideally, wound management would
have included the use of negative pressure wound management systems; however, the extent of Mrs C’s
wound and the inability to seal the wound negated this as an option. Use of prostan-soaked dressings with
4-hourly irrigation kept the wound clean and moist between returns to the operating theatre for debridement.
Because of the involvement of the perineum in the wound area, the wound was compartmentalised and
dressed in sections. Undertaking frequent wound care in a manner that was safe and effective for both
Mrs C and the nursing team meant good preparation of wound care supplies and planning of various
nursing roles for participation in the dressing and re-positioning of Mrs C a number of times during the
dressing procedure. As well as pain management, comfort and reassurance were provided for Mrs C
during this time-consuming and intrusive procedure. A faecal containment system was inserted to manage
faecal incontinence but, due to lack of rectal tone, leakage occurred and it was removed. As with any
transport of a critically ill patient outside the ICU, returns to theatre for wound debridement required
patient preparation, appropriate equipment and liaison with the theatre personnel for timing, so that other
activities related to Mrs C’s care could continue.
Positioning Mrs C for pressure injury prevention, wound care and comfort required good planning and
appropriate equipment and sufficient personnel.
After six daily returns to the operating theatre for wound debridement, Mrs C’s clinical condition
had improved sufficiently and she was extubated. And 3 days afterward, she was stable enough for
transfer to the surgical ward with ongoing infectious diseases review regarding the duration of antibiotic
therapy.

CASE STUDY QUESTIONS

1 What is necrotising fasciitis and what are the most common bacteria involved?
2 Outline the extrinsic and intrinsic factors of tissue tolerance that may have had significance for Mrs C
during her stay in ICU.

RESEARCH VIGNETTE

Duncan CN, Riley TV, Carson KC, Budgeon CA, Siffleet J. The effect of acidic cleanser versus
soap on the skin pH and micro-flora of adult patients: a non-randomised two group crossover
study in an intensive care unit. Int Crit Care Nurs 2013;29:291–296

Abstract
Objective: To test the effects of two different cleansing regimens on skin surface pH and micro-flora, in adult patients
in the intensive care unit (ICU).

Methods: Forty-three patients were recruited from a 23-bed tertiary medical/surgical ICU. The 19 patients in
group one were washed using soap for daily hygiene care over a 4-week period. In group two, 24 patients were
washed daily using an acidic liquid cleanser (pH 5.5) over a second 4-week period. Skin pH measurements
and bacterial swabs were sampled daily from each patient for a maximum of 10 days or until discharged from
the ICU.

Results: Skin surface pH measurements were lower in patients washed with a pH 5.5 cleanser than those washed
with soap. This was statistically significant for both the forearm (p = 0.0068) and leg (p = 0.0015). The bacterial count
was not statistically significantly different between the two groups. Both groups demonstrated that bacterial counts
were significantly affected by the length of stay in ICU (p = 0.0032).

Conclusions: This study demonstrated that the product used in routine skin care significantly affects the skin pH of
ICU patients, but not the bacterial colonisation. Bacterial colonisation of the skin increases with length of stay.
158 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Critique
This small study was a single site non-randomised and unblinded study. The study was labelled a prospective
descriptive crossover design. The design was used to prevent product substitution with the intervention (soap or a
pH 5.5 liquid cleanser). However, this study appears to be an A-B intervention design, where a group of participants
received treatment A over a 4-week period and the next group of participants received treatment B over a 4-week
period. In a crossover design participants serve as their own controls (i.e. they receive the intervention and crossover
to receive the placebo), but this did not occur in this study; therefore, the term ‘crossover’ appears misleading.
Comparing the same participants also provides less statistical variance in the results; however, this would be difficult
to manage in the critically ill patient population.

All patients admitted to the ICU during the study period (n = 344) were screened. Those with an anticipated length of
stay of greater than 48 hours were recruited. Patients were excluded if they had pre-existing skin conditions or known
allergies to the skin cleanser. Forty-three patients were recruited to the study over an 8-week period, with 19 patients
in group one and 24 patients in group two. It would have been helpful if participant progress through the phases of the
two groups (that is, enrolment, intervention allocation, follow-up and data analysis) was provided diagrammatically.
Transparent reporting of trials is an important issue. Given only 12.5% (43/344) of potential patients were enrolled in
the study it would have been interesting to note the reasons for exclusion.

A clear description of the study procedures was provided. Details about the study procedures, processes and
interventions allow others to replicate them in future research. However, the researchers did not mention collecting
data on intervention fidelity, or the extent to which the bed-bathing protocol was performed as was planned. Further,
it is not clear what ‘usual care’ for bed-bathing was at the study site.

The study results were presented clearly. Importantly, this study did not use methods of randomisation. Randomisation
is a method to try to ensure the groups are similar in all known and unknown characteristics, which is important in
that this will control for the effect of potential confounders. The researchers noted the characteristics between the two
groups were similar but these specific characteristics were not reported. Only the potential confounder of length of
stay was acknowledged and found to be associated with increased bacterial colonisation. In other words, the longer
the patient remained in ICU, the greater the chance of the skin becoming colonised with bacteria.

The researchers acknowledged and explained study findings, identifying the importance of the relationship between
skin pH and potential disruption of the skin integrity, the stratum corneum, through critical illness. Overall, the
researchers should be commended on undertaking this important small descriptive study. Finally, and very importantly,
other researchers interested in this work could use the results of this study to inform a larger three-arm randomised
controlled trial.

Lear ning a c t iv it ie s
1 List the benefits and risks of faecal containment devices.
2 Outline ICU patient preparation for transfer to the operating theatre.
3 What criteria do you use to evaluate the positioning in bed of your patients?
4 Name some of the significant infection risks for patients in ICU.

Online resources
Australian Department of Health, www.health.gov.au
Australian Wound Management Association, www.awma.com.au
Cochrane Collaboration, www.cochrane.org
College of Intensive Care Medicine of Australia and New Zealand (CICM), www.cicm.org.au
Communicable Diseases Network Australia (CDNA), www.health.gov.au/cdna
 CHAPTER 6 ESSENTIAL NURSING CARE OF THE CRITICALLY ILL PATIENT 159

European Pressure Ulcer Advisory Panel, www.epuap.org

Hand Hygiene Australia, www.hha.org.au
National Health and Medical Research Council, www.nhmrc.gov.au
National Institute of Clinical Studies (NICS), www.nhmrc.gov.au/nics/index.htm
Skin Tear Advisory Panel, www.skintears.org/pdf/Skin-Tear-Resource-Kit.pdf
Therapeutic Goods Australia, www.tga.gov.au/index.htm
US Centers for Disease Control and Prevention, www.cdc.gov
World Health Organization, www.who.int/en

Further reading
College of Intensive Care Medicine Australia and New Zealand (CICM). Guidelines for transport of critically ill patients,
<http://www.cicm.org.au>; 2013 [accessed 06.14].
Khoury J, Jones M, Grim A, Dunne WM Jr, Fraser V. Eradication of methicillin-resistant Staphylococcus aureus from a
neonatal intensive care unit by active surveillance and aggressive infection control measures. Infect Control Hosp Epidemiol
2005;26(7):616–21.
Wright MO, Hebden JN, Harris AD, Shanholtz CB, Standiford HC, Furuno JP et al. Concise communications: aggressive control
measures for resistant Acinetobacter baumannii and the impact on acquisition of methicillin-resistant Staphylococcus aureus
and vancomycin-resistant Enterococcus in a medical intensive care unit. Infect Control Hosp Epidemiol 2004;25(2):167–8.

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Chapter 7

Psychological care
Leanne Aitken, Rosalind Elliott

Learning objectives KEY WORDS

After reading this chapter, you should be able to: anxiety

• implement appropriate evidence-based strategies to reduce patient delirium
anxiety
pain assessment
• describe the different instruments available to assess sedation needs in and pain
critically ill patients and discuss the benefits and limitations of each management
• describe the subtypes of delirium sedation
• recognise risk factors for the development of delirium in the critically ill assessment and
management
• implement and evaluate delirium assessment screening instruments for
the critically ill sedation protocols

• implement appropriate evidence-based strategies to manage patients’ sleep promotion

sedative needs
• integrate best practice into pain assessment and management
• determine methods to promote rest and sleep for critically ill patients.

Introduction
Care of the psychological health and wellbeing of patients is essential in the
complex and multifactorial care of critically ill patients. Patients experience
ongoing compromise of their psychological health well beyond hospitalisation,
with this psychological compromise also affecting their physical health. Aspects
of psychological health most relevant in the care of the critically ill include
the recognition and management of anxiety, delirium, sedation needs, pain and
sleep and inclusion of the patient’s family in promoting psychological health.
Although each of these concepts is reviewed sequentially through this chapter,
in reality it is often difficult to separate the issues as their effects are often
additive or synergistic. While it is important to ensure that assessment incor-
porates each of the individual concepts, management may often target multiple
aspects concurrently.
 CHAPTER 7 PSYCHOLOGICAL CARE 165

Anxiety early in their stay and others reporting high anxiety later
in their ICU stay.5 The presence of anxiety appears to be
Anxiety can occur both during and following a period of an international issue, with the presence of anxiety in
critical illness. Anxiety has been defined as an unpleasant acute myocardial patients being reported as similar across
emotional state or condition.1 Within that broad definition multiple cultures.4
Spielberger recognises two related, but conceptually differ- There are both physiological and psychological
ent constructs, specifically state and trait anxiety. Trait responses to anxiety, associated with feelings of appre-
anxiety, a personality characteristic, refers to the relatively hension, uneasiness and dread from a perceived threat.
stable tendency of people to perceive stressful situations as These responses reflect a stress response and incorpo-
stressful or anxiety-provoking.1 In contrast, and of more rate avoidance behaviour, increased vigilance and arousal,
immediate concern during the care of critically ill patients, activation of the sympathetic nervous system and release
is state anxiety, an emotional state that exists at a given of cortisol from the adrenal glands.7 The humoral response,
moment in time and is characterised by ‘subjective feel- mediated by the hypothalamic–pituitary–adrenal (HPA)
ings of tension, apprehension, nervousness, and worry’.1 axis, regulates this activity. Physiological changes occur to
In addition, activation of the autonomic nervous system is multiple body systems, with the most relevant including
present during state anxiety. inhibition of salivation and tearing, constriction of blood
Factors that have been identified as precipitating vessels, increased heart rate, relaxation of airways, increased
anxiety include:2,3 secretion of epinephrine and norepinephrine as well as
increased glucose production,7 all of which contribute to
• concern about current illness as well as any the range of clinical indicators outlined in Table 7.1.These
underlying chronic disease
physiological manifestations illustrate the importance of
• current experiences and feelings such as pain, early identification, active reduction and minimisation
sleeplessness, thirst, discomfort, immobility of anxiety in critically ill patients.
• current care interventions including mechanical Clinical indicators of anxiety are broad and relate to
ventilation, indwelling tubes and catheters, four major categories including physiological, behavioural,
repositioning and suctioning psychological/cognitive and social (Table 7.1).8–10 Appro-
• medication side effects priate recognition of anxiety is important as there is
beginning evidence that the physiological effects of
• environmental considerations such as noise and light anxiety can have important effects on outcomes for critical
• concern about the ongoing impact of illness on care patients. Many of the clinical signs listed in Table 7.1,
recovery. for example increased blood pressure and respiratory rate,
Anxiety has been identified in approximately half are likely to lead to poorer outcomes for the critically ill
of critically ill patients, with the majority of patients patient. In addition, in acute myocardial infarction patients,
reporting moderate-to-severe anxiety in most cohorts.4–6 anxiety has been identified as a significant predictor of
Patients have reported varying patterns of anxiety over in-hospital complications such as recurrent ischaemia,
their ICU stay, with some patients reporting high anxiety infarction and significant arrhythmias.11,12

TABLE 7.1
Clinical indicators of anxiety

PSYCHOLOGICAL/
PHYSIOLOGICAL B E H AV I O U R A L COGNITIVE SOCIAL

• Heart rate • Restlessness • Confusion • Seeking reassurance

• Blood pressure • Agitation • Anger • Need for attention/
• Chest pain • Sleeplessness • Negative thinking companionship
• Respiratory rate • Hypervigilance • Verbalisation of anxiety • Limiting interaction
• Shortness of breath • Fighting ventilator • Crying
• Altered O2 saturation • Facial grimacing/tension • Inability to retain and
• Coughing/choking feeling • Uncooperative process information
• Diaphoresis • Rapid speech
• Pallor • Difficulty verbalising
• Cold and clammy • Distrustful/suspicious
• Dry mouth • Desire to leave stressful
• Pain area
• Headache
• Nausea and vomiting
• Swallowing difficulty
166 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Anxiety assessment FIGURE 7.1 Faces anxiety scale.

The importance of anxiety assessment, with the aim of
reducing or preventing the adverse effects it produces,
is supported by the literature. However, recognition and
interpretation of anxiety is complex, particularly when
signs and symptoms are masked by critical illness, the effects
of medications and/or mechanical ventilation. Further,
alterations in levels of biochemical markers such as cortisol
and catecholamines that are frequently associated with Adapted from McKinley S, Coote K, Stein-Parbury J.
Development and testing of a Faces Scale for the assessment
anxiety may also be attributed to physiological stress.13
of anxiety in critically ill patients. J Adv Nurs 2003;41(1):73–9,
Thus, anxiety rating scales are advocated and may offer with permission.
benefits not found with unstructured clinical assessment.
The relationship between a patient’s self-report of
anxiety and clinician assessment of anxiety has been incon- Anxiety Inventory) with 200 mechanically ventilated
sistent.When chart reviews were undertaken to determine patients.15 The VAS – anxiety comprises a 100-millimetre
the relationship between clinicians’ routinely documented vertical line, with the bottom marker labelled ‘not anxious
anxiety and patient self-report of anxiety, no relationship at all’ and the top marker labelled ‘the most anxious I have
was found.14 In contrast, when clinicians were prompted ever been’. Patients were able to successfully mark, or
to assess anxiety in intensive care patients their rating of indicate, their present level of anxiety.
the severity of anxiety did have moderate correlation with The Faces Anxiety Scale, another single-item scale that
patients’ self-report of anxiety.6 has been developed by a group of Australian researchers,
A number of self-reporting scales exist for measuring has five possible responses to assess anxiety (see Figure
anxiety (Table 7.2). These scales require cognitive inter- 7.1).16 Testing in critically ill patients indicates that the
pretation and an ability to communicate responses, which self-reporting single-item scale appears to accurately
presents challenges to many critically ill patients. In detect a patient’s anxiety.17,18
addition, some of these scales have up to 21 items, making
them both time-consuming and unmanageable for regular Anxiety management
use in the critical care setting. Patients with visual and Critical care nurses recognise that anxiety is detrimental
auditory impairments will require additional assistance, to patients and that anxiety management is important.26
such as larger print, hearing aids or glasses in order to Although pharmacological interventions such as anxiolytic
complete the forms. and pain-relieving medication are well-recognised and are
The visual analogue scale (VAS) – anxiety is fast and frequently used to reduce anxiety, non-pharmacological
simple to complete as it is a single-item measure. It has treatments are also useful, and can be divided into envi-
been evaluated against a recognised anxiety scale (the State ronmental and nurse-initiated interventions.

TABLE 7.2
Anxiety self-report scales

SCALE NUMBER OF ITEMS COMMENTS

Hospital Anxiety and Depression 14 (including Easy and fast to complete

Scale (HADS)19 7 anxiety items) Extensively used and therefore international comparisons are available
Demonstrated validity20
Depression Anxiety and Stress 21 (including Items measured on scale of 0 (did not apply to me at all) to 3 (applied
Scale 21 (DASS 21)21,22 7 anxiety items) to me very much or most of the time)
Demonstrated validity in clinical populations17
Spielberger State Anxiety 20 items Items measured on a scale of 1 (not at all) to 4 (very much so)
Inventory (SAI)1 Validity demonstrated in various populations1
Too long for routine clinical use, but may be useful in associated research;
attempts to shorten the SAI have provided inconsistent results24,25
Visual Analogue Scale – Anxiety 1 item 10 cm/100 mm line from ‘not at all anxious’ to ‘very anxious’
(VAS–A) Demonstrated validity23
Faces Anxiety Scale16 1 item 5 possible responses or ‘faces’ to reflect anxiety
Fast and easy to use
Validity has been demonstrated in a small number of ICU cohorts17,18
 CHAPTER 7 PSYCHOLOGICAL CARE 167

Non-pharmacological treatments Pharmacological treatment for anxiety

An advantage of the non-pharmacological treatments is Treatment for pain and other reversible physiologi-
that they can be nurse-initiated or implemented when cal causes of anxiety and agitation should be a priority.
units are designed or refurbished (see Table 7.3). Although Should anxiety and agitation continue, despite the
the benefits of some non-pharmacological treatments may incorporation of non-pharmacological interventions,
be widely accepted in the community, incorporation of pharmacological treatment with relevant agents may be
complementary therapies into critical care is dependent on initiated. A brief overview of these medications in the
their acceptance within the clinical context and appropriate treatment of unrelieved anxiety is provided in Table 7.4.
patient consent. Beneficial effects that have been reported In general, non-benzodiazepine sedative medications such
include lowered blood pressure, heart rate and respira- as propofol are recommended over benzodiazepines.35
tory rate; improved sleep; and reduced stress, anxiety and
pain,27 although the benefits of some therapies have only Delirium
been demonstrated in hospitalised, rather than critical care,
patients. As with any therapy, each non-pharmacological Delirium is a significant concern for critically ill patients
treatment may have different effects on individual patients; and the clinicians who care for them. It is a category of
consequently, ongoing assessment is essential. In addition, central nervous dysfunction where behaviours and phys-
the safety of these therapies within the critical care environ- iological responses are not conducive to healing and
ment has not been well demonstrated, necessitating a high recovery. Early detection and treatment of delirium is vital,
level of monitoring throughout administration. as it is associated with adverse clinical outcomes such as
prolonged duration of ventilation and length of ICU and
Practice tip hospital stay and higher rates of morbidity and mortality.37–40
Furthermore, increased duration of delirium has been
Ask your patient or their family if they like music to help associated with long-term cognitive impairment41,42
relax. Have the family bring in a music player with some and an increase in delusional memories.43 Arguably, the
favourite music and headphones. Prepare the patient condition has been under-recognised and under-treated44
for a rest period. Ensure that pain relief is sufficient, and has only recently received the attention it deserves.
all interventions are complete, and the patient is Under-recognition is probably related to a number of
comfortable. Assess the anxiety or level of sedation factors including the high incidence of the hypoactive
beforehand and then commence at least 30 minutes of subtype as well as lack of use of formal screening instru-
uninterrupted music. Reassess after the session, and ments – without which there exists a high degree of
record and report results. subjectivity when assessing delirium.
There are three subtypes of delirium: hypoactive,
hyperactive and combined (a combination of both).45,46
Practice tip
Disturbances in attention (e.g. reduced ability to direct,
Prioritise the assessment and treatment of discomfort, focus, sustain and shift attention) and awareness (e.g. reduced
pain and anxiety. This will greatly reduce sedative orientation to the environment) that develop over a short
medication requirements. period of time (e.g. hours to a few days) are characteristic
of all subtypes of delirium.47 This is in contrast to dementia
Other strategies to reduce anxiety include inter- in which cognitive decline occurs over months and years.
personal interventions such as communication and Cognitive and perceptive ability often fluctuates through the
information sharing by the healthcare team and inclusion day worsening at night. A change in an additional cognitive
of family members in care processes. The presence of a domain such as memory deficit, disorientation or language
family member can provide additional reassurance and can disturbance that is not better accounted for by a pre-
facilitate communication between the health team and existing, established or evolving other neurocognitive
patients (see Chapter 8 for additional information). disorder and does not occur in the context of a severely
reduced level of arousal such as coma is diagnostic of
delirium. There should also be evidence from the patient’s
TABLE 7.3 history, physical examination or laboratory findings that the
Non-pharmacological measures to reduce anxiety disturbance is a direct physiological consequence of another
medical condition or substance intoxication or withdrawal.47
N U R S E - I N I T I AT E D
Lethargy, slow quiet speech and reduced alertness are
T R E AT M E N T S E N V I R O N M E N TA L FA C T O R S
typical behaviours of hypoactive delirium.46 It is hypo-
Patient massage28,29 Provision of natural light30 thesised that clinicians may not recognise the ‘quietly’
Aromatherapy31,32 Calming wall colours such as blue, confused patient so the condition may be untreated or
green and violet misdiagnosed as depression.46 Behaviours evident in hyper-
Music therapy27,33 Noise reduction with consideration of active delirium such as hyperactivity and agitation cannot
alarms, paging systems, talking etc34 go unnoticed by clinicians and present overt risks of self
harm such as unintentional extubation/decannulation and
168 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 7.4
Anxiety drug therapy35,36

DRUG GROUP DRUG/DOSE RANGE ACTION SIDE EFFECTS COMMENT

Sedative hypnotic Propofol General • Hypotension • Dedicated intravenous line
agent 10–100 mcg/kg/min anaesthetic agent • Respiratory depression • Infusions recommended
(infusion) • Myocardial depression • High metabolic clearance
when given as bolus • Patients wake quickly once
• Reported to affect memory drug is ceased
• May cause dreams • Expensive
Non-benzodiazepine Dexmedetomidine Highly selective • Initial hypertension may be • Minimal respiratory
sedative 0.2–0.7 mcg/kg/h alpha-2- experienced depression
(infusion)36 adrenoceptor • Hypotension • No amnesic effect
agonist • Bradycardia may persist • Rapid onset
• Hyperglycaemia • Infusions preferred
• Role as first line agent not
yet demonstrated
Benzodiazepine Diazepam Block encoding • Long-acting metabolites • No analgesia properties
sedative 5–10 mg bolus on GABA • Hypotension
receptors • Respiratory depression
Midazolam • Less likely to have above • Useful as continuous
0.5–10 mg/h (infusion) side effects, but they may infusion
1–2 mg (bolus) still occur • Rapid onset
• No analgesia properties
• Amnesic effect
Lorazepam • Less likely to have above • Not licensed for use in
0.01–0.1 mg/kg/h side effects, but they may some countries
(≤10 mg/h) still occur • Strong anxiolytic

intravenous/arterial device removal. Combined delirium understood; however, imbalances in brain cholinergic
is characterised by fluctuations in activity and attention and dopaminergic neurotransmitter systems are thought
levels including the behaviours of both hyperactive and to be responsible.46 Many predisposing and precipitating
hypoactive subtypes. risk factors have been identified (Table 7.5) and current
Reports in the healthcare literature about the opinion suggests that there is an additive effect: patients
prevalence of delirium in ICU vary widely from 10% to with more than one predisposing factor will require less
80%,48–51 an unsurprising finding given that it is notori- noxious precipitating factors to develop delirium than
ously difficult to diagnose in patients who are unable to patients who have none. Predisposing risk factors are
communicate verbally. The prevalence in other critical those that exist prior to the occurrence of critical illness,
care areas such as emergency departments is generally while precipitating risk factors occur during the course
documented to be lower, likely because of the varying of critical illness and may be disease-related or iatrogenic.
illness severity of patients.39,52 Prevention and therapeutic management of risk factors is
The exact pathophysiology of delirium is not yet fully the mainstay of treatment for delirium.

TABLE 7.5
Risk factors for delirium

P R E D I S P O S I N G R I S K FA C T O R S 3 8 , 5 1 , 5 3 , 5 4 P R E C I P I TAT I N G R I S K FA C T O R S 51,53,55–58

• Advanced age Increased severity of illness

• Dementia Metabolic, fluid and electrolyte disturbance
• Illicit substance use Infection
• Excessive intake of alcohol Hypoxia
• Smoking Acute injury affecting the CNS
• Sensory deficits Medications that affect acetylcholine transmission, e.g. atropine, fentanyl
• Renal insufficiency Psychoactive medications, e.g. benzodiazepines, opioids
• Previous cerebral damage Prolonged pain
• Hypertension Excessive noise
• Congestive heart failure Sleep deprivation
• History of depression Immobility
• Genetic propensity
 CHAPTER 7 PSYCHOLOGICAL CARE 169

in routine care. Delirium is diagnosed when both the

Practice tip
features of acute onset of mental status changes or
Interview the patient or their family to identify pre- fluctuating course and inattention are present, together
disposing risk factors for delirium. Document your with either disorganised thinking or altered level of
findings and incorporate these into the plan of care. consciousness. A practical delirium assessment screening
instrument for the critically ill cannot be reliant on
patient–assessor verbal communication. Both the
Assessment of delirium Intensive Care Delirium Screening Checklist (ICDSC)59
The higher morbidity and mortality associated with (Figure 7.2) and the Confusion Assessment Method for
delirium and the relative ease of assessing its occurrence the Intensive Care Unit (CAM–ICU)60 (Figure 7.3) have
make it imperative to incorporate relevant assessment been shown to fulfil these requirements, although clinical

FIGURE 7.2 Intensive care delirium screening checklist (ICDSC).

7(;0,5;,=(3<(;065 +(@ +(@ +(@ +(@ +(@

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Adapted from Bergeron N, Dubois MJ, Dumont M, Dial S, Skrobik Y. Intensive Care Delirium Screening Checklist: evaluation of a new
screening tool. Intensive Care Med 2001;27(5):859–64, with permission.
170 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

FIGURE 7.3 Confusion Assessment Method – Intensive Care Unit (CAM-ICU).

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Adapted from Ely EW, Margolin R, Francis J, May L, Truman B, Dittus R et al. Evaluation of delirium in critically ill patients: validation of
the Confusion Assessment Method for the Intensive Care Unit (CAM-ICU). Crit Care Med 2001;29:1370–9, with permission.

judgement should also be retained in the diagnostic a five point scale (A–E). Only patients who are adequately
process.61,62 conscious, that is, responsive to moderate physical stimuli
The ICDSC contains eight items based on the (C–E on the scale), are able to be assessed. The eight items
Diagnostic and Statistical Manual of Mental Disorders of the ICDSC are rated present (1) or absent (0). A score of
(DSM-IV) criteria for delirium and was validated in a four or higher is considered to be indicative of delirium.59
study conducted within ICU.59 It is also simple to use and The CAM–ICU has also been shown to be valid for
easily integrated into existing patient documentation. All diagnosing delirium in the ICU population (see Further
features of delirium are incorporated such as sleep pattern reading for more information).60 Acute onset of mental
disturbances and hypo- or hyperactivity. The first step in status changes or fluctuating course is assessed using
using the ICDSC is an assessment of conscious level using neurological observations conducted over the previous
 CHAPTER 7 PSYCHOLOGICAL CARE 171

24 hours. Inattention is tested in patients who are unable to side effects (e.g. Q-T interval prolongation); therefore
communicate verbally by using either picture recognition any psychoactive medication should be used judiciously
or a random letter test. Disorganised thinking is assessed in the critically ill.
by listening to the patient’s speech and, for patients who
are unable to verbally communicate, a simple instruction Sedation
is administered such as asking the patient to hold up some Maintaining adequate levels of sedation is a core
fingers. Any conscious level other than ‘alert’ is considered component of care in critical care environments, where
‘altered’. Scores are not derived from the CAM–ICU; patients are treated with invasive and difficult-to-
delirium is either present or absent.60 tolerate procedures and treatments. A primary aim
of nursing critically ill patients is to provide comfort,
Prevention and treatment of delirium and adequate sedation is fundamental to this. Individ-
As previously stated, prevention and management of risk ualising sedation management is crucial to the effective
factors is the mainstay of delirium treatment; therefore management of each patient, with accurate assessment
patients’ risk factors should be identified and where a core nursing skill. An appropriate level of sedation
possible modified (even in the absence of delirium). is essential for all patients – this may be no sedation
Potential preventative measures include: for some patients while other patients may require a
• adequate pain relief significant level. The provision of adequate sedation is
paramount for those patients receiving muscle relaxants.
• reassurance to reduce anxiety In association with sedation management, it is essential
• judicious use of sedative medications, particularly that adequate pain relief and anxiolysis are provided to
benzodiazepine medications all critically ill patients.
• correction of the physiological effects of critical There has been growing evidence of the detrimental
illness (for example hypoxia, hypotension and fluid effects of sedation on outcomes in critically ill patients.
and electrolyte imbalance) A light, rather than deep, level of sedation in critically ill
• optimisation of the sleep cycle patients is associated with shorter duration of mechanical
ventilation and shorter length of ICU stay.35 There is also
• early mobilisation beginning, although sometimes conflicting, evidence to
• treatment of the underlying illness. suggest that lighter levels of sedation are beneficial for
Research into preventative interventions that target improved psychological recovery.35 Strategies to achieve
delirium on its own has not been conducted in ICU; light sedation are now the mainstay of sedation assessment
however, trials conducted in acute care with the elderly and management for critically ill patients.
show that many risk factors are potentially modifiable. In
one trial a multifaceted intervention that included reori- Assessment of sedation
entation strategies, a non-pharmacological sleep regimen, Assessment of the effect of all sedative treatments is
frequent mobilisation, provision of hearing devices and essential. When pharmacological agents are used there is
glasses and early treatment of dehydration led to a signifi- always a risk of over- or under-sedation, and both can have
cant reduction in the incidence of delirium.63 There is also significant negative effects on patients.65 Over-sedation
beginning evidence that bundles of interventions directed may lead to detrimental physiological effects including
towards prevention of delirium among other aspects of cardiac, renal and respiratory depression and can result
care in ICU patients can be beneficial,34,64 although both in longer duration of mechanical ventilation, associated
of these studies were before and after cohort studies complications and recovery. Under-sedation has the
that do not represent high level evidence. Despite these opposite effect on the cardiac system, with hyperten-
methodological concerns, the creation of environmental sion, tachycardia, arrhythmias, ventilator dyssynchrony,
conditions that are conducive to rest and sleep, in particular agitation and distress, with the potential for incidents
noise reduction and adjusting light levels appropriate for concerning patient safety. There is beginning evidence
the time of day, as well as sedation minimisation, delirium to suggest that heavy sedation is associated with psycho-
monitoring and early mobilisation, have not been shown logical recovery, particularly in relation to delusional
to cause harm and therefore represent good practice for memories.66,67
any critically ill patients. Objective sedation scales provide an effective method
In cases where non-pharmacological strategies have of assessing and monitoring a patient’s level of conscious-
not succeeded atypical antipsychotic medications (e.g. ness or arousal, as well as evaluating parameters such as
olanzapine) may reduce the duration of delirium in adult cognition, agitation and patient–ventilator synchrony
ICU patients.35 Although frequently used, it should be (Figures 7.4 and 7.5). A number of different sedation scales
noted that there is no evidence indicating the benefit have been developed for use in the intensive care environ-
of haloperidol in reducing the duration of delirium in ment (Table 7.6), with variable strengths and weaknesses
adult ICU patients.35 It should also be noted that any of each.68 Essential requirements of an effective sedation
medication designed to enhance cognition has the scale include that it measures what is intended, is reliable
potential to make it worse and there are many unwanted and is easy to use.69
172 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 7.6
Sedation scales

SCALE DESCRIPTION COMMENT

Ramsay sedation scale73 • Scores from 1 (agitated/restless) to 6 • Easy to administer

(no response) • No differentiation between different levels of
• 4 levels of sedation, 1 level of ‘cooperative, anxiety, restlessness and agitation
oriented and tranquil’ and 1 level of ‘anxious, • Unable to distinguish between a light plane of
agitated or restless’ unconsciousness and a deep coma
• Lack of clarity between each score
• Limited testing of psychometric properties
Richmond Agitation– • Scores from −5 (unarousable) to +4 (combative) • Assesses patient’s responses in relation
Sedation Scale (RASS)74 • 4 levels of agitation, 1 level for ‘calm and alert’, to the type of stimulus given (i.e. verbal or
5 levels of sedation physical), plus consideration of cognition and
sustainability
• Thorough testing of psychometric properties
with positive results including good inter-rater
reliability
Sedation–Agitation Scale • Scored from 1 (unarousable) to 7 (dangerous • Multiple criteria for each level which,
(SAS)75 agitation) although increase complexity, result in better
• 3 levels of agitation, 1 level of ‘calm and discrimination between scores
cooperative’, 3 levels of sedation • Thorough testing of psychometric properties
with positive results including good inter-rater
reliability
Motor Activity • Scored from 0 (unresponsive) to 6 (dangerously • Very similar to SAS
Assessment Scale agitated) • Multiple criteria for each level which,
(MAAS)76 • 3 levels of agitation, 1 level of ‘calm and although increase complexity, result in better
cooperative’, 3 levels of sedation discrimination between scores
• Limited psychometric testing
Vancouver Interactive • Two domains (interaction and calmness) each • Thorough assessment of calmness (in contrast
and Calmness Scale containing 5 questions to agitation) with multiple levels of scoring
(VICS)77 • Each question is scored on a 6-point scale available
from ‘strongly agree’ to ‘strongly disagree’, • Differentiation between each of the points on
resulting in a potential total score of 30 for the 6-point scale difficult
each domain • Moderate psychometric testing completed,
with positive results
Adaptation to the • Designed to measure the level of adaptation • Different scales for assessment of each item
Intensive Care of mechanically ventilated patients to the ICU • Moderate psychometric testing completed,
Environment (ATICE)72 environment with positive results
• Two domains – consciousness (awakeness
and comprehension items) and tolerances
(calmness, ventilator synchrony and face
relaxation items)
Minnesota Sedation • Two domains – motor activity (assessed on • Good descriptive differentiation of points on
Assessment Tool 4-point scale) and arousal (assessed on scales
(MSAT)78 6-point scale) • Moderate psychometric testing completed,
• Assessed over previous 10 min with positive results

Bispectral index monitoring is an assessment tool that Sedation protocols

provides an objective measure of sedation. It uses a self-
adhesive pad secured to the patient’s forehead to continu- The sedation needs of patients are complex, with various
ously record cortical activity that is scored on a scale from reports of patients receiving sub-optimal care and incon-
0 (absence of brain activity) to 100 (completely awake). sistent practice in this area.79,80 One of the responses to
There is not yet consensus on the most appropriate level this gap in nursing practice has been the development of
of activity for intensive care patients or what role bispectral protocols.
index might offer in their care.70,71 Continued studies to Sedation protocols offer a framework, or algorithm,
evaluate the efficacy of bispectral index are required. within which health professionals can manage specific
 CHAPTER 7 PSYCHOLOGICAL CARE 173

FIGURE 7.4 Richmond Agitation–Sedation Scale (RASS).

9PJOTVUK(NP[H[PVU:LKH[PVU:JHSL9(::
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M7H[PLU[OHZUVYLZWVUZL[VHU`Z[PT\SH[PVU ZJVYL−

Adapted from Sessler CN, Gosnell M, Grap MJ, et al. The Richmond Agitation–Sedation Scale: validity and reliability in adult intensive
care patients. Am J Respir Crit Care Med 2002;166:1338–44, with permission.

FIGURE 7.5 Sedation–Agitation Scale (SAS).

9PRLY:LKH[PVU(NP[H[PVU:JHSL:(:
:JVYL ;LYT +LZJYPW[PVU
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 ZOHRPUN[VHX\LZ[PVUVYMVSSV^ZJVTTHUKZ[OH[»ZH:(:ZHTLHZJHSTHUKHWWYVWYPH[L¶
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3P[[SLVYUVYLZWVUZL[VUV_PV\ZWO`ZPJHSZ[PT\SPYLWYLZLU[ZH:(:

Adapted from Riker RR, Picard JT, Fraser GL. Prospective evaluation of the Sedation–Agitation Scale for adult critically ill patients.
Crit Care Med 1999;27(7):1325–9, with permission.
174 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

patient care with prearranged outcomes. Protocol- agents and greater nurse workload was required for patients
directed sedation is ordered by a doctor or advanced in this group.85 Given this evidence, daily interruption of
practice nurse with prescribing rights, contains guidance sedation cannot be recommended. Instead, the mainstay
regarding sedation management and is usually imple- of achieving good practice in this area is setting and main-
mented by nurses although it may have input from taining appropriate targets for sedation levels based on the
pharmacists or other members of the healthcare team. individual needs of the patient.
Aspects of sedation management that are incorporated
into sedation protocols include: Pain
• the sedation scale to be used, as well as frequency of Pain is an unobservable, inherently subjective, experience.
assessment
The nebulous multifaceted nature of pain has led to
• an algorithm-based process for selecting the most significant difficulties in not only understanding the
appropriate sedative agent mechanisms underlying the experience for individuals but
• the range of sedative agents that might be considered also assessing and managing the phenomenon.
and associated administration guidelines Pain is almost certainly a sensation widely experi-
• when to commence, increase, decrease or cease use of enced by critical care patients as it is one of the stressors
sedative agents most commonly reported by former and current ICU
patients.86,87 In particular, procedures such as chest drain
• when to seek review by a medical officer. removal and the insertion of arterial catheters are reported
Many sedation protocols will also incorporate an to be painful (median 5/10 and 4/10 respectively).88
analgesia component. Arguably, pain management is not always afforded the
The aim of sedation protocols is to improve sedation same emphasis as more ‘life-threatening’ conditions such
management by encouraging regular discussion of sedation as haemodynamic instability in critical care. However, its
goals among the healthcare team, while enabling nurses to alleviation is an essential element of critical care nursing.
manage the ongoing sedative needs of the patient. Not all Myths such as the possibility that patients may become
patients’ sedative needs will be met within the sedation addicted to analgesics and that the very young and elderly
protocol; in these instances specific care should be planned have higher tolerance for pain, and our cultural tendency
and implemented by the multidisciplinary healthcare team. to reward high pain tolerance may lead to inadequate
Although sedation protocols have widespread support, pain management. In critical care, nurses assume a fairly
there is mixed evidence regarding the benefits of imple- autonomous role in titrating pain-relieving medication.
mentation of such protocols. A number of studies have With this increased autonomy comes a responsibility to be
demonstrated the benefits associated with nurse-led knowledgeable and aware of effective pain management
sedation protocols, yet other studies do not demonstrate and assessment of the ‘fifth vital sign’.
a benefit.81 Until further research is undertaken, sedation
protocols should be considered on a local basis where Pathophysiology of pain
current practice conditions indicate potential benefit Pain is defined as ‘an unpleasant sensory and emotional
from standardisation of care. Appropriate evaluation of the experience associated with actual or potential tissue
impact of protocol implementation should be undertaken. damage’.89,p.250 Although unpleasant it has a role in
protecting against further injury.90 There are three
Daily interruption of sedation categories of pain receptors or nociceptors: mechanical
A specific form of sedation protocol is the daily inter- nociceptors, which respond to damage such as cutting and
ruption of sedation. This intervention has been used in crushing; thermal nociceptors, which respond to tempera-
practice in some settings for more than 10 years based on ture; and polymodal nociceptors, which respond to all
the original study by Kress and colleagues of 128 patients types of stimuli including chemicals released from injured
in a single centre in the USA.82 In this study improved tissue. Prostaglandins released from fatty acids in response
patient outcomes were seen in the form of reduced to tissue damage reduce the threshold for activation of the
duration of mechanical ventilation and ICU length of stay. nociceptors.90
In a sub-study of 18 patients from this cohort and a further Pain is transmitted to the central nervous system
14 patients from a similar time period no adverse psycho- via one of two pathways. The fast pain pathway occurs
logical outcomes were noted.83 These initial benefits have when the stimuli are carried by small myelinated A-delta
not been demonstrated in subsequent work. In both a fibres, producing a sharp, prickling sensation that is easily
meta-analysis of data from studies including 699 patients localised. The slow pathway acts in response to polymodal
and a multicentre study of 423 patients in 16 centres across nociceptors, is carried by small unmyelinated C fibres and
Canada and the USA, no improvement in duration of produces a dull, aching or burning sensation. It is difficult
mechanical ventilation, ICU or hospital length of stay or to locate, acts after fast pain, and is considered to be more
rates of delirium was seen.84,85 Further, in the multicentre unpleasant than fast pain.90
study patients who received daily interruption of sedation Perceptions of pain are thought to occur in the
required higher daily doses of some sedative and analgesic thalamus, whereas behavioural and emotional responses
 CHAPTER 7 PSYCHOLOGICAL CARE 175

occur in the hypothalamus and limbic system.90 Percep- If at all possible, a history of the patient’s health status,
tions of pain are influenced by prior experience, and by including any existing painful conditions, should be
cultural and normative practices, which helps to explain taken. A family member or close friend may be willing
individual reactions to pain.90 to assist if the patient is unable to provide one. Quite apart
There are negative physiological effects of pain that from the presenting condition, which may be painful,
include a sympathetic response with increased cardiac many critical care patients have significant comorbid-
work, thus potentially compromising cardiac stability.91 ities such as rheumatoid/osteoarthritis and chronic
Respiratory function may be impaired in the critically ill back pain. It is imperative that the patient’s usual pain
undergoing surgical procedures when deep-breathing and management strategies are identified and implemented
coughing is limited by increased pain, thus reducing airway if possible. For example, factors that relieve the pain or
movement and increasing the retention of secretions and increase its intensity should be recorded, along with its
possibility of nosocomial pneumonia. Other known effects relationship to daily activities such as sleep, appetite and
of unrelieved pain are nausea and vomiting. physical ability.
Adverse psychological sequelae of poorly-treated Regardless of the patient’s communication capability,
pain include diminished feelings of control and self- strategies to ensure consistent objective assessment and
efficacy and increased fear and anxiety. Inattention with an management should be implemented. Laminated cards
inability to engage in rehabilitation and health-promoting displaying body diagrams, words to describe pain and
activities is not uncommon. Pain is commonly cited by pain intensity measures (including visual analogues and
patients as a significant negative memory of their ICU numerical scales) are useful instruments in meeting these
experience.86,87,92,93 The long-term effects of pain are not requirements. Verbal numerical scales and visual analogue
clearly understood but they almost certainly impact on scales (VAS) are commonly used. These are outlined in
recovery and may even lead to worsening chronic pain.94 Table 7.7. VAS can be difficult to administer to critically
When these unwanted outcomes are considered alongside ill patients; however, a combined VAS and numerical scale
the physiological effects of poorly treated pain, the vital includes the benefit of a visual cue with the ability to
importance of pain management is evident. quantify pain intensity.
Other physiological and behavioural pain indicators
Pain assessment may be used to assess pain in less responsive or uncon-
‘Pain is whatever the experiencing person says it is, existing scious patients.97 Research indicates that consistent
whenever he says it does.’95,p.26 The nebulous quality and assessment of a number of indicators together provides
subjective nature of the pain experience lead to consid- an adequate substitute for self-assessments.97,98 Several
erable problems in assessing it. Compounding this is the instruments have been developed and validated for use in
challenge of assessment in the critically ill who often have the critically ill adult patient including the Behavioural
insufficient cognitive acumen to articulate their needs Pain Scale (BPS) (Figure 7.6),99 Checklist of Nonverbal
and an inability to communicate verbally. A common Pain Indicators (CNPI)100 and the Critical Care Pain
language and process in which to assess pain is essential Observation Tool (CPOT)101 (Figure 7.7). Briefly,
in ameliorating some of these challenges. Furthermore, scores are assigned to categories such as altered body
accurate assessment and consistent recording are funda- movements, restlessness and synchronisation with the
mental aspects of pain management. Without these vital ventilator, providing a global score for comparison after
components, it is impossible to evaluate interventions pain relief interventions. The BPS and the CPOT are
designed to reduce pain.96 Despite the importance of considered to be the most valid and reliable behavioural
assessing pain there is evidence to suggest that formal pain assessment instruments,102 and the BPS is one of the
assessment (or at least documentation of that assessment) most widely used scales for patients unable to communi-
only occurs about 50% of the time.50 cate verbally.99,103,104
Since the pain experience is subjective, all attempts Nurses are urged not to solely rely on changes
should be made to facilitate communication by the in physiological parameters, including cardiovascular
patient of the nature, intensity, body part affected and (elevated blood pressure and heart rate) and respiratory
characteristics of their pain. For example, the patient’s recordings, as other pathophysiological or treatment-
usual communication aids such as glasses and hearing related factors may be responsible.97 Classic reactions to
aid should be used. Whenever patients cannot verbally stressors (e.g. pain), such as increased heart rate and blood
communicate other strategies must be established and used pressure, do not always occur in critically ill patients and
consistently. For example, strategies involving nodding, are therefore unreliable methods of assessing pain in this
hand movements, facial expressions, eye blinks, mouthing patient group.105 A potential explanation is that autonomic
answers and writing can be highly effective, not only for tone may be dysfunctional in a large proportion of ICU
the self-assessment of pain but also to express other feelings patients.106 In haemodynamically-stable long-term critical
and concerns. In extremely challenging cases when there patients, vital signs may be useful if used in conjunction
is very limited motor function but the patient is cogni- with other forms of assessment.97
tively able, the speech pathologist may be able to advise on In addition, it is particularly important to regularly
alternative communication strategies. consider and search for potential sources of pain in
176 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 7.7
Pain scales

SCALE DESCRIPTION COMMENTS

Verbal numeric scale • Self-rating scale • Patient has to be able to communicate

• Single-item scale verbally
• Scale from 0 (no pain) to 10 (worst pain ever) • Needs to understand concept of rating pain
• Dependent on prior pain experiences
• Simple, easy to use
Visual Analogue Scale • Self-rating scale • Patient can communicate by pointing
(VAS) • Single-item • Needs to understand concept of rating pain
• A horizontal line with equal divisions is used • Dependent on patient’s prior pain experiences
for the patient to rate current pain level (no • Simple, easy to use
pain is on far left and worst pain is far right)
McGill short pain • Measures quality of pain • Gives more information about the patient’s
questionnaire167 • Uses 15 descriptor words to measure sensory pain107
effect of pain • Takes longer to administer
• Can be used in conjunction with a pain
intensity scale
Behavioural Pain Scale • Based on pain-related behaviours: the sum of • Patient does not have to communicate
(BPS) (Figure 7.6)99 three items • Simple, easy to use
• Higher scores indicate higher pain intensity • Includes ‘ventilator compliance’ (may no
(range: 3–12) longer be relevant for pain assessment when
using modern ventilators)
Checklist of Nonverbal • Developed for cognitively impaired adults • Patient does not have to communicate
Pain Indicators (CNPI)100 • Based on the presence/absence of 5 non- • Simple, easy to use
verbal pain behaviours (one is non-verbal • No patient report at all
vocalisation, e.g. groaning) and verbal • Not as reliable for immobile patients100
complaints
• Score 0 to 6 (score of 1 allocated for
the presence of a pain behaviour/verbal
complaint), higher scores indicate more pain
Critical Care Pain • Based on previously developed instruments • Patient does not have to communicate
Observation Tool (CPOT)101 using pain-related behaviour to assess pain, • Simple, easy to use
(Figure 7.7) e.g. BPS • Includes ‘ventilator compliance’ (may no
• 4 items: facial expression, body movements, longer be relevant for pain assessment when
muscle tension and compliance with ventilator using modern ventilators) or vocalisation in
or vocalisation extubated patients
• Higher scores indicate more pain (range: 0–8)

unresponsive patients and those who are unable to commu- favour the concurrent use of both sedative and analgesic
nicate. Nurses are implored to assume pain is present if forms of medication.96 This practice therefore makes it
there is a reason to suspect pain. If pain is suspected an difficult to assess the single effect of each medication on
analgesic trial may assist in diagnosing sources of pain. As a the patient’s pain, and highlights its multidimensional
general rule, analgesia medication should be administered properties. In addition to pharmacological treatment of
to patients who are heavily sedated or receiving muscle pain, non-pharmacological strategies can prove effective
relaxants as a precaution. as an adjunct to drug therapy or as an alternative.
Pain relief may be required for pre-existing injuries
Pain management or prior to specific procedures to prevent the occurrence
Although pain management is discussed here inde- of pain. Being turned is often cited as the most painful
pendently, in practice pain management is often procedure; however, wounds, drain removal, tracheal
combined with sedative administration to reduce anxiety. suction, femoral catheter removal, placement of a
However, pain management should always be the first central-line catheter and non-burn wound dressings and
goal for achieving overall patient comfort. Efforts to coughing may also cause considerable discomfort.91,107
improve patient comfort for intubated patients often Guidelines and written protocols for procedures such as
 CHAPTER 7 PSYCHOLOGICAL CARE 177

FIGURE 7.6 Behavioural Pain Scale.

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Adapted from Payen JF, Bru O, Bosson JL, Lagrasta A, Novel E, Deschaux I et al. Assessing pain in critically ill sedated patients by
using a behavioral pain scale. Crit Care Med 2001;29(12):2258–63, with permission.

FIGURE 7.7 Critical Care Pain Observation Tool.

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-HJPHSL_WYLZZPVU 5VT\ZJ\SHY[LUZPVUVIZLY]LK 9LSH_LKUL\[YHS 
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)VK`TV]LTLU[Z +VLZUV[TV]LH[HSSKVLZUV[ULJLZZHYPS`TLHUHIZLUJLVMWHPU (IZLUJLVMTV]LTLU[Z 

:SV^JH\[PV\ZTV]LTLU[Z[V\JOPUNVYY\IIPUN[OLWHPUZP[LZLLRPUN 7YV[LJ[PVU 
H[[LU[PVU[OYV\NOTV]LTLU[Z
7\SSPUN[\ILH[[LTW[PUN[VZP[\WTV]PUNSPTIZ[OYHZOPUNUV[MVSSV^PUN 9LZ[SLZZULZZ 
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,]HS\H[PVUI` 9LZPZ[HUJL[VWHZZP]LTV]LTLU[Z ;LUZLYPNPK 
WHZZP]LMSL_PVUHUK :[YVUNYLZPZ[HUJL[VWHZZP]LTV]LTLU[ZPUHIPSP[`[VJVTWSL[L[OLT =LY`[LUZLVYYPNPK 
L_[LUZPVUVM\WWLY
L_[YLTP[PLZ

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[OL]LU[PSH[VY TV]LTLU[ 
PU[\IH[LKWH[PLU[Z (SHYTZZ[VWZWVU[HULV\ZS` *V\NOPUNI\[[VSLYH[PUN 
(Z`UJOYVU`!ISVJRPUN]LU[PSH[PVUHSHYTZMYLX\LU[S`HJ[P]H[LK -PNO[PUN]LU[PSH[VY 
69
=VJHSPaH[PVU ;HSRPUNPUUVYTHS[VULVYUVZV\UK ;HSRPUNPUUVYTHS[VUL 
L_[\IH[LKWH[PLU[Z VYUVZV\UK 
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;V[HSYHUNL  ¶

Adapted from Gélinas C, Fillion L, Puntillo KA, Viens C, Fortier M. Validation of the critical-care pain observation tool in adult patients.
Am J Crit Care 2006;15(4):420–7, with permission.

femoral sheath removal and insertion of a central-line Pain-relieving medication can be given via a number
catheter can significantly reduce pain intensity as they of routes, including oral, enteral feeding tube, intravenous,
often contain reminders to provide analgesia.108 Some rectal, topical, subcutaneous, intramuscular, epidural and
procedures, such as insertion of a central-line catheter, intrathecal. For all routes of administration, assessment
require additional pain management and considerations of the patient’s suitability and contraindications for use
such as administration of local anaesthetic. This highlights are an essential part of the decision-making process.
the potential need for additional pain protocols linked to Patient-controlled analgesia for intravenous and, more
key standard procedures (e.g. patient turning) to reduce recently, epidural analgesia is commonly part of critical
patients’ pain experience. care nursing.
178 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Epidural pain management requires additional

evaluation, including sensory and functional assessment, TABLE 7.8
due to the use of local anaesthetic agents in addition Non-pharmacological treatment for pain
to opioid drugs. Sensory function should be regularly
COMFORT MEASURES DIVERSIONAL MEASURES
checked using a dermatome chart to gauge segments that
35
are blocked by the local anaesthetic agent. In addition to • Repositioning • Relaxation
sensory blockade, regular assessment for lower limb motor • Oral and endotracheal • Breathing exercises
deficit is required to detect changes in motor response, suctioning • Visual imagery
• Mouth, oral and/or wound • Music therapy168
which may impair the ability to mobilise safely. Sudden
care • Family presence109
or subtle changes may also indicate a complication such
• Reassurance and
as epidural haematoma. The Bromage Assessment Scale is information
often used for assessing motor response. Regular checks • Massage
of the catheter site are essential to identify complications
such as bleeding, haematoma and infection early but also
to ensure catheter patency. Intrathecal administration Pharmacological treatment for pain
of analgesic medications has similar contraindications Pharmacological treatment for pain in critically ill patients
and complications to epidural analgesia and requires centres on opioid medications, which act as opioid agonists
similar precautions. It is important to note that intra- binding to the μ-receptors in the brain, central nervous
thecal (as compared to intravenous) administration
system and other tissues.35 Opioid medications have a
does not eliminate all of the side effects of opioids
rapid action and are readily titrated, and their metabo-
(see Further reading).
lites, if present, are less likely to accumulate. Morphine
sulfate and fentanyl are routinely used in critical care, and
Practice tip
their properties, side effects and nursing implications are
Epidural administration of medication does not preclude outlined in Table 7.9. For ischaemic chest pain, nitrates
mobilisation. However, certain safety measures should will be used together with morphine sulfate as first-line
be taken. Ensure that the epidural catheter is well pain measures (see Chapter 10).
secured: view the site before mobilising and apply extra Other medications such as non-steroidal anti-inflam-
tape. Monitor blood pressure and heart rate before and matory drugs (NSAIDs) act by inhibition of an enzyme
during the initial stages of mobilising. Two healthcare within the inflammatory cascade, and may produce
personnel should assist during the first attempt to analgesia (especially when combined with opioids) for
mobilise. bone and soft tissue injuries. As with all medication, side
effects and contraindications for use can be serious and,
Non-pharmacological treatment for in the case of NSAIDs, include gastrointestinal bleeding,
renal insufficiency and exacerbation of asthma. Para-
pain
cetamol is another medication that may be highly effective
Non-pharmacological strategies to reduce pain are linked for mild pain and, when combined with opioid medica-
to some key strategies to reduce stress. Excessive pain may tions, provides analgesia for bone and soft tissue injuries.
lead to stress as the body attempts to maintain homeo- An alternative to opioid medication for procedural
stasis and stress can exacerbate pain. Strategies to reduce pain is ketamine.112,113 Single doses of the medication are
stress and pain include both comfort measures and diver- effective in achieving analgesia during severely painful
sional interventions, which require the critical care nurse
interventions such as deep wound care (for example, a burn
to individualise and adapt strategies to match the patient’s
injury). Ketamine is usually administered in conjunction
needs and preferences. Diversional methods may include
strategies to distract the patient, and aim to refocus the with midazolam to reduce any potential emergent effects.
patient’s thinking away from the pain and on to other Pain relief is a primary goal for critical care nursing
more pleasant thoughts or activities. Research has high- and requires regular assessment of pain intensity using
lighted the importance patients place on the presence reliable, objective, patient friendly instruments. No single
of family members in the facilitation of emotional and medication is ideal for all patients, and clinicians need
physical strategies of pain management.109,110 Some inter- to carefully select, monitor and titrate the doses of any
ventions that may be effective are listed in Table 7.8. agent selected. In the case of, for example, cardiac surgery
Non-pharmacological interventions have the benefit patients, patient-controlled analgesia may provide the
of being nurse-initiated, non-invasive and able to be most effective pain management strategy (see Chapter 12).
personalised for each patient. These strategies alone may Non-pharmacological strategies add to the relief of pain
not achieve a pain-free experience but they have the and come under the domain of nursing care. Without
capacity to enhance the effects of analgesic medication adequate pain management, patients will be unable to
and humanise the critically ill patient’s experience, partic- achieve adequate rest and sleep, both essential to healing
ularly when family members are included.110,111 processes and wellbeing.
 CHAPTER 7 PSYCHOLOGICAL CARE 179

TABLE 7.9
Analgesics

DRUG/DRUG DOSE PROPERTIES SIDE EFFECTS N U R S I N G I M P L I C AT I O N S

Morphine sulfate • Water-soluble • Vasodilatory effect • Intermittent doses, rather the

1–10 mg/h (IV infusion), • Peak effect 30 min • Decreased gastric motility need for continuous infusions35
1–4 mg (IV bolus) • Half-life: 3–7 h • Respiratory depression
• Sedative effect and release of • Nausea and vomiting88
histamines35
Fentanyl 25–200 • Lipid-soluble • Respiratory depression Useful where:
mcg/h (IV infusion), • Synthetic opioid • Bradycardia • Hypotension or tachycardia
25–100 mcg/h • 80–100 times more potent • Muscular rigidity needs to be avoided
(IV bolus) than morphine • Gastric and/or histamine side
• Peak effect in 4 min effects occur with morphine
• Half-life: 1.5–6 h35
Tramadol • Soluble in water and ethanol • Nausea, vomiting • Intermittent doses only
hydrochloride 100 mg • Synthetic • Dizziness, dry mouth
(IV bolus), then • Centrally acting opioid-like • Headache
50–100 mg 4–6/24 h analgesic • Sweating
NSAIDs • Analgesia and antipyretic • Gastrointestinal • Oral or rectal
• Some have anticoagulant side • Renal clearance
effects
Ketamine 20 mg (IV • Analgesic and dissociative • Hypertension and respiratory • Use for painful procedures
bolus), then 10–20 mg anaesthetic for painful depression (administer slowly) e.g. wound dressings
every 5–10 min90 procedures • Increased intracranial pressure • Administer 2 mg of midazolam
• Onset of action 1–2 min • Hallucinations at the start of the procedure or
• Analgesic/anaesthetic effects continue midazolam infusion
last 5–15 min to minimise the dysphoric and
• Half-life 3 h hallucinogenic side effects

NSAIDs = non-steroidal anti-inflammatory drugs.

Sleep Many factors are thought to affect the patient’s ability

to sleep, including discomfort, treatment, medications,
The function of sleep is not yet fully understood; however, environmental noise and illness.123
it is considered to be required for many bodily functions.114 Sleep in the healthy adult comprises one consolidated
It is vital for wellbeing and sleep disruption or depriva- period of 6–8 hours (mean 7.5 hours) in each 24-hour
tion leads to psychological and physical ill health.115–117 period occurring at night according to natural circadian
Sleep is considered to be physically and psychologically rhythms.129 There are two main sleep states: rapid eye
restorative and essential for healing and recovery from movement sleep (REM) (approximately 25% of total
illness. Arguably, critically ill people are in greater need of sleep time [TST]) and non-rapid eye movement sleep
undisrupted sleep but are more likely to experience poor
(non-REM) (approximately 75% of TST). Non-REM
quality sleep.118
sleep is composed of four stages: stages 1 and 2 or
Evidence suggests that, although critically ill patients
may experience normal quantities of sleep, the quality light sleep and stages 3 and 4 or slow wave sleep (SWS)
is poor with very few experiencing deep or rapid eye or deep sleep, which must be completed in sequence in
movement sleep.119–121 Sleep is highly disrupted and order to enter REM sleep. The consolidated sleep period
distributed across 24 hours with roughly equal amounts consists of four to six sleep cycles: stages 1–4 followed
occurring in the day and at night.122,123 These findings, by REM sleep, which lasts 60–90 minutes. (More recent
obtained using polysomnography (PSG), have been sleep staging guidelines have combined stages 3 and 4 so
corroborated by patients’ self-reports of their sleep in that there are now only 3 stages of non-REM sleep;130
critical care.124,125 Patients consistently rate the overall however, the foremost textbook on sleep medicine uses
quality of their sleep as poor and, more specifically, they the conventional 1–4 staging nomenclature.129) Time spent
report light sleep with frequent awakenings and consid- awake during the sleep period is less than 5% of TST.129
erable difficulty falling asleep and returning to sleep.126–128 All sleep stages are important to health and, unfortunately,
180 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

critically ill patients commonly experience very little deep and interpretation.129 In addition, recently sleep research-
or REM sleep. ers have highlighted the difficulties applying standard
There are changes in sleep architecture over the adult R & K sleep criteria to critically ill patients’ sleep data:
lifespan that require consideration in the context of critical for example, EEG waveforms may be abnormal as a result
care nursing. TST and the percentage of SWS decline of sedative medications, mediators of systemic inflamma-
(TST by 10 minutes and SWS by 2% per decade) and tory response and the disease process.134 These drawbacks
light sleep increases slightly (only by 5% between 20 and preclude its routine use in clinical practice in critical care.
70 years) with age.131 REM sleep remains fairly constant Actigraphy is another method of recording sleep that has
with an approximate 0.6% decline per decade until age been attempted in the critically ill. Modern actigraphs are
70 when REM increases with a simultaneous decrease in small wristwatch devices (they may also be located on
TST.132 Time spent awake after sleep onset increases with the trunk or leg) containing accelerometers that detect
age by 10 minutes per decade after age 30.131 motion in a single axis or multiple axes.135,136 Data obtained
from actigraphy provides an overestimation of sleep time
Sleep assessment/monitoring (critically patients are typically immobile for long periods
An assessment of the patient’s sleep history should be regardless of sleep state). The other objective method that
performed as soon as possible after admission. The person has been attempted in critical care is bispectral index mon-
closest to the patient (ideally living in the same home) itoring.137,138 At present, considerable algorithm development
may be willing to provide a sleep history if the patient using comparisons with PSG data are required before it is
is unable to communicate verbally. The requirement for a viable option to measure sleep accurately in any setting.
nocturnal non-invasive ventilation or sleep medication The most reliable option for the critical care clinician
should be conveyed to the medical team for consid- to assess sleep is a patient self-report (in any case, the
eration. Particular attention should be paid to reports patient is best placed to judge the quantity and quality
of daytime sleepiness, dissatisfaction with sleep and bed of their sleep if they are able). Two instruments have
partner reports of excessive snoring as these may indicate been specifically developed for use in critical care: the
an undiagnosed sleep disorder. Usual sleep habits such as Richards-Campbell Sleep Questionnaire (RCSQ)139 and
‘going to bed’, ‘getting up’ and shower times should be the Sleep in Intensive Care Questionnaire (SICQ).125 The
accommodated while the patient is treated in critical care RCSQ comprises five 100-mm visual analogue scales
whenever possible. (VAS): sleep depth, latency, awakenings, time awake and
Unfortunately, few objective methods of assessing sleep quality of sleep. It was pilot-tested in medical ICU patients
reliably in the critically ill are available. PSG, a method (n = 9, 100% male)140 and validated in a more extensive
of recording electroencephalography, electrooculography investigation involving 70 male patients.139 There was a
and electromyography, is the ‘gold standard’ for assessing moderate correlation between total RCSQ score and
sleep. PSG data are analysed according to Rechtschaf- PSG sleep efficiency index, r = 0.58, (p < 0.001).139 The
fen and Kales’ (R & K)133 criteria and provide TST and SICQ is better suited for use when assessing a unit/
sleep stage times. However, a trained operator is required organisation-wide change in practice rather than for
to ensure satisfactory signal quality, continuous recording individual patient’s sleep (see Table 7.10).

TABLE 7.10
Sleep assessment instruments

INSTRUMENT DESCRIPTION COMMENTS

Richards Campbell Sleep • Five visual analogue scales (0–100 mm) • Patient does not need to be able to write
Questionnaire139 • Total score derived from average of the (nurse can mark the line as instructed by
5 scales (high scores indicate good sleep) patient)
• Patient requires sufficient level of cognitive
function to use it
Sleep in Intensive Care • Seven questions (some have more than one • Patient does not need to be able to write
Questionnaire125 item) (nurse can circle the response as instructed
• Likert scales 1–10 by patient)
• No global score • Patient requires sufficient level of cognitive
• Good for organisational changes in practice function to use it
• Not yet validated
Nurses’ observation • Tick box table • No training required
checklist141 • Assignment of a category: ‘awake’, ‘asleep’, • Typically, nurses tend to overestimate sleep
‘could not tell’ and ‘no time to observe’ every • Better for trend over several nights
15 min
 CHAPTER 7 PSYCHOLOGICAL CARE 181

Up to 50% of all patients treated in critical care may be reposition with suitable pressure support
unable to complete a self-assessment of their sleep, in which measures
case the only remaining option is nurse assessment.126,136
level the transducer at the phlebostatic axis to
The Nurses’ Observation Checklist (NOC)141 can be used
ensure accurate haemodynamic monitoring so you
to obtain the bedside nurses’ assessments of the quantity of
do not need to disturb the patient again later
the patient’s sleep. It is a relatively simple instrument to use.
However, evidence from many studies suggests that nurses ensure intravenous lines and drains are accessible.
tend to overestimate sleep time, so sleep time derived from • Plan care activities to allow the patient 1.5–2-hour
the NOC may be better used as a trend rather than a periods of undisturbed time during the night.
definitive report for an individual night’s sleep.136,142–144 (Negotiate with other healthcare personnel to allow
these uninterrupted periods at night and during
Sleep promotion and maintenance daytime rest times). ‘Cluster care’, for example, time
In the absence of conclusive evidence to support sleep- medication administration and blood samples to
promoting interventions in ICU, recommendations are coincide with pressure area care.
based on practices that would be likely to improve sleep
and health, e.g. noise reduction, limiting the number of • Provide the daily bath to suit patient needs rather
than organisational needs (either before settling for
interruptions to which patients are subjected and main-
the night or during normal waking hours).
tenance of an environment that is generally conducive to
normal night-time sleep. Individualised approaches to all
aspects of care are best and this is particularly important Practice tip
when promoting and maintaining sleep in the critically ill. The importance of sleep to critically ill patients cannot
The following information, based on research and expert be overstated. Enabling the patient to experience good
opinion, provides some general advice that may promote quality and quantities of sleep should be a major priority
and maintain sleep and, at the very least, create conditions for critical care nursing. Demonstrate your commitment
conducive to rest. to improving rest and sleep for intensive care patients
Comfort measures by incorporating sleep into the treatment reminder
system used in the unit you work in (e.g. FASTHUG
• Ensure pain relief is offered and administered if pain becomes FASSTHUG).
is suspected.
• Reduce anxiety by providing information and the
opportunity to have questions answered. Anxiolytics Environmental
such as benzodiazepines may also be required.
• Provide night-time sedation as required (remember • Reduce noise levels especially during rest times
and at night (this may require a unit-wide change
sedation is not natural sleep and patients may only in practice) as several studies conducted in critical
appear to be asleep; however, it is possible to be care have highlighted the association between noise
sedated and asleep). levels and sleep disruption.34,119,147–149 Continuous
• Provide a light massage unless contraindicated.140 noise levels in adult critical care areas consistently
• Offer guided relaxation and imagery (audio-guided exceed hospital noise standards, for example, the
relaxation and imagery sessions may be purchased).145 Environmental Protection Agency 35 dB(A) at night
• Provide an extra cover for warmth (metabolic rate and 45 dB(A) during the day150 and the Australian
typically drops during sleep). Standard AS/NZS 2107/2000 minimum 40 dB(A)
• Request the patient’s family to provide some of the and maximum 45 dB(A).151–153
patient’s own personal belongings such as pillows and • Ensure lights are sufficiently dimmed and window
toiletries. blinds drawn during rest times and at night and that
• Ear plugs and eye covers may assist some patients; lighting is bright and blinds opened at all other times.
however, it should be highlighted that studies have It is known that critically ill patients’ melatonin
shown that neither provides protection from excessive metabolism is non-circadian so it is particularly
noise and light levels.146 Patients provided with important to attempt to use lighting that encourages
ear plugs and eye covers should have the ability to normal circadian rhythm.154,155 Generally, critical care
remove them without assistance if they wish. areas contain fluorescent lights that may emit up to
600 lux.156 Light levels between 50 and 100 lux at
Care activities night, even for relatively brief periods, are known to
• Attend to nursing care at the beginning of the night suppress melatonin production, a vital hormone in
to reduce the likelihood of disturbing sleep during the promotion of sleep and maintenance of circadian
the night, for example: rhythm.129 It is well known that artificial lights emit
redress wounds and empty drainage bags light with sufficient short wave content to affect
wash, clean teeth and change gown and sheets melatonin secretion.
182 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

as adrenaline have the capacity to affect the quality

Practice tip of sleep. Sedatives, especially benzodiazepines and
Ask your patient (or their relatives) about their usual opioids, reduce time in stages 3 and 4 and REM,
night-time ‘settling routine’ for sleep. Try to emulate thus reducing the amount and quality of sleep.158,159
the routine as closely as possible. Ask the patient if this However, pain relief and anxiolysis may be essential
improved their sleep. for sleep to occur, but an awareness of potential
adverse medication reactions is important in the
prevention of escalating sleep disturbances.
Treatments
• Specific sleep-promoting medications may be
• Discuss the need for alternative mechanical venti- administered once non-pharmacological
lation settings at night with the medical team. interventions have been attempted. Table 7.11
Hyperventilation caused by inappropriately high contains a summary of the commonly used
inspiratory pressure can cause hypocapnia, which may medications for the general management of insomnia.
lead to central apnoeas and sleep disturbance.157 It should be noted that investigations of the
• Many medications administered in critical care affect effectiveness of these medications have not been
sleep architecture. Even vasoactive medications such undertaken in the critically ill.

TABLE 7.11
Summary of commonly used sleep-promoting medications

M E D I C AT I O N TYPICAL HYPNOTIC DOSE RANGE

M E D I C AT I O N CLASS ( A D U LT ) CAUTIONS

Temazepam Benzodiazepine Oral/enteral: 10–20 mg once per night Reduce dose in liver failure
(30 min before settling) Check liver function
Propofol Intravenous sedative/ Intravenous: Short-term use only
anaesthetic agent Mechanical ventilation: 1.0–3.0 mg/kg/h Continuous respiratory monitoring
Self-ventilating: no greater than 0.5 mg/kg/h Check liver function
Zolpidem Non-benzodiazepine Oral/enteral: 5–10 mg once per night Short-term use only (2–4 weeks)
hypnotic (immediately before settling) Associated with hallucinations
Extended half-life in liver impairment
Zopiclone Nonbenzodiazepine Oral/enteral: 3.75–7.5 mg once per night Short-term use only (2–4 weeks)
hypnotic (immediately before settling) Associated with hallucinations
Extended half-life in liver impairment
Haloperidol Typical antipsychotic Provide maintenance doses used for Monitor QT interval and liver function
treatment of delirium for night-time Observe for extrapyramidal symptoms
settling No more than 100 mg/day
Intravenous (slow): 2–10 mg which can be
repeated
Oral/enteral: 5–15 mg per day
Olanzapine Atypical Oral/enteral: 2.5–20 mg once per night Short-term use only
antipsychotic several hours before settling May cause hypotension
Quetiapine Atypical Oral/enteral: 25–200 mg once per night 1 h Short-term use only
antipsychotic before settling May cause hypotension
Monitor QT interval
Amitriptyline Tricyclic Oral/enteral: 25–150 mg once per night Monitor QT interval and for anticholinergic
antidepressant 1–2 h before settling effects
Increased seizure risk
Doxepin Tricyclic Oral/enteral: 25–150 mg once per night Monitor QT interval and for anticholinergic
antidepressant 1– 2 h before settling effects
Increased seizure risk
Mirtazapine Noradrenergic and Oral/enteral: 15–60 mg once per night Higher doses may have a stimulatory effect
specific serotonergic 1–2 h before settling
antidepressant
Dexmedetomidine Alpha agonist Intravenous: Loading dose 1 mcg/kg Not to be used as a continuous infusion for
over 10–20 min followed by maintenance more than 24 h
infusion 0.2–1 mcg/kg/h titrated to effect Continuous respiratory monitoring
 CHAPTER 7 PSYCHOLOGICAL CARE 183

Practice tip A note on melatonin

Melatonin is used for the short-term alleviation of insomnia.
Next time you are at work in ICU take the time to attend This naturally-occurring hormone is both sleep-promoting
to the noise level. At an appropriate time and position and -maintaining. Despite its use as a treatment for primary
in the ICU, close your eyes for 1 minute and consider insomnia, e.g. jet lag and shift work, the effectiveness of
whether you would be able to rest. In addition, find exogenous melatonin as a treatment for most sleep disorders
a patient who is well enough to be discharged to the has not been established.160,161 Investigations performed in
hospital ward and ask them about the factors that they ICU did not use polysomnography and were largely incon-
found most disruptive to rest and sleep while they were clusive.162–164 Difficulties occur in emulating the typical
being treated in ICU. endogenous pulsatile secretion of the hormone165 and,
together with its short half-life, these probably explain why
many study results are inconclusive.The high doses required
Practice tip to achieve an adequate plasma level overnight when admin-
istered once at the beginning of the night are likely to persist
If after interviewing the patient or their family about
in the body and may upset normal circadian rhythm. Some
their usual sleep and assessing their sleep in ICU
studies investigating the effect of melatonin on insomnia
you suspect they might have an existing untreated
suggest that it may be more effective when administered to
sleep disorder, request the treating medical team to
adults older than 55 years as there is an age-related decrease
make a sleep medicine referral. Research indicates
in endogenous melatonin.166 The typical dose is 2 mg once
that untreated sleep problems long-term are associ-
a day (1–2 hours before settling).
ated with increased risk of cardiovascular disease
The current advice of the authors is that it is better to
and cancer.
provide conditions that encourage the normal circadian
secretion of endogenous melatonin (i.e. provide lighting
and activity levels appropriate for the time of day) than to
administer exogenous melatonin.

Summary
Meeting the psychological needs of patients is essential in the care of critically ill patients. This chapter outlines various
methods that are available to assess and then effectively manage aspects of patient care related to anxiety, delirium, pain,
sedation and sleep. Assessment of these aspects of patient condition requires thorough clinical assessment, with a range
of instruments available to help improve consistency over time and between clinicians, as well as to inform decisions
regarding the most appropriate interventions. Although these aspects of care have been reviewed sequentially in this
chapter, in reality they are closely interrelated and should be considered concurrently.

Case study
A 49-year-old woman, Violet Jones, was admitted to the intensive care unit (ICU) with community-acquired
pneumonia. Her twin sister visited her at home after Violet’s employers expressed their concern that she had
not attended work for 2 consecutive days and had not called them. Violet’s sister found her unconscious at
her home in bed and called an ambulance.
On arrival in the emergency department Violet was unresponsive to voice but groaned to sustained tactile
stimulation, and was profoundly hypotensive and pyrexial. She was intubated and initially stabilised in the
emergency department before being transferred to the ICU. There were widespread infiltrates on her chest
X-ray.
Despite initial stabilisation in the emergency department her blood pressure on arrival in ICU remained low;
therefore, several litres of intravenous saline were administered and a vasopressor was started. Her peak
airway pressures were high and arterial blood gases poor so pressure control ventilation was instigated with
a high fraction of inspired oxygen and machine-delivered respiratory rate. Whenever the rate of sedative
medication infusion was reduced she became agitated and reached for her endotracheal tube. Over the
next day Violet’s lungs were increasingly difficult to ventilate and she experienced several hypoxic episodes.
On day 3 in ICU she was diagnosed with acute respiratory distress syndrome (ARDS). In an attempt to
improve gaseous exchange she was placed in a prone position for long periods of the day. Throughout
184 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

this time high-dose benzodiazepine medication with low-dose opioid medication was administered along
with vasopressors. On day 4 her family was informed that she had a high risk of dying. By day 6 Violet
had improved so she was returned to a supine position. However, the sedative medication infusion rate
could not be reduced appreciably without her becoming tachypnoeic and agitated. A head CT scan was
performed but showed no abnormalities.
On day 8 Violet’s respiratory condition had improved sufficiently for her to undergo a tracheostomy, which
enabled the sedative medication to be reduced. It took several days for the ventilator support to be reduced;
she remained on pressure control with pressure support until day 16 when she was placed on pressure
support exclusively. By day 18 Violet was breathing spontaneously without ventilator support for several
hours of the day.
Once she received her tracheostomy Violet was no longer agitated but was withdrawn and tearful; she
was rarely seen to close her eyes and was hypervigiliant and non-communicative, even with her family.
Her family, in particular her sister, was very distressed. She said, ‘She is not herself. This is not like her’.
Serial delirium assessments (using the CAM-ICU) revealed that Violet was not likely to be experiencing
delirium. The tracheostomy was still in situ and, although Violet could tolerate the cuff being deflated for
short periods, she struggled to speak loudly enough to be heard and did not have enough ‘huff’ to complete
long sentences. In addition, she was too weak to write and was frustrated and easily tired using alphabet
boards. Therefore, in order to facilitate a more meaningful assessment of Violet’s psychological wellbeing
the speech pathologist was consulted to explore alternative communication strategies. A specialised
swallowing and speaking (Passy-Muir®) valve was provided to allow Violet to speak.
After careful questioning it transpired that Violet was feeling acutely anxious and frightened (Faces Anxiety
Scale =5/5). She described memories of ‘voices of concern’ (ICU healthcare personnel talking at her
bedside) and times when she was ‘gasping for breath’ when she was acutely unwell earlier during her ICU
stay. She was fearful and pessimistic about her future.

TREATMENT
Violet was provided with information about the likely recovery trajectory after critical illness. The
physiotherapist reassured her that her current level of physical weakness was not permanent. Violet’s
primary nurse validated her feelings and provided additional information about the emotional and
psychological recovery process. In addition, Violet’s primary nurse developed a care plan in consultation
with Violet to address her acute anxiety:

• Violet was moved to a quieter area of the intensive care unit.

• Violet was provided with regular opportunities to express her feelings verbally and describe her
memories: the tracheostomy cuff was deflated and the Passy-Muir valve used for as long as she could
tolerate it.
• A daily routine was negotiated in which several periods of the day were dedicated to sleep/rest and
listening to music.
• A masseur was employed by the family to provide a head and neck massage each evening.
• A small dose of diazepam (2 mg) was provided prior to chest physiotherapy as Violet found this
particularly frightening.
• Her dog was brought in to visit by her sister twice a week (this arrangement was negotiated with the
hospital infection control department and hospital governance).
Violet’s mood and emotional wellbeing improved and she became more engaged in her rehabilitation in
ICU. She was transferred to the hospital ward after 30 days in ICU. Approximately 2 weeks after this she
was discharged home.

RECOVERY
Violet’s recovery was complicated by a pulmonary embolism 2 months after her return home but this did
not necessitate treatment in hospital. However, she fully recovered psychologically. She visited the ICU and
expressed her gratitude for the assistance she had been given to overcome her anxiety.

DISCUSSION
Violet’s illness and recovery trajectory are not uncommon. She was severely unwell and the respiratory
nature of her illness placed her at risk of becoming acutely anxious. She was provided with the means to
 CHAPTER 7 PSYCHOLOGICAL CARE 185

communicate verbally and several strategies both pharmacological (benzodiazepine medication is anxiolytic)
and non-pharmacological were implemented to reduce her anxiety. Her mood improved dramatically and,
subsequently, her ability to engage in rehabilitation increased. This may have been a result of the ability
to fully express herself, the other interventions or, most likely, a combination of both. The multifaceted
multidisciplinary healthcare team approach to addressing her obvious psychological distress while she was
a patient in ICU was highly likely to have contributed to her full psychological long-term recovery.

CASE STUDY QUESTIONS

1 When Violet was able to communicate verbally she expressed her fear and anxiety related to memories of
‘voices of concern’ (ICU healthcare personnel talking at her bedside) and times when she was ‘gasping
for breath’ when she was acutely unwell earlier during her ICU stay. Outline some nursing interventions
that could have been implemented when she was acutely unwell that may have ameliorated her fear and
reduced the likelihood of her having unpleasant memories of that time.
2 One of the non-pharmacological interventions used to treat Violet’s anxiety was massage. Describe the
proposed underlying physiological mechanism(s) for the relaxing effect of massage.

RESEARCH VIGNETTE

Rose L, Fitzgerald E, Cook D, Kim S, Steinberg M, Devlin JW, et al. Clinician perspectives on protocols designed to
minimize sedation. J Crit Care 2015;30:348–52

Abstract
Purpose: Within a multicenter randomized trial comparing protocolized sedation with protocolized sedation plus
daily interruption (DI), we sought perspectives of intensive care unit (ICU) clinicians regarding each strategy.

Methods: At 5 ICUs, we administered a questionnaire daily to nurses and physicians, asking whether they liked using
the assigned strategy, reasons for their responses, and concerns regarding DI.

Results: A total of 301 questionnaires were completed, for 31 patients (15 protocol only and 16 DI); 117 (59 physicians
and 58 nurses) were the first questionnaire completed by that healthcare provider for that patient and were included
in analyses. Most respondents liked using the assigned strategy (81% protocol only and 81% DI); more physicians
than nurses liked DI (100% vs 61%; P < 0.001). Most common reasons for liking the assigned sedation strategy
were better neurologic assessment (70% DI), ease of use (58% protocol only), and improved patient outcomes
(51% protocol only and 44% DI). Only 19% of clinicians disliked the assigned sedation strategy (equal numbers for
protocol only and DI). Respondents’ concerns during DI were respiratory compromise (61%), pain (48%), agitation
(45%), and device removal (26%). More questionnaires from nurses than physicians expressed concerns about DI.

Conclusions: Most respondents liked both sedation strategies. Nurses and physicians had different preferences and
rationales for liking or disliking each strategy.

Critique
ICU clinicians’ (nursing and medical) perspectives regarding the use of protocolised sedation with and without daily
interruption (DI) of sedation were sought in this survey-based study. This study was conducted within the framework
of the SLEAP trial (randomized controlled trial of protocolised sedation alone versus protocolised sedation with
DI). Clinicians in 5 of the 16 hospitals participating in the SLEAP trial were provided with questionnaires at the time
they were caring for study participants. In the SLEAP trial, where no differences in patient outcomes were identified
between the two sedation strategies, perceived workload was assessed as significantly higher for nurses in the
protocol only group compared to the protocolised sedation plus DI group.84

Clinicians participating in this sub-study generally liked both the protocol only and protocol with DI strategies,
although clinicians from different professions had differing views in relation to the strategy that incorporated DI with
fewer nurses (only 61%) indicating support compared to 100% of medical clinicians. In addition, more nurses raised
186 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

concerns with the strategy incorporating DI in relation to aspects such as patient discomfort and the potential for
respiratory compromise, pain and cardiac instability. The most common reason for liking the strategy that incorporated
DI was the improved neurological assessment that was possible.

Strengths of this study include that clinicians from 5 centres across Canada participated, although no participants
from the SLEAP trial centres in the USA participated. Further, as identified by the investigators, asking participants
to answer questions in regard to a specific patient being managed by one of the strategies helps provide real-time
perspectives rather than general opinions. This is the first examination of how clinicians view protocolisation of
sedation, particularly with the addition of DI, and is essential information to inform effective implementation of such a
strategy in practice. Given the evidence and associated guidelines35 it is essential that we identify effective methods
to minimise sedation levels in critically ill patients; understanding clinicians’ views of the benefits and challenges of
procolised sedation as one method to achieve this is vital.

The investigators of both this survey and the parent SLEAP trial have made the assertion that nurse led sedation
protocols provide one method to minimise sedation and have therefore designed both this and the parent SLEAP
study with protocolised sedation as the standard care. This is unfortunate given the lack of evidence of effectiveness
of nurse led sedation protocols.82 Despite this, the responses to the survey provide differentiation between the two
alternatives of the protocolisation that were offered in this setting and therefore give some general guidance on
clinicians’ views of protocolisation, as well as the incorporation of DI.

In summary, this study represents an important element of the larger issue of how best to achieve sedation minimization
when caring for critically ill patients. Results demonstrate that, although both nursing and medical clinicians were
generally supportive of using protocolised sedation with or without DI, nursing clinicians in particular raised a number
of concerns. In the context of the overall results of the SLEAP trial, where protocolised sedation with DI provided
no additional benefits over procolised sedation alone, daily sedation interruption should not be used as a routine
component of caring for critically ill patients.

Lear ning a c t iv it ie s
1 The assessment of anxiety, sedation and pain intensity is integral to critical care nursing.
• Discuss the assessment strategies you would use to differentiate between anxiety and pain. List any special
considerations associated with your choices.
• Suggest a non-pharmacological strategy you could employ to reduce pain.
• Consider how family could help with the management of the patient’s anxiety.
2 Critically ill patients who experience delirium require highly skilled and informed nursing. The following exercises
may enhance your ability to manage delirium:
• Identify nursing interventions that may reduce the potential for delirium, including some interventions that
involve the family in care.
• Describe the rationale for your selection of nursing interventions using current research.
• Outline the differences between delirium and dementia.
• Develop a nursing plan for a patient you cared for previously with delirium. Identify interventions you did not
use but would use in the future.
3 Compare and contrast the various sedation assessment instruments, and discuss the relative merits and
disadvantages of using each of these instruments. Now repeat the exercise for each of the pain assessment
instruments and the delirium assessment instruments.
4 Using the references provided in this chapter:
• highlight the importance of good quality sleep in health and illness
• identify theories that explain the function of sleep.
 CHAPTER 7 PSYCHOLOGICAL CARE 187

5 Think about the last time you experienced fragmented sleep or insufficient sleep and describe how you felt in
terms of your:
• mood
• cognitive function
• physical function
• appetite
• motivation.

Online resources
Australasian Sleep Association, www.sleep.org.au
ICU Delirium and Cognitive Impairment Study Group, www.icudelirium.org

Further reading
Ballantyne J, Bonica JJ, Fishman S. Bonica’s management of pain. Philadelphia: Lippincott Williams & Wilkins; 2009.
Barr J, Fraser GL, Puntillo K, Ely EW, Gelinas C, Dasta JF et al. Clinical practice guidelines for the management of pain,
agitation, and delirium in adult patients in the intensive care unit. Crit Care Med 2013,41:263–306.
Bergeron N, Dubois MJ, Dumont M, Dial S, Skrobik Y. Intensive Care Delirium Screening Checklist: evaluation of a new
screening tool. Intensive Care Med 2001;27:859–64.
Ely EW, Inouye SK, Bernard GR, Gordon S, Francis J, May L et al. Delirium in mechanically ventilated patients: validity and
reliability of the confusion assessment method for the intensive care unit (CAM-ICU). JAMA 2001;286:2703–10.
Hardin KA. Sleep in the ICU: potential mechanisms and clinical implications. Chest 2009;136:284–94.
Kyranou M, Puntillo K. The transition from acute to chronic pain: might intensive care unit patients be at risk? Ann Intensive
Care 2012;2:36.

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 Chapter 8

Family and cultural care

of the critically ill patient
Marion Mitchell, Denise Wilson, Robyn Aitken

KEY WORDS Learning objectives

bereavement After reading this chapter, you should be able to:
communication • describe models of care and evaluate how they meet patient and family
needs
continuity of care
cultural care and • recognise appropriate resources to enhance communication
cultural safety • develop an understanding of the needs of families and patients who die in
end of life the ICU
family care • evaluate and implement appropriate strategies for working with families
from a diversity of cultures
Indigenous or
Aboriginal • recognise and implement the needs of the critically ill and/or dying patient
Australians who is either an Aboriginal or Torres Strait Islander person or Ma-ori
Ma–ori people • recognise the various religious considerations for patients who are dying
or who have died.
models of care

Introduction
Care of critically ill patients is complex and multifactorial. Although
management of the haemodynamic parameters and healthcare interventions
is an essential component of effective care of the critically ill, the psycho-
social health and wellbeing of patients are intimately related to their wellness
and eventual illness outcome. There is a tendency, due to the technologi-
cally complex nature of nursing in critical areas, for novice nurses to focus
their attention on the management of medical treatment regimens. This is an
important part of their learning trajectory. However, nurses need to be guided
to see beyond the waveforms and physical parameters to see the patient in the
bed as an individual with unique needs.The previous chapter examined specific
aspects of the psychological wellbeing of the critically ill with strategies to
improve patient outcomes. This chapter extends the focus to incorporate the
family into the caring paradigm and introduces the concept of person-centred,
patient-centred and family-centred care. Nursing practices that incorporate the
patient’s family into the care of the critically ill acknowledge the vital part
families play in the illness continuum.
The assessment, understanding and incorporation of the patient’s and
family’s cultural needs are essential elements of nursing the critically ill, and
involve the entire multidisciplinary team. These elements are important for
194 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

both the recipients of the care (the patient and family) Implementation of patient-centred care requires a
and the critical care nurse, as the practice of nursing all culture change and therefore needs support at an individual
aspects of the patient’s wellbeing brings humanity into professional level and at an organisational level.11 A study
critical care nursing. Cultural factors include social in the USA examined how critical care nurses commu-
factors and human behaviours associated with emotional nicate with patients and families within a patient-centred
and spiritual needs.1 In this chapter, models of nursing care framework that was operating within their unit. They
are examined with particular reference to the philosophy found that nurses predominantly communicated infor-
of family-centred care, which may be an appropriate mation related to the patient’s acute biophysical status.
nursing model for use within critical care settings. The Although the nurses in the study supported the importance
specific needs of the families of critically ill patients are of shared power and responsibility, they exhibited few
discussed, also the implications for critical care nursing. examples in practice. They reflected that they felt sharing
The differing world views on health and illness are power fell within the domain of intensivists’ discussions
highlighted for consideration of appropriate care. Many with patients and families rather than theirs.12 Nurses
of the populations where we practise exhibit diversity deferring responsibility for communication in such a way
of ethnicity, country of origin and cultural practices. highlights the importance of a whole-of-team approach
Effective communication is crucial to meet both family to patient-centred care where healthcare professionals
members’ needs and those of the patient. The complexity share the responsibility of meaningfully involving patients
of patient communication together with the addition of and their families in decisions and care options.
linguistically diverse patients is outlined and suggestions
for clinical practice provided. End-of-life care is discussed Person-centred care
in general terms and specific cultural considerations More recently, the term person-centred care has gained
are highlighted with particular reference to Aboriginal favour over patient-centred care.13–15 The Oxford Dictionary
and Torres Strait Islander people of Australia and New defines ‘patient’ in passive terms as the receiver of care
Zealand Ma-ori patients and families. whereas a ‘person’ is acknowledged as being an individual.16
Those who read about patient-centred care (as outlined
above) will understand that the word patient in the
Overview of models of care context of patient-centred care is far from the passive role
The ways that nurses manage their daily activities and in this dictionary definition. However, if consumers are to
patient care are affected by both the critical care unit’s understand healthcare organisations’ working paradigms,
model of care delivery and the nurse’s personal philosophy semantics and first impressions are important. The term
of what and how nursing is constructed. Alternative ‘person-centred care’ emphasises the individual nature of
models of care are examined in this section and their use the person with the illness. It promotes the perception
in critical care areas discussed. Nursing models define (and reality) of equal power and a shared partnership
shared values and beliefs that guide practice. Various between the person and healthcare provider/s. Here, the
philosophies and models of nursing care delivery have person is an acknowledged expert for their own health
evolved over the decades and contrast with the ‘medical values and goals. The partnership is both collaborative
model’, which focuses on the diagnosis and treatment and respectful and highlights the importance of knowing
of disease.2 Models such as primary nursing and team the person behind the patient and understanding that the
nursing include organisational or management properties, patient is more than their illness.4,13
whereas patient-centred practice is another model in No evaluations of person-centred care in critical
which a partnership relationship is developed between care areas could be found. However, some evidence is
health professionals and the patient and family.3–8 coming out of the Centre for Person-centred Care in the
University of Gothenburg in Sweden. In one in-hospital
Patient-centred care study of chronic heart failure patients, length of stay
Patient-centered care shifts control in health-related was reduced by a third with no compromise in their
decisions from the healthcare professional to the patient – perceived quality of care when person-centred care was
the recipient of care, thus challenging some existing compared to usual care.The individualised care plan based
paradigms.9 This model has patient empowerment as the on understanding each patient’s needs was seen to be a
core element. To facilitate empowerment, patients need to major contributing factor in reducing hospital stay.14 In
be well informed in such a way that they can understand another study of patients with chronic heart failure in the
the information to help with their decisions.6 It is USA, person-centred care was explored in five wards in
incumbent upon critical care nurses to ask patients about a single hospital that implemented a person-centred care
their illness perceptions, priorities and future plans. Having approach.12 Person-centred care was evaluated in relation
a clear understanding of patients’ concepts of illness, their to how it reduced patients’ uncertainty about their illness.
cultural beliefs and intent is vital.3,6 Treating patients with The differing organisational and operational features of
respect and providing care that is responsive to individual the ward were examined. In wards where goal setting,
patient preferences, needs and values is fundamental to planning, control and stability were evident, patients’
acknowledging empowerment.10 uncertainty in illness was reduced, which the authors
 CHAPTER 8 FAMILY AND CULTURAL CARE OF THE CRITICALLY ILL PATIENT 195

linked to a person-centred approach to care.12 Within an information about care were rated the highest. The famil-
ICU environment, however, a truly shared partnership iarity of nurses with the special needs of patients was rated
with the patient may be problematic, where critical illness highest in the area of support.28
restricts patient involvement in decision making and care Many nurses also value family involvement in the care
planning.17 In reality, it is generally family members who of their own sick relative.31,32 Strategies to improve family-
provide the link between the patient and healthcare team. centred care within adult critical care areas include
During the 1980s, the role of the family was one involving family members in partnering with the nursing
focus of nursing debate and discussion. Friedman believed staff to consider the involvement they would like, which
families were the greatest social institution influencing may include providing fundamental care to their sick
individuals’ health in our society.18 A worldwide trend is relative.33 Family members can decide in consultation and
for health professionals to value the role of family members negotiation with the bedside nurse the care that they want,
in providing ongoing, post-acute care,19 with the reality and are able to provide. This care may vary from moistur-
being that families provide considerable support during ising their relative’s skin to a full sponge and will require
rehabilitation phases of critical illnesses.20–22 The family negotiation. Such acts of caring allow family members to
is strongly incorporated within the three philosophies of connect in what they see as a meaningful way with their
patient-centred, person-centred and family-centred care. sick relative. In addition, it can also improve communica-
Whichever model is selected, it must be practical and tion with critical care nurses and facilitate close physical
understood in the clinical setting for which it is intended.2 and emotional contact with their relative.34 An indepen-
dent nursing intervention such as partnering with family
Family-centred care to provide care constitutes an example of how to opera-
Family-centred care shares the responsibility of patient tionalise a family-centred care model in the clinical setting
care decisions with the family and thus highlights the and assists in the evaluation of other future interventions
importance of family in critical care areas. The family- directed to improve an area’s family-centred approach.
centred model of care, developed during the early 1990s, Further research on the benefits of family-centred care is
primarily in North America in the area of children’s needed in all critical care areas.33,35,36
nursing, considered incorporating the family was funda- It is acknowledged that taking care of critically ill
mental to the care of the patient.23 Over the past two patients requires considerable knowledge and skill. When
decades, the scope and extent of family-centred care has family members are incorporated into the caring paradigm,
broadened and the Institute for Family-Centered Care as advocated within family-centred care, health profes-
defines family-centred care as ‘an innovative approach sionals equally need specific knowledge and skills.28 This
to the planning, delivery, 24 and evaluation of healthcare information should be initiated in foundation degrees,
that is governed by mutually beneficial partnerships postgraduate studies and via ongoing professional devel-
among healthcare providers, patients and families’.25 opment opportunities.12,37
Patient-and-family-centred care applies to patients of all Beyond the educational needs for nurses there is an
ages, and it may be practised in any healthcare setting. international policy drive to include families as a quality
Family-centred care is founded on mutual respect and safety measure in patient care.38–40 The family knows
and partnership among patients, families and healthcare the patient best, has their best interest foremost and is
providers. It incorporates all aspects of physical and the one constant throughout the critical illness. Family
psychosocial care, from assessment to care delivery and members provide ongoing care and involving them during
evaluation.26 Healthcare providers that value the family/ the critical illness phase supports their ability to provide
patient partnership during a critical illness strive to immediate feedback and prolonged care to their relative.
facilitate relationship building and provide amenities and Involving and supporting families is not necessarily
services that facilitate families being near their hospitalised time-consuming but, to be able to do this, an understand-
relative.19 When a clinical unit’s staff embrace a family- ing of the needs of families is required.18,41
centred care philosophy and partner with families to make
changes to the physical environment, such as improved Needs of family during critical illness
privacy and aesthetically pleasing decor, it can have the Family members of critically ill patients contribute a signif-
added advantage of positive culture changes for the staff. icant and ongoing involvement to patients’ wellbeing.42
Such outcomes indicate there is a benefit beyond the Patients need and want their family members with them43
family members for whom the changes were initiated.27 and healthcare professionals also need family members’
In trying to understand family-centred care, neo- input.44 Family members’ satisfaction with the care their
natal and paediatric ICU studies have focused on parents’ relative receives is considered a legitimate quality indicator
perceptions of care in the three key components of in many areas that routinely assess family satisfaction.45,46
family-centred care: respect, collaboration and support.28– On a very practical level within a critical illness
30
In the area of respect, families rated most highly ‘feeling situation, family members are often the decision makers
welcome when I come to the hospital’ and ‘I feel like a on treatment options due to the impaired cognitive state
parent, not a visitor’.28 Within the area of collaboration, of the patient. Their contribution to healthcare decisions
feeling well-prepared for discharge and being given honest is sought in both acute and ongoing care situations
196 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

as they have insight and knowledge of the patient on 2) reassurance, 3) closeness, 4) support and 5) comfort.52
an entirely different level to health professionals.47 In More specifically, families’ needs include the following:52
addition, family members provide not only support • to know their relative’s progress and prognosis
in the critical illness situation, but also continuity of
care through rehabilitation. This responsibility together • to have their questions answered honestly
with the often sudden critical illness may create stress, • to speak to a doctor at least once a day
anxiety, depression and/or post-traumatic stress disorder • to be given consistent information by staff
(PTSD) for family members.48,49 A primary aim of family- • to feel their relative is looked after by competent and
centred care is to reduce the risk of stress-related reactions caring people
to the ICU experience, which is often traumatic for family
members.50,51 • to feel confident that staff will call them at home if
changes occur in their relative’s condition
Practice tip • to be given a sense of hope
• to know about transfer plans as they are being made.
Suggest to a family member(s) that they might like to
remain by the bedside (when you would normally ask Meeting information needs
them to leave). At first it may feel daunting, as the Families’ needs for information and reassurance are
family member may seem to watch your every move paramount during a critical illness, which is often
and action, but if you start doing this when you are unexpected or unexplained. Seven out of the top ten
performing interventions with which you feel confident, needs of families are related to information needs.64 When
you will find that having them there seems natural. There information is provided, it is important to spend sufficient
is less fuss with family coming and going and talking time with family members.65 A self-designated family
about what you are doing, and it promotes information member can act as the primary receiver of information
sharing and understanding. and take the responsibility of relaying the information
to others. However, the information has to make sense
Stress and anxiety associated with having a critically to them and it is imperative that healthcare professionals
ill relative can hinder a family’s coping ability, adaptation, check their understanding.59 It is not sufficient to think,
decision making52 and long-term health with the possi- ‘But I told them all that yesterday’. Communication is a
bility that post-traumatic stress disorder (PTSD) may two-way process and as such needs to be received in a
develop in family members of ICU patients.50 Families meaningful way as well as given appropriately. Repeated
that experience stress before the critical illness do not and current information is suggested as it helps to reduce
cope as well, and may need additional assistance.53 family members’ anxiety.59 In a case study report of a
As many as half of family members report symptoms mother and her adult war-injured son, the mother tells
of anxiety and depression, indicating it is a very real how she tried to remember things the staff told her. She
problem.32 These figures are concerning, particu- said, ‘I loved how my questions would be answered when
larly when symptoms continue beyond 6 months post we asked (except for the daily one about his brain damage)
ICU.50,54 In addition, post-traumatic stress symptoms are and how most people did not take offense at me writing
reported by family members, which is consistent with a down everything. I know that I was scared to death most
moderate-to-major risk of PTSD, resulting in ongoing of the entire time’.48, p.18
health-related concerns for the family members.50 Early Strategies to improve communication with family
identification and prevention strategies are an important members include nurse-led education sessions designed
area for further research.50,55 Meeting the needs of to identify and meet the needs of family members. Once
families during this stressful and demanding time has the needs have been identified, a specific program can be
the capacity to reduce their stress and promote positive developed to meet those needs. This strategy was found
coping strategies. to be effective when two 1-hour sessions were conducted
A combined healthcare team approach is needed to with family members who reported significantly lower
meet the family’s needs, as differing perceptions among levels of anxiety and higher levels of satisfaction.60 Other
the healthcare team can result in non-unified approaches56 units may choose to have a designated critical care nursing
that are potentially confusing. The needs of families with position in their unit that focuses on family advocacy
critically ill relatives are complex and multifactorial, rein- within a family-centred care philosophy.66
forcing the need for an all-of-team approach.56 Family Multidisciplinary patient rounds that meaningfully
members’ needs were recognised in Molter’s influential include the family show an inclusive and open commu-
study in 1979 in which she researched the specific needs of nication process that values all contributors as they make
ICU patients’ family members. Although Molter’s sample an individual plan of care for the patient.48 Alternatively,
was small (n = 40), 45 potential needs of family members consider routine family meetings with the healthcare
were identified and ranked in order of importance.57 team aimed at improving communication and under-
Family needs continue to be researched48,58–63 and can standing.61,62 Frequently, family meetings are called when
be generally grouped into the need for: 1) information, the family is needed to make critical decisions about the
 CHAPTER 8 FAMILY AND CULTURAL CARE OF THE CRITICALLY ILL PATIENT 197

ongoing care of their relative rather than as a proactive and of critical care nurses and medical officers for them to
positive strategy that allows for patient and family prefer- work effectively.75 This is particularly relevant for patients’
ences to be integrated into patient care.62 families who live large distances from the hospital and
Family conferences with the interdisciplinary team have to travel for many hours in order to be with their
should be organised in a staged and planned manner with sick relative. Flexible visiting policies have been found to
the first occurring within the first 48 hours of admission, improve quality indicators with higher patient and family
the second after 3 days and a third when there is a signif- satisfaction levels and fewer formal complaints.76 Restric-
icant change in treatment goals.24,64 Fundamental topics tive visiting policies limit families’ access to their relatives
for the interdisciplinary meetings with the family could and restrict their involvement. Family members are
include the patient’s condition and prognosis together different from other visitors in critical care areas because
with short- and long-term treatment goals.24,45,67 Family of their intimate relationship, which helps to form crucial
conferences provide time for discussion among family components of the patient’s identity.77–79 Remember
members with the healthcare team as a resource and that there are often different meanings or interpreta-
also for the team to make an assessment of the family’s tions of ‘family’, with family often meaning more than
understanding of the situation. In addition, they provide just the immediate nuclear family (e.g. the Ma-ori wha-nau
an opportunity to develop an awareness of specific [extended family] and the Aboriginal ‘compound’ family).
family needs that the team can endeavour to meet.45 Negotiation of visiting processes that take into account
Unhurried family conferencing allows opportunities these cultural understandings is imperative and is discussed
for families to pose questions and longer family confer- later in this chapter.
ences can result in families feeling greater support and There is a genuine concern by some parents or
significantly reduced PTSD symptoms.68 Some authors carers that children should not visit family members who
suggest the family should be given a meeting guide prior are critically ill as they may find the ICU environment
to the family conference that outlines the purpose of and visit traumatic. However, this needs to be balanced
the meeting and points for discussion relating to current against a child who experiences separation anxiety,
and future patient care. A meeting guide prompts family which can be intense and have a negative impact on their
members to jot down their questions prior to coming adaptive functioning. In addition, when children are
to the conference to ensure these are discussed,69 as it is appropriately supported in visiting a critically ill close
well recognised that families forget, or are hesitant to ask family member, they are more likely to be not frightened
their questions. but rather curious about their surroundings.37 Children
Although family conferencing has been found bene- may have questions and it is recommended that they be
ficial, it is advocated that multiple modes of communication prepared well with adequate information before, during
and information sharing are required. Individualised or and after their time with their relative in the critical
general information via leaflets, brochures and internet- care area.
based information and support strategies are also helpful.45,68,70 Patients, however, may want visiting restricted as some
To promote communication, nurses can discuss with patients find them stressful or tiring.21 Contrary to popular
the family whether they would like a phone call at night belief, unrestricted visiting hours are not associated with
updating them on their relative’s condition. Alternatively, long visits. In two separate European studies where unre-
nurses can give them a time to phone before change of stricted visiting hours were introduced, the number of
shift. This will help to allay their anxiety and promotes hours family members spent with the patient was low.
positive communication and trust.When patients are trans- They stayed for 1 to 2 hours per day and usually came
ferred from critical care, families and patients may become during the day. This suggests that when family members
anxious or concerned by the reduced level of care in the have free access to their sick relative they do not perceive
new ward area.This can be alleviated by providing families a sense of duty to be there all day and night.14,80
with verbal and individualised written transfer informa- Barriers that restrict family presence require attention
tion as a means to help prepare them for transfer.71 In as family attendance is beneficial to the patient43 and a
addition, a structured transferring plan helps critical care primary need for family members.70 Although some
nurses feel better equipped to ensure they give families the critical care staff indicate they experience performance
information they need at this important time of transfer.72 anxiety with the family present during procedures43,81 or
with extended family visits,21 many nurses are comfortable
Visiting practices providing care with the family present.82 Staff who do not
One of the primary needs of families is the need to be feel comfortable with this methodology require support
physically close to their sick relative. Patient confidenti- and mentoring to facilitate this fundamental aspect of
ality and privacy remain central and need to be balanced family-centred care.
with family presence.73 Patients find that family provides Participating in patient care is one way for
a link with their pre-illness self and provides support and family members to feel closer to their critically ill family
comfort.74 member74,83,84 and at the same time promotes family
Family-friendly policies with few restrictions that integrity.83 Most family members, however, will not ask
centre on genuine patient care issues require the support if they can help with care32 as this is seen as the nurses’
198 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

communication difficulties due to either mechanical

TABLE 8.1 devices (e.g. endotracheal tubes),90 cognitive impairment
Family participation in patient care from the disease and/or pharmacological medications or
language difficulties.94 Therefore, effective communica-
PRINCIPLE PROCEDURE
tion is challenging, and nurses need additional knowledge
Consent Gain patient consent beforehand where and understanding of these complex situations to meet
possible medico-legal obligations and to assist in meeting the key
Building of Introduce the concept of family members’ information needs of patients and families.95 As many
trust involvement in care after a period during critically ill patients are unconscious, it is important
which a rapport is developed to understand the need for verbal communication
Individualise Offer suitable options from which family to continue. Such communication did not occur in
for patient and members can choose: for example, one Jordanian setting where in-depth interviews and
family massaging feet and hands, cleaning teeth observations in three critical care areas identified that
and feeding may be appropriate options nurses communicated less with unconscious patients
for short-term patients, whereas additional than with conscious patients.96 It has been known for
options may exist for long-term patients decades that sedated and unconscious patients can hear
Safety The registered nurse should remain and recall some verbal communication once they regain
physically close by at all times consciousness.97,98
Promote Provide sufficient information to the family Meeting information needs builds trust between
achievement member to support successful completion the nurse and patient and their family as a relationship
of goals of the care develops.95 The nurse’s understanding of the person
behind the patient is important to families, and can be
Reflect on Provide feedback to family members on
outcomes how they performed the task
achieved by talking to the family about the patient’s life
before the illness.99
Continuity of Document the care the family members
Good communication is a prime patient need and
care participated in and any relevant information
inspires patient confidence, making patients feel safe.100
When nurses reassure patients they provide a sense of
domain in adult critical care areas.85,86 Nurses, therefore, hope and a feeling of safety, which is further supported
should invite family members to be part of the patient’s by family members’ presence and the patients’ religious
care, with massaging and providing a sponge being popular beliefs, which may include the desire to have their priest
activities.6,33,86 Providing care allows the family members or religious leader visit.93,100 Constructive strategies
to feel connected emotionally with their relative and should be identified to overcome difficulties with
provides a means to get to know and communicate with patient communication.This is worthwhile pursuing as it
the nurses, which families consider important. Family reduces both nurse and patient frustration and improves
nursing care.91 The following methods of communica-
members appreciate invitations from nurses as this allows
tion may be used individually or together to enhance
them to feel more in control24 in a situation where family
communication, and should be readily employed in
members do not often experience this.87,88
critical care settings:90,101
For family participation to work effectively and
safely, a number of guiding principles should be incorpo- • body language
rated, as outlined in Table 8.1. It is useful for critical care • lip reading
nurses to explore their beliefs and practices concerning • writing
family participation, as many support family participa-
tion but do not always implement these beliefs in their
• alphabet boards
practice.89 • communication boards
• pictures
Communication • gestures, including nodding and blinking of the eyes.
The ability to communicate effectively is an underlying Although electronic voice output communication aids
tenet of nursing practice and a fundamental need for are used with disabled children and adults, they have not
people. As mentioned previously in the context of caring been evaluated sufficiently with an ICU population.These
for family members, for communication to occur, there aids use prerecorded digitalised voice messages or synthe-
needs to be a two-way passage of ideas or information. sised speech, with the phrases accessed by the patient via
In the patient context the inability to communicate a computer screen or keyboard.101 This device would be
causes, or adds to, anxiety, frustration and stress90–92 as restricted to those patients who are dexterous and able
they lose control over their life and decisions.93 It is to select an appropriate key, which limits its utility in
therefore imperative for healthcare professionals to find the ICU setting. However, some patients in a small study
ways to communicate with patients in simple non- found electronic voice output beneficial, particularly
technical language. Critically ill patients commonly have when communicating with family.101
 CHAPTER 8 FAMILY AND CULTURAL CARE OF THE CRITICALLY ILL PATIENT 199

summary: ‘[Subject’s name], we find her this and that’, and

Practice tip they’d be saying stuff and I’d think, ‘Oh no!’ They would
Routinely, both document and inform the nurse taking ask me, ‘Do you understand?’, ‘Are there any questions?’
over the patient’s care of any points of patient and family And I would think ಹ ‘I don’t even know what you just
discussion and any codes that have been developed said; how do I know if I have questions or not?’93 In this
during the shift to promote communication. This fosters case, both parties were trying to communicate with each
continuity of care and consistency in information other, but it is apparent that the patient was not able to
sharing and is useful to the entire healthcare team. take in and process the information about her current
condition and therefore had difficulty comprehending.
Basic principles of patient autonomy and respect need
An effective strategy to promote good communica-
to be used cautiously with critically ill patients who may
tion is for health professionals to seek and maintain eye
appear competent, when in reality their cognitive ability
contact (if culturally appropriate). This may mean the
is impaired.17 Effective communication with the family
nurse or doctor sitting down on a chair beside the bed
is vital in order to determine the cultural beliefs and
to facilitate face-to-face communication.95 This act also
practices of patients and their family to further enhance
conveys a sense of the importance the health professional
communication and understanding.
is placing on the interaction by taking time to ensure they
understand each other. Associated with this is the need
to use commonly understood language. One method of Cultural care
checking patients’ responses is to repeat these back to The challenge for critical care nurses is to establish positive
them. A quiet environment reduces extraneous noise and working relationships with the patient (when possible) and
potential interruptions, and may promote communication the family so their important values, beliefs and practices
and concentration. Codes may also be developed by the can be shared and incorporated in plans of intervention
nurse and patient, with facial expression, head nods and and treatment. It is not always possible to ‘know’ another
eye blinks used to respond to questions.91 These codes
person’s culture in any great depth, or ‘know’ all cultural
should be passed on to the next nurse and recorded in the
beliefs and practices of the patients and families a critical
patient’s notes to promote continuity of care.
care nurse comes into contact with. Therefore, establish-
When communication seems unsuccessful, talking
ing relationships with the patient and the family during
loudly will not improve the interaction; one good strategy
their critical care experience is crucial, and also demon-
is for the nurse and patient to agree to try again later.91
strates both respect for, and valuing of, patients and their
Communication can also occur through physical contact,
families and the cultural beliefs and practices they hold.
and touch often communicates empathy and provides
This enables critical care teams to better meet their needs.
spiritual comfort.1 Spiritual needs may further be met by
Although people’s ethnicities may provide a clue to
providing comfort, reassurance and respect for privacy, and
their culture, it is not a reliable indicator and ignores the
by helping patients relate to others.102
multiple cultural groups people belong to that extend
beyond ethnicity, such as age and gender. Furthermore,
Practice tip
with increasing migration globally and inter-ethnic
Communication with the family is essential. When family marriages, some people identify with more than one
members describe the patient, Ling-Chi, as the 55-year- ethnic group. Making assumptions about a person’s culture
old wife of Lee and mother of two adult children, June and reliance on universal approaches to direct nursing
and Maggie, who works full-time as an enrolled nurse, practice engenders risks to nursing practice and potentially
they help the staff to see the person beyond the patient compromises the outcomes of interactions and interven-
with an illness. This assists the critical care nurse to tions. Even within cultural groups (e.g. indigenous and
individualise care. immigrant groups), variations in beliefs and practices can
exist. Such differences result from factors such as colonisa-
Language barriers may necessitate the assistance of an tion, interactions with the various groups a person belongs
interpreter with knowledge of healthcare terminology to to, responses to societal changes and the socialisation of
ensure the content is adequately translated. An indepen- immigrants into a new country. Thus, person-centred care
dent person ensures that the patient receives the message of patients and their families is imperative to incorporat-
in its entirety from the health professional.95 Interviews ing specific cultural needs in the planning and delivery
with previously intubated patients after discharge from of interventions. This section outlines important strategies
the ICU capture, from the patients’ perspective, issues critical care nurses can develop for working with patients
with communication and highlight the need for further and their families to identify the essential beliefs and
improvement and understanding of the two-way process. practices they need to have incorporated into treatment
An example of this is from an ex-patient, who related her and intervention plans during a stressful time in an
situation: ‘They would come into the room in masses to unfamiliar environment. Such actions can optimise their
talk to me. One doctor would stand there and read off a spiritual wellbeing and lessen some of the stress they feel.
200 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Defining culture and diagnoses, risks excluding what is important for the
patient and family.108 This contrasts with indigenous
Wepa describes culture: ‘Our way of living is our culture.
cultures, for example, which tend to have a holistic
It is our taken-for-grantedness that determines and defines
eco-spiritual world view, with a strong spiritual dimension
our culture.The way we brush our teeth, the way we bury
that extends beyond a disease and illness focus.109 The
people, the way we express ourselves through art, religion,
world view of critical care nurses is influenced by the
eating habits, rituals, humour, science, law and sport; the
cultural beliefs, practices and life circumstances of each
way we celebrate occasions ಹ is our culture. All these
nurse, and the ‘world view’ of the critical care service that
actions we carry out consciously and unconsciously’.103,p.31
drives its service delivery. The result is that, consequently,
Simply, culture refers to the values, beliefs and practices
patients and their families become sandwiched between
that patients, family members and nurses undertake on a
differing world views.
daily basis. It determines how they view the world, and
Research highlights the lack of alignment that can occur
their orientation to health, illness, life and death.104,105
between the needs of consumers of health services and the
Culture involves a shared set of rules and perspectives
intentions of healthcare providers such as nurses.110 It is
acquired through the processes of socialisation and inter-
the potential for the non-alignment between patients and
nalisation. These provide a frame of reference to guide families and healthcare providers that critical care nurses
how members interpret such phenomena as health and need to be aware of, as dissatisfaction with the care being
illness and death and dying. This, in turn, influences their delivered may arise when the patient’s and family’s needs
actions and interactions.105 Culture is a more specific way are not recognised or attended to,111 leading to unneces-
of describing how groups of people function on a daily sary tensions and conflicts between patients, families and
basis, influenced by their beliefs, relationships and the nurses. A nurse’s willingness to acknowledge and respect
activities they engage in. patients’ world views and the things that are important to
Understanding that culture, ethnicity and race are not them minimises the occurrence of any dissatisfaction,108
the same thing is crucial to meeting the cultural needs of as it values their specific needs during their critical care
patients and their families. Race is generally determined experience.
on the basis of physical characteristics and is often used to
socially classify people broadly as Caucasians, Europeans, Practice tip
Polynesians or Asians, for example.106 However, assigning
people to a homogeneous group is problematic, the Being able to deliver culturally responsive nursing care
antithesis of cultural diversity,103 particularly as globally requires the nurse to undergo a process of education
countries are becoming increasingly ethnically diverse. and self-examination of culture, own cultural beliefs and
Furthermore, homogenisation does not account for the practices, and the possible influences these may have
diversity that exists within many groups in contemporary on practice.
society. Ethnicity extends beyond the physical charac-
teristics associated with race to include such factors as Where the world views of patients and families are
common origins, language, history and dress – it is usually considerably different from that of the nurse, nurses should
associated with nations,103 although a number of ethnic identify the beliefs they hold about the patient and family,
groups may exist within a nation. the impact of these interactions on the patient and family
and the power the nurse can utilise during such inter-
Differing world views actions.103 Sometimes the nurse’s personal beliefs will be in
Culture influences how people view the world, what conflict with professional nursing beliefs, which necessi-
they believe in and how they do things, particularly with tates choosing between personal and professional beliefs
regard to practices around health, dying and death. The in the practice setting. For example, a nurse’s personal
critical care environment is unfamiliar for patients and beliefs about life, death and body tissues may be compro-
families, especially as health professionals’ beliefs, practices mised by the duty to care for a patient with brain death
and world views may not align with their own. What is awaiting the removal of organs for transplant. This may
important for critical care nurses may not be important also be compounded by nursing staff shortages, less-than-
for the patient or the family, and may lead to tension desirable skill mixes and the acuity and complexity that
and dissatisfaction when patients’ and families’ views are critical care nurses are faced with on a daily basis.Therefore,
at variance. This does not mean that one world view is it is vital, not only for the individual nurse, but also for the
necessarily more right or wrong – they are different. team of critical care nurses to develop strategies, such as
The biomedical model influences the way healthcare processes and procedures, that can optimise the develop-
services are structured and delivered.107 As a dominant ment of working relationships with patients from different
model it heavily influences the necessary focus on the cultural backgrounds.112
physical wellbeing of patients within critical care envi-
ronments. Focusing on the management of disease and Cultural responsiveness
illness, and using processes that lead to health issues being Cultural responsiveness refers to strategies for responding
fragmented and reduced to presenting signs and symptoms to a patient’s and their family’s cultural backgrounds, and
 CHAPTER 8 FAMILY AND CULTURAL CARE OF THE CRITICALLY ILL PATIENT 201

depends on the cultural competence of nurses so that diversity that exists both among and within groups.118
they feel cultural safety. Different models exist to assist Therefore, critical care nurses are advised to critically
in the integration of the cultural beliefs and practices of examine theories and models to guide their practice, to
patients and their family in critical care nursing practice. ensure they deliver appropriate and effective care for the
For example, Leninger’s cultural care diversity and patients and families they work with.
universality theory113 requires nurses to deliver culturally Competence is an important dimension of nursing
congruent nursing care for people of varying or similar practice, as it provides users of nursing services with
cultures. Ramsden’s work on cultural safety114,115 focuses confidence in nurses’ knowledge, skills and attitudes
on the delivery of nursing care to patients (whose cultural necessary to undertake their practice. Given the importance
beliefs and practices differ from that of the nurse) that is of culture in the delivery of nursing care, the measure-
determined appropriate and effective by the patients and ment of cultural competence is also important. There is
families who are the recipients of that care. These models evidence of numerous variations on the concept of cultural
have been used to guide nursing practice in Australia, competence.118–120 The attributes of cultural competence
New Zealand and North America. Such models require include cultural awareness, cultural knowledge, cultural
that critical care nurses recognise patients’ and families’ understanding, cultural sensitivity, cultural interaction
views of their health experience107 and any that subse- and cultural skill.119–121 However, the inherent need for
quently have discordant priorities. Wood and Schwass the acquisition and use of culturally specific information
have described three levels at which a nurse may practise limits the application of these attributes: the collation of
with respect to cultural issues (see Table 8.2).116 These culturally specific information is becoming increasingly
levels, ranging from cultural awareness to cultural safety, problematic as our communities become more diverse in
describe the differing characteristics of nurses’ cultural their composition.
care. For example, a nurse practising in an organisation
where cultural safety is required would need not only to Practice tip
recognise differences between groups of people, but also to
The ability to deliver culturally competent nursing
deliver differing cultural care to patients and their families practice involves self-awareness, the nurse’s actions
after undergoing appropriate education. undertaken to improve the patient’s and family’s health
From a transcultural nursing perspective, culturally experience and integrating their beliefs and practices
responsive nursing care requires the nurse to incorporate into treatment and intervention plans.
cultural knowledge, the nurse’s own cultural perspective
and the patient’s cultural perspective into intervention Cultural responsiveness is about practising in a sound
plans.117 However, it is not possible to collate cultural manner rather than about behaving correctly.122 Durie
knowledge specific to various groups owing to the encouraged the development of cultural safety (which
focuses on the patient’s and their family’s experience and
TABLE 8.2 determination of the appropriateness of care received),
to a construct that can measure the capability of the
Levels of cultural practice
health worker, such as the critical care nurse.122 Culturally
L E V E L O F C U LT U R A L competent nursing practice is about:
PRACTICE I N D I C AT O R S
• the nurses’ knowledge about their own cultural beliefs
1 Awareness Recognition that differences and practices and the impact these may have on others
between groups of people
extend beyond socioeconomic
• the actions of the nurse to improve the patient’s
health experience, and the integration of culture in
differences
clinical practice
2 Sensitivity Recognition that difference is
valid, which initiates a critical
• delivering culturally competent and safe care.123
exploration of personal cultural Cultural competence provides a framework to objec-
beliefs and practices as a tively measure the nurse’s performance, although there is
‘bearer’ of culture that may variation in frameworks.112 Fundamental for the critical
affect others care nurse to deliver culturally responsive care, which is
3 Safety Delivery of a safe service as a
competent and safe, is determining the cultural needs of
result of undergoing education patients and families, and the provision of patient-centred
about culture and nursing care that focuses on their individual needs.
practice, and reflecting on their
own and others’ practice
Determining the cultural needs of
patient and family
Adapted from Wood PJ, Schwass M. Cultural safety: a
framework for changing attitudes. Nurs Prax NZ 1993;8(1):
The concepts of health and illness are generally constructed
4–15, with permission. within the context of people’s sociocultural environment
and the groups they belong to; these vary from person to
202 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

person and group to group. To this end, culture influences as a result of communication problems with the family;
how health and illness experiences are constructed and communicating information in a clear and understandable
lived. When people become critically ill, their cultural manner helps prevent these problems from occurring.
beliefs and practices can be just as important as their
physical health status.124 Yet cultural beliefs and practices are An Indigenous health workforce
often compromised when healthcare providers’ concern Increasing the representation of indigenous people within
about physical health takes precedence – invariably, health the health workforce has been recognised internationally
services also do things differently than patients and families as an important mechanism for improving cultural safety
would do them.While the importance of psychosocial and within healthcare facilities.129 Research has demonstrated
cultural needs is the focus of this chapter, the presence of that indigenous people are more likely to access mainstream
life-threatening events or crises experienced by the patient health services if there is an indigenous workforce.130
in critical care must rightfully take precedence. However, on In Australia, there have been efforts to increase the
stabilisation of the patient, establishing a positive working number of Aboriginal registered nurses to improve the
relationship with the family can facilitate the determina- competency of the Australian nursing workforce in
tion of their perspectives and needs and negotiation about delivering appropriate care to Aboriginal people. This
how these can be included in a potentially complex plan move is supported by the ‘getting ’em ‘n’ keeping ’em’
of care. Incorporating cultural requirements becomes vital report of the Indigenous Nursing Education Working
in a delivery of nursing care that is both appropriate and Group.131 Similar strategies for improving culturally
acceptable. Therefore, given the nature of critical care responsive care by increasing the participation of First
settings, the quality of interactions with the patient’s family Nations people within the healthcare workforce exist in
is just as crucial as interactions with the patient. North America (see, for example, the National Aboriginal
Promoting a genuine, welcoming atmosphere and the Health Organization132 and the First Nations Authority133).
use of effective communication invite the family to be
involved early in the patient’s critical care experience, and Cultural responsiveness and patient-
are essential to determine the cultural needs of the patient
and family. While communication has been mentioned
centred, individualised care
earlier, interpreting cultural needs requires the critical care ‘Individualised care requires the patient and nurse to work
nurse to be attentive to communication. Nurses are advised together to identify a path towards health that maintains
to talk less, attend to details that may arise and simply the integrity of the patient’s sense of self and is compatible
listen. The need to intervene and to dominate discus- with their personal circumstances’.134,p.46 This means the
sions and ‘interviews’ with the family125 from the nurse’s critical care nurse ideally working in collaboration with
perspective needs to be curbed, so time is made available the family to identify important cultural needs and the
for cultural beliefs and practices to be shared.27,108,125 inclusion of beliefs and practices that need to be observed
Understanding and supporting the patient and family can during the patient’s critical care experience; in other
be improved by the nurse’s empowering them through the words, eliciting a patient’s view to ensure person-centred
processes of listening, understanding and validating what care.135 It is recognised that ‘the work’ of the nurse involves
they have to say.124,126 Conning and Rowland’s research responding, anticipating, interpreting and enabling, all of
on the attitudes of mental health professionals towards which are crucial for individualised care.136 Indeed, part-
management practices and the process of assessing patients nership requires the nurse not only to work with the
and decision making found that those who had a greater patient and family but also to identify the power that
‘client orientation’ (versus management orientation) were the nurse possesses and the potential for its inadvertent
more likely to engage in assessment processes that facilitate misuse.108 Patient- and family-centred care requires critical
patient-centred care that focuses on the individual needs care nurses to observe each of the following:
of patients and their family.127,128
Working in partnership with a family can bridge the • respectfully interacting with the patient and their
family, and treating them with dignity
cultural ‘gap’. However, this is not always easy to achieve
in challenging situations, such as when various members • communicating clearly, without jargon
of a large family come and go, compounded by changing • sharing information fully and honestly
nurses with shift changes. Receiving clear and consistent
information about the patient, including his/her progress,
• using the strengths of the family to enhance their
sense of control and independence
from all members of the healthcare team can reduce
cross-cultural confusion and misunderstanding, especially • working with patients and their family collaboratively.136
as messages are prone to distortion and change when Facilitating the inclusion of cultural beliefs and
many are involved. A strategy to manage this may involve practices requires identification and then incorporation
discussing the management of information dissemination in the patient’s plan of care. However, given the resource
with the family, and the identification of one or two family constraints and the culture of some health services,
members who become the point of contact through universal approaches to planning care may be adopted for
which staff discuss and communicate information about convenience. The critical care nurse is discouraged from
the patient.108 Often, apparent ‘cultural conflicts’ will arise adopting a ‘one-size-fits-all’ approach to nursing practice,
 CHAPTER 8 FAMILY AND CULTURAL CARE OF THE CRITICALLY ILL PATIENT 203

as this disregards the cultural systems of the patient and Working with culturally and
family.108 Patient-centred care is optimised by nurses
having sufficient information about the patient and family linguistically diverse patients and
in order to identify their needs and plan interventions. families
Incorporating each family’s cultural beliefs and practices Globalisation has resulted in increasing immigration and
provides a ‘bigger picture’ of the patient124 than would migration to both Australia and New Zealand, similar to
have been gained by simply focusing on the presenting other countries, thus populations are increasing in their
disease or illness and its management. Such an approach cultural and linguistic diversity. Thirty-three percent
to patient-centred care enables the critical care nurse to of Australians,140 25% of New Zealanders,141 20.6% of
become familiar with the context of the patient’s life Canadians142 and 13% of Americans143 were born overseas.
circumstances and how they interpret illness, and also Immigrants arrive from various countries globally, but
improves the quality of care and interactions they have especially the European, Asian and African continents.
with patients and families.137,138 Labels assigned to groups of ‘immigrants’, such as Asians,
Sometimes the nurse will want to have a full under- are misleading and far from the homogeneity they infer.
standing of a cultural belief or practice before being Added to the complexity of trying to determine ways
willing to incorporate it. For example, several years ago of working with culturally and linguistically diverse
a Ma-ori patient was dying and the family wanted to patients and families is the variation in their degree of
organise the patient’s expedient removal from the hospital acculturation – for example, some may be second- or
environment on the patient’s death. This was necessary so third-generation Australian- or New Zealand-born and
that the spiritual and cultural grieving processes could be highly acculturated into the respective culture, or they
commenced. But the nurse blocked the family’s desire to may be new immigrants with traditional cultural beliefs
plan and organise a prompt postmortem on death because and practices. Therefore, given this diversity it is difficult
the patient had not yet died. This created unnecessary to provide specific guidelines on working with culturally
tension and conflict between the nurse and the family. and linguistically diverse patients and their families,
Clearly, the nurse’s and the family’s beliefs about death and although some common principles exist.
dying were different, and the apparent position of ‘power’ A fundamental starting point for working with
adopted by the nurse did not encourage communication culturally and linguistically diverse patients is to establish
and negotiation about how this situation could be resolved their capacity to communicate in English. Determining
to the satisfaction of both parties. This is an example of the language a patient uses on a daily basis, and whether
where the identification and acceptance of cultural beliefs they can speak and write in English, will indicate whether
and practices of the family (to the extent that they will an interpreter is needed. Family members or friends can
not deliberately harm the patient), and working with the be used as interpreters when care is being undertaken on
family on how these are incorporated in an interven- a daily basis, although a professional or accredited inter-
tion plan, can be beneficial to all parties. Once this has preter should be used when important information is to
occurred, it is crucial this information is documented, be shared or when decisions need to be made. This avoids
thereby making visible the patient’s individualised care.139 the potential for family members or friends ‘censoring’
the information conveyed during discussions. How the
Practice tip patient prefers to be addressed, cultural values and beliefs
related to communication (e.g. eye contact, personal
Determining cultural needs means the critical care
space or social taboos), preferences related to healthcare
nurse must:
providers (that is culture, gender or age), the nature of
• identify a spokesperson to communicate information family support and usual food and nutrition are other
to so the messages the family receives are consistent areas that should be explored with the patient or family,
• engage in genuine communication and partnership whichever is appropriate.
with the patient and family Given the great diversity that occurs within contempo-
• be willing to listen, understand and validate rary cultural groups, it is crucial to develop a relationship
information received. so important cultural values, beliefs and practices can be
identified and incorporated into the patient’s plan of care.
Critical care nurses can then better understand a patient’s
Practice tip or family’s behaviours when the patient is critically
unwell. Discovering the values and beliefs a patient and
To optimise interactions with people from a culture their family have about health, illness, death and dying,
different from yours as a critical care nurse: and what they believe may make their health worse, is a
• avoid making assumptions good starting point, and will provide insight into the type
• avoid culturally offensive practices that are known of support and caring behaviours that may be observed. In
and learned addition to this, identifying how health and illnesses are
• remember that actions speak louder than words. managed will provide an indication of whether traditional
healers are used, along with healing remedies such as herbs
204 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

and prayer, for example. Understanding the patient’s locus diverse people should be based on the following framework:
of control can also provide an indication of whether they 1 Partnership: aim to work in partnership with the
will play an active role in the outcome of an illness, or patient and family. Prior negative experiences
whether there is a fundamental belief that illnesses are may influence the development of a productive
caused by some external force. relationship. A respectful, genuine, non-judgemental
For many cultural groups the presence of family is attitude is necessary to develop a productive
vital to both the patient’s and family’s spiritual wellbeing. relationship with the patient and family, and
Therefore, facilitating family presence at the patient’s providing time for responses is important.
bedside and possibly including them in the care of the
2 Participation: where possible involve the patient
patient is important. For some cultures there is a belief
that family members should shoulder the burden of infor- and family in their care, if this is appropriate. This
mation and decision making so the patient can expend will involve the critical care nurse explaining the
their energy and focus on getting better. In some cases to treatment and intervention routines.
burden the patient with information about their condition, 3 Protection: determine specific cultural and spiritual
especially its gravity, or having to make decisions, is values, beliefs and practices, and enable these to be
believed to contribute to a negative outcome. Thus, practised during the patient’s time in the critical care
positively engaging families and, where practical, patients unit. Where possible these should be accommodated,
in collaborative relationships, involving them in the care although there may be instances when this is not
and decision making and ensuring their cultural values, possible. In such situations, the patient and family
beliefs and practices are protected are ways critical care should be fully informed of the rationale for this.
nurses can respect the cultural traditions of those patients Considerations when caring for Aboriginal and Ma-ori
who are from different cultural and linguistic backgrounds. peoples are reviewed in the next sections. Closely related
Campinha-Bacote’s144 mnemonic, ASKED, provides to cultural aspects of care is spirituality, which for some is
a process for self-reflection to make explicit your based in religion. Aspects to consider when patients have
knowledge and skills and desires to work with people religious needs are reviewed later in this chapter.
Working with Ma-ori patients and
who are culturally and linguistically diverse.The following
questions can be asked:
• Awareness: what awareness do you have of the stereo- families
types, prejudices and racism that you hold about those Ma-ori are the indigenous people of New Zealand and,
in cultural groups that are different from your own? like other indigenous people who have survived the
• Skill: what skills do you have to undertake a cultural processes of colonisation, they experience poorer health
assessment in an appropriate and safe manner? status and health outcomes and socioeconomic disad-
vantage compared to other groups in the New Zealand
• Knowledge: how knowledgeable are you about the population.145 Ma-ori were not a homogeneous group
world views of the various cultural and ethnic groups
within your community? of people before settlement by European people, and
contemporary Ma-ori continue to be diverse in their iwi
• Encounters: what face-to-face interactions have you (tribal) affiliations, cultural identity, backgrounds, beliefs
initiated with people from different cultural groups and practices,146 and in the colour of their hair, eyes and
than yourself? skin. The critical care nurse ideally needs to recognise the
• Desire: what is the extent of your desire to be diversity that exists, and have a sociopolitical and historical
culturally safe or competent in your nursing practice? perspective of contemporary Ma-ori. This positions the
When critical care nurses understand their position critical care nurse to understand the importance of and
on nursing people from other cultures, strategies can be respect the need to undertake assessments with Ma-ori
adopted to improve their responsiveness and the quality of patients and wha-nau regarding their cultural needs (see
care delivered. Working with culturally and linguistically Table 8.3).

TABLE 8.3
Considerations for working with Aboriginal or Ma-ori people
-
ISSUE A B O R I G I N A L C O N S I D E R AT I O N M AO R I C O N S I D E R AT I O N

Holistic, spiritual • Health is not just the physical • Most Ma-ori have a holistic and spiritual world view, this means
world view wellbeing of the individual but wha- nau (extended family) and their wairua (spiritual wellbeing) are
the social, emotional and cultural important
wellbeing of the whole community • Wha- nau members generally have a strong connection and sense
of obligation to each another, which means that they want to be
present with patient, especially when they are unwell
 CHAPTER 8 FAMILY AND CULTURAL CARE OF THE CRITICALLY ILL PATIENT 205

-
ISSUE A B O R I G I N A L C O N S I D E R AT I O N M AO R I C O N S I D E R AT I O N

Beliefs around • Identify any previous encounters • Many Ma-ori have had negative experiences in hospitals with
hospitalisation with family members dying, or wha- nau dying. They have also been subjected to judgemental staff
and places to stories from communities that and discriminatory attitudes and behaviours. Therefore,
die reinforce these views Ma-ori wha- nau may be wary and possibly defensive – approaching
• Provide honest responses to them in consistent, genuine and non-judgemental ways can instill
questions about a patient’s condition confidence that the patient will be cared for well
• Avoid communication that expects • Talk to wha- nau about concerns they may have about the patient
people to ‘read between the lines’ and the care they will be receiving, and any specific cultural
practices they would like observed
• It is important to avoid doing things that may breach tapu: by
keeping body tissues and fluids, and body parts, away from food
and utensils; removing food and drink when undertaking cares,
not putting food where hairbrushes are, for instance. Body parts
(particularly the head for some Ma-ori), tissues and fluids are
considered tapu (spiritually restricted)
Traditional • Explore how traditional medicine can • Explore how traditional healing and medicines can complement
healing complement western medicine western medicine. Traditional healers (tohunga) may play an
• Facilitate access by traditional important role
healers when requested • Discuss with the wha- nau any specific healing modalities that
need to be considered, e.g. a tohunga to be present or the use of
rongoa- or karakia (prayer)
Connections • Acknowledge Aboriginal people’s • Acknowledge that connections with other people and the land
needs to connect to the land and may be important
possible need to return to their land • Whakapapa and kinship may be important, so having wha- nau
to die present may be very important
• Compound families are common and • Note that wha- nau is broader than the nuclear concept of family,
identifying kinship relationships is and kaupapa wha- nau (wha- nau groups formed between those
important members who do not share genealogical connections) are equally
important for some as whakapapa wha- nau
• Enquire whether body tissue/fluids/parts need to be returned for
burial
Elders • Respect of community elders • Elders are respected members of society that hold mana and
• Elders are often spokespersons important status. Thus, an unwell elder may have a lot of visitors
for the family so the spokesperson because of his/her respected status
needs to be identified • Elders may be the spokesperons for the wha- nau, or will designate
spokesperson(s) for staff to communicate with
Establishing • Aboriginal health workers and • Showing attitudes and actions that are genuine, and a willingness
relationships liaison officers provide vital links to to listen and to share where you have come from and who you are,
Aboriginal communities are helpful in establishing relationships with Ma-ori wha- nau
• Establish relationships with • The principles of the Treaty of Waitangi, partnership, participation,
Aboriginal people through sharing protection, provide a useful framework for working with Ma-ori
community knowledge: family, • Establish and maintain a positive partnership relationship that
friends, football, food promotes participation of wha- nau and that protects their values
and beliefs
• Develop a relationship with the Ma-ori health service within the
hospital
Diversity • Aboriginal communities have • Ma-ori are diverse, so patient-centred assessment and planning
different lores is important. This recognises the diverse values, beliefs and
• Talk to family, community elders practices of Ma-ori
about community lore
Language • Facilitate use of interpreters • Facilitate use of interpreters for Ma-ori whose main language is te
• Cautiously engage family or trained reo Ma-ori
community members • Always check out understanding of the information shared
• Have culturally appropriate • Avoid using healthcare jargon when explaining things
resources developed
206 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

The Treaty of Waitangi (commonly known as ‘the care nurses often have to explore how they manage rela-
Treaty’) is based on an agreement between Ma-ori and tionships with large numbers of people within confined
the Queen of England, Queen Victoria, which estab- physical spaces, which may necessitate establishing rela-
lished the rights of Ma-ori as tangata whenua, or people tionships and identifying one or two people who will be
of the land. There are two versions of the Treaty – one the point of contact through which information can be
in English and one in te reo Ma-ori (Ma-ori language). communicated.124 Establishing connections and links can
Ma-ori understood that, while they gave governorship to be a positive way of engaging with Ma-ori patients and
the Queen under Article One of the Treaty, they would wha-nau; this is often called whanaungatanga, and Ma-ori will
retain their right to control and self-determination over often do this by sharing their whakapapa, or genealogy.
their lands, villages and taonga (which includes health) This means identifying where you have come from and
under Article Two. Under Articles Three and Four Ma-ori who you are. It is crucial that the critical care nurse be able
are guaranteed protection and the same rights as British to demonstrate a genuine intent and a willingness to listen
citizens, including the protection of beliefs and customs. to what the wha-nau feel is important. Forming effective
Nurses working within the New Zealand health setting working relationships with Ma-ori wha-nau can never be
can be considered agents of the Crown;147 therefore they underestimated. It is also useful for critical care nurses to
have a responsibility and obligation to honour the Treaty establish working relationships with Ma-ori health services
when working with Ma-ori. The principles of partnership, within their health service and to get to know the local
participation and protection148 are used to apply the Treaty Ma-ori community.
in practice within health settings such as critical care.
The commitment that critical care nurses have to Practice tip
establish, and maintain, a positive relationship with Ma-ori
patients and their families is as important as being willing Often when a wha- nau member is seriously or critically
to facilitate the inclusion of cultural beliefs and practices in ill, the wider wha- nau members will have a strong sense
the care of the patient. Such a commitment can influence of obligation to want to visit and to manaaki (care for)
the outcome of the critical care experience for Ma-ori the immediate wha- nau members. This may mean
patients and their wha-nau. It is not the purpose of this many wha- nau members will be present at the hospital.
section to provide a ‘recipe’ for working with Ma-ori in In situations such as this it is often important to get
the critical care setting. An overview of the fundamen- the wha- nau to identify a spokesperson with whom
tal issues to consider, and the importance of critical care to engage in explanations and discussions about
nurses establishing working relationships with local Ma-ori the patient, and the needs of the critical care staff to
health services and/or local iwi and Ma-ori community care for the patient and other patients. This assists in
groups, is stressed. meeting the needs of both the wha- nau and the critical
Ma-ori have a collective, rather than an individual, care staff.
orientation, with whakapapa and kinship having an
important place.149 Reilly outlines the variations that Many Ma-ori view themselves as spiritual beings,146,149
occur in the contemporary social organisation of and ill health may therefore be seen to have a spiritual as
Ma-ori.149 The wha-nau is the social group that critical care opposed to a physical cause. The way Ma-ori interpret the
nurses will generally interact with. Wha-nau encompasses world is a unique blend of cultural artefacts from the past
more than the common notion of the family.150 Wha-nau and present, and also reflects the nature of their interac-
are inclusive and are made up of multiple generations, tions within contemporary society.146 Despite the diversity
extending widely to include those who have ‘kinship’ ties. that exists, many Ma-ori have a world view that is holistic
This contrasts with the ‘nuclear’ family concept. Elders, and eco-spiritual in nature.150 This holistic and spiritual
especially kuia (older respected women) and kaumatua world view interconnects the physical world and the
(older respected men) possess mana (power, authority world of others.149 Ma-ori creation stories are cosmologi-
and prestige) and important status that commands cal in nature, and establish the link Ma-ori have to the atua
respect. Because of the status of kuia and kaumatua in (gods) and tupuna (ancestors) who created the world and all
Ma-ori society, if they become ill it is especially important living things through the separation of Ranginui (the ‘sky
for the wha-nau and wider Ma-ori community to support father’ in mythology) and Papatuanuku (the ‘earth mother’
them during this time. in mythology).151 For some Ma-ori, acknowledging atua
and tupuna in karakia (ritual chants or prayer) is spiritu-
Practice tip ally important, as well as maintaining their strong links
to others and the land. Some Ma-ori also have religious
Ma-ori elders may prefer to speak in te reo Ma-ori (Ma-ori faiths originating from the processes of colonisation, and
language). In these instances, a wha-nau member may may include Christianity or the Ma-ori-based Ratana
be able to assist in interpreting explanations about care. and Ringatu faiths.149
The activities of individuals and groups of Ma-ori that
Because of the collective orientation of many Ma-ori, serve to control human activities and life, and maintain
wha-nau support is exceedingly important. Thus, critical health and wellness, are restricted spiritually and
 CHAPTER 8 FAMILY AND CULTURAL CARE OF THE CRITICALLY ILL PATIENT 207

practically (through rituals) by the concept of tapu (sacred

or restricted).122,149 Breaches of tapu, while spiritual in Practice tip
nature, often manifest in physical forms such as illness. Acknowledging identity is an important contributor to
Often illness is seen as a failure to observe tikanga (custom) establishing respectful cross-cultural relationships.
and tapu,149 and is known as makatu (a spell or curse) or Be mindful of Australia’s history of colonisation of
mate Ma-ori (sickness or death). Traditional healers and Aboriginal and Torres Strait Islander people and take
healing practices (such as the use of rongoa [medicine] the time to ask Aboriginal people what community/
and karakia [ritual chant or prayer]) play an important traditional name they identify with, e.g. Koori, Yolngu,
role in healing someone who is ill. Accessing traditional Kaurna, Barundji, Gurindji etc.
healers, such as a tohunga (expert), may be an important
part of the critically ill person’s recovery or dying process. The contribution of Aboriginal people as a small com-
However, cultural expressions of spirituality differ among ponent of the overall Australian population means that
Ma-ori and, for some, traditional cultural approaches critical care nurses will have varying levels of interaction
may not be acceptable. The critical care nurse needs to with them. For example, Aboriginal people represent 30%
identify the beliefs and practices related to wellbeing of the population of the Northern Territory and between
and illness. 45% and 65% of intensive care admissions.153,154 There-
There are some things that are done in one culture that fore, working with Aboriginal people is core business for
are perceived to be offensive in another, and thus disrupt critical care nurses in the Northern Territory. In contrast,
the formation of relationships.The concept of tapu (sacred 6.4% of patients admitted to a tertiary intensive care unit
or restricted), mentioned above, is also associated with the in Western Australia identify as Aboriginal,155 which is
concept of noa (common), or to make ordinary. Thus, a slightly higher than the national figures where Aboriginal
person’s body, body fluids and body parts are considered people represent on average 5.6% of intensive care admis-
tapu, whereas food is often used to make something sions.156 This section therefore aims to provide information
ordinary. In practical terms this means that food should that will assist critical care nurses to understand some of
be kept separate from the person’s body and body fluids. the complexities of care unique to Aboriginal people no
For example, do not put urine in urinals or collecting matter where they work and to improve the experience
chambers for faeces in pans on surfaces where food will for both nurses and patients regardless of whether this is a
be put. Body tissues and body parts and their placement familiar or unfamiliar situation for all concerned.
and disposal are a major consideration in the care of The information presented is broadly applicable to
Ma-ori. For some Ma-ori, having their body parts and any the diverse cultural and language groups of Aboriginal
tissues removed returned to them so they can bury them is people and their communities in Australia. However, it is
spiritually important: they are returning these to Papatu- essential that each episode of nursing care provided for an
anuku (the Earth Mother). However, again it is important Aboriginal person and his/her family is individualised to
to identify what is important for each patient and their the person, their distinct cultural heritage, local Aboriginal
wha-nau, as some Ma-ori may not want their body tissues or law, identified family relationships and unique connection
parts returned to them. with particular land and country.

Practice tip
Health status of Aboriginal people
Critically ill Aboriginal people vary from their non-
Before proceeding with care that involves touching the indigenous counterparts. Aboriginal persons admitted to
head or disposal of body fluids, for instance, ask the Australian ICUs are on the whole younger (mean age 40
patient or family member if there are any considerations compared to 48 years) and sicker than non-indigenous
that need to be observed. people. Emergency admissions for sepsis, septic shock,
pneumonia, cardiopulmonary arrest and trauma are most
common for Aboriginal people. The high rates of infection
Working with people of Australia are reflective of the high burden of chronic disease within
Aboriginal and Torres Strait Islander peoples are the Aboriginal population and the challenging socioeco-
the traditional owners of Australia but currently nomic setting in which Aboriginal people live.153 Injury,
represent only 3% of the entire population. Of this poisoning, motor vehicle accidents, assaults, self-inflicted
population 90% identify as Aboriginal, 6% identify as harm and falls are the second most common causes of
Torres Strait Islander people and 4% identify as both hospitalisation for Aboriginal people.157 Hospitalisation for
Aboriginal and Torres Strait Islander people.152 In line assault is 34 times higher for Aboriginal women than other
with culturally acceptable practices, excepting for women. Aboriginal men aged 15–24 years have the highest
when distinctions between Aboriginal and Torres Strait rate of trauma of any age group and experience violence
Islander people are required, the term Aboriginal will be twice as frequently as non-indigenous men.158 Aboriginal
used for the remainder of this section to refer to both people also have disproportionately higher rates of presen-
population groups. tation to ICU following suicide attempts compared to their
208 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

proportion of the overall population.159 Aboriginal males particularly important impact on the patient themselves
are also more likely to choose hanging as a method of and their accompanying family members.
suicide, survive and require a subsequent admission to ICU The concept of ‘culture shock’ provides an explana-
following hanging than non-indigenous people. tion for the tension and anxiety, feelings of isolation and
Although mortality rates for Aboriginal people admitted sensations of loss, confusion and powerlessness that people
to intensive care units are comparable to outcomes for encounter when entering an environment characterised
non-indigenous people, the reality is that they have a higher by an unfamiliar culture.162,163 The critical care environ-
severity of illness (APACHE II score), which is related to ment is unfamiliar to most people. However, in the case
their high levels of chronic disease.153,154 Rates of diabetes of Aboriginal people an admission to critical care may be
are three times higher for Aboriginal people than for the first time the patient and their family has encountered
non-indigenous people, and they are also 3.9 and 5.7 times this level of invasive healthcare treatment and/or city life.
more likely to be hospitalised for diabetes than non-indig- The conditions in remote communities where one-quarter
enous males and females, respectively. In 2012, Aboriginal of Aboriginal people live are very different to the circum-
people died from diabetes at almost seven times the rate of stances encountered in a major city or even regional hospital.
non-indigenous people. Between 2008 and 2012 the rate of For example, most Australian hospitals are multistorey.
end stage renal disease was 7.3 times higher for Aboriginal Travelling in a lift may be a significant challenge164 for family
people than for non-indigenous people.The most common members. Being ‘up in the air’ away from direct contact
reason for hospitalisation of Aboriginal persons was care with the earth and enclosed in an air-conditioned envi-
involving dialysis. Chronic liver disease is also high amongst ronment can be unsettling so that frequent visits outside
Aboriginal people, with the hospitalisation rate for alcoholic are often necessary to renew contact with the natural and
liver disease six times the rate for non-indigenous people. more familiar external environment. The highly technical
Rheumatic heart disease, which is rare among non-indig- environment of the critical care unit adds another layer of
enous Australians, is prevalent amongst Aboriginal people unfamiliarity and contributes further to a sense of anxiety.
aged 45–54 years.157,160 There are specific hospital routines, corridors and spaces,
Each of these chronic diseases is preventable. The unfamiliar smells, technology, restraints on movement,
high incidences reflect the socioeconomic disadvantage protocols for safety, limitations to visiting, biomedical
experienced by Aboriginal people and the decreasing customs and practices, professional and personal relation-
access to primary health care the further people live from ships to negotiate and language and jargon to interpret,
major cities.158 In broad terms, the ‘social determinants of along with expectations of compliance to systems and pro-
health’ reflect the disadvantage Aboriginal people suffer in cedures that reinforce the dominance of western medicine.
terms of employment, physical infrastructure (including Critical care nurses have a significant role in deter-
running water and housing), education, connection to mining how well Aboriginal patients and their families
land, racism and incarceration.161 Together, these factors manage such culture shock. A first step is being aware of
result in Aboriginal people presenting to hospital further the contributing factors and the feelings these may invoke
along the trajectory of their disease process than non- for Aboriginal people. The authors of Binan Goonj165
indigenous people. In the critical care setting many have identified factors characteristic of six cross-cultural
chronic health conditions, including severe cardiovascular stressors within institutions such as hospitals. Figure 8.1
disease, may not have been diagnosed until the person depicts these stressors and some of the concerns and
presents with life-threatening complications. Similarly, reactions experienced by Aboriginal people. Acknowledg-
life-threatening complications of acute illness exacerbate ing these stressors and reactions is a first step in assisting
underlying chronic disease and result in more complicated the patient and their family to adapt to the unfamiliar
and often longer lengths of stay in critical care.155 With culture of the critical care unit.
even this very brief overview of the status of Aboriginal Establishing trust to promote adaptation165 should be
health, it should be clear that understanding both the phys- a priority of the critical care nurse. Understanding the
iological and social determinants of health is essential for conditions that underpin culture shock for Aboriginal
optimal nursing care of the critically ill Aboriginal person. patients and their families is a particularly good starting
point for developing trust. Understanding the importance
A long way from home and family in an of family within Aboriginal culture and how the culture
unfamiliar environment influences beliefs about health and illness is also essential
The geographical distribution of the Aboriginal population for developing a therapeutic relationship and minimising
not only impacts on how much contact the critical care the impact of culture shock during the critical care
nurse might have with them, but also impacts on people’s experience. Elements of family relationships and health
experiences of an admission to critical care. Only 32% of beliefs that are particularly relevant to the critical care
Aboriginal people live in major cities. An estimated 43% of setting are discussed in the next section.
Aboriginal people live in regional areas and 25% in remote
areas.157 Therefore, most Aboriginal people admitted to Family
critical care units have come from somewhere else, and ‘Family’ is cited as one of the most enabling and enduring
are often a long way from home. This demographic has a pillars of Aboriginal culture, and the fundamental unit of
 CHAPTER 8 FAMILY AND CULTURAL CARE OF THE CRITICALLY ILL PATIENT 209

FIGURE 8.1 Bridging cultures in Aboriginal health.

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࠮SHUN\HNLQHYNVU ࠮YLZ[YPJ[PVU!ILPUNZ[\JR ࠮WYV[VJVS
࠮WH[[LYUVMZWLLJO ࠮\UJVTMVY[HISLWLYZVUHSZWHJL ࠮ZHML[`
࠮SL]LSVM\UKLYZ[HUKPUN ࠮KLWLUKLUJ`WV^LYSLZZULZZ ࠮LMMPJPLUJ`

࠮KLWLUKLUJ`WV^LYSLZZULZZ ࠮^P[OKYH^HS
࠮MLHYHU_PL[` ࠮MLHYZ[PNTH
࠮^P[OKYH^HS ࠮KLWYLZZPVUZLNYLNH[PVU
࠮HJJLW[HUJLVMWYVMLZZPVUHSRUV^SLKNL

*VTWSPHUJL *\Z[VTZ
࠮WYVMLZZPVUHSWV^LY ࠮KVTPUHUJLVMIPVTLKPJHS
࠮ºKVJ[VYRUV^ZILZ[»  TVKLS
࠮ISHTPUN[OL]PJ[PT ࠮PUZ[P[\[PVUHSVYNHUPZH[PVU
࠮WYVMLZZPVUHSZ\IJ\S[\YLZ

࠮Z\ITPZZPVU ([[P[\KLZILSPLMZ ࠮UL^YVSLZ

࠮YLZPZ[HUJL ࠮WYVMLZZPVUHSZVJPHSPZH[PVU ࠮UL^YV\[PULZ
࠮^P[OKYH^HS ࠮JVTTP[TLU[[VILZ[WYHJ[PJL ࠮UL^Y\SLZ
࠮JVUMPKLUJLPUL_WLY[PZL

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Adapted from Eckermann A-K, Dowd T, Chong E, Nixon L, Gray R, Johnson B. Binan Goonj: bridging cultures in Aboriginal health.
3rd ed. Sydney: Churchill Livingstone; 2010, with permission.

contemporary Indigenous society.166 Concepts of family but would not usually fulfill this role for non-indigenous
are, however, a potential point of cultural tension between people.
Aboriginal people and health professionals educated in Another feature of traditional Aboriginal kinship
dominant models of health that emphasise a strong ethical systems is avoidance relationships. Kinship laws determine
and legal commitment to individual rights, confidentiality who can and cannot speak to each other, associate with
and autonomy. In contrast, health may not be an individual each other or have physical contact with each other. This
issue within Aboriginal family constructs. The construct might mean that certain visitors are not able to be present
of an extended family with a complex set of kinship rules in the room at the same time – an important consider-
and different levels of sharing and support is often cited as ation for the critical care nurse when convening a family
distinguishing Aboriginal from western culture.165 conference. Some Aboriginal communities also have
Within the Aboriginal extended family, relationships lores that dictate that only women speak about ‘women’s
are defined through the traditions of culture so that the business’ or only men speak about ‘men’s business’.
biological mother’s sisters are also called mother, while
her brothers are uncles. The sisters’ children become Practice tip
brothers and sisters rather than cousins. The children
It is important to identify who is the spokesperson of the
of the father’s brothers are also considered brothers and
patient from the outset and who is the right person to
sisters rather than cousins and the father’s brothers are
talk to about all aspects of the patient’s care. Identifying
called uncle.This system carries over to grandparents and
the right person is of additional importance when the
grandchildren.
patient is a long way from home. Early notification of
In the critical care environment, the kinship system
family when an important decision is to be made is
has significance in terms of the western concept of ‘next
essential if they are required to travel long distances to
of kin’. Spokespeople such as ‘aunties’ or ‘uncles’ are often
join their critically ill family member.
nominated to speak on behalf of the Aboriginal family,
210 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Kinship systems also mean that Aboriginal people colonisation, significant changes to the traditional lifestyles
may have a number of names. A person may have a of Aboriginal people and the cultural diversity among
European first name and surname, a bush name, a skin Aboriginal groups and communities themselves, ‘tradi-
name and maybe a nickname. A person’s name may also tional’ beliefs regarding the cause of illness appear to have
change over the period of their life. If a person shares a persisted in a consistent way.169 The interconnected aspects
name with a person who dies, they may be given a new of connection to country and kinship obligations place
name at that time. an emphasis on social and spiritual dysfunction causing
illness. Mobbs170 proposes that there are five categories
Practice tip of illness causation. Natural causes (diet, physical assault,
injury and emotions such as homesickness, anger and
Retrieving past results/records may be essential to jealousy) and environmental causes (including the wind,
inform current care, so knowing if the patient has the moon and excessive heat or cold) may be considered
multiple names or medical histories is important, responsible for temporary states of weakness such as loss
particularly if these need to be retrieved from regional of appetite, weight loss, diarrhoea, coughs, lung complaints
hospitals or remote health clinics. and headaches. Suicide and attempted suicide are also
considered to be the result of such emotional factors.
Respecting kinship structures may assist in relieving Alternatively, these ailments may be associated with
some culture shock experienced by Aboriginal patients and more serious ‘direct supernatural’ causes that result from
their families. However, it is also important to acknowl- transgressing Aboriginal law. Such transgressions include
edge that the traditional ‘extended’ family has been breaching taboos relating to place (sacred sites), ceremony,
somewhat eroded through forcible removal of Aboriginal relationships (parenthood, childhood, avoidance, incest and
children from their families (the ‘stolen generation’); mortuary), women’s business (pregnancy and menstru-
policies of assimilation; disconnection from traditional ation) or spirits of the dead. Persistent sickness, mental
lands, community, family and cultural values; and socio- illness and death may also result from transgressing these
economic disadvantage. The latter has particularly led to lores/laws.
disruption of Aboriginal family structures, gravitation of ‘Indirect supernatural’ causes of illness result from
youth to regional centres and capital cities and family more serious offences involving transgressions of social or
structures being disrupted by incarceration, domestic spiritual law or intergroup or intragroup conflict and are
violence and drug and alcohol abuse.167 ‘Compound believed to have multiple effects including death, serious
families’ are the urban and contemporary equivalent to illness and injury, sterility, congenital abnormalities and
the traditional extended family. A compound family is physical deformities. Illnesses in this category may have
a group of people who share a dwelling and where the been precipitated by ‘pointing the bone’, ‘singing’ and
household head agrees to accept cohabitation with a ‘painting’.171 The concept of supernatural intervention
diversity of relatives and other persons not related biolog- provides a culturally embedded explanation for why one
ically, but who are considered ‘kin’. Another new form of person and not another becomes sick or dies.172 It links
family structure is the grandparent family where grand- illness and death to personal and social conflict and the
mothers, in particular, take responsibility for child-rearing. breach of cultural and spiritual lores.173
This occurs due to parents being unable to look after their The final category of illness causation is ‘western
children because of the need to relocate for work, parents influences’, deemed responsible for alcohol-related illnesses,
who misuse drugs, family violence or parents who are too substance abuse, infectious diseases, heart disease, cancer and
young to cope. Regardless, individual decision making sexually transmitted diseases, which fall into this category.
continues to be influenced by communal relationships and On the other hand, for Aboriginal people preventative
family groupings that may go beyond a specific locality, measures to ensure wellbeing include actions that avoid
and shared health beliefs. repercussions such as observing kinship obligations to
others; containing anger, violence or jealousy; respecting
Aboriginal view of health and and honouring elders and the dead; and leading a moral life.
health beliefs Traditional treatment includes the use of bush
Aboriginal people have a view of health that incorpo- medicines, involvement of a traditional healer, singing/
rates notions of body, spirit, family and community. The chanting or employing counter spells and charms to
National Aboriginal Health Strategy (1989)168 identifies remove evil influences. Traditional healers provide strong
that: ‘Health to Aboriginal peoples is a matter of deter- spiritual support and can identify the underlying causes
mining all aspects of their life, including control over of a serious injury or illness. In contrast to the western
their physical environment, of dignity, of community biomedical model, upon which most western health care is
self-esteem, and of justice. It is not merely a matter of based, the Aboriginal world view does not see the primary
…. the absence of disease and incapacity’. In the context function of the western healthcare provider as being able to
of these beliefs, understanding how Aboriginal people remove the cause of the illness, except for illnesses relating
conceptualise disease and illness is particularly important to colonisation. Instead, the role of western medicine is
in the critical care environment. Despite 200 years of often that of relieving symptoms and hastening the cure,
 CHAPTER 8 FAMILY AND CULTURAL CARE OF THE CRITICALLY ILL PATIENT 211

provided it does not conflict with traditional beliefs. 174 Communication

For the critical care nurse, this means that making an effort Aboriginal culture is based on a deep sense of spirituality
to understand and assist patients and families to link into and oral history. Traditionally, knowledge has been passed
Aboriginal health beliefs (such as facilitating the presence down from generation to generation through storytelling
of a healer), while at the same time explaining western and yarning. In some communities traditional languages
interventions, can ensure maximum effect of critical care
are still being used, and English may be a second or third
therapies.
language for many Aboriginal people. Critical care nurses
‘Payback’ is a traditional physical or psychological
should therefore identify interpreters to optimise commu-
punishment for transgressing Aboriginal laws. Whereas a
nication with patient and family. Family members are
person sustaining an injury as a result of payback may never
engage with western medicine, the fear of being blamed for frequently the first choice and there are advantages and
failure of a medical intervention and suffering payback as a disadvantages of this practice.176 On the positive side, family
result may influence decision making by families in relation may be the most expedient choice for interpreting because
to consenting to treatment of a critically ill patient. For this they are immediately available, and can translate culture and
reason, it is important that the correct family members are context as well as language. If the family member has the
consulted. For example, Western Australian desert people appropriate cultural authority there may also be significant
divide themselves into two separate groups for important trust, which an interpreter would not be able to foster. On
cultural occasions, including when someone dies or is the negative side, there is the potential for bias, inaccurate
critically ill. The tilitja belong to the same generation as information, selective transfer of information, transgress-
the ill/dying person and are the activists and the yirrkapirri, ing laws relating to gender and kinship, and for relatives
the partners and children, are the mourners. In the case of receiving information that the person would prefer they
an unconscious or dying relative, when serious healthcare did not know.177 Utilising the important cultural brokerage
interventions or procedures are being considered, the tilitja abilities of Aboriginal health practitioners, health workers
are the ones that should be consulted first and it is their or liaison officers is an important strategy to enhance
duty to then consult with family members before final communication between Aboriginal patients, their families
decisions can be made. Being aware of, and respecting, and health professionals.178 However, health professionals
this process encourages the right people to come forward, have been known to use health workers to excuse their
allows those who wait and mourn to be able to do so and own deficits in communication,179 rather than observing
ensures decisions become shared according to cultural laws some basic verbal and non-verbal communication cues and
and not the decision of one person who may be at risk of principles when working with Aboriginal people.Table 8.4
recriminations.175 provides some guidance in this respect.

TABLE 8.4
Communication cues and principles

PRINCIPLE C O N S I D E R AT I O N S

Establish a The first few minutes of your initial interaction with an Aboriginal person are critical for effective communication
relationship Avoid perpetuating Aboriginal people’s experiences with western systems where language has reinforced
dominant and submissive power relationships
Obtaining information is regarded as a privilege, not a right
This may mean a person has to prove they are worthy and can be trusted with the receipt of knowledge
Spend time building rapport and establishing common ground before exploring the ‘business at hand’
Be prepared to share information about yourself. As family and country are important to Aboriginal people,
positioning yourself within your family context and your ‘place’ is important. For example, sharing where
you are from, relationships you are comfortable talking about (children, brothers, sisters, grandparents), the
football team you support and food you like is culturally appropriate
Consider kinship Certain people will have rights to access particular knowledge and make specific decisions within family and
relationships community
The passing of information often depends on a person’s position in the family/community or relationship with
the holder of information
Find out the relationships between the Aboriginal patient, and his/her attending family and friends and the
relationships between family and friends
Identify any avoidance relationships
Establish spokespersons – remembering that there might be different spokespersons for different elements of
the person’s life
Identify who can make decisions on behalf of the patient (e.g. in the capacity of next of kin)
Consider what might constitute ‘women’s and men’s business’ in conversations
212 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 8.4 continued

PRINCIPLE C O N S I D E R AT I O N S

Body language Become familiar with non-verbal forms of communication amongst Aboriginal people, e.g. hand signs and
facial gestures
Don’t assume Aboriginal people do not make direct eye contact. However, if the person is avoiding eye
contact this does not mean that they are not listening or are being rude
Body language may also extend into close proximity within the client’s personal space, this is particularly
evident when the opposite sex is conducting the consultation; ask for permission to conduct any physical
examinations
Use of silence Use of silence is a key feature of communication with and between Aboriginal people. Pauses or silence
during an interaction may mean that a person is thinking carefully before speaking or divulging information. It
may also be a time for translation between languages. Pauses may be quite pronounced and time should be
allowed for responses before seeking to fill in the silence by repeating the question
Cultural protocols may also mean there are times when it is culturally inappropriate to respond
Try reframing the question in a different way, or ask if the person may like someone else to respond
Shame Shame is a term often used in Aboriginal society. ‘Shame’ describes a person’s feeling of utmost
embarrassment about something. It is used in both serious and humorous terms
Providing ‘Reading between the lines’ is a concept that is difficult to understand if English is not your first language and
information and western culture is unfamiliar
asking questions Be direct in your communication – carefully consider how to describe clinical progression, while at the same
time not diminishing the severity of a situation because family may need to be informed and travel long
distances to join the patient
Don’t assume nodding or saying yes means that a message is understood – it is often easier to say yes – this
is known as gratuitous concurrence. Perceived/actual power relationships between the health professional
and Aboriginal person may prompt the person not to contradict or disappoint and may lead to the person
providing what they think is an agreeable response
Improve communication outcomes by:
• providing opportunities for more than one person to ask questions
• following up on individual messages in different ways to ensure full understanding has been gained
• using open rather than closed questions
• avoiding compound questions (e.g. ‘Is it this way, that way or the other way?’)
• avoiding asking questions in a way that is framed in expectation of a positive response
• asking only one question at a time

Issues around death and dying and the

Practice tip
importance of country
Developing a relationship with Aboriginal patients Aboriginal people also have a strong connection to
and their families is an invaluable start to good the land they live on. Community is linked to land, a
communication and establishing trust. Introducing shared history and mutual responsibility and is the basis
yourself in a conversation based on the four ‘F’s’ of physical, social, spiritual and emotional wellbeing.181
may be useful: family, food, football and fun.180 Not ‘People talk about country the same way they would talk
only does this approach open up shared space for about a person: they speak to country, sing to country, visit
conversation, it also positions you as a nurse within a country, worry about country, feel sorry for country and
family and community of your own, which is important long for country.’ 182,p.7
to Aboriginal people. The ties Aboriginal people have to their people and
land are so strong that, rather than receiving life-saving
A major complaint of Aboriginal people is that care, many prefer to refuse the treatment and die on the
communication occurs too late, particularly when a health land that they belong in, with their family and community
professional has attempted to deliver bad news gently, present. This means that patients often do not present to
oblivious to the recipient not being able to ‘read between healthcare settings until their illness is very advanced.
the lines’ within the subtleties of English language.179 When transfer to hospital occurs it is often traumatic for
‘People need the full story so they can die with dignity, both patients and accompanying family. The following
with their family members fully involved … it is a good research quote summarises some of the stresses experi-
way to let them drive the process’ (p 156). enced: ‘They split the family up, one family in one hostel,
 CHAPTER 8 FAMILY AND CULTURAL CARE OF THE CRITICALLY ILL PATIENT 213

one family in another …. So how can you lean on one reactions from Aboriginal people.154 Currently, there are
another in time of grieving and in that time and if it low rates of both organ donation and organ transplanta-
comes the time to turn something off.’183,p.3 The reality tion amongst Aboriginal people. This situation has been
is that Aboriginal people frequently die in hospital. Stress attributed to beliefs relating to the importance of a body
relating to hospital admissions for many Aboriginal people being buried whole and issues relating to transference
is that their knowledge of city hospitals draws upon of the spirit of the donor into the body of the recipient.
previous encounters with family members dying, or of Both concerns are related to transgressing the connection
hospitals as places where you go to die.179,183 between a person and their own country. Discussing the
In this situation the most important consideration for principles and purpose of organ donation with identified
Aboriginal families may be the need for the patient to go family decision makers well before an expected death
‘back to country’, back to their traditional lands to die occurs, rather than approaching an individual family
or to heal. The critical care nurse should allow time and member with a request for consent when death occurs, is
facilitate discussion with the team around these issues. recommended.150 This discussion should take place within
However, return to country is rarely medically possible. a culturally supportive environment where collective
Instead, ensuring the relevant family or community decision making is possible.
members are present is a priority. However, financial When death occurs, it is associated with a period of
constraints and geographical distance may make family intense grieving. Although many western nurses associate
visiting difficult. singing after death with ‘wailing’ in anguish, death is often
For those members of Aboriginal families who do accompanied by singing to help the spirit move on to
manage to gather around the dying person, having the the traditional place of rest.179 ‘Sorry business’ is the term
opportunity to pass on knowledge through stories to commonly used to describe the complex bereavement
family members is important. The critical care nurse can practices and protocols that occur in Aboriginal commu-
facilitate this by allowing time and space for storytelling nities.There is no set time for sorry business to conclude, but
to occur and should also be aware of the culture shock to avoid prolonging the grief, the name of the deceased
described earlier, kinship relationships and the logistical person is not used again once they have passed away. A
practicalities in the critical care unit. The following quote discussion with the family will establish how critical care
demonstrates the interrelationship of these issues and the personnel can refer to the deceased person in a culturally
negative impact nurses can have on the family’s experience. acceptable way.
Aboriginal people have a distinct history, health
It was really hard to sit down and talk … they are all close
profile, culture and health beliefs that affect their experi-
together, very close and … you haven’t got the privacy.You say
ences of western medicine and health care in the critical
something and … it might offend the person next to you or
care environment. It cannot be stressed enough that the
whatever … And this does happen you know. I mean when integration of the patient’s culture into the critical care
they are in the intensive care part, there are little rooms that setting is important to achieving optimal health outcomes
can only have about 4 people … because the machines are and improved relationships between patients, family and
everywhere hooked up to the ceiling. And you have some in healthcare professionals. Critical care nurses are placed in
there, some outside the door you know, and then we have nurses an ideal situation where the experiences of Aboriginal
say ‘We can’t have that many in here’ …. That’s family, that’s people and their families who are critically ill or dying
a son, that’s a daughter, that’s the other son, you can’t chuck can be positive while maintaining their cultural integrity.
them out.183,p.6 To achieve these aims critical care nurses need to be
It is anticipated that the information presented in this culturally safe, become familiar with specific factors influ-
chapter will assist in overcoming such dissonance between encing Aboriginal patient’s and their family’s experiences
nurses’ and Aboriginal people’s expectations in the critical of hospitalisation, pay attention to verbal and non-verbal
care setting.When an Aboriginal patient dies in the critical communication cues and develop therapeutic relation-
care setting there are also certain protocols that need to be ships built on trust.
considered. Gender-appropriate care may be needed, as
often male elders will not allow women into their room,
and a male nurse may be required to provide care. Some
Religious considerations
Aboriginal communities may not allow health profes- Religious beliefs and practices contribute to a person’s
sionals to handle the body after death. The critical care spiritual wellness, on one hand, while on the other a
nurse needs to discuss with the family issues that relate to critical care nurse’s religion may influence how care is
handling of the body, whether cremation is acceptable and delivered.184 Religious beliefs can be closely aligned with
arrangements for the person to be returned home. a person’s culture and vary in how life, dying and death
The potential for organ donation may also be raised. are viewed, and may dictate how life is conducted.1,185,186
Despite anecdotal reports that broaching this subject is Any breaches can have profound effects on a patient’s
inappropriate for Aboriginal people, research has identified wellbeing and, in some cases, how a family member may
that culturally sensitive discussion about organ donation consequently interact with the patient. This has important
and transplantation may not be met with any negative implications for critical care nurses undertaking everyday
214 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

practices and common procedures where religious beliefs mechanism in terms of making sense of the experience,
dictate a different approach. A common example is blood as well as being a source of faith and hope. While it can
transfusions for those belonging to the Jehovah’s Witness be helpful to the critical care nurse to have an overview
religion. Having a standardised list of religions and of the main religious beliefs and practices (see Table 8.5),
procedural considerations is flawed due to the variations caution must be used, and should not preclude working
that exist, and in some instances the variations are great. with the patient’s family to ascertain exactly what their
Thus, as part of the initial assessment the critical care nurse beliefs and preferences are. Having said this, a patient may
should determine whether the patient has religious beliefs have adopted a religion that is separate from their family’s.
and practices that must be observed or not, and incorpo- In such circumstances family cannot be relied upon as
rate these into the care plan. informants and, in some situations, there may be a conflict
When a family member becomes critically ill, religious between the religious values and practices of the patient
beliefs and practices become an important coping and those of the family. Religious beliefs and practices, like

TABLE 8.5
Overview of key religious beliefs and practices

RELIGION PRACTICES TO BE AWARE OF B E L I E F S A B O U T I L L N E S S , L I F E A N D D E AT H

Protestantism Prayer and the Bible are important for support. Illness is an accepted part of life, although
Minister, vicar or pastor may visit the sick person euthanasia is not allowed. There is a belief in the
and the family afterlife, with the dead being buried or cremated
Roman Catholicism Prayer and the Bible are important. Some may have Illness is an accepted part of life, although
restrictions on eating meat on Fridays of Lent, Ash euthanasia is forbidden. There is a belief in the
Wednesday and Good Friday. Priest may undertake afterlife, with the dead being buried or cremated
communion with and anoint the sick person
Judaism There are orthodox and non-orthodox forms of Illness is an accepted part of life, with euthanasia
Judaism. Procedures should be avoided on the being forbidden, thus prolonging life is important
Sabbath (from sundown on Friday to sundown on and those on life support stay on it until death. The
Saturday). Dietary restrictions around pork, shellfish Sabbath is a time that is considered sacred and
and the combination of meat and dairy products when restrictions on activities are observed. There is
extend to the use of dishes and utensils. Frequent a belief that the human spirit is immortal. There are
praying, especially for the sick person who should special processes for managing the dead person,
not be left alone. The Rabbi will attend the sick who should be buried as soon as possible after
person death. Thus, consultation with the Rabbi is important.
Postmortem examination is allowed only if necessary
Buddhism Prayer and meditation are important, using prayer Illness originates from a sin in a previous life. There
books and scriptures, supported by teacher is a belief in afterlife, and the dead are buried or
and Buddhist monks. The Buddhist is generally cremated. Living things should not be killed; this
vegetarian. Patients may refuse treatments (e.g. belief extends to euthanasia
narcotic medications) that alter consciousness
Hinduism Prayer and meditation are important, and are Illness is usually a punishment and must be
supported by a Guru. Some Hindus are vegetarian. endured. Some Hindus have healing practices
The dying patient may have threads tied around the based on their faith. There is a belief that the dead
neck or wrist and be sprinkled with water; these are reincarnated; they are usually cremated
threads are sacred and are not removed after death.
The body is not washed after death
Islam (Muslims) Private prayer, facing Mecca several times a day, Life and death are predetermined by Allah, and any
requires a private space. The patient may like to be suffering must be endured in order to be rewarded
positioned towards Mecca. Guided by the Qur’an in death. It is believed that dying the death of
(Koran), which outlines the will of Allah (the creator a martyr will be rewarded in death by going to
of all) as given through Muhammad (the prophet). paradise. Thus, staying true to the Qur’an is crucial.
Muslims fast during Ramadan, and eating pork and There is a belief in the afterlife, and the dead are
drinking alcohol are forbidden. Stopping treatment buried as soon as possible after death, on the side
goes against Allah. Talking about death should be facing Mecca
avoided; designated male relatives will decide what
information patient and family should receive

Adapted from Blockley C. Meeting patients’ religious needs. Kai Tiaki Nurs NZ. 2001/2002;7(11):15–7, with permission.
 CHAPTER 8 FAMILY AND CULTURAL CARE OF THE CRITICALLY ILL PATIENT 215

cultural beliefs and practices, will vary between orthodox during their time in the critical care setting.1,187 Once
or traditional and contemporary interpretations. the spiritual or religious beliefs and practices have been
Patients generally fall into three groups with regard to determined, the critical care nurse can facilitate oppor-
their religious practices.187 There are those who: tunities for the patient and/or family to carry out their
1 practise their religious beliefs regularly beliefs and practices, and avoid any insensitive actions and
2 practise their religious beliefs on an irregular basis, pay attention to any spiritual distress evident in the patient
often in times of need and stress and family members.187
A person’s spirituality, whether informed by religion
3 have no religious interests.
or some other basis, manifests in a variety of relation-
All patients should have access to religious support
ships with self, others, nature and ‘divine’ beings. It is the
where they indicate a need. Therefore, it is beneficial for
critical care nurses to have knowledge of how to access essence of who a person is, or who groups of people are.
the relevant religious resources if needed. The focus of While assessing spiritual or religious needs is one aspect,
the critical care setting often involves going to extreme presence and being with, empathetic listening, reality
lengths to keep patients alive, which may well be in orientation of the family and enabling visiting and contact
direct opposition to some religious beliefs. Religious are all important nursing activities that can support the
beliefs can either facilitate or disrupt the process of living spiritual and religious needs of patients and their families.1
or dying.185,186 There are a number of useful principles When families are confronted with the possibility of
underpinning practice when nursing patients with specific death, the documentation of a death plan that outlines
religious needs (see Table 8.6). the preferred care during the process of dying and death
In addition to these principles, contact and commu- is recommended.187 Death plans are about empower-
nication between the patient, family and the critical care ment, and differ from advance directives, which outline
nurse are important,1 and can enable a person’s spiritual or what is not wanted (e.g. cardiopulmonary resuscitation).
religious needs to be determined. The critical care nurse Through formal discussion with the patient and/or family,
should ascertain whether the patient and family have any religious and end-of-life needs can be determined and a
spiritual or religious beliefs and practices to be observed management plan developed for implementation.

TABLE 8.6
Principles for recognising religious needs

PRINCIPLE A R E A S F O R C O N S I D E R AT I O N

Diversity exists between and within the various religions Determine values and beliefs related to health, illness, dying, death
and any specific requirements for undertaking everyday nursing
cares and procedures
Spirituality is an essential part of care planning and the Spiritual and religious needs should be documented in the care plan
delivery of quality care to ensure continuity and quality of care
Interpersonal skills and therapeutic use of self are Approach the patient with a genuine, non-judgemental attitude
essential to engaging and being present with the patient Avoid imposing own religious or spiritual beliefs on the patient and
and family family
Being knowledgeable about a patient’s religious values Consult family, if they share same religion, and/or consult
about life, health, illness, death and dying enables the appropriate representative of the patient’s religion. Areas to explore
critical care nurse to be respectful and accommodating should include the following to determine:
in their care • religious values regarding life, health, illness, dying and death
• nature of the ideal environment
• processes surrounding dying, if appropriate to the patient
• beliefs regarding nutrition and hydration
• use of touch
• gender-specific care
• family presence, involvement and support
• care after death
Philosophies and policies should be cognisant of the Policies should be cognisant of cultural and religious diversity, and
cultural and religious diversity within the critical care include management of the following:
patient population • visiting
• modesty
• gender-specific care
• communication
• language and the use of interpreters
216 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

End-of-life issues and the most appropriate form, and an oral airway may improve
patient comfort and aid secretion clearance. Atropine and
bereavement scopolamine have been reported to successfully reduce
copious oral secretions and enhance comfort.198
Internationally, mortality rates in ICUs vary considerably
The attainment of humane nursing care must include
and are a feature of the models of care including admission
heightened efforts in achieving quality indicators, such
criteria and discharge destinations.188 Specifically, within
as mentioned above – adequate management of pain
Australia and New Zealand the Intensive Care Society
and nausea, agitation and restlessness. Both critical care
Centre for Resource and Evaluation reported on data
staff and families should continue to communicate with
from 140 Australasian ICUs about discharge of 128,095
the patient by speaking and touching as this can have a
patients. The mortality rates across these tertiary, metro-
calming influence. Comfort measures to enhance holistic
politan, rural, paediatric and private ICUs ranged from
care delivery should continue and may include:
2% to 8%. The impact is that 6000 families in these two
countries alone were bereaved during the reporting year • hygiene care
of 2010/2011.189 End-of-life questions and bereave- • position changes
ment in critical care areas are therefore important issues • foot and hand massages
involving patients, families and staff. Death can occur as
a result of sudden decline in the patient’s condition, or • hair washes and other individual preferences
as a result of withdrawal of life support in anticipation of • artificial nutrition and hydration.195
demise. Patient death in critical care areas is found to have Patient dignity should be a priority, with gowns or
a significantly different effect on family members from a personal attire essential elements of care. The management
death in another in-hospital area.190 This is perhaps due of symptoms further allows patients to maintain their dignity.
to the heightened anxiety associated with a critical care Privacy for patients and their families allows an opportun-
environment190 or to the perception of an ability to cure ity for them to communicate without the constraints of
in highly medicalised areas.191 Where possible, family- observers.199 As indicated in previous sections of this chapter,
centred decision making with patient involvement, patient and family culture, beliefs and spiritual values are
together with effective communication and attention to important considerations that underpin care.193
symptom management, is optimal. Practical and emotional
support for family and patients is important and scrutiny Family care
of the way we manage these important areas provides Care of the family is supported by proactive palliative care
quality indicators for critical care areas.45,192 interventions that include empathic, informative commu-
nication with interdisciplinary team meetings and family
Patient comfort and palliative care conferences that are not rushed where families are integral
Maintaining patient comfort and support for families to decision making and goal planning.45,70,200 The desire to
and staff are primary requirements of nursing patients participate in decision making varies from family to family,
during the end stages of life. Advanced directives and and cannot be assumed. Ascertaining individual families’
‘not for resuscitation’ orders should be in place to prevent needs for decision making is therefore recommended201
mismanagement and misunderstanding of patient care (see as families are best placed to have an understanding of
Chapter 5).45 Maintenance of patient comfort through patients’ wishes, which can be taken into account when
care guidelines to facilitate a ‘good death in ICU’193 is decisions are made.202 Structured communication between
designed to control symptoms such as agitation, pain and the healthcare team and families can assist with earlier
breathlessness and is extremely important from the patient, decisions and goal formation about care.203 Emotional and
family and nurses’ perspective.194–196 Although this may practical support can be given to families by providing
seem fundamental, there is evidence to suggest this is not written material about the critical care area, local facilities
always achieved, with 78% of over 900 North American and specific information on bereavement.70 Privacy is not
critical care nurses perceiving that patients received always possible in the busy critical care environment, but
inadequate pain medications ‘sometimes’ or ‘frequently’ maximising efforts in this regard for dying patients and
during end-of-life nursing in critical care areas.197 their families provides a more conducive environment for
Collaboration and early involvement by palliative care strengthening patient–family relationships and commu-
teams is one way to integrate end-of-life care for patients who nication.204 Communication is enhanced with family
either remain in critical care areas or are transferred from the conferences, which provide a structured process where
unit to other areas.195 Withdrawal of mechanical ventilator family members and patients’ healthcare teams can share
support requires adequate provision for management of goals and understanding of end-of-life care.
potential agitation, pain and hypoxia.196 Opioid and benzo- Family conferences are a way to meet family needs,
diazepine agents should be considered for administration and enhance communication and understanding of the
before and after extubation to prevent agitation and pain. patient situation. These become an essential element of
Choices of bolus or infusion administration need to be based care when end-of-life discussions are needed. Privacy,
on patient comfort issues. Oxygen therapy is continued in away from the direct clinical environment, is important to
 CHAPTER 8 FAMILY AND CULTURAL CARE OF THE CRITICALLY ILL PATIENT 217

allow uninterrupted time for families to meet with their family members. Reassurance that the patient will not be
relative’s healthcare team.205 When family conferences abandoned and care will remain of the highest quality is
have been instituted early in the admission, a family/staff important to families.210,211
relationship will be established that supports ongoing A well-organised critical care team will meet prior to
communicating about end-of-life care.24,206 the family conference and ensure all relevant information
It is important to have the interprofessional team (for is gathered and that there is a shared understanding. Curtis
example: intensivist, social worker, case manager, direct and colleagues212 suggest the use of a five-point approach
care nurse, chaplain) meeting with the patient’s family during the family conference, which may be useful around
at this time to ensure a comprehensive approach to the end-of-life meetings. This approach is termed ‘VALUE’:
coordination of patient care and family support.67,207 1) valuing family statements, 2) acknowledging emotion,
This approach enhances understanding and information 3) listening, 4) understanding the patient as a person and
consistency.Where possible, involving all significant family 5) eliciting questions. The critical care team’s ability to
members in the family conference allows them to hear listen to the family is a key element and has been found
the same information, ask individual questions and discuss to significantly increase a family’s satisfaction with end-of-
options. These collectively reduce family and/or family/ life care.200,213,214
staff conflict87 and support those families that prefer to The healthcare team that provides information and
make decisions as a collective. discusses palliation and end-of-life care needs to clearly
Family members of ICU patients are at a high risk of indicate to families that, although they are involved in
anxiety and depression. In a large ICU multicenter French much of the decision making,24 the decision to withdraw
study, 73% of family members had anxiety and 35% were treatment is a medical one in Australia. This notwith-
diagnosed with depression around the time of discharge standing, consensus and shared decision making is the
or death of their relative.208 This mental health morbidity aim as careful consideration of the patient’s wishes, the
is likely related to the burden of the critical illness and family perspective and the futility or otherwise of further
potential or imminent demise of a loved one. Family treatment are considered within an ethical framework.24,205
member’s depression, grief and anxiety can be manifested While the family grapple with the process of
by physiological, behavioural, psychological/cognitive and grieving,215 nurses need to provide physical and psycho-
social indicators. The physiological stress response with logical care for patients and families.216 This can be
increased cortisol excretion and poor sleep patterns51 can achieved when there is patient- and family-centred
affect family interactions with each other and with staff. decision making, good communication, continuity of care
At times of end-of-life discussions, family members may and emotional and practical support; and spiritual support
exhibit confusion, anger and/or threatening behavior, can assist with this.217 Individualising the care to the family
making it difficult for everyone involved. Importantly, is essential, and support measures should be instituted after
these emotions make it difficult for family to grasp and a full assessment of their needs. This should be informed
understand the often complex patient situation. Strategies by the notion that grief manifests in different ways, and
such as family conferences are important as they improve that grieving is a complex process. Bereaved families in
communication channels and promote understanding, intensive care demonstrate complex bereavement processes
thereby reducing conflict situations.209 and, without support, prolonged grief reactions can occur.
Planning for the family conference around end-of-life In a longitudinal study nearly half (46%) of bereaved
issues involves ensuring a common time for significant family members had complicated grief 1 year later when
family members and the critical care team to meet. If a key measured by the Inventory of Complicated Grief Scale.218
family member is away or overseas, a conversation over the Complicated grief patterns decrease the family’s ability to
internet may be the best option as video facilities will allow cope with everyday needs, increase the need for health
better communication than with a telephone call. Where services and may progress to unresolved grief.219,220
there are complex family situations with extended families The detrimental effects of long-term unresolved grief
or previous partners, care must be taken to try to avoid a after the death of a loved one are well documented.220
poorly functioning group. There may also be an estranged Current terminology favours the term ‘prolonged
partner who wants to be included, which may add to the grief disorder’ (previously called complicated grief),
dynamics of the situation. The critical care team will need which has clinically disabling grief symptoms including,
to exhibit great diplomacy in such complex situations to amongst others, a preoccupation with thoughts of the
keep the group and meeting meaningful and productive. loss, avoidance of reminders of the loss, disbelief over the
There is no rule as how to manage these situations but the person’s death, feeling lonely since the loss, feeling that the
foremost consideration is how to serve the best interests of future holds no purpose and feeling stunned or shocked
the patient. Family members unable to attend the family by the loss.221 These symptoms can result in elevated
conferences should be relayed information in a timely way morbidity and mortality levels associated with depression,
by a self-designated family spokesperson. This person is cardiac events (including a higher risk of sudden cardiac
generally one who is more resilient and coping better than death), hypertension, neoplasms, ulcerative colitis, suicidal
others with the end-of-life discussions who can take the tendencies and social dysfunction (including alcohol
responsibility for communicating the situation to other abuse and violence).51,220,222 These potentially harmful
218 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

outcomes provide strong motivation for critical care care and death in the critical care environment, and a
clinicians to initiate family support mechanisms such as specific educational program and unit guidelines on
bereavement services.195 Bereavement programs aim to palliative care may provide support and reduce burnout
reduce the immediate physical and emotional distress for and caregiver burden.193,195,229,230
those grieving, while improving the long-term morbidity Once the patient has died, nurses may not have the
associated with unresolved grief.223 opportunity to mourn publicly and may feel they are acting
Although critical care clinicians in the UK,224,225 unprofessionally if they show overt signs of grief.227 Dealing
USA,195 Europe and Canada201 are conducting dialogue with the death of patients may be exacerbated in some
and developing guidelines for bereavement care in critical critical care environments, particularly in the rural setting,
care, little evidence-based research has been conducted on where the nurse may know the patient outside the work
bereavement care strategies.195 An exception is a bereave- environment. Collaboration with colleagues from oncology
ment program developed by a group of nurses from a areas or palliative care teams will provide guidance and
British ICU, who instituted a booklet on ‘coping with support to critical care nurses as they develop better organ-
bereavement’, an after-care form for the clinical nurse to isational and emotional support for each other.231 Effective
complete with details for follow-up with the family and palliation occurs when the multidisciplinary team, including
a sympathy card and letter inviting family to participate senior management, collectively develops a philosophy for
in support group meetings.224 Although initial evaluation palliative care and bereavement services.195,217
of the program through feedback from participating Nurses depend on colleagues and friends for support
family members was positive, the team acknowledges that when patients die, and value debriefing sessions.224
this does not constitute rigorous research. Evaluation of ‘Debriefing’ sessions can have a number of interpretations.
bereavement services in Australian adult ICUs was also For example, debriefing in critical care often takes the form
reported to be inadequate, as no data could be located of an opportunity to share feelings. Alternatively, it may
concerning bereavement services in other areas of critical involve a procedural clinical review of events where the
care. Only 30% of ICUs provided some follow-up objective is to understand and learn from the situation.231
care, and only four units had any evaluation other than Both components of debriefing are important, together
anecdotal evidence.226 It is imperative to assess new and with the opportunity to provide mutual support within
existing bereavement interventions and how well they the multidisciplinary team. The effectiveness of sessions
meet the needs of families through rigorous evaluation. should be evaluated.
Legitimising research on this vulnerable group is required A ‘grief team’ provides more formalised support from
to improve end-of-life care for families and patients.224 colleagues that have been given additional education on
grief, dying and death.227 This enables a program of care,
Care of the critical care nurse and may include such strategies as assessing the welfare
The two previous sections have focused on care for the of the staff immediately after the death of the patient,
dying patient and the patient’s family. Critical care nurses being present for staff members to express their feelings
who care for both patients and families also require care and providing follow-up and information on coping
in bereavement situations. Caring for dying patients is mechanisms during grief.227 Accessing experts from outside
emotionally draining and highly demanding of the critical the unit’s usual resources may be helpful with debriefing
care nurse, who often fails to notice or acknowledge the in especially challenging situations.231 Dealing with death
need to grieve.227,228 In addition, critical care nurses may is never easy; however, an awareness of colleagues’ needs is
not have the knowledge and understanding of palliative the key to providing the support they require.

Summary
The psychosocial, cultural and religious needs of critically ill patients and their families are just as important as their
physical needs, and care needs to be taken not to overlook these.This chapter presents a holistic and person-, patient- and
family-centred approach to practice, which enables individualised plans of care that include specific psychosocial, cultural
and religious needs of critically ill patients and their families. Ma-ori and Aboriginal people generally have a holistic and
spiritual world view, and consequently have specific cultural practices that are vital to their spiritual wellbeing. Culturally
and linguistically diverse patients and families also have specific cultural values, beliefs and practices that critical care
nurses need to determine, which may involve the assistance of an interpreter. These patients require the critical care
nurse to interact with them in a manner that facilitates the identification of their needs on an individual basis. The old
adage ‘actions speak louder than words’ is worthy of consideration when working with these patients in the critical care
setting. It is important that individual plans of care be developed that include the participation of Ma-ori, Aboriginal
and culturally and linguistically diverse patients and wha-nau or family, reflecting the beliefs and practices that need to be
included in their critical care experience. In order to meet the needs of the critically ill patient and family, the critical care
nurse is advised to identify personal beliefs, practices and expectations that may influence professional decision making
and interactions with the patient and family.
 CHAPTER 8 FAMILY AND CULTURAL CARE OF THE CRITICALLY ILL PATIENT 219

Case study
Mereana is a 40-year-old woman who has just been admitted to the critical care unit post-bariatric surgery.
In the past, Mereana has been an active member of her community advocating for the support of young
families with limited resources. However, she has been unwell for some time, as a consequence of being
morbidly obese and having diabetes, hypertension, sleep apnoea and restricted mobility. During her
bariatric surgery (Roux-en-Y), Mereana had significant blood loss and cardiac arrhythmias. At the bedside
the critical care nurse is challenged by a number of concerned family members, including Mereana’s
partner, children, siblings, cousins, aunties and uncles, who all want to be with Mereana. Some of the
family members are exhibiting defensive and negative attitudes, and the critical care nurses are somewhat
concerned. Aware of the problem with having too many people within the restricted space of the critical
care unit, the critical care nurse’s immediate thought is to restrict visitors to her partner and children – as per
the critical care visitation policy. This action is also reinforced by the need to assess Mereana, and ensure
she gets the necessary rest she needs post-surgery. Nevertheless, the critical care nurse is aware that the
family has indicated that this is totally unacceptable and that they need to be with the patient. Instead of
acting on her immediate thoughts to restrict the family, the critical care nurse instead opts to explain to
the family what she needs to do in the interim for Mereana and requests that, while this is occurring, they
decide upon someone to be the spokesperson for the family, and who could be the person that staff then
communicate with. She also asks them to consider what cultural needs that Mereana and the family have
that should be included in Mereana’s plan of care.

MAJOR ISSUES
There are a number of issues evident within this situation:
1 The family’s request to be present will impact on the critical care environment, given the number of
people wanting to be with Mereana.
2 The critical care nurse does not fully appreciate or understand the need for the wider group of
family members to be present and support the patient, although she recognises it is important
for them.
3 The critical care nurse is concerned about a potentially volatile situation, particularly with some family
members.

DISCUSSION
This situation is not uncommon for people belonging to indigenous or other minority groups who culturally
have collective world views that contrast with dominant biomedical approaches to health care, which
predominately focus on individuals. For these cultural groups, the individual has less prominence; instead,
the predominant focus is collectively on ensuring the wellbeing of family members. This means, as in the
case of Mereana (and not dissimilar to many Ma-ori and Indigeneous Australian families), family members
who are both close and distant relatives will come from near and far to be with an unwell person. This
creates tension for critical care nurses who have to manage visitation, particularly when their mind is on
keeping the patient stable and improving his or her outcome. Critical care nurses may be concerned about
the increased traffic caused by large families within the critical care environment, especially when there
is restricted space, and the need for the patient to rest is uppermost in their minds. On the other hand,
the family may be interested in having unrestricted access to the patient and somewhere to sleep.232 The
critical care nurse in this case study managed an immediate situation prudently – she explained the work
that she had to do, and asked the family to decide on a spokesperson. Having a spokesperson is one
way that critical care nurses can manage family needs, in particular their cultural needs. Communicating
and working with the family through the spokesperson can defuse potentially volatile situations whereby
family members feel the critical care nurses are obstructing their need to be with the patient. Foci of
communication with families should be on: 1) understanding the family’s cultural and general needs,
2) explaining the critical care unit functioning and needs and other patients’ needs and the reasons and
3) negotiating the specifics of how the family members can be with the patient. For example, this may mean
that the numbers of family members are restricted unless there are important cultural practices, such as
karakia (prayer), when more people may be able to be present for this short time. Such approaches enable
the facilitation and balancing of the family needs to be with the patient with the family’s cultural needs, the
patient’s needs and the nurses’ needs.
220 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

CASE STUDY QUESTIONS

1 When confronted by large family groups, reflect on 1) how this makes you feel, think and act and 2) how
this is similar or different to your own family of origin. Identify how your own personal cultural orientation
impacts on working with patients and their families within the critical care setting, particularly when their
requests and activities may differ markedly from your own views.
2 When confronted by large family groups, reflect on your thoughts, the actions you undertake and how
you evaluate whether your actions are driven by your personal and/or professional values and beliefs,
and if you are being culturally responsive in such situations.
3 Having worked with the family, how will you ensure that their needs are integrated into the patient’s plan
of care, and communicated to other critical care nurses and staff?

RESEARCH VIGNETTE

Henrich NJ, Dodek P, Heyland D, Cook D, Rocker G, Kuitsogiannis D et al. Qualitative analysis of
an intensive care unit family satisfaction survey. Crit Care Med 2011;39(5):1000–5

Abstract
Objectives: To describe the qualitative findings from a family satisfaction survey to identify and describe the themes
that characterize family members’ intensive care unit experiences.

Design: As part of a larger mixed-methods study to determine the relationship between organizational culture and
family satisfaction in critical care, family members of eligible patients in intensive care units completed a Family
Satisfaction Survey (FS-ICU 24), which included three open-ended questions about strengths and weaknesses of the
intensive care unit based on the family members’ experiences and perspectives. Responses to these questions were
coded and analyzed to identify key themes.

Setting: Surveys were administered in 23 intensive care units from across Canada.

Participants: Surveys were completed by family members of patients who were in the intensive care unit for
>48 hours and who had been visited by the family member at least once during their intensive care unit stay.

Interventions: None.

Measurements and main results: A total of 1381 surveys were distributed and 880 responses were received.
Intensive care unit experiences were found to be variable within and among intensive care units. Six themes emerged
as central to respondents’ satisfaction: quality of staff, overall quality of medical care, compassion and respect shown
to the patient and family, communication with doctors, waiting room, and patient room. Within three themes, positive
comments were more common than negative comments: quality of the staff (66% vs 23%), overall quality of medical
care provided (33% vs 2%), and compassion and respect shown to the patient and family (29% vs 12%). Within the
other three themes, positive comments were less common than negative comments: communication with doctors
(18% vs 20%), waiting room (1% vs 8%), and patient rooms (0.4% vs 5%).

Conclusions: The study provided improved understanding of why family members are satisfied or dissatisfied with
particular elements of the intensive care unit and this knowledge can be used to modify intensive care units to better
meet the physical and emotional needs of the families of intensive care unit patients.

Critique
Although the research question was not overtly stated, the aim of the study was to gain insight into the ICU experience
from the perspective of family members to improve the capacity of ICU staff to meet their emotional needs. The
authors note that most evaluations of family satisfaction in the ICU involve quantitative data assessing characteristics
of the ICU experience such as satisfaction with overall care, the decision making process and communication. The
survey tool used in this study included both closed and open-ended questions. This paper reports on the data
 CHAPTER 8 FAMILY AND CULTURAL CARE OF THE CRITICALLY ILL PATIENT 221

analysis of the open-ended questions. The mixed-methods approach is appropriate to both compare the results
with previous quantitative surveys and generate new knowledge by exploring known themes in greater depth. For
example, a qualitative approach can explore why families are satisfied or dissatisfied with specific aspects of ICU
care that they rated on the Likert scale as ‘excellent’ or ‘poor’, respectively.

The authors compare and contrast their results with five other quantitative studies and provide references for five
qualitative studies to support the inclusion of free-text questions as a way to improve understanding of experiential
aspects of ICU. It is unclear from these short précis the depth and breadth of other studies about patient satisfaction
in the ICU and what is already known about this topic. The paper would therefore have benefited from including more
information about the existing literature and results of previous studies when comparing and contrasting the findings
to their own.

In the absence of this more comprehensive information it appears from the introduction that the quantitative element
of the survey tool is based on the previously validated 24-item Family Satisfaction Survey (FS-ICU), but that this study
included three new, yet to be validated questions seeking suggestions and comments about things that were done
well and ways to improve.

Despite the qualitative element of the survey tool appearing not to have been validated or even piloted prior to
use, the sample size adds validity and reliability to the tool. Surveys to 40 family members of ICU survivors and
40 family members of ICU non-survivors who had spent a minimum of 48 hours in the ICU and who had a family
member visit them at least once during the stay were distributed in participating units. The family members of
surviving patients were recruited in person when their relative was ready for discharge. The family members of non-
surviving patients were recruited by mail 2–3 weeks after the death of their relative. It would have been beneficial
to include a definition of ‘family member’ given the potential variety of family composition across Canada, which
has both a multicultural population and a First Nations population.

Almost half (48%) of respondents identified as the patient’s spouse, with the other relationships being husband,
partner, sibling or parent. Interestingly, there were no respondents who identified as the children of the ICU patient,
although there are missing data in relation to this variable for 250 respondents. Of the reported relationships, 69%
were female with the highest number (34% of all respondents) identifying as the patient’s wife, then mother (8%)
and sister (4%). It is unclear from the paper how many family members of each patient were represented, i.e. did a
wife, mother and sister of some patients all respond to the survey, or just one member of each family? Although the
size of the ICU where the respondent’s family member stayed is reported (1–10 beds, 11–20 beds or >20 beds), it
would also have been pertinent to identify the types of ICUs and their distribution across the country. Given the aim
of the study is to improve families’ experiences, these characteristics may have important ramifications in terms of
recommendations for improving care.

The qualitative components of the surveys were analysed using the qualitative software NVIVO, which is an
appropriate tool for thematic analysis. Twenty-two themes were identified, each of which were coded according
to the positive or negative nature of the responses. Six themes were mentioned by at least 5% of all respondents
across all sites and are those themes discussed in this paper. The six themes included: 1) staff quality and quantity;
2) overall care: competency and quality; 3) compassion/respect for family and patient: kindness meeting individual
patient/family needs; 4) communication: quality, frequency, directness, timing; 5) waiting rooms: characteristics;
6) patient rooms: characteristics. These themes are set out in tables that make it easy to gain a sense of the results
at a quick glance. The narrative provides more detail.

The most common theme identified by 66% of respondents was the high quality of staff, their competency,
professionalism, concern and positive attitudes. Negative comments related to lack of interpersonal skills including
rudeness, abruptness, insensitivity and ‘dodging’ interaction with family members as well as ‘unprofessional’
conversations between each other. Respondents also worried about shortages of nurses compared to patient
demands. Competency ranked as the second most common positive theme, with only 2% of respondents making
negative comments. Staff treating patients/family with kindness contributed to the third most common theme of
compassion and respect for family/patient, with only 12% of respondents reporting negative experiences such as not
being provided adequate space or time to grieve their family member’s death.
222 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Slightly more respondents were not happy with communication from ICU staff (20%) compared to those who were
(18%). Negative communication experiences included infrequent communication/invisibility of doctors, excluding
family from decision making and not being informed how long they may have to wait for a procedure to take or how
long they would be excluded from the room when asked to leave. They also wanted to know logistical information
to reduce the ‘scariness’ of ICU as a place. Family members wanted communication to be honest, particularly when
it comes to discussing death. Positive comments appreciated clinicians who made communication with family a
priority, made themselves available, were honest and direct and answered questions thoroughly. Waiting room
conditions such as phones, couches, television, décor and a generally unwelcoming environment were ranked
negatively. Lack of privacy and not catering for large numbers of people were the primary complaints relating to
the patient room.

The authors identified that themes and subthemes were interconnected but that, when attempting to address overall
dissatisfaction or improve satisfaction, breaking themes into their individual parts is useful for achieving change.
Recommended changes included: establishing regular clinician/family meetings; improving doctors’ interpersonal
skills and decreasing inappropriate communication through education; providing more chairs in patient rooms;
providing more informational pamphlets about the ICU environment; and making waiting rooms more welcoming.
The authors identified that most of these recommendations are consistent with the American College of Critical Care
Medicine/Fellow of the American College of Critical Care Medicine Guidelines.233

The authors also noted the insight qualitative responses gave to quantitative assessment of family satisfaction, and
that these findings confirmed results from previous quantitative studies. Having said this, it was disappointing that
the authors did not relate the two elements of their survey in this paper.

Strengths of this study are identified by the authors as providing an opportunity for respondents to articulate their
opinions and the large size of the sample, which means that these comments most likely are representative of the
diversity of families across Canadian ICUs. Limitations of the research were poorly identified. The authors identified
that there were different recruitment techniques between survivor and non-survivor families. They also identified
that the perspectives of families who opted not to respond may have been different to those who did. Additional
limitations include the absence of information related to whether there were versions of the survey in both French and
English, as would be expected in bi-lingual Canada, and the potential shortcoming of failure to identify responses
from specific cultural groups in the multicultural Canadian environment. The degree of illness of the patient was not
analysed, which has previously been identified as impacting on satisfaction rates. Similarly, it would have been good
to know if there were differences in satisfaction based on length of stay and survival.

Overall, this paper provides an interesting perspective on family satisfaction. The quotations drawn from the data
powerfully illustrate the family’s perspective. The six identified themes are significant because, as the authors note,
they reveal that, for each element that can be handled poorly, elements that contribute to family satisfaction can also
be handled well with some awareness and effort informed by research such as this paper.

Lear ning a c t iv it ie s
1 Delivering patient- and person- or family-centred nursing care can be assisted by working through your own
philosophy for nursing practice. To develop and articulate your own nursing philosophy, or way of doing things,
complete the following activities:
• List any organisational practices you can identify in the clinical practice setting in which you most recently
worked that might influence the model of nursing.
• Write out a list of characteristics of a clinician you admire and indicate how these complement good nursing
care.
• If you were a patient in the critical care unit in which you recently worked, what would be important to you
about the nursing care you received?
 CHAPTER 8 FAMILY AND CULTURAL CARE OF THE CRITICALLY ILL PATIENT 223

• If you had a family member in a critical care unit, write down the top eight things you consider most
important about the care that you and your family member receive. Compare this with the list provided
earlier in the chapter in the section Needs of family during critical illness.
• Having completed the above four activities, write three sentences that reflect your desired way of nursing
that can constitute your philosophy of nursing.
2 Ascertain the personal and professional beliefs you hold as a critical care nurse about 1) health and illness and
2) life, death and dying, by identifying situations when your personal and professional beliefs are in conflict.
Once these beliefs have been identified, the critical care nurse may ask:
• ‘How do these personal and professional beliefs influence my practice?’
• ‘What strategies do I need to implement to minimise negative impacts?’
• ‘When faced with a conflict between personal and professional beliefs and practices, which one is more
likely to direct practice decisions, and why?’
3 Using the information established in Learning activity 2, identify:
• your personal cultural beliefs and practices, and the impact these have on the patients and families that use
the services of critical care
• what actions you take to meet the patient’s and family’s needs during their critical care experience
• how you can integrate culture into nursing practice and the critical care setting that you work in. This
information can serve as a baseline for the development of strategies to improve practice.
4 The patient you are caring for today is to be the focus of a family conference that you will attend. Consider the
following:
• What would you do if this was your first ever family conference?
• What information would you prepare in readiness for the family conference?
• If you have not cared for the patient before, how and from whom would you seek additional information?
• How would you vary your approach if children were to be present?
• What would you record in the patient’s notes following the family conference?

Online resources
Australian Indigenous Health InfoNet, www.healthinfonet.ecu.edu.au
Cooperative Research Centre for Aboriginal Health, www.crcah.org.au/index.cfm
eMedical Journal of Australia articles on Aboriginal health, www.mja.com.au/Topics/Aboriginal%20health.htm
Hauora: Ma-ori standards of health IV: A study of the years 2000–2005, www.Maori.org.nz/tikanga/?d=page&pid=sp44&
parent=42
Information about Ma-ori protocol and beliefs, www.Maori.org.nz/tikanga/?d=page&pid=sp44&parent=42)
New Zealand Ministry of Health website (access to Ma-ori health-related publications and resources), www.moh.govt.nz
Office of Aboriginal Health–WA, http://www.aboriginal.health.wa.gov.au/home
Patient-centred care: Improving quality and safety by focusing care on patients and consumers, www.safetyandquality.gov.
au/wp-content/uploads/2012/01/PCCC-DiscussPaper.pdf

Further reading
Carson B, Dunbar T, Chenhall RD, Bailie R, eds. Social determinants of Indigenous health. Crows Nest, NSW: Allen and
Unwin; 2007.
Durie M. Whaiora. Auckland, NZ: Oxford University Press; 1998.
Eckermann A-K, Dowd T, Chong E, Nixon L, Gray R, Johnson SM. Binan Goonj: Bridging cultures in Aboriginal health.
3rd ed. Sydney: Churchill Livingstone; 2010.
Wepa D. Cultural safety in Aotearoa New Zealand. Auckland, NZ: Pearson Education; 2004.
Wright LM, Leahey M. Nurses and families: A guide to family assessment and intervention. 5th ed. Philadelphia: FA Davis; 2009.
224 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

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226 Valks K, Mitchell ML, Inglis-Simmons C, Limpus A. Dealing wth death: an audit of family bereavement programs in Australian intensive care
units. Aust Crit Care 2005;18:257–68.
227 Brosche TA. Death, dying and the IC nurse. DCCN 2003;22(4):173–9.
228 Main J. Management of relatives of patients who are dying. J Clin Nurs 2002;11:794–801.
229 Shaw DJ, Davidson JE, Smilde RI, Sondoozi T, Agan D. Multidisciplinary team training to enhance family communication in the ICU. Crit Care
Med 2014;42:265–71.
230 Quenot JP, Rigaud JP, Prin S, Barbar S, Pavon A, Hamet M et al. Suffering among carers working in critical care can be reduced by an
intensive communication strategy on end-of-life practices. Intens Care Med 2012;38(1):55–61.
231 Rogers S, Babgi A, Gomez C. Educational interventions in end-of-life care: part 1. Adv Neonatal Care 2008;8(1):56–65.
232 Wallace M, Sarles S. EB49 Changing culture to cultivate patient- and family-centered care. Crit Care Med 2012;32(2):e30-e.
233 Henrich NJ, Dodek P, Heyland D, Cook D, Rocker G, Kutsogiannis D et al. Qualitative analysis of an intensive care unit family satisfaction
survey. Crit Care Med 2011;39:1000–5.
 Chapter 9

Cardiovascular assessment
and monitoring
Thomas Buckley, Frances Lin

KEY WORDS Learning objectives

cardiovascular After reading this chapter, you should be able to:
assessment • describe the normal blood flow through the cardiovascular system
cardiovascular • define each stage of the cardiac action potential and its application to
electrophysiology electrocardiography
cardiovascular • describe the determinants of cardiac output and their interpretation in
macrostructure cardiovascular assessment and monitoring
chest X-ray • describe the reasons for the assessment and monitoring of critically ill
coronary perfusion patients
diagnostic imaging • summarise the key principles underpinning cardiac assessment and
electrocardiography monitoring
haemodynamic • identify the recommended anatomical landmarks for cardiac auscultation
monitoring and identify normal and common abnormal heart sounds
heart sounds • describe the physiological bases and reasons for different types of
haemodynamic monitoring
• critique and evaluate current clinical practice on haemodynamic
monitoring and integrate best evidence in clinical practice.

Introduction
This chapter reviews the support of cardiovascular function in the face of many
compromises to the system. It is essential for the reader to have a thorough
knowledge of both electrical and mechanical functions of the cardiac system.
Methodology for assessment of cardiovascular elements is discussed, along with
best practice ideas and diagnostic techniques.

Related anatomy and physiology

The cardiovascular system is essentially a transport system for distributing metabolic
requirements to, and collecting byproducts from, cells throughout the body. The
heart pumps blood continuously through two separate circulatory systems: to the
lungs and to all other parts of the body (see Figure 9.1). Structures on the right
side of the heart pump blood through the lungs (the pulmonary circulation) to be
oxygenated. The left side of the heart pumps oxygenated blood throughout the
232 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

remainder of the body (the systemic circulation).1,2 The two form the two separate pumps. The upper chambers, the
systems are connected, so the output of one becomes the atria, collect blood and act as a primer to the main pumping
input of the other. chambers, the ventricles. As the atria are low-pressure
chambers, they have relatively thin walls and are relatively
Cardiac macrostructure compliant. As the ventricles propel blood against either
The heart is cone-shaped and lies diagonally in the media- pulmonary or systemic pressure, they have much thicker
stinum towards the left side of the chest. The point of the and more muscular walls than the atria. As pressure is
cone is called the apex and rests just above the diaphragm; higher in the systemic circulation, the left ventricle is much
the base of the cone lies just behind the mediastinum. The thicker than the right ventricle. Dense fibrous connective
adult heart is about the size of that individual’s fist, weighs tissue rings provide a firm anchorage for attachments of
around 300 g and is composed of chambers and valves that atrial and ventricular muscle and valvular tissue.1,4

FIGURE 9.1 The systemic and pulmonic circulations.3

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Adapted from Novak B, Filer L, Latchett R. The applied anatomy and physiology of the cardiovascular system. In: Hatchett R, Thompson
D, eds. Cardiac nursing: a comprehensive guide. Philadelphia: Churchill Livingstone Elsevier; 2002, with permission.
 CHAPTER 9 CARDIOVASCULAR ASSESSMENT AND MONITORING 233

One-way blood flow in the system is facilitated by The heart wall has three distinct layers: the outer
valves.Valves between the atria and ventricles are composed protective pericardium, a medial muscular layer or
of cusps or leaflets sitting in a ring of fibrous tissue and myocardium and an inner layer or endocardium that
collagen. The cusps are anchored to the papillary muscles lines the heart. The pericardium is a double-walled, firm
by chordae tendinae so that the cusps are pulled together fibrous sac that encloses the heart. The two layers of the
and downwards at the onset of ventricular contraction. pericardium are separated by a fluid-filled cavity, enabling
The atrioventricular valves are termed the tricuspid valve the layers to slide over each other smoothly as the heart
in the right side of the heart and the mitral or bicuspid beats. The pericardium provides physical protection for
valve in the left side of the heart. Semilunar valves prevent the heart against mechanical force and forms a barrier to
backflow from the pulmonary artery (pulmonic valve) and infection and inflammation from the lungs and pleural
aorta (aortic valve) into the corresponding right and left space. Branches of the vagus nerve, the phrenic nerves and
ventricles. The muscles in the ventricles follow a distinct the sympathetic trunk enervate the pericardium.
spiral path so that, during contraction, blood is propelled The myocardium forms the bulk of the heart and is
into the respective outflow tracts of the pulmonary artery composed primarily of myocytes.5 Myocytes are the contrac-
and aorta. The aortic valve sits in a tubular area of mostly tile cells, and autorhythmic cells, which create a conduction
non-contractile collagenous tissue, which contains the pathway for electrical impulses. Myocytes (see Figure 9.2)
opening of the coronary arteries. The coronary arteries are cylindrical in shape and able to branch to intercon-
run through deep grooves that separate the atria and nect with each other. The junctions between myocytes
ventricles. The two sides of the heart are divided by a are termed intercalated discs and contain desmosomes and
septum, which ensures that two separate but integrated gap junctions.6 Desmosomes act as anchors to prevent the
circulations are maintained.1,4 myocytes from separating during contraction. Gap junctions

FIGURE 9.2 Diagram of an electron micrograph of cardiac muscle showing mitochondria, intercalculated discs,
tubules and sarcoplasmic reticulum.

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Mosby/Elsevier; 2010, with permission.
234 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

contain connexons, which allow ions to move from one support cardiac myocytes. Anastomoses between branches
myocyte to the next. The movement of ions from cell to of the coronary arteries often occur in mature individuals
cell ensures that the whole myocardium acts as one unit, when myocardial hypoxia has been present. These anasto-
termed a functional syncytium.When ischaemia occurs, the moses are termed collateral arteries, but the contribution
gap junctions may uncouple, so ions do not move as freely. to normal cardiac perfusion during occlusion of coronary
Uncoupling may also contribute to the poor conduction arteries is unclear.1
evidenced on ECG during ischaemia. The cardiac veins collect venous blood from the
The endocardium is composed primarily of squamous heart. Cardiac venous flow is collected into the great
epithelium, which forms a continuous sheet with the coronary vein and coronary sinus and ultimately flows
endothelium that lines all arteries, veins and capillaries. into the right atrium. Lymph drainage of the heart follows
The vascular endothelium is the source of many chemical the conduction tissue and flows into nodes and into the
mediators, including nitric oxide and the endothelin superior vena cava.
involved in vessel regulation. It has been theorised that the
endocardium may also have this function.1,4 Physiological principles
An understanding of the principles of cardiac physiology
Coronary perfusion is essential for safe management of the critically ill
The heart is perfused by the right and left coronary patient. While the primary role of the circulatory system
arteries that arise from openings in the aorta called the is to provide sufficient blood flow to meet metabolic
coronary ostia (see Figure 9.3). The right coronary artery demands, this requires adequate myocardial contraction,
(RCA) branches supply the atrioventricular node, right coordinated electrical conduction and adequate intravas-
atrium and right ventricle, and the posterior descending cular volume.
branch supplies the lower aspect of the left ventricle.
The left coronary artery divides into the left anterior Mechanical events of contraction
descending artery (LAD) and the circumflex artery (CX) Energy is produced in the myocytes by a large number of
shortly after its origin. The LAD supplies the interven- mitochondria contained within the cell. The mitochon-
tricular septum and anterior surface of the left ventricle. dria produce adenosine triphosphate (ATP), a molecule
The CX supplies the lateral and posterior aspects of the that is able to store and release chemical energy. Other
left ventricle. This is the most common distribution of the organelles in the myocyte, called sarcoplasmic reticulum,
coronary arteries, but it is not uncommon for the right are used to store calcium ions.The myocyte cell membrane
coronary artery to be small and the CX to supply the (sarcolemma) extends down into the cell to form a set
inferior wall of the left ventricle. The coronary arteries of transverse tubules (T tubules), which rapidly transmit
ultimately branch into a dense network of capillaries to external electrical stimuli into the cell. Cross-striated

FIGURE 9.3 Location of the coronary arteries.

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Mosby/Elsevier; 2010, with permission.
 CHAPTER 9 CARDIOVASCULAR ASSESSMENT AND MONITORING 235

FIGURE 9.4 Actin and myosin filaments and other FIGURE 9.5 A Action potential in a ‘fast response’,
cross-bridges responsible for cell contraction. non-pacemaker myocyte: phases 0–4, resting
membrane potential -80 mV, absolute refractory period
(ARP) and relative refractory period (RRP). B Action
potential in a ‘slow response’, pacemaker myocyte.
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critical care nursing: Diagnosis and management. 6th ed.  7KUHVKROG
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muscle fibrils, which contain contractile units, fill up the Adapted from Bersten AD, Soni N, Oh TE. Oh’s intensive care
myocyte. These fibrils are termed sarcomeres. manual. 7th ed. Oxford: Butterworth-Heinemann; 2013, with
The sarcomere contains two types of protein permission.
myofilaments, one thick (myosin) and one thin (actin,
tropomyosin and troponin) (see Figure 9.4). The myosin Cell membrane pumps create concentration gradients
molecules of the thick filaments contain active sites that across the cell membrane during diastole to create a
form bridges with sites of the actin molecules on the thin resting electrical potential of –80 mV. Individual fibres are
filaments. These filaments are arranged so that during separated by membranes but depolarisation spreads rapidly
contraction, bridges form and the thin filaments are pulled because of the presence of gap junctions. There are five
into the lattice of the thick filaments. As the filaments are key phases to the cardiac action potential:
pulled towards the centre of the sarcomere, the degree
of contraction is limited by the length of the sarcomere. 0 depolarisation
Starling’s law states that, within physiological limits, the 1 early rapid repolarisation
greater the degree of stretch, the greater the force of 2 plateau phase
contraction. The length of the sarcomere is the physiolog- 3 final rapid repolarisation
ical limit because too great a stretch will disconnect the
myosin–actin bridges. 4 resting membrane phase.8
The contractile response begins just after the start of
Electrical events of depolarisation, depolarisation and lasts about 1.5 times as long as the
resting potential and action potential depolarisation and repolarisation (see Figure 9.6).
Automaticity and rhythmicity are intrinsic properties of The action potential is created by ion exchange
all myocardial cells. However, specialised autorhythmic triggered by an intracellular and extracellular fluid
cells in the myocardium generate and conduct impulses trans-membrane imbalance. There are three ions involved:
in a specific order to create a conduction pathway. This sodium, potassium and calcium. Normally, extracellular
pathway ensures that contraction is coordinated and fluid contains approximately 140 mmol/L sodium and
rhythmical, so that the heart pumps efficiently and contin- 4 mmol/L potassium. In intracellular fluid these concen-
uously. Electrical impulses termed action potentials are trations are reversed. The following is a summary of
transmitted along this pathway and trigger contraction physiological events during a normal action potential:
in myocytes. Action potentials represent the inward and • At rest cell membranes are more permeable to
outward flow of negative and positive charged ions across potassium and, consequently, potassium moves slowly
the cell membrane (see Figure 9.5). and passively from intracellular to extracellular fluid.
236 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

FIGURE 9.6 Action potential.

Phase 1
⫹20 mV
Phase 2

Mechanical
Phase 3
contraction
Phase 0

ACTION
POTENTIAL ⫺90 mV Phase 4 ⫺90 mV

QRS
T
ECG

Depolarisation Repolarisation

Adapted from Urden L, Stacy KL, Lough ME, eds. Thelan’s critical care nursing: Diagnosis and management. 6th ed. St Louis:
Mosby/Elsevier; 2010, with permission.

At this time fast sodium and slow calcium channels atrioventricular (AV) node; atrial depolarisation normally
are closed and the resting membrane potential is very takes 0.1 second. There is a short delay at the AV node
negative (-90 mV). (0.1 s) before excitation spreads to the ventricles. This
• During depolarisation (phase 0), rapid ion movement delay is shortened by sympathetic activity and lengthened
caused by sodium flowing into the cell alters the by vagal stimulation. Ventricular depolarisation takes
electrical potential from -90 mV to +30 mV. At this 0.08–0.1 sec, and the last parts of the heart to be depolar-
time potassium channels close. ised are the posteriobasal portion of the left ventricle, the
pulmonary conus and the upper septum.8
• In phase 1 the sodium channels close and potassium The electrical activity of the heart can be detected
begins to leave the cell.This is followed by a brief influx
of calcium via the fast channel and then more via the on the body surface because body fluids are good
slower channel to create a plateau (phase 2), the duration conductors; the fluctuations in potential that represent
of which determines stroke volume due to its influence the algebraic sum of the action potentials of myocardial
on the contractile strength of the muscle fibres. fibres can be recorded on an electrocardiogram (see later
in this chapter).
• The third phase occurs when the calcium channels
are inactivated allowing potassium to leave the cell Cardiac macrostructure and conduction
more rapidly, restoring the negative charge and The electrical and mechanical processes of the heart differ
causing rapid depolarisation. but are connected. The autorhythmic cells of the cardiac
• The final resting phase occurs when slow potassium conduction pathway ensure that large portions of the
leakage allows the cell to increase its negative heart receive an action potential rapidly and simultane-
potential or charge (phase 4) to ensure that it is more ously. This ensures that the pumping action of the heart is
negative than surrounding fluid, before the next maximised. The conduction pathway is composed of the
depolarisation occurs and the cycle repeats.6 sinoatrial (SA) node, the atrioventricular (AV) node, the
Cardiac muscle is generally slow to respond to bundle of His, right and left bundle branches and Purkinje
stimuli and has relatively low ATPase activity. Its fibres fibres (see Figure 9.7). The cells contained in the pathway
are dependent on oxidative metabolism and require a conduct action potentials extremely rapidly, 3–7 times
continuous supply of oxygen. The lengths of fibres and faster than general myocardial tissue. Pacemaker cells of
the strength of contraction are determined by the degree the sinus and atrioventricular nodes differ, in that they
of diastolic filling in the heart. The force of contraction is are more permeable to potassium, so that potassium easily
enhanced by catecholamines.2 ‘leaks’ back out of the cells triggering influx of sodium
Depolarisation is initiated in the sinoatrial (SA) node and calcium back into cells. This permits the spontaneous
and spreads rapidly through the atria, then converges on the automaticity of pacemaker cells.
 CHAPTER 9 CARDIOVASCULAR ASSESSMENT AND MONITORING 237

FIGURE 9.7 Cardiac conduction system. AV = atrioventricular; LBB = left bundle branch; RBB = right bundle branch.

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Mosby/Elsevier; 2010, with permission.

At the myocyte, the action potential is transmitted to the Determinants of cardiac output
myofibrils by calcium from the interstitial fluid via channels. In the healthy individual, the most immediate change in
During repolarisation (after contraction), the calcium ions cardiac output is seen when heart rate rises. However,
are pumped out of the cell into the interstitial space and into in the critically ill, the ability to raise the heart rate in
the sarcoplasmic reticulum and stored. Troponin releases response to changing circumstances is limited, and a rising
its bound calcium, enabling the tropomyosin complex to heart rate may have negative effects on homeostasis, due
block the active sites on actin, and the muscle relaxes. to decreased diastolic filling and increased myocardial
The cardiac conduction system and the mechanical oxygen demand.
efficiency of the heart as a pump are directly connected. Preload is the load imposed by the initial fibre length
Disruption to conduction may not prevent myocardial of the cardiac muscle before contraction (i.e. at the end of
contraction but may result in poor coordination and lower diastole).The primary determinant of preload is the amount
pump efficiency. Interruption to flow through the coronary of blood filling the ventricle during diastole and, as indicated
arteries may alter depolarisation. Disrupted conduction in Figure 9.8, it is important in determining stroke volume.
from the SA to the AV node may allow another area in the Preload influences the contractility of the ventricles (the
conduction system to become the new dominant pacemaker strength of contraction) because of the relationship between
and alter cardiac output. Although the autonomic nervous myocardial fibre length and stretch. However, a threshold
system influences cardiac function, the heart is able to is reached when fibres become overstretched, and force of
function without neural control. Rhythmical myocardial contraction and resultant stroke volume will fall.
contraction will continue because automaticity and rhyth- Preload reduces as a result of large-volume loss (e.g.
micity are intrinsic to the myocardium. haemorrhage), venous dilation (e.g. due to hyperther-
mia or drugs), tachycardias (e.g. rapid atrial fibrillation
Cardiac output or supraventricular tachycardias), raised intrathoracic
Cardiac performance is altered by numerous homeostatic pressures (a complication of intermittent positive pressure
mechanisms. Cardiac output is regulated in response to ventilation [IPPV]), and raised intracardiac pressures (e.g.
stress or disease, and changes in any of the factors that cardiac tamponade). Some drugs such as vasodilators can
determine cardiac output will result in changes to cardiac cause a decrease in venous tone and a resulting decrease in
output (see Figure 9.8). Cardiac output is the product of preload. Preload increases with fluid overload, hypother-
heart rate and stroke volume; alteration in either of these mia or other causes of venous constriction, and ventricular
will increase or decrease cardiac output, as will alteration failure. Body position will also affect preload, through its
in preload, afterload or contractility. effect on venous return.
238 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

FIGURE 9.8 Determinants of cardiac function and oxygen delivery.9

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1994, with permission.

The volume of blood filling the ventricles is also (SVR), as this is just one factor determining left ventricu-
affected by atrial contraction: a reduction in atrial contrac- lar afterload. Factors that increase afterload include:
tion ability, as can occur during atrial fibrillation, will result
in a reduction in ventricular volume, and a corresponding
• increased ventricular radius
fall in stroke volume and cardiac output. • raised intracavity pressure
Preload of the left side of the heart, assessed at the • increased aortic impedance
end of filling of the left ventricle from the left atrium • negative intrathoracic pressure
using the pulmonary capillary wedge pressure (PCWP),
is assumed for clinical purposes to reflect left ventricu- • increased SVR.
lar end-diastolic volume (LVEDV). Due to the non-linear As afterload rises, the speed of muscle fibre shortening
relationship between volume and pressure,10 caution must, and external work performed falls, which can cause a
however, be taken when interpreting these values, as rises decrease in cardiac output in critically ill patients.Afterload
in LVEDP may indicate pathology other than increased of the right side of the heart is assessed during the ejection
preload. Preload of the right side of the heart is indirectly of blood from the right ventricle into the pulmonary
assessed at the end of filling of the right ventricle from artery. This volume is indirectly assessed by calculating
the right atrium through central venous pressure (CVP) pulmonary vascular resistance.Ventricular afterload can be
monitoring. altered to clinically affect cardiac performance. Reducing
Afterload is the load imposed on the muscle during afterload will increase the stroke volume and cardiac
contraction, and translates to systolic myocardial wall output, while also reducing myocardial oxygen demand.
tension. It is measured during systole, and is inversely However, reductions in afterload are associated with
related to stroke volume and therefore cardiac output, lower blood pressure, and this limits the extent to which
but it is not synonymous with systemic vascular resistance afterload can be manipulated.
 CHAPTER 9 CARDIOVASCULAR ASSESSMENT AND MONITORING 239

Contractility is the force of ventricular ejection, or volume and cardiac output. Increasing contractility will
the inherent ability of the ventricle to perform external increase myocardial oxygen demand, which could have
work, independent of afterload or preload. It is difficult a detrimental effect on patients with limited perfusion.
to measure clinically. It is increased by catecholamines, Stroke volume is the amount of blood ejected from each
calcium, relief of ischaemia and digoxin. It is decreased ventricle with each heartbeat. For an adult, the volume is
by hypoxia, ischaemia and certain drugs such as thiopen- normally 50–100 mL/beat, and equal amounts are ejected
tone, beta-adrenergic blockers, calcium channel blockers from the right and left ventricle.
or sedatives. Such changes affect cardiac performance, Cardiac output is dependent on a series of mechanical
with increases in contractility causing increased stroke events in the cardiac cycle (see Figure 9.9). As normal

FIGURE 9.9 The cardiac cycle.

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Mosby/Elsevier; 2010, with permission.
240 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

average heart rate is maintained at approximately 70 beats/ depends on venous return from systemic and pulmonic
min the average phases of the cardiac cycle are completed veins and varies according to tissue metabolism, total
in less than a second (0.8 s). Electrical stimulation of blood volume and vasodilation.Venous return contributes
myocardial contraction ensures that the four chambers of to end-diastolic volume (preload) and pressure, which are
the heart contract in sequence. This allows the atria to act both directly related to the force of contraction in the
as primer pumps for the ventricles, while the ventricles next ventricular systole. The intrinsic capacity of the heart
are the major pumps that provide the impetus for blood to respond to changes in end-diastolic pressure can be
to flow through the pulmonary and systemic vascular represented by a number of length–tension curves and the
systems. The phases of the cardiac cycle are characterised Frank-Starling mechanism (see Figure 9.10). According to
by pressure changes within each of the heart chambers, this mechanism, within limits, the greater the stretch of
resulting in blood flow from areas of high pressure to areas the cardiac muscle fibre before contraction, the greater
of lower pressure. the strength of contraction.The ability to increase strength
During late ventricular diastole (rest), pressures are of contraction in response to increased stretch exists
lowest in the heart and blood returns passively to fill the because there is an optimal range of cross-bridges that
atria. This flow also moves into the ventricle through the can be created between actin and myosin in the myocyte.
open AV valves, producing 70–80% of ventricular filling. Under this range, when venous return is poor, fewer
The pulmonic and aortic valves are closed, preventing cross-bridges can be created. Above this range, when heart
backflow from the pulmonary and systemic systems into failure is present, the cross-bridges can become partially
the ventricles. Depolarisation of the atria then occurs, disengaged, contraction is poor and higher filling pressures
sometimes referred to as atrial kick, stimulating atrial are needed to achieve adequate contractile force.
contraction and completing the remaining 20–30% of Ventricular contraction is also intrinsically influenced
ventricular filling. by the size of the ventricle and the thickness of the
During ventricular systole (contraction), the atria ventricle wall. This mechanism is described by Laplace’s
relax while the ventricles depolarise, resulting in ventric-
law, which states that the amount of tension generated
ular contraction. Pressure rises in the ventricles, resulting
in the wall of the ventricle required to produce intra-
in the AV valves closing. When this occurs, all four
ventricular pressure depends on the size (radius and wall
cardiac valves are closed, blood volume is constant and
thickness) of the ventricle.1 As a result, in heart failure,
contraction occurs (isovolumetric contraction). When
the pressure in the ventricles exceeds the pressure in when ventricular thinning and dilation are present, more
the major vessels the semilunar valves open. This occurs tension or contractile force is required to create intra-
when pressure in the left ventricle reaches approximately ventricular pressure and therefore cardiac output.
80 mmHg and in the right ventricle approximately
27–30 mmHg. During the peak ejection phase, pressure FIGURE 9.10 The Frank-Starling curve. As left
in the left ventricle and aorta reaches approximately ventricular end-diastolic pressure increases, so does
120 mmHg and in the right ventricle and pulmonary ventricular stroke work.
artery approximately 25–28 mmHg.
During early ventricular diastole, the ventricles
repolarise and ventricular relaxation occurs. The pressure
Increased
in the ventricles falls until the pressures in the aorta and contractility
pulmonary artery are higher and blood pushes back
Ventricular stroke work (mmHg)

125
against the semilunar valves. Shutting of these valves
prevents backflow into the ventricles, and pressure in the Normal
ventricles declines further. During ventricular contraction, 100 contractility
the atria have been filling passively, so the pressure in the
atria rises to higher than that in the ventricles and the AV 75
valves open, allowing blood flow to the ventricles. Any Decreased
contractility
rise in heart rate will shorten the resting period, which 50
may impair filling time and coronary artery flow as these
arteries fill during diastole.1 25

Regulation of cardiac output

The heart is a very effective pump and is able to adapt to
0 4 8 12 16
meet the metabolic needs of the body. The activities of
the heart are regulated by two responsive systems: intrinsic Left ventricular end-diastolic filling pressure (LVEDP)
regulation of contraction and the autonomic nervous Adapted from Urden L, Stacy KL, Lough ME, eds. Thelan’s
system. critical care nursing: Diagnosis and management. 6th ed.
Intrinsic regulation of contraction responds to the rate St Louis: Mosby/Elsevier; 2010, with permission.
of blood flow into the chambers. Blood flow into the heart
 CHAPTER 9 CARDIOVASCULAR ASSESSMENT AND MONITORING 241

The heart’s ability to pump effectively is also strong muscular walls that can contract (vasoconstrict)
influenced by the pressure that it is required to generate to the point of closure and relax (vasodilate) to change
above end-diastolic pressure to eject blood during the artery lumen rapidly in response to tissue needs. The
systole. This additional pressure is usually determined by lumen created by the arterioles is the most important
how much resistance is present in the pulmonary artery source of resistance to blood flow in the systemic circu-
and aorta, and is in turn influenced by the peripheral lation (just under 50%).
vasculature. This systemic vascular resistance, known Capillaries function to allow exchange of fluid,
and measured as afterload, causes resistance to flow in nutrients, electrolytes, hormones and other substances
relation to the left ventricle and is influenced by vascular through highly permeable walls between the blood
tone and disease. plasma and interstitial fluid (see Figure 9.11). Just before
the capillary beds are precapillary sphincters, bands of
Autonomic nervous system control and regulation smooth muscle that adjust flow in the capillaries. Venules
of heart rate collect blood from the capillaries to veins. Excess tissue
Although the pacemaker cells of the heart are capable fluid is collected by the lymphatic system. Lymphatic veins
of intrinsic rhythm generation (automaticity), inputs have a similar structure to the cardiovascular system veins
from the autonomic nervous system regulate heart rate described below, with lymph returning to this system at
changes in accordance with body needs by stimulating the right side of the heart.
or depressing these pacemaker cells. Cardiac innervation Veins collect and transport blood back to the heart at
includes sympathetic fibres from branches of T1–T5 and low pressure and serve as a reservoir for blood. Therefore,
parasympathetic input via the vagus nerve.11 The heart veins are numerous and have thinner, less muscular walls,
rate at any moment is a product of the respective inputs which can dilate to store extra blood (up to 64% of total
of sympathetic stimuli (which accelerate) and parasympa- blood volume at any time). Some veins, particularly
thetic stimuli (which depress) on heart rate. Rises in heart in the lower limbs, contain valves to prevent backflow
rate can thus be achieved by an increase in sympathetic and ensure one-way flow to the heart. Venous return is
tone or by a reduction in parasympathetic tone (vagal promoted during standing and moving by the muscles
inhibition). Conversely, slowing of the heart rate can be of the legs compressing the deep veins, promoting blood
achieved by decreasing sympathetic or increasing para- flow towards the heart.1,4
sympathetic activity.4
Hormonal, biochemical and pharmacological inputs
also exert heart rate influences by their effects on FIGURE 9.11 The structure of arteries, veins and
capillaries.
autonomic neural receptors or directly on pacemaker
cells. In mimicking the effects of direct nervous inputs,
these influences may be described as sympathomimetic &DSLOODU\ &DSLOODU\
or parasympathomimetic. Sympathomimetic stimula- (QGRWKHOLDOFHOOV QHWZRUN
tion (e.g. through the use of isoprenaline) achieves the
same cardiac end points as direct sympathetic activity,
increasing the heart rate, while sympathetic antagonism
(e.g. beta-blockade therapy) slows the heart through
receptor inhibition. By contrast, parasympathomimetic
agonist activity slows the heart rate, while parasympa-
thetic antagonism (e.g. via administration of atropine
sulfate) raises the heart rate by causing parasympathetic
receptor blockade.4
The vascular system /XPHQ
9DOYH
The vascular system is specialised according to the 7XQLFDLQWLPD
different tissues it supplies, but the general functions (QGRWKHOLXP
and characteristics are similar. All vessels in the circu- 6XEHQGRWKHOLDOOD\HU
latory system are lined by endothelium, including the ,QWHUQDOHODVWLFODPLQD
heart. The endothelium creates a smooth surface, which $UWHU\ 9HLQ
reduces friction and also secretes substances that promote 7XQLFDPHGLD
contraction and relaxation of the vascular smooth muscle. 7XQLFDDGYHQWLWLD
Arteries function to transport blood under high pressure
and are characterised by strong elastic walls that allow Adapted from Novak B, Filer L, Latchett R. The applied
anatomy and physiology of the cardiovascular system.
stretch during systole and high flow. During diastole, the
In: Hatchett R, Thompson D, eds. Cardiac nursing: a
artery walls recoil so that an adequate perfusion pressure comprehensive guide. Philadelphia: Churchill Livingstone
is maintained. Arterioles are the final small branches Elsevier; 2002, with permission.
of the arterial system prior to capillaries, and have
242 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Blood pressure on blood vessels, the bronchi, gastrointestinal tract, skeletal

Blood flow is maintained by pulsatile ejection of blood muscle, liver and mast cells (inflammatory cells). Activation
from the heart and pressure differences between the blood results in vasodilatation of small coronary arteries,
vessels. Traditionally, blood pressure is measured from bronchodilation, relaxation of the gastrointestinal tract,
the arteries in the general circulation at the maximum glycogenolysis (breakdown of glycogen to glucose) in the
value during systole and the minimum value occurring liver, tremor in skeletal muscle and inhibition of histamine
during diastole. The cardiovascular system must supply (an inflammatory amine responsible for increased perme-
blood according to varying demands and in a range of ability of capillaries).
circumstances, with at least a minimal blood flow to be Noradrenaline binds to both beta and alpha receptors.
maintained to all organs. At a local level this is achieved by Alpha-1 and alpha-2 adrenoreceptors are found in the
autoregulation of individual arteries, such as the coronary central and peripheral nervous system and are located
arteries, in response to the metabolic needs of the specific on vascular and non-vascular smooth muscle. Alpha-1
tissue or organ. The exact mechanism is unknown, but it adrenergic stimulation causes vasoconstriction and is the
has been proposed that increased vascular muscle stretch main mechanism of the vasopressor action of noradrena-
and/or metabolites and decreased oxygen levels are line. Presynaptic alpha-2 receptors inhibit the release of
detected and cells release substances such as adenosine.4 noradrenaline and thus serve as an important receptor in
These substances result in rapid vasodilation and increased the negative feedback control of noradrenaline release.
perfusion. The vascular endothelium actively secretes Postsynaptic alpha-2 receptors are located on liver cells,
prostacyclin and endothelial-derived relaxing factor (nitric platelets and the smooth muscle of blood vessels and,
oxide), both vasoactive agents. when activated, cause platelet aggregation and blood vessel
There are three main regulatory mechanisms of blood constriction. Noradrenaline results in very little beta-2
pressure control: (a) short-term autonomic control, (b) activity. Clinically, the positive inotropic and chrono-
medium-term hormonal control and (c) long-term renal tropic effects of noradrenaline, from beta-1 simulation, are
system control. counterbalanced by the increased afterload from elevated
systemic vascular resistance (alpha-1 adrenergic agonist
Autonomic control effect).
The cardiovascular control centre connects with the
hypothalamus to control temperature, the cerebral cortex Renal control
and the autonomic system to control cardiac activity Renal control of blood pressure in the long term occurs
and peripheral vascular tone. Information about blood via control of blood volume. Generally, as blood pressure or
pressure and resistance is sensed by neural receptors volume rises, the kidneys produce more urine; conversely,
(baroreceptors) in the aortic arch and the carotid sinuses, as blood pressure or volume falls, the kidneys produce less
which detect changes in blood supply to the body and urine.
the brain. Impulses from these receptors initiate a blood- In addition to longer term fluid regulation, during acute
pressure regulating reflex in the cardiovascular centre, which illness or time of acute hypotension, the renin–angiotensin–
activates the parasympathetic system and sympathetic aldosterone system (RAAS) plays an important role in
system to alter cardiac activity and dilation or constriction maintaining blood pressure.This negative feedback system
of arterioles and veins to lower or raise blood pressure. The both reabsorbs intravascular fluid and increases peripheral
cardiovascular system also maintains a constant resting tone resistance, in an effort to increase blood pressure. Further
of intermediate tension in the arteries. details on the RAAS system can be found in Chapter 18.
Hormonal control
Changes in blood pressure are also detected by the
Assessment
adrenal medulla, which secretes catecholamines as cardiac It is essential that the critical care nurse conducts a compre-
output declines. The two main catecholamines, adrenaline hensive cardiac assessment on a critically ill patient. The
(epinephrine) and noradrenaline (norepinephrine), mimic nursing assessment aims to define patient cardiovascular
the action of the sympathetic system by binding to and status as well as inform implementation of an appropriate
stimulating adrenergic receptors. Adrenergic receptors are clinical management plan. The focus of the cardiovascular
located in smooth muscle cells of vascular beds including assessment varies according to the setting, clinical presen-
the peripheral veins and arterioles supplying the skin, tation and treatments commenced, if any. However, the
kidneys, skeletal muscles and mucosa. main priority should be to determine whether the patient
The main action of adrenaline occurs by binding to is haemodynamically stable or requiring initiation or
the beta-1 adrenoreceptors (located mainly in the heart adjustment of supportive treatments.
but also found in platelets and the non-sphincter part of A thorough cardiac assessment requires the critical care
the gastrointestinal tract), causing an increase in the rate nurse to be competent in a wide range of interpersonal,
and contraction of the heart, aggregation of platelets and observational and technical skills. A cardiac assessment
relaxation of the non-sphincter part of the gastrointesti- should be performed as part of a comprehensive patient
nal tract. Adrenaline also binds to beta-2 receptors, located assessment and should consider the following elements.
 CHAPTER 9 CARDIOVASCULAR ASSESSMENT AND MONITORING 243

It is important to create a health history, if not already ‘tachycardia’ (tachy is Greek meaning swift). An important
obtained. This history should aim to elicit a description of aspect of pulse assessment involves assessment for regularity.
the present illness and chief complaint. A useful guide in Detection of an irregular pulse should trigger further
taking a specific cardiac history is to use direct questions investigation and prompt ECG assessment for atrial fibril-
to seek information regarding symptom onset, course, lation, a condition in which atrial contraction becomes
duration, location and precipitating and alleviating factors. lost due to chaotic electrical activity with variable ventric-
Some common cardiovascular disease-related symptoms ular response. In addition to rate and rhythm, assessment
to be observed for include: chest discomfort or pain, of pulse, especially if palpated in the carotid or femoral
palpitations, syncope, generalised fatigue, dyspnoea, cough, artery, can reveal a bounding pulse that may be indicative
weight gain or dependent oedema. Chest pain, discomfort of hyperdynamic state or aortic regurgitation. An alternat-
or tightness should be initially considered indicative of ing strong and weak pulse, known as pulsus alternans, may
cardiac ischaemia until proven otherwise by further exam- be observed in advanced heart failure.
ination and diagnostic assessment. Additionally, a health
history should be inclusive of known cardiovascular risk Auscultation of heart sounds
factors, such as hyperlipidaemia or hypertension, and any Auscultation of the heart involves listening to heart sounds
medications the patient may be taking including over-the- over the pericardial area using a stethoscope. While chal-
counter medications. lenging to achieve competence in, cardiac auscultation
Prior to inspecting or palpating the patient, the nurse is an important part of cardiac physical examination and
should observe the patient’s general appearance noting relies on a sound understanding of cardiac anatomy, cardiac
whether the patient is restless, able to lie flat, in pain or cycle and physiologically associated sounds. For accurate
distress, is pale or has decreased level of consciousness. auscultation, experience in assessment of normal sounds
Patients with compromised cardiac output will likely is critical and can only be obtained through constant
have decreased cerebral perfusion and may have mental practice. When auscultating heart sounds, normally two
confusion, memory loss or slowed verbal responses. Addi- sounds are readily audible and they are known as the first
tionally, assessment of any pain should be noted. (S1) and second (S2) sounds. A useful technique when
Specific physical assessment in relation to cardiovascu- listening to heart sounds is to feel the carotid pulse at the
lar function should be inclusive of: same time as auscultation, which will help identify the
heart sound that corresponds with ventricular systole.
• vital signs
• respiratory assessment for signs of pulmonary oedema Practice tip
(shortness of breath or basal crepitations)
When learning to interpret heart sounds, feel the carotid
• assessment of neck vein distension for signs of right- pulse at the same time as auscultation of the heart,
sided venous congestion
which will help identify the heart sound that corresponds
• assessment for signs of peripheral oedema with ventricular systole (S1 will be heard simultaneously
• capillary refill time with >3 s return indicative of with the pulse).
sluggish capillary return
• 12-lead ECG for signs of ischaemia or cardiac The first heart sound (S1) occurs at the beginning of
pathology ventricular systole, following closure of the intracardiac
valves (mitral and tricuspid valves). This heart sound is
• appearance and temperature of the skin for signs of best heard with the diaphragm of the stethoscope and
peripheral constriction or dehydration
loudest directly over the corresponding valves (4th inter-
• core body temperature measurement costal space [ICS] left of the sternum for the tricuspid
• urine output with <0.5 mL/kg/h a potential and 5th ICS left of the mid-clavicular line for the mitral
indicator of decreased renal perfusion.12 valve). Following closure of these two valves, ventricular
contraction and ejection occurs and a carotid pulse may
Assessment of pulse be palpated at the same time that S1 is audible.
In the critical care environment, the heart rate can be The second heart sound (S2) occurs at the beginning
observed from a cardiac monitor; however, this does of diastole, following closure of the aortic and pulmonary
not give qualitative information about the arterial pulse. valves and can be best heard over these valves (2nd ICS
Routinely performed as part of most patient assessments, to the right and left of the sternum, respectively). It is
information gathered from pulse assessment can give important to remember that both S1 and S2 result from
useful cues and direct further assessments. Although the events occurring in both left and right sides of the heart.
radial pulse is distant from the central arteries, it is useful As left-sided heart sounds are normally loudest and occur
for gathering information on rate, rhythm and strength. slightly before right-sided events, careful listening during
Heart rate below 60 beats per minute is defined as ‘brady- inspiration and expiration may result in left and right
cardia’ (brady is Greek for slow, and kardia means heart). events being heard separately. This is known as physiolog-
A heart rate greater than 100 beats per minute is called ical splitting of heart sounds, a normal physiological event.
244 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 9.1
Guide to placement of the stethoscope when listening to heart sounds

STETHOSCOPE PLACEMENT A U D I TA B L E R E G I O N O F H E A R T

2nd intercostal space right of sternum Aortic valve

2nd intercostal space left of sternum Pulmonary valve
4th intercostal space left side of sternum Tricuspid valve
5th intercostal space Mid-clavicular line Mitral valve

A guide to placement of the stethoscope when listening stenosis or regurgitation at these locations. Murmurs are
to heart sounds is presented in Table 9.1. best thought of as turbulent flow or vibrations associated
In assessment of the critically ill patient extra heart with the corresponding valve and can be of variable pitch.
sounds, labelled S3 and S4, may be heard during times of Specialist cardiac referral is indicated upon detection of
extra ventricular filling or fluid overload. Often referred cardiac murmurs to differentiate pathological murmurs, as
to as ‘gallops’, these extra heart sounds are accentuated seen during valvular dysfunction or myocardial infarction,
during episodes of tachycardia. S3, ventricular gallop, from innocent systolic ‘high flow’ murmurs detected in
occurs during diastole in the presence of fluid overload. children or adolescents as a result of vigorous ventricular
Considered physiological in children or young people, contraction. Murmurs may be classified using the Levine
due to rapid diastolic filling, S3 may be considered patho- scale,12 shown in Table 9.2.
logical when due to reduced ventricular compliance and
associated increased atrial pressures. As S3 occurs early Continuous cardiac monitoring
in diastole, it will be heard and associated more closely In the case of the critically ill patient, there are two main
with S2. forms of cardiac monitoring, both of which are used to
S4 is a late diastolic sound and may be heard shortly generate essential data: continuous cardiac monitoring and
before S1. S4 occurs when ventricular compliance is the 12-lead ECG. Internationally, a minimum standard
reduced secondary to aortic or pulmonary stenosis, mitral for an ICU requires availability of facilities for cardio-
regurgitation, systemic hypertension, advanced age or vascular monitoring.13,14 Continuous cardiac monitoring
ischaemic heart disease. In patients with severe ventricu- allows for rapid assessment and constant evaluation with,
lar dysfunction, both S3 and S4 may be audible although, when required, the instantaneous production of paper
when coupled with tachycardia, these may be difficult to recordings for more detailed assessment or documenta-
differentiate and will require specialist assessment. tion into patient records. In addition, practice standards for
The critical care nurse auscultating the heart should electrocardiographic monitoring in hospital settings have
also listen for a potential pericardial rub. This ‘rubbing’ been established.15
or ‘scratching’ sound is secondary to pericardial inflam- It is now common practice for five leads to be
mation and/or fluid accumulation in the pericardial used for continuous cardiac monitoring, as this allows
space. To differentiate pericardial rub from pulmonary
rub, if possible the patient should be instructed to hold
their breath for a short duration as pericardial rub will TABLE 9.2
continue to be audible in the absence of breathing, Classification of heart murmurs using the Levine scale
heard over the 3rd ICS to the left of the mid sternum.
Detection of pericardial rub warrants further investiga- Grade 1 Low intensity and difficult to hear
tion by ultrasound. Grade 2 Low intensity, but audible with a stethoscope
but no palpable thrill
Practice tip 2 Grade 3 Medium intensity and easily heard with a
stethoscope
To differentiate pericardial rub from pulmonary rub, ask
the patient to hold their breath for a short duration, as Grade 4 Loud and audible and with palpable thrill
pericardial rub will continue to be audible in the absence Grade 5 Very loud but cannot be heard outside the
of breathing and pleural rub will not be audible while the praecordium and with palpable thrill
patient is not breathing. Grade 6 Audible with the stethoscope away from the
chest
In addition to pericardial rub, murmurs may also be
audible. Murmurs are generally classified and charac- Adapted from Johnson K, Rawlings-Anderson K. Oxford
handbook of cardiac nursing. 2nd ed. New York: Oxford
terised by location with the most common murmurs University Press; 2014, with permission.
associated with the mitral or aortic valves, due to either
 CHAPTER 9 CARDIOVASCULAR ASSESSMENT AND MONITORING 245

a choice of seven views. The five electrodes are placed

as follows: FIGURE 9.12 Einthoven’s triangle formed by standard
limb leads.
• right and left arm electrodes: placed on each shoulder
• right and left leg electrodes: placed on the hips or
level with the lowest ribs on the chest
• V-lead views can be monitored: for V1 place the
electrode at the 4th ICS, right of the sternum;
for V6 place the electrode at the 5th ICS, left 5$ ⫺
, ⫹
/$
mid-axillary line. ⫹ ⫹
⫺ ⫺
The monitoring lead of choice is determined by the D9 /
5 D9
patient’s clinical situation. Generally, two views are better
than one. V1 lead is best to view ventricular activity and ⫺
differentiate right and left bundle branch blocks; therefore, ,, ,,,
one of the channels on the bedside monitor should display D9)
a V lead, preferably V1, and the other display lead II or III
for optimal detection of arrhythmias. When the primary ⫹
purpose of monitoring is to detect ischaemic changes, ⫹
//
⫹
leads III and V3 usually present the optimal combination.15
The skin must be carefully prepared before electrodes
are attached, as contact is required with the body surface
and poor contact will lead to inaccurate or unreadable Adapted from Urden L, Stacy KL, Lough ME, eds. Thelan’s
recordings, causing interference or noise. Patients who are critical care nursing: Diagnosis and management. 6th ed.
sweaty need particular attention, and it may be necessary St Louis: Mosby/Elsevier; 2010, with permission.
to shave the areas where the electrodes are to be placed in
very hairy people. such as left arm, right arm or left leg), with the centre of
12-lead ECG Einthoven’s triangle acting as the negative electrode. The
The Dutch physiologist Einthoven was one of the first waveforms of these leads are usually very small; therefore,
to represent heart electrical conduction as two charged they are augmented by the ECG machine to increase the
electrodes, one positive and one negative.16 The body size of the potentials on the ECG strip.17 These three leads
can be likened to a triangle, with the heart at its centre, view the heart at different angles:
and this has been called Einthoven’s triangle. Cardiac • Lead aVR produces a negative reflection because the
electrical activity can be captured by placing electrodes electrical activity moves away from the lead. Lead
on both arms and on the left leg. When these electrodes aVR does not provide a specific view of the heart.
are connected to a common terminal with an indifferent • Lead aVL produces a positive deflection because the
electrode that remains near zero, an electrical potential electrical activity moves towards the lead. Lead aVL
is obtained. Depolarisation moving towards an active views the electrical activity from the lateral wall.
electrode produces positive deflection.
The 12-lead ECG consists of six limb leads and six • Lead aVF also produces a positive deflection on the
chest leads. The limb leads examine electrical activity ECG because the electrical activity flows toward
along a vertical plane. The standard bipolar limb leads this lead. It views the electrical activity from the
(I, II, III) record differences in potential between the two inferior wall.
limbs by using two limb electrodes as positive and negative The six unipolar chest leads (precordial leads) are
poles (see Figure 9.12):17 leads I, II, and III all produce designated V1–6 and examine electrical activity along
positive deflections on the ECG because the electrical a horizontal plane from the right ventricle, septum, left
current flows from left to the right and from upwards to ventricle and the left atrium. They are positioned in the
downwards. Placement should be: following way (see Figure 9.13):
• I = negative electrode in right arm and positive • V1 = 4th ICS, to the right of the patient’s sternum
electrode in left arm
• V2 = 4th ICS, to the left of the patient’s sternum
• II = negative electrode in right arm and positive • V3 = equidistant between V2 and V4
electrode in left leg
• III = negative electrode in left arm and positive • V4 = 5th ICS on the mid-clavicular line
electrodes in left leg. • V5 = 5th ICS, anterior axillary line
The three unipolar limb leads (aVR, aVL, aVF) record • V6 = 5th ICS on the mid-axilla line
activity of the heart’s frontal plane. Each of these unipolar Amplitude (voltage) in the ECG is measured by a series
leads has only one positive electrode (the limb electrode of horizontal lines on the ECG trace (see Figure 9.14).
246 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Lines are 1 mm apart and represent increments of 0.1 mV. Duration of activity within the ECG is measured by a series
Amplitude reflects the wave’s electrical force and has no of vertical lines also 1 mm apart (see Figure 9.14).The time
relation to the muscle strength of ventricular contraction.8 interval between each line is 0.04 s. Every 5th line is printed
in bold, producing large squares. Each represents 0.5 mV
FIGURE 9.13 Position of chest leads. (vertically) and 0.2 s (horizontally).
Key components of the ECG
$QWHULRU
YLHZ
Key components of the cardiac electrical activity are
termed PQRST (see Figure 9.15):
$QJOHRI/RXLV
• The P wave represents electrical activity caused by
spread of impulses from the SA node across the atria
and appears upright in lead II. Inverted P waves
indicate atrial depolarisation from a site other than
9 9 the SA node. Normal P wave duration is considered
9
9 9 9 to be less than 0.12 s.
• The P–R interval reflects the total time taken for the
atrial impulse to travel through the atria and AV node.
It is measured from the start of the P wave to the
beginning of the QRS complex, but is lengthened
by AV block or some drugs. Normal P–R interval is
0.12–0.2 s.
5 / • The QRS complex is measured from the start of the
Q wave to the end of the S wave and represents the
time taken for ventricular depolarisation. Normal
Adapted from Urden L, Stacy KL, Lough ME, eds. Thelan’s
QRS duration is 0.08–0.12 s. Anything longer than
critical care nursing: Diagnosis and management. 6th ed.
St Louis: Mosby/Elsevier; 2010, with permission. 0.12 s is abnormal and may indicate conduction
disorders such as bundle branch block. The deflections

FIGURE 9.14 ECG graph paper.

3 sec

0.20 sec

10 mm

0.04 sec

5 mm

1 mm

0.20 sec

Adapted from Urden L, Stacy KL, Lough ME, eds. Thelan’s critical care nursing: Diagnosis and management. 6th ed. St Louis:
Mosby/Elsevier; 2010, with permission.
 CHAPTER 9 CARDIOVASCULAR ASSESSMENT AND MONITORING 247

seen in relation to this complex will vary in size, • The ST segment is measured from the J point
depending on the lead being viewed. However, small (junction of the S wave and ST segment) to the start
QRS complexes occur when the heart is insulated, as of the T wave. It is usually isoelectric in nature, and
in the presence of pericardial effusion. Conversely, an elevation or depression indicates some abnormality
exaggerated QRS complex is suggestive of ventricu- in the onset of recovery of the ventricular muscle,
lar hypertrophy. Normal, non-pathological Q waves usually due to myocardial injury.
are often seen in leads I, aVL,V5,V6 from septal
depolarisation, which are less than 25% of the • The U wave is a small positive wave sometimes seen
R height and 0.04 s. A ‘pathological’ Q wave (>0.04 s following the T wave. Its cause is still unknown but
plus >25% of R wave height) may indicate a previous it is exaggerated in hypokalaemia. Inverted U waves
myocardial infarction; however, not every myocardial may be seen and are often associated with coronary
infarction will result in a pathological Q wave18 and heart disease (CHD), and these may appear transiently
some abnormal Q waves, in combination with other during exercise testing.18
ECG changes and patient symptoms, may indicate a
current myocardial infarction.19 Pathological Q waves Practice tip
could also be seen in non-ischaemic conditions such The 6-second measurement for heart rate calculation
as Wolff-Parkinson-White syndrome (WPW).20 is particularly useful when the patient’s heart rate is
• The Q–T interval is the time taken from irregular. Count the R waves on a 6-s strip and multiply
ventricular stimulation to recovery. It is measured by 10 to calculate the rate for 1 minute.
from the beginning of the QRS to the end of the
T wave. Normally, this ranges from 0.35 to 0.45 s,
but shortens as heart rate increases. It should be less ECG interpretation
than 50% of the preceding cycle length. Interpretation of a 12-lead ECG is an experiential skill,
requiring consistent exposure and practice. Some steps to
• The T wave reflects repolarisation of the ventricles.
aid interpretation are noted below.
A peaked T wave indicates hyperkalaemia, myocardial
infarction (MI) or ischaemia,21 while a flattened • Calculate heart rate
T wave usually indicates hypokalaemia. An inverted There are many ways to calculate the heart rate.
T wave occurs following an MI, or ventricular One way is to count the R waves on a 6-s strip and
hypertrophy. A normal T wave is 0.16 s. The height of multiply by 10 to calculate the rate (the top of the
the T wave should be less than 5 mm in all limb leads, ECG paper is usually marked at 3-s intervals).
and less than 10 mm in the precordial leads.17 Use an ECG ruler if one is available.

FIGURE 9.15 Normal ECG.

Atrial Ventricular Ventricular

depolarisation depolarisation repolarisation

Atrial Ventricular
systole systole
T
P

Q S

PR QRS ST
interval segment

QT interval

Adapted from Urden L, Stacy KL, Lough ME, eds. Thelan’s critical care nursing: Diagnosis and management. 6th ed. St Louis:
Mosby/Elsevier; 2010, with permission.
248 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

• Check R–R intervals (rhythm) Haemodynamic monitoring

Are the rhythms regular?
To assess regularity, mark the duration of two The dynamic movement of the blood in the cardio-
neighbouring R waves (R–R interval) on a plain vascular system is referred to as haemodynamics.
piece of paper and move this paper to check other Haemodynamic monitoring is performed to provide the
R–R intervals on the ECG strip. R–R intervals clinician with a greater understanding of the pathophysi-
should be uniform in a normal ECG, which means ology of the problem being treated than would be possible
the patient has a regular ECG rhythm. with clinical assessment alone. Knowledge of the evidence
that underpins the technology and the processes for inter-
• Locate P waves (check atrial activity) pretation is therefore essential to facilitate optimal usage
Observe for the presence or absence of P waves. and evidence-based decisions.22
Check regularity and shape. This section explores the principles related to haemo-
Is the P wave positive? dynamic monitoring and the different types of monitoring
The relationship between P waves and QRS available, and introduces the most recent and appro-
complexes: is there a P wave preceding every QRS priate evidence related to haemodynamic monitoring.
complex? The reasons for haemodynamic monitoring are generally
What is the duration of the P wave? threefold:
• Measure P–R interval (check AV node activity) 1 to establish a precise health-related diagnosis
What is the duration of the P–R interval?
2 to determine appropriate therapy
• Measure QRS duration (check ventricular
3 to monitor the response to that therapy.
activity)
Is the ventricular electrical activity normal? Haemodynamic monitoring can be non-invasive or
Is the QRS complex too wide or narrow? invasive, and may be required on a continuous or inter-
Check the presence of a Q wave. If present, is it mittent basis depending on the needs of the patient.23 In
normal or pathological? both cases, signals are processed from a variety of physio-
logical variables, and these are then clinically interpreted
• Note other clues
within the individual patient’s context.22
Observe whether the isoelectric line is present
between the S and T waves. Non-invasive monitoring does not require any device
Examine the T wave to see whether it is positive, to be inserted into the body and therefore does not breach
negative or flat: is it less than 0.16 s? the skin. Directly measured non-invasive variables include
Examine the duration of the Q–T interval: is it too body temperature, heart rate, blood pressure, respiratory
long? rate and urine output, while other processed forms can
Observe for any extra complexes and note their be generated by the ECG, arterial and venous Dopplers,
rate and shape, and whether they have the same or transcutaneous pulse oximetry (using an external probe
different morphology. on a digit such as the finger or on the ear) and expired
carbon monoxide monitors.
Practice tip Invasive monitoring requires the vascular system to
be cannulated and pressure or flow within the circula-
The presence of Q waves does not always indicate past tion interpreted. Invasive haemodynamic monitoring
myocardial infarction. Q waves may be secondary to: technology includes:
• physiological and positional effects • systemic arterial pressure monitoring
• myocardial injury or replacement • central venous pressure
• ventricular enlargement • pulmonary artery pressure
• altered ventricular conduction.
• cardiac output.
Other patient clinical information is needed to interpret Invasive monitoring has also facilitated greater use of
the significance of Q waves. ECG interpretation blood component analyses, such as arterial and venous
should always take a patient’s clinical information blood gases.
(patient symptoms, complaints, other haemodynamic The invasive nature of this monitoring allows the
information) into account. pressures that are sensed at the distal ends of the catheters
to be transduced, and to continuously display and monitor
the corresponding waveforms. The extent of monitoring
Practice tip
should reflect how much information is required to
Think of the leads I, II, III, aVR, aVL, aVF, V1–V6 as the optimise the patient’s condition, and how precisely the
‘eyes’ that are looking at the heart’s electrical activity data are to be recorded. As Muller argues, a great deal of
from different angles and view the heart’s different information is generated by this form of monitoring, and
areas. the clinical value of this is questionable.23 It is important
to note that these invasive monitoring strategies are not
 CHAPTER 9 CARDIOVASCULAR ASSESSMENT AND MONITORING 249

substitutes for careful examination and do not replace the Haemodynamic accuracy
clinicians’ clinical decision making. The accuracy of the Accuracy of the value obtained from haemodynamic
values obtained and the critical care professionals’ ability
monitoring is essential as this information is used to guide
to interpret the data and choose an appropriate interven-
patient care.23 Electronic equipment for this purpose has
tion directly affect the patient’s condition and outcome.23
four components (see Figure 9.16):
Principles of haemodynamic monitoring 1 an invasive catheter attached to high-pressure tubing
A number of key principles need to be understood in 2 a transducer to detect physiological activity
relation to invasive haemodynamic monitoring of critically
3 a flush system
ill patients. These include haemodynamic accuracy, the
ability to trend data and the maintenance of minimum 4 a recording device, incorporating an amplifier to
standards. These are reviewed below. increase the size of the signal, to display information.

FIGURE 9.16 Haemodynamic monitoring system.

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Adapted from Urden L, Stacy KL, Lough ME, eds. Thelan’s critical care nursing: Diagnosis and management. 6th ed. St Louis:
Mosby/Elsevier; 2010, with permission.
250 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

High-pressure (non-distensible) tubing reduces dis-

tortion of the signal produced between the intravascular FIGURE 9.17 Normal dynamic response test.
device and the transducer; the pressure is then converted
into electrical energy (a waveform). Fluid (0.9% sodium
chloride) is routinely used to maintain line patency using
a continuous pressure system; the pressure of the flush
system fluid bag should be maintained at 300 mmHg,
which normally delivers a continual flow of 3 mL/h.
Accuracy is dependent on levelling the transducer to
the appropriate level (and altering this level with changes
in patient position as appropriate), then zeroing the
transducer in the pressure monitoring system to atmo-
spheric pressure (called calibration) as well as evaluating
the response of the system by fast-flush wave testing. The
transducer must be levelled to the reference point of the
phlebostatic axis, at the intersection of the 4th intercostal
space and the mid-thoracic anterior–posterior diameter
(not the mid-axillary line). Error in measurement can
occur if the transducer is placed above or below the
phlebostatic axis. Measurements taken when the patient
is in the lateral position are not considered as accurate
as those taken when the patient is lying supine or semi- FIGURE 9.18 Over-damped dynamic response test.
recumbent up to an angle of approximately 60°.24
Zeroing the transducer system to atmospheric pressure
(calibration of the system) is achieved by turning the
three-way stopcock nearest to the transducer open to the
air, and closing it to the patient and the flush system. The
monitor should display zero (0 mmHg), as this equates
to current atmospheric pressure (760 mmHg at sea
level). With the improved quality of transducers, repeated
zeroing is not necessary as, once zeroed, the drift from the
baseline is minimal.25 Some critical care units, however,
continue to recalibrate transducer(s) at the beginning of
each clinical shift.
Fast-flush square wave testing, or dynamic response
measurement, is a way of checking the dynamic response
of the monitor to signals from the blood vessel.25 It is also Data trends
a check on the accuracy of the subsequent haemodynamic The ability to trend data via a monitor or a clinical infor-
pressure values. The fast-flush device within the system, mation system is essential for critical care practice. Current
when triggered and released, exposes the transducer to monitoring systems can retain data for a period of time,
the amount of pressure in the flush solution bag (usually produce trend graphs and link to other devices to allow
300 mmHg). The pressure waveform on the monitor will review of data from locations other than the immediate
show a rapid rise in pressure, which then squares off before
bedside. The data trends can be used to assess the pro-
the pressure drops back to the baseline (see Figure 9.17).
gression of a patient’s clinical condition and monitor the
Interpretation of the square wave testing is essential;
the clinician must observe the speed with which the patient’s response to treatment.
wave returns to the baseline as well as the pattern Haemodynamic monitoring standards
produced. One to three rapid oscillations should occur
immediately after the square wave, before the monitored There are stated minimum standards for critical care units
waveform resumes. The distance between these rapid worldwide. The standards require that patient monitor-
oscillations should not exceed 1 mm or 0.04 s.25 Absence, ing include circulation, respiration and oxygenation, with
or a reduction, of these rapid oscillations, or a ‘square the following essential equipment available for every
wave’ with rounded corners, indicates that the pressure patient: an ECG that facilitates continual cardiac moni-
monitoring system is overdamped; in other words, its toring; a mechanical ventilator, pulse oximeter; and other
responsiveness to monitored pressures and waveforms is equipment available where necessary to measure intra-
reduced (see Figure 9.18). An underdamped monitoring arterial and pulmonary pressures, cardiac output, inspiratory
system will produce more rapid oscillations after the pressure and airway flow, intracranial pressures and expired
square wave than usual. carbon dioxide.26
 CHAPTER 9 CARDIOVASCULAR ASSESSMENT AND MONITORING 251

Blood pressure monitoring • accidental drug administration through the arterial

Indirect and direct means of monitoring blood pressure catheter; all arterial lines and connections should
are widely used in critical care units. These are outlined in be clearly identified as such (e.g. marked with red
more detail below. stickers or have red bungs).
Blood pressure is the same at all sites along a vertical
Non-invasive blood pressure monitoring level but when the vertical level is varied, pressure will
Non-invasive blood pressure monitoring requires the use change. Consequently, referencing is required to correct
of a manual or electronic sphygmomanometer. Oscillation for changes in hydrostatic pressure in vessels above and
in the pressure generated by alterations in arterial flow is below the heart; if not, the blood pressure will appear to
captured either through auscultation or automatic sensing. rise when this is not really the case. It is important to zero
On auscultation, a number of Korotkoff sounds can be the monitoring system at the left atrial level.24
heard as the cuff pressure is released:27
Arterial waveform
• a sharp thud that is heard when the patient’s systolic A steep upstroke (corresponding to ventricular systole) is
pressure is reached
followed by brief, sustained pressure (anacrotic shoulder).
• a soft tapping, intermittent in nature At the end of systole pressure falls in the aorta and left
• a loud tapping, intermittent in nature ventricle, causing a downward deflection (see Figure 9.19).
• a low, muffled noise that is continuous in nature and A dicrotic notch can be seen in the downward deflection
is heard when the diastolic pressure is reached; as the which represents the closure of the aortic valve. The
cuff pressure diminishes further, the sound disappears. systolic pressure corresponds to the peak of the waveform.
For critically ill patients, this method of blood pressure The arterial pressure waveform changes its contours
monitoring has limitations and is often used when invasive when recorded at different sites. It can become sharper in
methods cannot be utilised.22 It is a less accurate alterna- distal locations.
tive, as results vary with the size of cuff used, equipment Disease process has an effect on waveforms: for
malfunction and incorrect placement of the sphygmoma- example, atherosclerosis causes an increase in systolic
nometer (this must be placed at heart level). In addition, waveform, as well as a decrease in the size of the diastolic
the pressures generated by the inflating cuff, particularly wave and dicrotic notch due to changes in elasticity.
those generated by automatic machines, can be high, and Cardiomyopathy causes reduced stroke volume and mean
frequent measurements of blood pressure by this method arterial pressure, and there is a late secondary systolic peak
may become uncomfortable for the patient. It is therefore seen on the waveform.
important that skin integrity be checked regularly to Invasive arterial pressure versus cuff pressure
prevent ischaemia and that the frequency of automated
At times, the accuracy of the invasive arterial pressure
inflations be minimised.22
reading may be checked by comparing the reading against
Invasive intra-arterial pressure that generated by a non-invasive device using an inflating
monitoring cuff. However, there is no basis for comparing these
values. Invasive blood pressure values are a measure of the
Arterial pressure recording is indicated when precise and actual pressure within the artery whereas those from the
continuous monitoring is required, especially in periods of cuff depend on flow-induced oscillations in the arterial
fluid volume, cardiac output and blood pressure instabil- wall. Pressure does not equal flow, as resistance does not
ity.22 An arterial catheter is commonly placed in the radial
artery, although other sites can be accessed, including
the brachial, femoral, dorsalis pedis and axillary arteries. FIGURE 9.19 Arterial pressure waveform.
Arterial catheter insertion is performed aseptically, and it
is important that collateral circulation, patient comfort and  6\VWROH
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risk of infection be assessed before insertion is attempted.

The radial artery is the most common site, as the ulnar 
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• arterial thrombosis 7LPH
• distal ischaemia
Adapted from Urden L, Stacy KL, Lough ME, eds. Thelan’s
• air embolism critical care nursing: Diagnosis and management. 6th ed.
• accidental disconnection (the insertion sites should be St Louis: Mosby/Elsevier; 2010, with permission.
always visible)
252 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

remain constant. Studies found that the non-invasive cuff continues to be used. Therefore, clinicians need to be
blood pressure method can be unreliable in measuring aware of possible limitations to this form of measurement
systolic blood pressure when the blood pressure is low, for and interpret the data accordingly. CVP monitoring can
example, when a patient is in shock.22 In addition, radial produce erroneous results: a low CVP does not always mean
arterial pressure is normally higher than that obtained by low volume and it may reflect other pathology, including
brachial non-invasive pressure monitoring because the peripheral dilation due to sepsis. Hypovolaemic patients
smaller vessel size exerts greater resistance to flow, and may have normal CVP due to sympathetic nervous system
therefore generates a higher pressure reading. 24 activity increasing vascular tone. An increase in CVP can
also be seen in patients on mechanical ventilation with
Invasive cardiovascular monitoring application of PEEP.31
For many critically ill patients, haemodynamic instability Central venous catheters used for haemo-
is a potentially life-threatening condition that necessitates dynamic monitoring are classed as short-term
urgent action. Accurate assessment of the patient’s intra- percutaneous (non-tunnelled) devices. Short-term percu-
cardiac status is therefore essential. A number of values taneous catheters are inserted through the skin, directly
can be calculated; the measurements commonly made are into a central vein, and usually remain in situ for only a
listed in Tables 9.3 and 9.4 . few days or for a maximum of 2–3 weeks.28 They are easily
removed and changed, and are manufactured as single- or
Preload multi-lumen types. However, they can be easily dislodged,
As noted earlier, preload is the filling pressure in the are thrombogenic due to their material and are associated
ventricles at the end of diastole. Preload in the right with a high risk of infection.28,32
ventricle is generally measured as CVP, although this A number of locations can be used for central venous
may be an unreliable predictor because CVP is affected catheter insertion. The two commonly used sites in
by intrathoracic pressure, vascular tone and obstruc- critically ill patients are the subclavian and the internal
tion.28 Left ventricular preload can be measured as the jugular veins. Other less common sites are the antecubital
pulmonary capillary wedge pressure (PCWP), but again, fossa (generally avoided but may be used when the patient
due to unreliability, this parameter provides an estimate cannot be positioned supine), the femoral vein (associated
rather than a true reflection of volume.29,30 In view of with high infection risk and the external jugular vein
this, other modalities are now being explored, including (although the high incidence of anomalous anatomy and
right ventricular end-diastolic volume evaluation via the severe angle with the subclavian vein make this an
fast-response pulmonary artery catheters, left ventricu- unpopular choice).32
lar end-diastolic area measured by echocardiography and Internal jugular cannulation has a high success rate for
intrathoracic blood volume measured by transpulmonary insertion; however, complications related to insertion via
thermodilution.22 this route include carotid artery puncture and laceration
of local neck structures arising from needle probing.32,33
Central venous pressure monitoring There are a number of key structures adjacent to the
CVP is defined as the pressure of the blood within the vein, including the vagus nerve (located posteriorly to
systemic venous return.23 Central venous catheters are the internal jugular vein), the sympathetic trunk (located
inserted to facilitate the monitoring of CVP; facilitate behind the vagus nerve) and the phrenic nerve (located
the administration of large amounts of IV fluid or blood; laterally to the internal jugular).34 Damage can also
provide long-term access for fluids, drugs, specimen occur to the sympathetic chain, which leads to Horner’s
collection and/or parenteral feeding. CVP monitoring syndrome (constricted pupil, ptosis and absence of sweat
has been used for many years to evaluate circulating gland activity on that side of the face). Central venous
blood volume, despite discussion as to its validity to do catheters inserted in the internal jugular vein pose a
so.22 However, it is a common monitoring practice and number of nursing challenges that can cause fixation

TABLE 9.3
Haemodynamic pressures

PA R A M E T E R R E S T I N G VA L U E S

Central venous pressure 0 to +8 mmHg (mean)

Right ventricular pressure +15 to +30 mmHg systolic; 0 to +8 mmHg diastolic
Pulmonary artery wedge pressure +5 to +15 mmHg (mean)
Left atrial pressure +4 to +12 mmHg (mean)
Left ventricular pressure 90 to 140 mmHg systolic; +4 to +12 mmHg diastolic
Aortic pressure 90 to 140 mmHg systolic; 60 to 90 mmHg diastolic; 70 to 105 mmHg (mean)
 CHAPTER 9 CARDIOVASCULAR ASSESSMENT AND MONITORING 253

TABLE 9.4
Normal haemodynamic values

PA R A M E T E R DESCRIPTION N O R M A L VA L U E S

Stroke volume (SV) Volume of blood ejected from left ventricle/beat 50–100 mL/beat
SV = CO/HR
Stroke volume index (SVI) Volume of blood ejected/beat indexed to BSA 25–45 mL/beat
Cardiac output (CO) Volume of blood ejected from left ventricle/min 4–8 L/min
CO = HR ⫻ SV
Cardiac index (CI) A derived value reflecting the volume of blood ejected 2.5–4.2 L/min/m2 (normal
from left ventricle/min indexed to BSA assumes an average weight
CI = CO/BSA of 70 kg)
Mean arterial pressure (MAP) [ (2 ⫻ diastolic) + systolic ] /3 70–105 mmHg
Flow time corrected (FTc) Systolic flow time corrected for heart rate 330–360 ms
Systemic vascular resistance Resistance left heart pumps against 900–1300 dyn•s/cm5
(SVR) SVR = [(MAP – RAP) ⫻ 79.9]/CO
Systemic vascular resistance Resistance left heart pumps against indexed to body 1700–2400 dyn•s/cm5/m2
index (SVRI) surface area
SVRI = [(MAP – RAP) ⫻ 79.9]/CI
Pulmonary vascular resistance Resistance right heart pumps against 20–120 dyn•s/cm5
(PVR) PVR = [(mPAP – LVEDP) ⫻ 79.9]/CO
Pulmonary vascular resistance Resistance right heart pumps against indexed to body 255–285 dyn•s/cm5/m2
index (PVRI) surface area
PVRI = [(mPAP – LVEDP) ⫻ 79.9]/CI
Mixed venous saturation (SvO2) Shows the balance between arterial O2 supply and oxygen 70%
demand at the tissue level
Left ventricular stroke work Amount of work performed by LV with each heartbeat 50–62 g-m/m2
index (LVSWI) (MAP – LVEDP) ⫻ SVI ⫻ 0.0136
Right ventricular stroke work Amount of work performed by RV with each heartbeat 7.9–9.7 g-m/m2
index (RVSWI) (mPAP – RAP) ⫻ SVI ⫻ 0.0136
Right ventricular end-systolic 50–100 mL/beat
volume (RVESV) The volume of blood remaining in the ventricle at the end of
Right ventricular end-systolic the ejection phase of the heartbeat 30–60 mL/m2
volume index (RVESVI)
Right ventricular end-diastolic 100–160 mL/beat
volume (RVEDV) The amount of blood in the ventricle immediately before a
Right ventricular end-diastolic cardiac contraction begins 60–100 mL/m2
volume index (RVEDVI)

BSA = body surface area; HR = heart rate; RAP = right atrial pressure.
Adapted from:
Leeper B. Monitoring right ventricular volumes: a paradigm shift. AACN Clinical Issues 2003;14(2):201–19, with permission.
Schummer W. Central venous pressure. Validity, informative value and correct measurement. Anaesthetist 2009;58(5):499–505,
with permission.

problems and the need for repeated dressing changes. positive pressure ventilation (IPPV).35 Complications of
These include beard growth, diaphoresis and poor control any central venous access catheter include air embolism,
of oral secretions. pneumothorax, hydrothorax and haemorrhage.22,23,32
The subclavian approach is used often, perhaps because
of a reported lower risk of catheter-related bloodstream Pulmonary artery pressure monitoring
infection.34,35 Coagulopathy is a significant contraindica- Pulmonary artery pressure (PAP) monitoring began in
tion for this approach, as puncture of the subclavian artery the 1970s, led by Drs Swan, Ganz and colleagues,36 and
is a known complication. There is also a risk of pneumo- was subsequently adopted in ICUs worldwide. Pulmonary
thorax, which rises if the patient is receiving intermittent artery catheterisation facilitates assessment of filling
254 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

FIGURE 9.20 Pulmonary artery catheter.

Thermistor
connector
Proximal injectate
lumen hub

Thermistor

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port @ 30 cm
Balloon
Distal lumen hub
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Thermistor
Balloon inflation port @ 31 cm
connector
valve

Thermistor

Distal Proximal injectate

lumen Proximal injectate port @ 30 cm Balloon
hub lumen hub
Proximal infusion
% lumen hub Distal lumen

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Thermistor
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Thermal filament
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Thermistor
connector
Balloon inflation Balloon
valve

PA distal
lumen
Proximal injectate Proximal infusion
lumen hub VIPTM port port @ 26 cm
Optical module
@ 30 cm
connector PA distal VIPTM lumen hub
& lumen hub

Adapted from Urden L, Stacy KL, Lough ME, eds. Thelan’s critical care nursing: Diagnosis and management. 6th ed. St Louis: Mosby/
Elsevier; 2010, with permission.

pressure of the left ventricle through the pulmonary artery The benefits of PAP monitoring have been scrutinised
wedge (occlusion) pressure (see Figure 9.20).22,33,37 By in recent years. A Cochrane systematic review on PAC use
using a thermodilution pulmonary artery catheter (PAC), by Rajaram et al38 suggests that there was no difference
cardiac output and other haemodynamic measurements in mortality rates, hospital length of stay and ICU length
can also be calculated. PAP monitoring is a diagnostic of stay in patients with or without PACs, and there was
tool that can assist in determination of the nature of a no difference in clinical benefit or harm in either group
haemodynamic problem and improve diagnostic accuracy. of patients. The PAC insertion is invasive, and increases
In addition to measuring PA pressures, PAC may also be the cost of patients’ hospitalisation.38 Consequently, the
used for accessing blood for assessment of mixed-venous use of PAC in clinical practice has dropped 50–65% in
oxygenation levels (see Chapter 13). recent years,38 although the PAC is still considered a
 CHAPTER 9 CARDIOVASCULAR ASSESSMENT AND MONITORING 255

useful monitoring tool that helps with diagnosis in clinical pulmonary capillary wedge pressure (PCWP), which is an
practice. estimate of left ventricular preload (LVEDV), or through
Thus, the indications of PAP monitoring are largely calculation of derived parameters such as cardiac output
based on health professionals’ clinical experience and (CO) and cardiac index (CI) (see Table 9.4 for descriptors
expertise. It has been suggested that PAP monitoring may and normal values).
be indicated for adults in severe hypovolaemic or cardio-
genic shock, where there may be diagnostic uncertainty, Pulmonary capillary wedge pressure (PCWP)
or where the patient is unresponsive to initial therapy.The monitoring
PAP is used to guide administration of fluids, inotropes and PCWP, or pulmonary artery occlusion pressure (PAOP),
vasopressors. PAP monitoring may also be utilised in other is measured when the pulmonary artery catheter balloon
cases of haemodynamic instability when the diagnosis is is inflated with no more than 1–1.5 mL air. The inflated
unclear. It may be helpful when clinicians want to differ- balloon isolates the distal measuring lumen from the
entiate hypovolaemia from cardiogenic shock or, in cases pulmonary arterial pressures, and measures pressures in the
of pulmonary oedema, to differentiate cardiogenic from capillaries of the pulmonary venous system, and indirectly
non-cardiogenic origins.39 However, in their Cochrane the left atrial pressure. The PAP waveform looks similar to
review, Rajaram et al38 concluded that more studies are that of the arterial waveform, with the tracing showing a
needed to investigate the benefit of PAC use in subgroup systolic peak, dicrotic notch and a diastolic dip (see Figure
patients including reversing shock states and improving 9.21). When the balloon is inflated, the waveform changes
organ function. Complications do arise from PACs, as shape and becomes much flatter in appearance, providing
these catheters share all the complications of central lines a similar waveform to the CVP. There are two positive
and are additionally associated with a higher incidence of waves on the tracing: the first reflects atrial contraction
arrhythmia, valve damage, pulmonary vascular occlusion, and the second reflects pressure changes from blood flow
emboli/infarction (reported incidence of 0.1–5.6%) and, when the mitral valve closes and the ventricles contract.40
very rarely, knotting of the catheter.32 The PCWP should be read once the ‘wedge’ trace stops
A number of measurements can be taken via the falling at the end-expiratory phase of the respiratory cycle
PAC, either by direct measurement, for example using (see Figure 9.21).

FIGURE 9.21 Pulmonary artery pressure and wedge waveforms.

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Adapted from Urden L, Stacy KL, Lough ME, eds. Thelan’s critical care nursing: Diagnosis and management. 6th ed. St Louis:
Mosby/Elsevier; 2010, with permission.
256 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

If balloon occlusion occurs with <1 mL of air, the Contractility

balloon is wedged in a small capillary and consequently Contractility reflects the force of myocardial contraction,
will not accurately reflect LA pressure. Conversely, if and is related to the extent of myocardial fibre stretch
1.5 mL air does not cause occlusion, the balloon may have (preload, see above) and wall tension (afterload, see above).
burst (which can result in an air embolus) or it may be It is important because it influences myocardial oxygen
floating in a larger vessel. If balloon rupture is suspected, consumption. Contractility of the left side of the heart is
no further attempts to inflate the balloon should be made, measured by calculating the left ventricular stroke work
and interventions to minimise the risk of air embolism index (LVSWI), although the clinical use of this value is
should be initiated.7 not widespread.
Note: it is essential that the balloon be deflated as soon Right ventricular stroke work index (RVSWI) can be
as the wedge has been recorded, as continued occlusion similarly calculated. Contractility can decrease as a result
will cause distal pulmonary vasculature ischaemia and of excessive preload or afterload, drugs such as negative
infarction.40 inotropes, myocardial damage such as that occurring after
Left atrial pressure monitoring MI and changes in the cellular environment arising from
acidosis, hypoxia or electrolyte imbalances. Increases in
Left atrial pressure (LAP) monitoring directly estimates contractility arise from drugs such as positive inotropes.44
left heart preload. It used to require an open thorax to
enable direct cannulation of the atrium. It was used only Cardiac output
in the postoperative cardiac surgical setting, although As discussed earlier in the chapter, the cardiac output
such use has been infrequent since the widespread use of (CO) refers to the blood volume ejected by the heart in
PAC. Recent advancement in cardiac implantable devices one minute. Stroke volume (SV) is the blood ejected by
development enables the patients to self-monitor LAP the heart in one beat. Therefore cardiac output can be
under their doctors’ guidance, which was found to be calculated as the heart rate multiplied by stroke volume.
a valuable tool to improve the management of patients Stroke volume is determined by the heart’s preload,
with advanced heart failure.41 Other modes of monitoring afterload and the contractility.
can also be used to achieve comprehensive left atrial The variety of cardiac output measurement techniques
assessment, such as Doppler echocardiography.42 has grown over the past decade since the development of
Afterload thermodilution pulmonary artery catheters, pulse-induced
contour devices, less invasive techniques such as Doppler
As previously noted, afterload is the pressure that the and non-invasive continuous haemodynamic monitoring
ventricle produces to overcome the resistance to ejection methods. As many critically ill patients require mechanical
generated in the systemic or pulmonary circulation by ventilation support, the associated rises in intrathoracic
the arteries and arterioles. It is calculated by cardiac pressure, as well as changing ventricular compliance, make
output studies: left heart afterload is reflected as systemic accurate haemodynamic assessment difficult with the
vascular resistance (SVR), and right heart afterload is older technologies. Therefore, volumetric measurements
reflected as pulmonary vascular resistance (PVR) (see of preload, such as right ventricular end-systolic volume
Table 9.4). (RVESV), right ventricular end-diastolic volume (RVEDV)
Systemic and pulmonary vascular resistance and index (RVESVI/RVEDVI) as well as measurements of
right ventricular ejection fraction (RVEF) are now being
Systemic vascular resistance (SVR) is a measure of used to more accurately determine cardiac output. The
resistance or impediment of the systemic vascular bed parameters RVEF, CO and/or CI and SV are generated
to blood flow. An elevated SVR can be caused by vaso- using thermodilution technology, and from these the
constrictors, hypovolaemia or late septic shock. A lowered parameters of RVEDV/RVEDVI and RVESV/RVESVI
SVR can be caused by early septic shock, vasodilators, can be calculated (see Table 9.4 for normal values).10 The
morphine, nitrates or hypercarbia. Afterload is a major availability of continuous modes of assessment has further
determinant of blood pressure, and gross vasodilation improved a clinician’s ability to accurately assess, and then
causes peripheral pooling and hypotension, reducing effectively treat, these patients.10
SVR. The precise estimation of SVR enables safer use of
therapies such as vasodilators (e.g. sodium nitroprusside) The Fick principle
and vasoconstrictors (e.g. noradrenaline).43 Several cardiac output measurement methods use the Fick
Pulmonary vascular resistance (PVR) is a measure of principle. In 1870, Fick proposed that ‘in an organ, the
resistance or the impediment of the pulmonary vascular uptake or release of an indicator substance is the product
bed to blood flow. An elevated PVR (‘pulmonary of the arterial-venous concentration of this substance
hypertension’) is caused by pulmonary vascular disease, and the blood flow to the organ’.45 Using oxygen as the
pulmonary embolism, pulmonary vasculitis or hypoxia. A indicator substance, the calculation of cardiac output is as
lowered PVR is caused by medications such as calcium follows:
channel blockers, aminophylline or isoproterenol, or by
the delivery of O2.43 CO = VO2/(CaO2 – CvO2)
 CHAPTER 9 CARDIOVASCULAR ASSESSMENT AND MONITORING 257

whereVO2 is oxygen consumption, CaO2 is arterial oxygen is artificially ventilated. Derived normal value for
concentration, and CvO2 is venous oxygen concentration. intrathoracic blood volume index, 850–1000 mL/m2.
Thermodilution methods • Extravascular lung water (EVLW): the amount of
water content in the lungs; allows quantification of
Thermodilution methods calculate cardiac output by the degree of pulmonary oedema (not evident with
using temperature change as the indicator in Fick’s X-ray or blood gases). Derived normal value for
method. Cardiac output and associated pressures such extravascular lung water index is 3–7 mL/kg. EVLW
as global end-diastolic volume can be calculated using has been shown to be useful as a guide for fluid
a thermodilution PA catheter. Cardiac output can be management in critically ill patients.46 An elevated
monitored intermittently or continuously using the PA EVLW may be an effective indicator of severity
catheter. Intermittent measurements obtained every few of illness, particularly after acute lung injury or in
hours produce a snapshot of the cardiovascular state over ARDS, when EVLW is elevated due to alterations
that time. By injecting a bolus of 5–10 mL of crystal- in hydrostatic pressures.49 Other patients at risk of
loid solution, and measuring the resulting temperature high EVLW are those with left heart failure, severe
changes, an estimation of stroke volume is calculated. pneumonia and burns. There may be an association
Cold injectate (run through ice) was initially recom- between high EVLW and increased mortality, the
mended, but studies now support the use of room need for mechanical ventilation and a higher risk
temperature injectate, providing there is a difference of nosocomial infection.49 A decision tree outlining
of 12° Celsius between injectate and blood tempera- processes of care guided by information provided by
ture.46 Three readings are taken at the same part of the PiCCO is provided in Figure 9.22.
respiratory cycle (normally end expiration), and any
measurements that differ by more than 10% should be PiCCO removes the impact of factors that can cause
disregarded (see Table 9.4 for normal values). Since the variability in the standard approach of cardiac output
1990s, the value of having continuous measurement of measurement, such as injectate volume and tempera-
cardiac output has been recognised37 and this has led to ture, and timing of the injection within the respiratory
the development of devices that permit the transference cycle.48 The additional fluid volume injected with the
of pulses of thermal energy to pulmonary artery blood – standard technique is significant in some patients;
the pulse-induced contour method.23 with the continuous technology, this is eliminated. A
further advantage is that virtually real-time responses to
Pulse-induced contour cardiac output treatment can be obtained, removing the time delay that
Pulse-induced contour cardiac output (PiCCO) provides was a potential problem with standard thermodilution
continuous assessment of CO, and requires a central techniques.48
venous line and an arterial line with a thermistor (not a An arterial catheter is widely used in critical care
PAC).47 A known volume of thermal indicator (usually to enable frequent blood sampling and blood pressure
room temperature saline) is injected into the central monitoring, and is used to measure beat-by-beat cardiac
vein. The injectate disperses both volumetrically and output, obtained from the shape of the arterial pressure
thermally within the cardiac and pulmonary blood. When wave. The area under the systolic portion of the arterial
the thermal signal is detected by the arterial thermistor, pulse wave from the end of diastole to the end of the
the temperature difference is calculated and a dissipation ejection phase is measured and combined with an
curve generated. From these data, the cardiac output can individual calibration factor. The algorithm is capable of
be calculated. These continuous cardiac output measure- computing each single stroke volume after being calibrated
ments have been well researched and appear to be equal by an initial transpulmonary thermodilution.
in accuracy to those produced by intermittent injections PiCCO preload indicators of intrathoracic blood
required for the earlier catheters.48 The parameters volume (ITBV) and global end-diastolic volume
measured by PiCCO47 include the following: (GEDV) are more sensitive and specific to cardiac pre-
load than the standard cardiac filling pressures of CVP
• Pulse-induced contour cardiac output (PiCCO): and PCWP, as well as right ventricular end-diastolic
derived normal value for cardiac index, 2.5–4.2 L/
volume. One advantage of ITBV and GEDV is that they
min/m2.
are not affected by mechanical ventilation and therefore
• Global end-diastolic volume (GEDV): the volume give correct information on the preload status under
of blood contained in the four chambers of the almost any condition. Extravascular lung water (EVLW)
heart; assists in the calculation of intrathoracic blood correlates moderately well with severity of ARDS,
volume. Derived normal value for global end- length of ventilation days, ICU stay and mortality,50 and
diastolic blood volume index, 680–800 mL/m2. appears to be of greater accuracy than the traditional
• Intrathoracic blood volume (ITBV): the volume of assessment of lung oedema by chest X-ray. Disadvantages
the four chambers of the heart plus the blood volume of PiCCO include its potential unreliability when heart
in the pulmonary vessels; more accurately reflects rate, blood pressure and total vascular resistance change
circulating blood volumes, particularly when a patient substantially.10,47
258 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

FIGURE 9.22 PiCCO decision tree.

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Doppler ultrasound methods output.53 This form of monitoring can be used perioper-
Oesophageal Doppler monitoring enables calculation of atively and in the critical care unit, on a wide variety of
cardiac output from assessment of stroke volume and heart patients.52 It should not, however, be used in patients with
rate, but uses a less invasive technique than those outlined aortic coarctation or dissection, oesophageal malignancy or
previously.51 Stroke volume is assessed by measuring the perforation, severe bleeding problems or with patients on an
flow velocity and the area through which the forward intra-aortic balloon pump.54
flow travels. Flow velocity is the distance one red blood The Doppler probe that sits in the oesophagus is approx-
cell travels forward in one cardiac cycle, and the measure- imately the size of a nasogastric tube, is semi-rigid and is
ment provides a time velocity interval. The area of flow inserted using a similar technique. The patient is usually
is calculated by measuring the cross-sectional area of the sedated but the method has been used in awake patients. In
blood vessel or heart chamber at the site of the flow velocity such cases, however, the limitation is that the probe is more
measurement.42 Oesophageal Doppler monitoring can be likely to require more frequent repositioning.54
performed at the level of the pulmonary artery, mitral The waveform that is displayed on the monitor is
valve or aortic valve. triangular in shape (see Figure 9.23) and captures the systolic
According to Doppler principles, the movement portion of the cardiac cycle – an upstroke at the beginning
of blood produces a waveform that reflects blood flow of systole, the peak reflecting maximum systole and the
velocity, in this case in the descending thoracic aorta (see downward slope of the ending of systole. The waveform
Figure 9.23), that is captured by the change in frequency captures real-time changes in blood flow and can therefore
of an ultrasound beam as it reflects off a moving object.23 be seen as an indirect reflection of left ventricular function.
This measurement is combined with an estimate of the Changes to haemodynamic status will be reflected in alter-
cross-sectional area of the aorta so that the stroke volume, ations in the triangular shape (see Figure 9.23).
cardiac output and cardiac index can be calculated, using
the patient’s age, height and weight.42 Ultrasonic cardiac output monitor
Oesophageal Doppler monitoring provides an alternative The ultrasonic cardiac output monitor (USCOM)
for patients who would not benefit from PAC insertion,42,52 monitors CO non-invasively using continuous Doppler
and can be used to provide continuous measurements under ultrasound waves by placing an ultrasound transducer probe
certain conditions: the estimate of cross-sectional area must supra- or parasternally. The principles of CO calculation
be accurate; the ultrasound beam must be directed parallel in this method are the same as for oesophageal Doppler
to the flow of blood; and there should be minimal variation monitoring. Empirical study suggests that the use of
in movement of the beam between measurements. There is non-invasive ultrasonic cardiac output monitor (USCOM)
some debate at present among clinicians about the accuracy provided adequate clinical data in patients in different shock
of oesophageal Doppler monitoring for calculating cardiac categories, and it was safe and cost effective.55
 CHAPTER 9 CARDIOVASCULAR ASSESSMENT AND MONITORING 259

should therefore be undertaken with the electrodes

FIGURE 9.23 Oesophageal Doppler waveforms. positioned in the same location as previous readings.
Caution is required for patients with high levels of perspi-
'HFUHDVHGSUHORDG ,QFUHDVHGSUHORDG ration (which reduces electrode contact), atrial fibrillation
(irregular R–R intervals make estimation of the ventric-
)OXLGV ular ejection time difficult) or pulmonary oedema, pleural
effusions or chest wall oedema (which alter bioimpedance
readings irrespective of any changes in cardiac output).The
use of transthoracic bioimpedance in critically ill patients
is variable, due in part to limitations of its usefulness in
patients who have pulmonary oedema.58,59
$
Practice tip
3RRUFRQWUDFWLOLW\ ,QFUHDVHGFRQWUDFWLOLW\
Current evidence-based literature suggests that haemo-
,QRWURSHV dynamic measurements such as CVP, PAWP and PAP
can be accurately measured with a patient position of
supine to head – up to 60°.

Diagnostics
% Apart from the haemodynamic monitoring methods to
facilitate cardiac assessment of a patient’s clinical condition,
+LJKDIWHUORDG KLJK695 'HFUHDVHGDIWHUORDG various diagnostic tests are often used. Echocardiography
and blood tests are the most commonly used in critical
9DVRGLODWRUV care. Other tests such as computerised tomography (CT)
and nuclear medicine cardiac examination are also used
when indicated. Exercise stress tests and cardiac angio-
graphy are also used and are reviewed in Chapter 10.
Echocardiography
& Echocardiography (frequently shortened to ECHO) is
often used in critical care to assess cardiovascular conditions
Impedance cardiography such as heart failure, hypertensive heart disease, valve disease
and pericardial disease in critically ill patients. It adopts a
Transthoracic bioimpedance (impedance cardiography) is technique of detecting the echoes produced by a heart
another form of non-invasive monitoring used to estimate from a beam of very high frequency sound – ultrasound.
cardiac output, and was first introduced by Kubicek in Two-dimensional, three-dimensional and contrast ECHO
1966.56 It measures the amount of electrical resistance images can be obtained using the non-invasive transthoracic
generated by the thorax to high-frequency, very-low- technique or the invasive transoesophageal technique
magnitude currents. This measure is inversely proportional (TOE). The transthoracic ECHO uses a transducer probe
to the content of fluid in the thorax: if the amount of externally to the heart to obtain images (same as a normal
thoracic fluid increases, then transthoracic bioimpedance ultrasound technique). This method is painless and does
falls.23 Changes in cardiac output can be reflected as a not require sedation. The TOE technique involves placing
change in overall bioimpedance. The technique requires a transducer probe into the oesophageal cavity to assess the
six electrodes to be positioned on the patient: two in the function and structure of the heart. This method produces
upper thorax/neck area and four in the lower thorax.These better images of the heart than the normal transthoracic
electrodes also monitor electrical signals from the heart. ECHO.45 However, this method requires sedation during
Overall, transthoracic bioimpedance is determined by: the procedure and the patient needs to fast for a few hours
1) changes in tissue fluid volume, 2) volumetric changes prior to the examination.
in pulmonary and venous blood caused by respiration Two-dimensional ECHO images are valuable
and 3) volumetric changes in aortic blood flow produced resources for assessment of the function and structure of
by myocardial contractility.57 Accurate measurements of the heart. Three-dimensional images offer more realistic
changes in aortic blood flow are dependent on the ability visualisation of its structure and function. Contrast ECHO
to measure the third determinant, while filtering out any provides enhanced images of left and right ventricular
interference produced by the first two determinants. Any definition to facilitate the diagnosis of complex cardiac
changes to position or to electrode contact will cause conditions such as congenital heart defects, valve stenosis
alterations to the measurements obtained, and recordings and regurgitation.60,61 The contrast ECHO technique
260 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

uses gas air microbubbles, produced by hand-agitating a conditions will also affect the haematocrit. WBC levels
syringe containing 10 mL of normal saline with a small will be elevated during episodes of infection, tissue
amount of air, injected into the peripheral vein to produce damage and inflammation. When infections are severe, the
images of the heart functions.45 full blood count will show a dramatic rise in the number
In the critical care setting, the preparation of critically of immature neutrophils. Platelets are easily lost during
ill patients for this examination is important. The nurse haemorrhage, and spontaneous bleeding is a danger when
needs to help the sonographer to position the patient to the count falls to below 20 ⫻ 109/L.62,63
achieve the best results. For TOE preparation, fasting time
must be followed to avoid complications such as respiratory Electrolytes
aspiration. The nurse will also need to assist the anaesthe- The assessment of electrolyte levels in critically ill patients
tist and the TOE operator, and continue to monitor the is important in diagnosing the patient’s condition. Elec-
patient’s clinical conditions during the procedure. trolyte imbalances, such as potassium and calcium level
changes, can cause cardiovascular abnormalities such as
Blood tests arrhythmias. Electrolyte levels are often checked regularly
A number of blood tests are often conducted to assist the in critically ill patients.
clinical assessment of critically ill patients in the critical The functions of electrolytes and their cardiac implica-
care setting. tions are listed in Table 9.5.
Full blood count Cardiac enzymes
The full blood count (FBC) assesses the status of three Cardiac biochemical markers, such as troponin, are proteins
major cells that are formed in the bone marrow: red that are released from damaged myocardial cells that are
blood cells (RBC), white blood cells (WBC) and platelets. detectable by performing blood tests. Troponin elevation
Although normal values have been given (see Appendix A), is considered a significant biomarker for patients with
for critically ill patients changes will occur under certain MI; however, it can also be elevated in non-MI patients.64
conditions. For example, haemoglobin (Hb) is reduced Thus, diagnosis for critically ill patients with elevated
in the presence of haemorrhage and also in acute fluid cardiac troponin levels should be made with support from
overload causing haemodilution. other data.64 See Table 9.6 for cardiac enzyme parameters
Haemoconcentration can occur during acute dehy- and normal values. For abnormal cardiac enzymes in MI,
dration, which would show up as a high Hb. Similar please refer to Chapter 10.

TABLE 9.5
Electrolyte functions and pathophysiology

E L E C T R O LY T E FUNCTIONS COMMON IMBALANCES AND CAUSES S I G N S A N D S Y M P T O M S

Potassium Maintains normal Hyperkalaemia Muscle weakness, ECG changes in cardiac

functions of nerve Renal failure, dehydration, diabetes, toxicity, severe hyperkalaemia (serum K
and muscle cells diuretic medications between 6 and 6.5 mEq/L) needs prompt
Acid–base balance attention because it can cause life-
threatening arrhythmia
Hypokalaemia Muscle weakness, respiratory failure, ECG
Kidney disease, diarrhoea, vomiting, changes
diuretic medications
Sodium Regulates body fluid Hypernatraemia Thirst, confusion, hyperreflexia, seizures
movement Renal failure, dehydration, diarrhoea,
Maintains cell vomiting
functions Hyponatraemia Altered personality, confusion, seizures,
Acid–base balance Acute renal failure, heart failure, coma, death
pancreatitis, peritonitis, burns
Calcium Bone metabolism Hypercalcaemia Polyuria, constipation, nausea, vomiting,
Blood coagulation Hyperparathyroidism, vitamin D toxicity, muscle weakness, confusion, coma, ECG
Muscle contraction cancer changes (shortened QT intervals)
Nerve conduction Hypocalcaemia Paraesthesias, tetany. In severe cases,
Hypoparathyroidism, vitamin D seizures, encephalopathy, ECG changes
deficiency, renal disease (prolonged ST and QT intervals), heart
failure
 CHAPTER 9 CARDIOVASCULAR ASSESSMENT AND MONITORING 261

E L E C T R O LY T E FUNCTIONS COMMON IMBALANCES AND CAUSES S I G N S A N D S Y M P T O M S

Magnesium Activates sodium– Hypermagnesaemia Hypotension, respiratory depression, AV

potassium pumps Renal failure conduction disturbances, which can lead to
Inactivates calcium cardiac arrest (often in renal failure patients)
channels Hypomagnesaemia Anorexia, nausea, vomiting, lethargy. It may
Neuromuscular Inadequate intake and absorption, contribute to hypokalaemia development
transmission or increased excretion, due to therefore cardiac arrhythmias may be
hypercalcaemia or diuretics present
Note: associated hypocalcaemia is
common in hypomagnesaemia
Phosphorus Intracellular energy Hyperphosphataemia Usually asymptomatic. However, when
production (ATP) and Kidney failure, metabolic and respiratory concurrent hypocalcaemia, symptoms of
enzyme regulation acidosis hypocalcaemia may be present
Tissue oxygen Hypophosphataemia Usually asymptomatic. Severe cases may
delivery Burns, diuretic medications, respiratory have muscle weakness, heart failure, coma
Bone metabolism alkalosis, acute alcoholism

For cardiac implications of electrolytes imbalances, see Chapter 10 and Chapter 11.
Adapted from:
Urden LD, Stacey KM, Lough ME, eds. Critical care nursing: diagnosis and management. St Louis, Mo: Elsevier; 2014, with permission.
Moser DK, Reigel B. Cardiac nursing: a companion to Brauwald’s heart disease. St Louis: Elsevier; 2008, with permission.

TABLE 9.6
Cardiac biochemical markers – description and normal values

ENZYME DESCRIPTION N O R M A L VA L U E

Troponin T (cTnT) Detected within 2–3 h after infarction, and may remain elevated for 7–10 d <0.1 ng/mL
Troponin I (cTnI) Detected within 2–3 h of infarction, and may remain elevated for up to 14 d <0.03 ng/mL
Creatine kinase (CK) Serum CK are elevated following muscle or neurological injury. Creatine kinase Adult female:
myocardial bound (CK–MB) is useful in quantifying the degree of infarction and 30–135 units U/L; Adult
timing of onset. Levels rise 3–6 h and peak 12–24 h after infarction male: 55–170 units U/L
CK-MB: 0–5% of
total CK
Aspartate Detection and monitoring of liver cell damage. No cardiac-specific isoenzymes; <40 U/L
aminotransferase (AST) today rarely used because it is released after renal, cerebral and hepatic damage
Lactate dehydrogenase Of no value in the diagnosis of myocardial infarction. Occasionally useful in the 110–230 U/L
(LDH) assessment of patients with liver disease or malignancy (especially lymphoma,
seminoma, hepatic metastases); anaemia when haemolysis or ineffective
erythropoiesis suspected. Although it may be elevated in patients with skeletal
muscle damage, it is not useful in this situation. Post-AMI, cardiac-specific
isoenzyme LDH1 peaks between 48 and 72 h
D-Dimer Presence indicates deep vein thrombosis, myocardial infarction, DIC <0.25 ng/L

DIC = disseminated intravascular coagulation.

Adapted from Pragana KD, Pragana TJ. Mosby’s diagnostic and laboratory test reference. 12th ed. St Louis: Elsevier; 2015.

Chest X-ray identify abnormality, and a basic understanding of the

Chest X-ray is the oldest non-invasive way to visualise the chest X-ray is essential. Please review the basic concepts,
heart and blood vessels, and is one of the most commonly such as what water, air and bone show on X-ray, and the
taken diagnostic procedures in critical care. To interpret concepts of anteroposterior (AP) and posteroanterior
a chest X-ray for cardiac diagnosis, basic knowledge of (PA) films, in Chapter 13 before you move on to the next
the normal anatomical cardiac structure is important to section.
262 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Cardiac chest X-ray interpretation 3 On the superior border the aortic arch and the
To interpret the chest X-ray for cardiac assessment, the pulmonary arteries should be identified next. The
following steps should be followed to ensure a thorough aortic arch is called the knob. The pulmonary
diagnosis: arteries and their branches radiate outward from
the hila (see Figure 9.24). The hilum in the
1 The heart size needs to be checked first to see if the
mediasternal region is formed by the pulmonary
size of the heart is appropriate. The cardiac silhouette
arteries and the main stem bronchi shadows on the
should be no more than 50% of the diameter of the
film. The focus of this step is to check for prominence
thorax; this is called the cardiothoracic ratio.65 The
of vessels in this region, as this suggests vascular
position of the heart should be 1⁄3 of the heart shadow
to the right of the vertebrae and 2⁄3 of the shadow to abnormalities.66
the left of the vertebrae.65 The size of the heart can
be determined in a matter of seconds, even by the
Chest X-ray in diagnosing cardiac
novice clinician, since this can be simply determined conditions
by visualising the cardiothoracic ratio. For coronary heart disease assessment, an initial
2 The shape of the heart should be inspected next. The chest X-ray film is useful to exclude other causes of
border of the heart on the X-ray film is determined chest pain, such as pneumonia, pneumothorax and
by the heart anatomy. The border is formed by: the aortic aneurysm, and to assess whether heart failure
right atrial shadow as the right convex cardiac border, and/or pulmonary congestion are present. Patients
the superior vena cava as the superior border and with chronic heart failure show cardiomegaly, Kerley B
the left ventricle as the left heart border and cardiac lines or pulmonary oedema. Cardiomegaly is seen as an
apex. In the frontal chest X-ray, the right ventricle is enlarged heart on the X-ray film. Kerley B lines on the
not a border-forming structure because it is directly X-ray film are the result of pulmonary congestion and
superimposed on the cardiac silhouette. Similarly, fluid accumulation in the interstitium. Although cardio-
the normal left atrium should not be visible on a megaly and pulmonary oedema indicate heart failure,
posteroanterior (PA) film. The border of the heart the chest X-ray alone cannot diagnose the condition.
should be sharp. If the left atrium is enlarged, a Other tests are needed to thoroughly assess patients for
convex superior left heart border is seen.65 accurate diagnosis.67

FIGURE 9.24 Chest PA radiograph. The convex right cardiac border is formed by the right atrium (thin arrows), and
the heavy arrows indicate the location of the superior vena cava.

Aortic arch (knob)

Main and left pulmonary

arteries

Left atrial appendage

Left ventricle

Adapted from Erkonen WE, Wilbur LS. Radiology 101: The basics and fundamentals of imaging. 3rd ed. Philadelphia, PA: Lippincott
Williams & Wilkins; 2009, with permission.
 CHAPTER 9 CARDIOVASCULAR ASSESSMENT AND MONITORING 263

Practice tip
Magnetic resonance imaging
Magnetic resonance imaging (MRI) is a non-invasive
Critical care nurses should take a systematic approach method that can provide cardiac-specific biochemical
to interpreting chest X-rays. The respiratory and cardiac information about factors such as tissue integrity, cardiac
structures, tubes, wires and other devices should all be aneurysms, ejection fraction and cardiac output. These
identified in the chest X-ray film. techniques are sometimes considered superior to radio-
graphy and ultrasound examination methods because the
A widened mediastinum and abnormal aortic contour MRI is not affected by bone structure. The techniques
may indicate aortic dissection. Similar to heart failure, include perfusion imaging, atherosclerosis imaging
further tests such as TOE, magnetic resonance imaging and coronary artery imaging.72 MRI is considered an
(MRI) or angiography are needed to confirm the accurate method for predicting the presence of significant
diagnosis. Subtle abnormalities in the hilar region may coronary artery disease.73 However, MRI use in critically
indicate pulmonary hypertension (PAH). A decrease in ill patients has its limitations. Because of the magnetic field
pulmonary vascular markings and prominent main and required for this method, the patient cannot be fitted with
hilar pulmonary arterial shadows in the lung fields on any pumps or machines that have metal parts in them.
the chest film are classic signs of pulmonary hyperten- Organising appropriate equipment for critically ill patients
sion. However, the sensitivity of this for excluding PAH who are undergoing this test can be a challenge.
is lacking.68 In pericardial disease, the chest X-ray often
appears normal unless the accumulated fluid in the peri- Nuclear medicine cardiac studies
cardial space is over 250 mL. Note that accumulation of There are several types of radionuclide imaging methods
fluid is indicated in many cardiac conditions; therefore, available to assess a patient’s cardiac status, including radio-
other tests need to be carried out to confirm the diagnosis.69 nuclide isotopes, thallium scan and stress test radionuclide
The positions of a pulmonary artery catheter, a central scan.17 The purpose of radionuclide imaging is to assess
venous catheter and pacing wires can be identified on the the perfusion status of cardiac muscle. When lowered
chest X-ray. The positions of these catheters need to be perfusion in cardiac muscle is identified this may indicate
checked regularly to ensure the catheters and wires are in heart muscle damage. Radionuclide imaging is often used
appropriate places. More details on how to identify the in patients who have been diagnosed with a myocardial
catheters and pacing wires are given in Chapter 13. infarction when further investigation is required to
Due to individual variations in shape, size and rotation of determine if interventions such as cardiac stent or coronary
the heart, and the complexity of cardiac signs, chest X-rays artery bypass surgery are likely to benefit the patient.
often play a minor role in cardiac diagnosis. A patient’s
clinical condition and other diagnostic test results must be Nursing care of patients undergoing
taken into account when diagnosing a cardiac condition.68 diagnostic tests
All of the above methods have advantages and benefits in
Practice tip assessing the cardiac condition of a patient. For the critical
care nurse, preparation of patients for these examinations
Comparison of earlier chest X-ray film(s) with the
is important because patients often need to be trans-
current film is important to diagnose a patient’s clinical
ported to the radiology or nuclear medicine departments.
progress, response to treatment and any movements of
Important considerations include:
catheter positions.
• Patient’s allergy profile in relation to imaging contrast
needs to be evaluated before the requests are made.
Other diagnostic tests of cardiac function
Since 2000, more non-invasive diagnostic imaging • These tests all require the patient to lie still for certain
periods of time; therefore, explanation is essential and
techniques are used to aid cardiac assessment. Some of
sedation may be required during the procedure.
these techniques have shown significant advantages, such
as lowered cost, but they also have their limitations.45 • Appropriate equipment, such as non-metal
equipment, needs to be organised beforehand if the
Cardiac computed tomography patient is having an MRI study.
Cardiac computed tomography (cardiac CT) is a recent
development in diagnosing cardiac conditions such as Practice tip
suspected coronary heart disease and in the evaluation Hearing aids and partial dental plates with metal parts
of coronary artery bypass grafts. It provides a method must be removed prior to MRI. Additionally, patients with
for visualising the anatomical structures of the heart and implantable devices such as permanent pacemakers
coronary arteries reliably and accurately in patients.70 cannot have an MRI. Critical care patients are at increased
However, limitations remain with this method including risk of adverse events during intra-hospital transport;
the inability to assess the haemodynamic relevance of a therefore, close monitoring and documenting the patient’s
coronary artery lesion. In addition, the most appropriate clinical condition during transport are imperative.
radiation and contrast doses have not been determined.71
264 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Summary
The cardiovascular system is essentially a transport system for distributing metabolic requirements to, and collecting
byproducts from, cells throughout the body. A thorough understanding of anatomical structures and physiological events
is critical to inform a comprehensive assessment of the critically ill patient. Findings from assessment should define
patient cardiovascular status as well as inform the implementation of a timely clinical management plan. A thorough
cardiac assessment requires the critical care nurse to be competent in a wide range of interpersonal, observational and
technical skills.
Current minimum standards for critical care units in Australia and New Zealand require that patient monitoring
include circulation, respiration and oxygenation. For many critically ill patients, haemodynamic instability is a potentially
life-threatening condition that necessitates urgent action. In the critical care environment two main forms of cardiac
monitoring are commonly employed: continuous cardiac monitoring and the 12-lead ECG. Accurate assessment of the
patient’s intracardiac status is frequently employed and often considered essential to guide management. Strong research
evidence has shown that there is no increased harm or benefit in using pulmonary artery monitoring in critically ill
patients; therefore the decision to use pulmonary artery monitoring as a diagnostic tool depends on the clinical need and
clinician expertise. In day-to-day management of critically ill patients, critical care nurses must ensure they are skilled and
educated in the techniques of non-invasive and invasive cardiovascular monitoring techniques and technologies, and be
able to synthesise all data gathered and base their practice on the best available evidence to date.

Case study
Mr Andrew is a 40-year-old man who was admitted to the intensive care unit 14 days ago via the emergency
department. He weighs 82 kg and is 173 cm tall. The following is a summary of the key events to date and
his haemodynamic status currently.
Past medical history:
1 Long history of thrombocythaemia
2 Portal vein thrombosis
Regular medications on admission to hospital:
• Warfarin (titrated to INR range 2.0–3.0)
• Propranolol (80 mg sustained-release once a day)
Drug, alcohol and smoking habits:
• Nil
Allergies:
• None known
Presenting symptoms:
Admitted to emergency department with a 2-day history of PR bleeding and haematemesis. Commenced
on Hartmann’s solution (active ingredients sodium lactate, sodium chloride, potassium chloride, calcium)
IV shortly after admission.
Sequence of events:
• Admitted to ICU 14 days ago from emergency with Sengstaken–Blakemore (SB) tube in situ and gastric
balloon inflated.
• Patient was sedated and ventilated (see settings below).
• Recurrent PR bleeding on day 2 and became haemodynamically unstable.
• Transferred to theatre: SB tube removed and surgical banding of oesophageal varices attempted and
failed. Gastrotomy performed and large clot removed from stomach. Actively bleeding varix over-sewn.
• Returned to ICU.
• Difficulties with ventilation 1 day postoperatively.
• Patient became haemodynamically unstable and pulmonary artery catheter inserted.
• Chest X-ray: bilateral pulmonary infiltrates.
 CHAPTER 9 CARDIOVASCULAR ASSESSMENT AND MONITORING 265

• Cultures taken and commenced on IV antibiotics.

• Spiking high temperatures despite negative cultures.
• Sedated on morphine and midazolam infusion and commenced on synchronised intermittent mandatory
volume (SIMV) control ventilation.
Patient observations and status currently:
Respiratory:
Size 8 ET tube, ET cuff pressure 17 mmHg
Ventilated SIMV + pressure support (PS)
Ventilator settings: rate 12, TV 500 mL, FiO2 0.6, PEEP 6 cmH2O, PS 10 cmH2O, flow 35 Lpm
Upper alarm (peak inspiratory pressure) set at 25 cmH2O
I:E = 1:2.3
Minimal secretions on suction
Last arterial blood gas:
pH 7.30
PCO2 49.0 mmHg
PO2 78 mmHg
HCO3 16 mmol/L
BE -6.5
SaO2 95%
Na 148 mmol/L
K 3.1 mmol/L
Cardiovascular:
BP 102/63 mmHg
ECG as follows (lead II)

Haemodynamic parameters from pulmonary artery catheter:

CI 4.4 L/min/m2
CVP 18 mmHg
PCWP 21 mmHg
SVRI 2311 dynes/s/cm5/m2
Neurological:
Opens eyes to command
Withdraws to painful stimuli
Pupils equal size 2–3 mm and reacting
Renal:
Urine output for last hour: 15 mL
Average urine output for past 6 hours 10–15 mL/h
266 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Hydration:
N/saline @ 120 mL/h
Heparin infusion (25,000 IU in 500 mL) @ 20 mL/h
Midazolam (50 mg in 50 mL) @ 2 mL/h
Morphine (60 mg in 60 L) @ 2 mL/h
Noradrenaline (8 mg in 100 mL) @ 18 mL/h
20% Albumex @ 10 mL/h
Mannitol @ 10 mL/h
Previous days’ balance + 3868
GIT/nutrition:
No nasogastric (NG) tube in situ
Blood sugar level (BSL) 6.1 mmol
Bowels: no record in patient notes
Integumentary/hygiene:
Temperature 38.4°C
Pressure areas intact
Currently supine
Dry dressing intact to abdominal wound
+2 pitting oedema in dependent areas
Sociopsychological:
Patient’s wife and 3 children visit daily

DISCUSSION
This case study illustrates the complexities of critical illness in the presence of several risk factors
and comorbidities. Initial non-invasive assessments following admission focused on assessment and
management of intravascular volume depletion secondary to blood loss. When the patient’s bleeding
was controlled during surgery, he was transferred to the intensive care unit and invasive monitoring
was required to guide patient management. As the patient’s haemodynamic status became unstable,
continuous invasive arterial monitoring aided titration of vasoconstrictor therapy and insertion of a central
venous line aided with directing fluid therapy. At this stage, it would have been easy to have continued
focusing on treating the patient’s hypovolaemia but, in this case, the value of invasive pulmonary artery
monitoring readings guided management direction with evidence of septic shock (hyperdynamic status,
low intravascular filling pressures and peripheral vasodilation), prompting the commencement of a
noradrenaline infusion.
For the critical care nurse at the bedside, this case demonstrates the need to be able to synthesise all
assessment findings, invasive and non-invasive, and titrate prescribed therapies to achieve optimal tissue
perfusion while providing holistic nursing care in a complex and changing environment. Without invasive
monitoring, management of this patient would have been technically challenging and required a trial-and-
error approach, especially with fluid and drug therapy, until a successful treatment plan was accomplished.
This patient did ultimately get discharged from ICU to the medical ward several weeks later and was
eventually discharged back home after 12 weeks hospitalisation.

CASE STUDY QUESTIONS

1 What is the patient’s MAP from the BP reading above and how is it calculated?
2 What is the patient’s rhythm on the rhythm strip above?
3 Calculate the patient’s heart rate from the rhythm strip above.
4 The patient in this case study required invasive arterial monitoring. Discuss some of the potential
complications of such monitoring and measures to prevent them.
5 In the case study above, the patient’s SVRI is 2311 dynes/s/cm5/m2. Discuss SVRI: how it is derived and
what high or low values indicate clinically.
 CHAPTER 9 CARDIOVASCULAR ASSESSMENT AND MONITORING 267

RESEARCH VIGNETTE

Sotomi Y, Sato N, Kajimoto K, Sakata Y, Mizuno M, Minami Y et al. Impact of pulmonary artery catheter
on outcome in patients with acute heart failure syndromes with hypotension or receiving inotropes:
From the ATTEND Registry. Int J Cardiol 2014;172(1):165–172

Abstract
Background: Randomized controlled trials concerning pulmonary artery catheters (PACs) use have yielded little
evidence of their beneficial effects on survival. This study aimed to evaluate the association between PACs and
in-hospital mortality in patients with acute heart failure syndromes (AHFS).
Methods: The Acute Decompensated Heart Failure Syndromes (ATTEND) Registry is a prospective, observational,
multicenter cohort study performed in Japan, since April 2007. We analyzed data from the ATTEND Registry and evaluated
the effectiveness of PAC in AHFS treatment using propensity score-matching and the Cox proportional hazards model.
Results: Final follow-up examinations of the 4842 patients were conducted in December 2012. During the study
period, 813 patients (16.8%) were managed with PACs, of which 502 patients (PAC group) were propensity score-
matched with 502 controls (Control group). Of the 1004 score-matched patients, 22 (4.4%) patients from the Control
group and 7 (1.4%) from the PAC group died. The risk of all-cause death was lower in the PAC group than that in
the Control group [hazard ratio (HR), 0.3; 95% confidence interval (CI), 0.13–0.70; p = 0.006]. PAC-guided therapy
decreased all-cause mortality in patients with lower systolic blood pressure (SBP ≤ 100 mmHg; HR, 0.09; 95% CI,
0.01–0.70; p = 0.021) or inotropic therapy (HR, 0.22; 95% CI, 0.08–0.57; p = 0.002).
Conclusions: This study revealed that appropriate PAC use effectively decreases in-hospital mortality in AHFS
patients, particularly those with lower SBP or receiving inotropic therapy, suggesting that real-world PAC use could
improve AHFS management.

Critique
In this paper the results of a multicentre, prospective observational study on the use of a pulmonary artery catheter
(PAC) in acute heart failure syndromes (AHFS) are reported. The aim of the study was to evaluate the impact of PAC
use in AHFS patients. The outcome measure was in-hospital mortality.
Data were collected using the Acute Decompensated Heart Failure Syndromes (ATTEND) Registry in Japanese hospitals
from April 2007 to December 2011. Patients were assigned to two groups: the study group (with PAC inserted) and
the control group (no PAC use). Please note, that the hospital follows the Japanese guidelines for treatment of AHFS,
which recommend PAC use in AHFS patients. The allocation of the two groups was not randomised. To overcome
the randomisation issue, the researchers used a propensity score-matching technique to eliminate the potential
confounding factors in both groups. In simpler terms, the groups were comparable in terms of diagnosis, severity of
illness and comorbidities. They score-matched a total of 502 patients in each group for final analysis.
The authors found that appropriate PAC use in AHFS patients effectively decreased in-hospital mortality, especially
for those patients who had lower systolic blood pressure or who received inotropic therapy. Recent strong evidence
suggests that PAC use does not alter mortality and hospital/ICU length of stay and that further study is needed to
study the usefulness of PAC use in subgroup patients, such as patients in shock states, and in improving organ
functions.38 This study adds to the literature on PAC use in heart failure patients.
In their Cochrane review, Rajaram and colleagures38 recommended that the PAC is a useful diagnostic tool to
assist with patient management. Insertion and management of a PAC requires the operator to have a high level of
clinical expertise to ensure patient safety. For the critical care nurse, competence in caring for patients with PACs is
important. Being able to understand and manage the PAC, and recognise potential PAC-associated complications, is
imperative. In recent years, the decreased use of PAC in clinical practice may be attributed to the available research
evidence that suggests a PAC does not improve patient survival. Some argued that this reduced PAC use may have
consequently contributed to the decrease in PAC clinical expertise.22 Subsequently, critical care nurses may not have
adequate exposure to PAC use in clinical practice, which adds challenge to managing staff training in PAC use.
268 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Lear ning a c t iv it ie s
1 Briefly discuss the main ion movement at each of the following phases of the cardiac action potential:
• depolarisation
• early rapid repolarisation
• plateau phase
• final rapid repolarisation
• resting membrane phase.
2 Describe the correct placement of the precordial leads when doing a 12-lead ECG.
3 Describe what PQRST represents on an ECG and identify what is the normal duration for each segment.
4 Describe what systematic vascular resistance (SVR) is and what clinical condition can cause an elevated or
lowered SVR.
5 Describe what are the limitations of central venous pressure (CVP) monitoring and why.

Online resources
American Heart Association, www.americanheart.org
Australian and New Zealand Intensive Care Society, www.anzics.com.au
Australian College of Critical Care Nurses, www.acccn.com.au
Australian Institute of Health and Welfare, www.aihw.gov.au
British Association of Critical Care Nurses, www.baccn.org.uk
Critical Care Forum, www.ccforum.com/home
Intensive Care, www.intensivecare.com
National Heart Foundation of Australia, www.heartfoundation.org.au
World Federation of Critical Care Nurses, www.wfccn.org

Further reading
Chung F-T, Lin S-M, Lin S-Y, Lin H-C. Impact of extravascular lung water index on outcomes of severe sepsis patients in a
medical intensive care unit. Resp Med 2008;102(7):956–61.
Erkonen WE, Wilbur LS. Radiology 101: the basics and fundamentals of imaging. 3rd ed. Philadelphia, PA: Lippincott
Williams & Wilkins; 2009.
Patil H, Vaidya O, Bogart D. A review of causes and systemic approach to cardiac troponin elevation. Clin Cardiol
2011;34(12):723–728.
Rajaram SS, Desai NK, Kalra A, Gajera M, Cavanaugh SK, Brampton W et al. Pulmonary artery catheters for adult patients
in intensive care. Cochrane Database Syst Rev 2013;2:CD003408.

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 Chapter 10

Cardiovascular alterations
and management
Robyn Gallagher, Andrea Driscoll

KEY WORDS Learning objectives

acute coronary After reading this chapter, you should be able to:
syndrome • explain the pathophysiology of coronary artery disease, clinical
acute heart failure manifestations of acute coronary syndromes and management of
events
aortic aneurysm
• discuss the collaborative care for a patient with chest pain
arrhythmia
cardiomyopathy • list the diagnostic tests used to assess myocardial ischaemia
endocarditis • outline the actions and contraindications of thrombolytic drugs
hypertensive • outline the clinical manifestations of right and left ventricular failure
emergencies • discuss the goals of heart failure treatment
left ventricular failure • discuss the pathophysiologies of the four different types of
myocardial cardiomyopathy and how they affect cardiac function
infarction • outline the actions of angiotensin-converting enzyme inhibitors, beta-
percutaneous blockers, loop diuretics and spironolactone and how they relate to the
coronary pathophysiology of heart failure.
intervention
right ventricular
failure Introduction
ventricular This chapter reviews the support of cardiovascular function in the face of
aneurysm many compromises to the system. It focuses on two of the most prevalent
and fatal diseases affecting the heart: coronary heart disease and heart failure.
These diseases are also a common comorbidity in elderly patients admitted
to critical care units. The first section on coronary heart disease reviews the
pathophysiological concepts of myocardial ischaemia and associated compli-
cations, with detailed consideration of the clinical implications, assessment and
associated management. Heart failure is discussed in terms of the body’s compen-
satory mechanisms and the clinical sequelae and associated clinical features
of heart failure. Nursing and medical management is outlined including the
management of acute exacerbations of heart failure. Finally, other cardiovascular
disorders commonly managed in critical care units are reviewed, ranging from
other forms of heart failure to hypertensive emergencies and aortic aneurysms.
The case study presented at the end of the chapter highlights the key aspects of
the management of coronary heart disease and heart failure in patients admitted
to critical care units.
272 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Coronary heart disease A fixed coronary artery lesion, causing limitation of

oxygen supply at times of increased demand, results in
Coronary heart disease (CHD) is the term used to describe stable angina. Therefore, symptoms arise during periods
the effects of a reduction or complete obstruction of blood of physical and emotional stress and resolve within 2–10
flow through the coronary arteries due to narrowing from minutes of rest. Symptoms tend to be worse in the morning
atherosclerosis and/or thrombus. Although some patients (coinciding with a peak in blood pressure), after heavy
may be asymptomatic, the most common manifestations meals and in cold weather. The severity of symptoms has
of CHD are chest pain due to angina, acute coronary little correlation with the progress of the disease. However,
syndrome (ACS, a term used to collectively describe a patient with a typical history of angina has a high prob-
acute myocardial infarction [AMI] and unstable angina) ability of CHD and a higher risk of AMI and coronary
and sudden death. CHD may also cause arrhythmias and death during the next 5 years.7
heart failure.1
CHD is now the leading single cause of death, premature Unstable angina and acute
death and disability both globally2 and in Australia and myocardial infarction
New Zealand.3–5 In 2011, more than 21,500 people died Unstable angina and AMI form a continuum on the basis of
of CHD in Australia, more than 5000 in New Zealand in reduction in coronary blood flow and subsequent damage
2006 and in 2010 more than 7 million worldwide.2–5 Death
to myocardial cells. Unstable angina may indicate transient
rates have fallen by about 76% since the 1960s, primarily
ischaemia, whereas AMI indicates myocardial tissue death.
due to improvements in risk factors and health care for
The term ‘acute coronary syndrome’ (ACS) is now used to
those at risk. However, the burden of CHD remains high,
represent this continuum.8,9 ACS results from the rupture
with 11% of males and 9% of females impacted by the
or erosion of an atherosclerotic plaque, leading to release of
disease in Australia.3 Furthermore, the impact of this disease
vasoconstrictor substances and potentially triggering coag-
worldwide is forecast to be substantial, with an increase of
ulation activity (see Figure 10.1). Formation of thrombi
28% in deaths between 1990 and 2010.2
results in intermittent and/or prolonged obstruction of
Myocardial ischaemia the coronary artery. Therefore, ACS typically presents as
When coronary blood flow is insufficient to meet a recent history of angina (within the past 4–6 weeks); a
myocardial tissue demand for oxygen, myocardial change in symptoms including increased frequency, more
ischaemia occurs. Critical restriction to blood flow occurs easily provoked or occurring in the absence of physical
when the diameter of the lumen of the blood vessel is or emotional stress, more severe or prolonged and/or less
reduced by more than half. Coronary blood flow is also responsive to nitrate therapy. ACS is a medical emergency,
determined by perfusion pressure, which can be adversely with up to a third of ACS patients at risk of AMI and
affected by abnormalities in blood flow (valvular disease), death within 3 months.9 There is a high risk of death if the
vessel wall (coronary spasm) and the blood (anaemia, poly- patient experiences more than 20 minutes of pain at rest
cythaemia).6 Myocardial oxygen demand is influenced (pain at rest is associated with changes in ST segment of
by heart rate, strength of myocardial contraction and left 1 mm or more on a 12-lead ECG), if there was myocardial
ventricular wall tension.The myocardium receives most of infarction within the previous 2 weeks or if pulmonary
its blood supply during diastole; hence a rise in heart rate oedema or mitral regurgitation is present.8
that decreases the duration of diastole will also decrease Myocardial infarction (MI) occurs when blood flow
coronary perfusion. Sympathetic stimulation increases to the myocardium is severely impaired for more than
the force of contraction and therefore oxygen demand. 20 minutes as myocardial cell necrosis begins. A coronary
Left ventricular wall tension increases with the changes in artery thrombus arising from an atherosclerotic plaque is
preload associated with filling and afterload associated with found in the majority of patients dying of AMI.10 Cellular
systemic vascular resistance. During activity, pyrexia and death begins in the subendocardial layer and progresses
arrhythmias, these effects may compound due to sympa- through the full muscle thickness, so that by 2 hours with
thetic stimulation, causing increased oxygen demand and total occlusion a full ‘transmural’ infarction will result.
reduced coronary perfusion. However, the full extent of tissue death may occur as a
single incident or evolve over several days, depending on
the degree of obstruction to blood flow.
Angina The size and location of the infarction will influence
Angina (angina pectoris) is the most common mani- the clinical manifestations and risk of death and determine
festation of CHD and is the term used to describe the treatment. The size of the infarction is determined by
symptoms of discomfort that occur during myocardial the extent, severity and duration of the ischaemic event,
ischaemia. The classic angina pattern consists of retroster- the amount of collateral circulation and the metabolic
nal constricting pain/discomfort, which may radiate to demands placed on the myocardium. Usually the ventricle
the arms, throat, jaw, teeth, back or epigastrium. Associated wall is affected, with a small infarction often resulting in
symptoms often include shortness of breath, nausea, a dyskinetic wall (altered movement), whereas a large
vomiting, sweating, palpitations and weakness. infarction may result in akinesis (no movement).
 CHAPTER 10 CARDIOVASCULAR ALTERATIONS AND MANAGEMENT 273

well as the AV node in most patients and the SA

FIGURE 10.1 (A) Plaque rupture exposes node in 50% of people. There is potentially severe
thrombogenic lipid. A white thrombus is formed by
impact on ventricular function if both the inferior
activated platelets adhering. This lesion is unstable
and may lead to thrombin activation. (B) Thrombin wall and the right ventricle are affected, as well as
activation leads to a mesh of fibrin and red blood cells, a high risk of arrhythmias due to SA and AV node
leading to a ‘red thrombus’. involvement.
Clinical features
3ODWHOHW 'LVWDOSODWHOHW Patients with AMI most often present with chest pain.
ZKLWHWKURPEXV HPEROL
This pain is described as central crushing retrosternal pain,
which lasts longer than 20 minutes and is not relieved
by nitrate therapy. The pain may radiate to the neck, jaw,
back and shoulders and is often accompanied by ‘feelings
%ORRGIORZ of impending doom’, sweating and pallor. Nausea is often
associated with the pain, due to vagal nerve stimulation.
Depending on the size and location of the AMI, patients
may also present as sudden death and with varying degrees
of syncope and heart failure. Women may present with
different symptoms.
(QGRWKHOLXP 5XSWXUHG /LSLG
$ SODTXH FRUH Patient assessment and diagnostic
features
A key feature of assessment of the patient with chest pain
)LEULQDQG5%&V is the use of protocols and guidelines to promote rapid
UHGWKURPEXV
assessment so that revascularisation procedures such as
thrombolysis and percutaneous coronary intervention
(PCI) can be implemented as soon as possible. This means
that assessment may begin as early as in the ambulance,
%ORRGIORZ with ECG transmission to the hospital emergency
department where rapid, early triage models of care are
in place.11 Additionally, assessment needs to determine
whether there are any contraindications for thrombolysis.
The assessment method used depends on the condition
of the patient but should occur within 10 minutes of
:KLWH 9HVVHORFFOXVLRQ arrival.10 This initial history will focus on the nature
% WKURPEXV of symptoms such as pain. Pain assessment is complex,
and the use of an acronym such as PQRST (see Table
Adapted from Bersten AD, Soni N, Oh TE. Oh’s intensive care 10.1) is useful to incorporate precipitating and palliative
manual. 5th ed. Oxford: Butterworth-Heineman; 2003, with
factors, qualitative descriptors, location, radiation,
permission.
severity and length of time. A pain scale is included
to help rate the intensity of pain. Asking patients for
The location and impact of the infarction will depend descriptive words is useful in assessment as many patients
on which coronary artery has been obstructed: will deny pain and instead use words such as pressure,
• Left anterior descending (LAD) affects the function tightness or constriction. It is essential not to ignore
of the left ventricle and interventricular septum, other presentations, as patients with atypical symptoms,
including ventricular conduction tissue. Patients such as women, often have a delayed diagnosis and
with anteroseptal MI are at high risk of heart treatment and a higher mortality (50%) than those with
failure, cardiogenic shock and mortality due to typical symptoms (18%).8 Differentiating this pain from
pump deficits. any previous pain is also useful. The brief history should
include a short cardiovascular risk profile: 1) previous
• Circumflex (CX) affects the left ventricle lateral cardiac history such as angina, MI, revascularisation and
and posterior walls and the SA node in 50% of 2) family history, smoking, hypertension, diabetes.
people.6 The impact on pump efficiency of lateral A more complete history, which includes detailed
and posterior wall necrosis is not as severe as information about risk factors, can be acquired when the
anteroseptal infarctions, although patients are at patient is stabilised. This information will be essential to
more risk of arrhythmias. guide patient education and rehabilitation and to plan
• Right coronary artery (RCA) affects the inferior discharge. Recurrent chest discomfort requires urgent
wall of the left ventricle and the right ventricle, as reassessment, including immediate ECG.
274 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

ischaemia, the risk of adverse events and to provide a

TABLE 10.1 baseline for subsequent changes.8 Most importantly,
The PQRST criteria for assessing chest pain12 the ECG is essential to determine whether emergency
reperfusion is required, and is recommended as the
P Precipitating Exercise and activity
Stress and anxiety
sole test for selecting patients for PCI or thrombolysis.
Cold weather
Where ST-segment monitoring is available, this should
be continuous. Alternatively, if chest discomfort persists,
Palliating Stop activity
ECGs should be repeated every 15 minutes. Even when
Rest
chest pain resolves it is important to record a series of
Nitroglycerin
12-lead ECGs during admission to determine changes
Q Quality Heavy, tight, choking, vice-like, over time. (The normal ECG is covered in Chapter 9,
constricting
whereas this section addresses ischaemic changes in
R Region, Left side of chest, shoulder, arm and jaw the ECG.)
Radiation Retrosternal and radiating to the neck Myocardial ischaemia, injury or infarction causes
S Severity Rate pain on scale of 1 (no pain) to 10 cellular alterations and affects depolarisation and repolar-
(worst pain possible) isation.13 Myocardial ischaemia may be a transient finding
T Time Pain lasts longer than 10 min despite on the ECG. Ischaemia results in T-wave inversion or
nitroglycerin ST-segment depression in the leads facing the ischaemic
Pain comes and goes but lasts longer area.14 Ischaemic T waves are usually symmetrical,
than 20 min narrower and more pointed. ST-segment depression of
1 mm for 0.08 seconds is indicative of ischaemia, especially
Adapted from Hudak CM, Gallo BM, Morton PG. Critical care
nursing, A holistic approach. 7th ed. Philadelphia: Lippincott;
when forming a sharp angle with an upright T wave.15
1998, with permission. These changes are reversible with reduction in demand
(e.g. by rest, nitrates).
On acute presentation, myocardial injury (infarction)
Practice tip is most commonly associated with ST-segment elevation
on the ECG, although this is not universal. In addition, a
Because of changes in neuroreceptors, older patients typical pattern of ECG changes over time (evolution of the
and diabetic patients may not describe the typical ST segments, Q-wave development and T-wave inversion)
anginal pain. Women also may not describe classic is often seen (described below), but these changes too
angina symptoms and may use different descriptors are not universal. The distinction between the various
from men.8 Be alert for prodromal symptoms, such as acute coronary syndromes, including ST-elevation acute
increased shortness of breath, weakness and fainting. coronary syndrome (STEACS), ST-elevation myocardial
infarction (STEMI) and non-ST-elevation myocardial
Physical examination infarction (non-STEMI), is important for ensuring appro-
priate assessment and protocol-based treatment16 for the
Physical manifestations vary and depend on the impact
various presentations.
of pain, size and location of the infarction in the
The location and extent of ischaemia or infarction
individual. Heart rate and blood pressure may be raised
may be evident on the ECG leads overlying the affected
due to anxiety. Impaired left ventricular function may
area, as follows:
result in dyspnoea, tachycardia, hypotension, pallor,
sweating, nausea and vomiting. Impaired right ventricu- • anteroseptal wall of left ventricle,V1–V4
lar function may be indicated by jugular vein distension • anterior wall of the left ventricle,V1–V6, I and aVL
and peripheral oedema. Abnormalities in heart sounds • lateral wall of left ventricle, I, aVL,V5 and V6
may be present, including a muffled and diminished
first heart sound due to decreased contractility. A fourth • inferior wall of left ventricle, II, III and aVF.
heart sound is common, whereas a third heart sound is Additional leads are needed to view the right ventricle
uncommon. Many patients develop a pericardial rub and posterior wall. Chest electrodes can be placed on
after about 48–72 hours due to an inflammatory response the right chest wall using the same landmarks as the left
to the damaged myocardium. Additional findings occur chest to view the right ventricle (see Chapter 9). Further
with complications, and these are discussed in the related electrodes,V7–V9, may be placed over the posterior of the
specific sections below. left chest to view the posterior wall. Other indicative signs
of posterior wall damage are a small r wave in V1 and/or
Electrocardiographic examination ST depression in V3 and V4, as these may be reciprocal
Patients with chest discomfort should be assessed by an changes.The endocardial surface of the posterior wall faces
appropriately qualified person and have a 12-lead ECG the precordial leads of the ECG so the signs of ischaemia
recorded within 5 minutes of arrival at a healthcare facility and infarction, such as ST depression or a small r wave, are
to determine the presence and extent of myocardial reversed or reciprocal. If these signs are present a left-sided
 CHAPTER 10 CARDIOVASCULAR ALTERATIONS AND MANAGEMENT 275

ECG, V7–V9, should be done to confirm or rule out a • Recent: Q waves have developed. ST-segment
posterior infarction. elevation may still be present. Evolution is underway.
Continuous ECG monitoring is essential to detect The infarction is more than 24 hours old.
arrhythmias, which often accompany AMI and are a • Old (fully evolved): Q waves and T inversion are
common cause of death. The arrhythmia may be due present. ST segments are no longer elevated. Infarction
to poor perfusion of the conduction tissue. More often, occurred anything from a few days to years ago.
arrhythmias occur because ischaemic tissue has a lower
fibrillatory threshold and ischaemia is not being managed. Biochemical markers
Arrhythmias also result from left ventricular failure. Intracellular cardiac enzymes enter the blood as
Typical ECG evolution pattern ischaemic cells die, and elevated levels are used to
confirm myocardial infarction and estimate the extent
The initial ECG features of myocardial infarction of cell death. The cardiac troponins T and I (cTnT and
are ST-segment elevation with tall T waves recorded cTnI) have been found to be both sensitive and specific
in leads overlying the area of damaged myocardium. measures of cardiac muscle damage.17 Troponin I is
These changes gradually change, or evolve, over time, rapidly released into the bloodstream, so it is especially
with ST segments returning to baseline (within hours), useful for the diagnosis and subsequent risk stratification
while Q waves develop (hours to days) and T waves of patients presenting with chest pain in the early stages.
become inverted (days to weeks). The time course for High sensitivity troponin T assays are being used increas-
the evolutionary changes is accelerated by reperfu- ingly, but lack specificity, especially when trauma and
sion, e.g. PCI, thrombolysis or surgery. Thus, an almost renal disease are present. Troponin I is also a more appro-
fully-evolved pattern may be seen within hours if priate marker to use in postoperative and trauma patients
successful reperfusion has been undertaken (see Figures than creatine kinase-MB (CK-MB), as CK-MB levels
10.2–10.4 for examples). Given the expected time will be affected by muscle damage. However, CK-MB is
course for evolution, it is possible to approximate how less costly and more readily available, and so is still often
recently infarction has occurred, which is essential in used, particularly in the presence of a non-diagnostic
determining management: ECG. C-reactive protein assays may prove to be useful, as
• Acute (or hyperacute): there is ST elevation but baseline and discharge levels are predictive of subsequent
Q waves or T inversion has not yet developed cardiac events. However, the laboratory facilities are not
(see Figure 10.5). readily available.

FIGURE 10.2 Acute inferoposterior infarction: ST elevation in indicative leads II, III and aVF. The ST-segment
depression in I and aVL is reciprocal to the inferior infarction. As well, ST depression in anterior leads (V1–V3) is
reciprocal to posterior wall infarction. Posterior leads (not shown here) were recorded and revealed ST elevation in V7,
V8 and V9. This patient had acute (100%) obstruction at the ostium of the right coronary artery.
276 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

FIGURE 10.3 The same patient as above, recorded only 1 hour later, after stenting of the right coronary artery with
an evolving inferoposterior infarction. Note the ST segments in II, III and aVF are still elevated but returning to baseline.
The reciprocal ST depression is likewise diminishing and can now be seen only in aVL, V1 and V2. Q waves have
already developed in inferior leads.

FIGURE 10.4 The same patient again, recorded a further 21 hours later. An almost fully evolved pattern is now
present. Note the ST segments inferiorly have almost completely returned to baseline (as have the reciprocal changes).
The Q waves remain, and T waves have now inverted inferiorly.
 CHAPTER 10 CARDIOVASCULAR ALTERATIONS AND MANAGEMENT 277

FIGURE 10.5 Acute anterolateral infarction in a patient with left anterior descending coronary artery obstruction.
Note the ST elevation and tall (hyperacute) T waves across the chest leads V1–V6. ECG recorded on admission.

Coronary angiography and left heart catheterisation (percutaneous coronary intervention [PCI], coronary
Coronary angiography gives a detailed record of coronary artery bypass grafting or medical therapy). The nursing
artery anatomy and pathophysiology. Specially designed care for coronary angiography is similar to PCI, and is
catheters are advanced with the assistance of a guidewire covered under that section.
into the ascending aorta via the femoral or brachial Exercise test
arteries and manoeuvred into the ostium of each coronary Exercise testing with ECG monitoring forms part of the
artery. Contrast media is then injected and images are diagnostic screen for patients suspected of stable angina.
taken from several views to provide detailed information The Bruce protocol is used most often and considered
on the extent, site and severity of coronary artery lesions positive for CHD if there is 1 mm or more of reversible
and the blood flow into each artery. This flow is graded ST-segment depression.19 False-positive tests are more
using the Thrombolysis in Myocardial Infarction (TIMI) common in populations with a lower incidence of CHD,
studies system (see Table 10.2).1 Typically, a left ventricu- including women.20
lar angiogram is performed during the same procedure
to assess the appearance and function of the left ventricle, Chest radiography
mitral and aortic valves. If CHD is present, treatment An initial chest X-ray film is useful to exclude other
is determined as appropriate according to the severity causes of chest pain, such as pneumonia, pneumothorax

TABLE 10.2
Thrombolysis in myocardial infarction (TIMI) flow grades in coronary arteries18

TIMI 0 No perfusion and no antegrade flow beyond the occlusion

TIMI 1 Penetration with minimal perfusion, and contrast does not opacify the entire bed distal to the stenosis during the
picture run
TIMI 2 Partial perfusion and contrast opacifies the entire coronary bed distal to the stenosis, although entry to this area is
slower than with unaffected coronary beds
TIMI 3 Complete perfusion and filling and clearance of contrast is rapid and comparable to other coronary beds

Adapted from Belenkie I, Knudtson ML, Roth DL, Hansen JL, Traboulsi M, Hall CA et al. Relation between flow grade after
thrombolytic therapy and the effect of angioplasty on left ventricular function: a prospective randomized trial. Am Heart J 1991;
121(2 Pt 1):407–16, with permission.
278 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

and aortic aneurysm, and to assess whether heart failure plasminogen activator (tPA), have been developed that
and/or pulmonary congestion are present. If the diagnosis trigger conversion of plasminogen to plasmin and
is clearly ACS or AMI, this step can wait until after throm- therefore break down clots. It is essential to screen
bolysis or PCI. patients for contraindications to thrombolysis quickly but
thoroughly so that therapy can be commenced as soon
Patient management as possible. Contraindications are given in the National
The management of stable angina patients is aimed at: Health Foundation of Australia (NHFA) Guidelines.8
1) secondary prevention of cardiac events, 2) symptom Tenecteplase is the most commonly prescribed throm-
control with medication, 3) revascularisation and 4) reha- bolytic agent and is a drug tissue-type plasminogen
bilitation (see Figure 10.6). (Revascularisation by coronary activator (tPA) that is available as alteplase, tenecteplase
artery bypass graft is reviewed in Chapter 12; revascular- and reteplase. These agents are of human origin, made by
isation by percutaneous coronary angioplasty is reviewed recombinant DNA techniques.26 The drug activates only
in the next section.) plasminogen present in blood clots, so the risk of haemor-
Treatment of acute coronary syndrome aims at rapid rhage is decreased. Unlike streptokinase, tPA can be given
diagnosis and prompt re-establishment of flow through the repeatedly without risk of anaphylactic reaction. Often
occluded artery to ensure myocardial perfusion and reduce patients with anterior ischaemic changes are treated with
the size of infarction. In addition, treatment aims to:21 tPA (alteplase) based on the GUSTO-1 trial that showed
• minimise the area of myocardial ischaemia by improved outcomes in terms of reduction of ischaemia.27
increasing coronary perfusion and decreasing Alteplase is usually given by infusion, whereas reteplase,
myocardial workload which has a longer half-life, can be given in two bolus
injections.
• maximise oxygen delivery to tissues Nursing management of patients post-thrombolysis
• control pain and sympathetic stimulation focuses on monitoring and detection of bleeding compli-
• counter detrimental effects of reperfusion cations and/or return of ischaemia. Care is as follows:
• preserve ventricular function • Observations: assess neurological state including
• reduce morbidity and mortality. orientation, any IV sites and urinalysis for the
The ideal place to manage ACS or MI patients is in the presence of bleeding. Along with vital signs, these
coronary care unit, where continuous, specialised nursing are attended every 15 minutes for the first hour,
care is available and there is rapid access to treatments.22 half-hourly for an hour and then hourly according
Secondary prevention of cardiac events includes the to the patient’s condition; however, patients are
provision of medications, such as antiplatelet therapy and advised to report any bleeding post-discharge
as well.
lipid-lowering therapy.23
• ECG monitoring: includes 12-lead ECG on return
Reperfusion therapy and ongoing ECG monitoring and chest pain
Reperfusion therapy includes coronary angioplasty, ideally assessment to detect reocclusion. Patients need to be
with stent and thrombolytic therapy (also termed fibrin- requested to inform nursing staff of any chest pain or
olysis). Patients fast-tracked for reperfusion therapy have discomfort.
one or more of the following indications: 1) ischaemic or • IV anticoagulants such as heparin and/or oral anti-
infarction symptoms for longer than 20 minutes; 2) onset of platelet drugs, such as clopidogrel or ticlopidine: may
symptoms within 12 hours; 3) ECG changes (ST elevation be given following thrombolysis to prevent reoc-
of 1 mm in contiguous limb leads, ST elevation of 2 mm in clusion in the stent. Assess International Normalised
contiguous chest leads; left bundle branch block). Ratio (INR), prothrombin (PT) and partial thrombo-
plastin time (PTT), as bleeding is more likely to occur
Thrombolytic therapy if anticoagulants are above the therapeutic range.
Thrombolytic therapy has been demonstrated to produce
a significant reduction in mortality in the high-risk group Coronary angioplasty
described above.24 The greatest reduction in mortality Percutaneous transluminal coronary angioplasty (PTCA)
occurs if the reperfusion occurs within the first ‘golden’ procedures are being used about twice as frequently as
hour of presentation.25 Thrombolysis can be delivered coronary artery bypass graft surgery, with 155 PTCA
effectively in many settings where other methods of procedures performed for every 100,000 population in
reperfusion are not available. Australia in 2008–09.3 PTCA rates have grown dramat-
Clots formed in response to injury normally dissolve ically in patients aged over 75 years. In this procedure, a
using the body’s fibrinolytic processes as tissue repair takes catheter is introduced by the brachial or femoral artery
place.This requires the presence of the proenzyme plasmin- into the coronary arteries and advanced into the area of
ogen, which is converted into the enzyme plasmin when occlusion or stenosis under the guidance of imagery and
activated by macrophages and degrades the clot. Throm- specifically designed catheters. A balloon attached to the
bolytic agents, including streptokinase and tissue-type end of the catheter is then inflated to widen the lumen
FIGURE 10.6 Management of acute coronary syndromes.

Acute coronary syndromes treatment algorithm Updated September 2011

Reperfusion therapy for ST segment elevation myocardial infarction (STEMI) Evolving risk stratification: clinical assessment, troponin assessment and time

• Start ECG monitoring Careful clinical history, examination, ECG, chest X-ray and investigations to High-risk NSTEACS
Symptoms consistent with ACS • Insert cannula
diagnose other causes of chest pain and evaluate clinical likelihood of evolving ACS* Presentation with clinical features consistent with ACS
• Pain relief and any of:
• Blood tests • repetitive or prolonged (> 10 minutes) ongoing chest
• Give aspirin 150–300 pain/discomfort
High-sensitivity troponin test all patients
mg unless already given • elevation of at least 1 cardiac biomarker (troponin or
Immediate 12-lead ECG or contraindicated CK-MB) Admit to coronary care
• persistent or dynamic ST depression ≥ 0.5 mm or new unit or other PCI or
T wave inversion ≥ 2 mm high-dependency unit CABG
• transient ST segment (≥ 0.5 mm) in more than • Estimate ischaemic risk
Doctor to see patient within 10 minutes of arrival At presentation Negative Positive 2 contiguous leads (risk score)
Refer for
(< 99th percentile) (≥ 99th percentile)† • haemodynamic compromise: systolic blood pressure • Estimate bleeding risk angiography
(national triage category 2) Monitor
< 90 mmHg, cool peripheries, diaphoresis, Killip class (bleeding score)
• Chest pain Medical
> 1 and/or new onset mitral regurgitation • Choose augmented
• ECG
• sustained ventricular tachycardia anti-thrombotic therapy
therapy
• Cardiac biomarkers
• syncope
Does patient meet indications for reperfusion • Pain relief 3 hours after presentation • LV systolic dysfunction (LVEF < 40%)
Note: the routine use of and at least 6 hours after Repeat
therapy? • prior PCI within 6 months or prior CABG surgery
supplemental oxygen is
the onset of symptoms troponin • presence of known diabetes (with typical symptoms
• Persistent ST elevation ≥ 1 mm in 2 contiguous limb leads or NO not recommended.
• ST elevation ≥ 2 mm in 2 contiguous chest leads or of ACS)
Oxygen therapy is
• chronic kidney disease – estimated GFR < 60 mL/min
• New left bundle branch block pattern indicated for patients
(with typical symptoms of ACS).
with hypoxia (oxygen
saturation < 93%) and YES + ive
YES where there is evidence Negative Positive#
of shock.1 ≥ 99th percentile or
≥ 50% increase Intermediate-risk NSTEACS
Presentation with clinical features consistent with ACS

CHAPTER 10 CARDIOVASCULAR ALTERATIONS AND MANAGEMENT

and any of:
Symptom onset • chest pain/discomfort within past 48 hours that
6 hours after Repeat troponin to evaluate occurred at rest, or was repetitive or prolonged (but
presentation cause of troponin elevation currently resolved)
• age > 65 years
• known CHD: prior MI with LVEF ≥ 40% or known Recurrent
coronary lesion > 50% stenosed ischaemia or Stress test (e.g.
3–12 hours ago • no high-risk ECG changes (see above) NO
< 1 hour ago 1–3 hours ago PCI available within 90 minutes elevated exercise ECG)
Significant change No change in • two or more of: known hypertension, family history,
PCI available within 1 hour? PCI available within 90 minutes? (onsite) or 2 hours (offsite, including in troponin level‡ troponin level troponin
active smoking or hyperlipidaemia
transport time)? • presence of known diabetes (with atypical symptoms
of ACS)
• chronic kidney disease – estimated GFR < 60 mL/min
YES NO NO YES NO Myocardial infarction MI likely: seek Not early MI: consider (with atypical symptoms of ACS)
YES • prior aspirin use.
(MI) unlikely: cardiac consultation late MI or other causes
proceed to early and further of chronic troponin
– ive
And not meeting the criteria for high-risk NSTEACS.
‘rule-out’ CAD testing investigation elevation
Fibrinolysis Fibrinolysis Fibrinolysis
PCI (unless contraindicated*)
PCI (unless contraindicated*)
PCI (unless contraindicated*) * This algorithm applies to patients with suspected ACS, in the absence of other plausible causes of troponin elevation (e.g. sepsis,
pulmonary embolus). Where other diagnoses are evident, management should be directed at these conditions.
† Substantial early elevations in troponin may indicate evolving MI or other diagnoses associated with increased risk – immediate Low-risk NSTEACS Discharge with
evaluation is required. Management decisions should not be delayed for repeat troponin testing at six hours. Presentation with clinical features consistent with ACS urgent cardiac
‡ Significant change: the Universal Definition of MI has recommended a change of 20% (3 SD) from baseline be considered significant without intermediate- or high-risk features, for example Appropriate
with contemporary assays. follow-up
one of the following: period of
Patients in whom fibrinolysis is contraindicated, or # Due to the increased sensitivity, a change of 50% or more may be required to make the diagnoses of evolving MI using the newer assays, (on upgraded
but the clinical significance of changes from very low baseline levels is uncertain. Research, currently ongoing, will clarify this • onset of anginal symptoms within the last month observation
with ongoing systems or instability after fibrinolysis, • worsening in severity or frequency of angina medical
recommendation.
should be transferred for PCI. • lowering in anginal threshold. therapy)
Note: This algorithm is based upon high-sensitivity troponin tests.1 If high-sensitivity troponin is unavailable, assessment should be based on
4- and 8-hour time points.

Note * Contraindications for fibrinolysis 1. Based on expert opinion

Reperfusion not Absolute Relative
Based on the ‘2011 Addendum to the National Heart Foundation of Australia/Cardiac Society of Australia and New Zealand Guidelines for the Management of Acute Coronary Syndromes (ACS), 2006’, published in Heart, Lung and Circulation, 2011;20:487–502. For
routinely • Active bleeding or bleeding diathesis • Current use of anticoagulants • Severe uncontrolled hypertension on more information, refer to this article or call our Health Information Service on 1300 36 27 87. Note
recommended after (excluding menses) • Noncompressible vascular punctures presentation (systolic ≥ 180 mmHg or
12 hours from © 2011 National Heart Foundation of Australia ABN 98 008 419 761 All patients with ACS should
• Significant closed head or facial trauma • Recent major surgery (< 3 weeks) diastolic ≥ 110 mmHg)
symptom onset if be given a written chest pain
within 3 months • Traumatic or prolonged (> 10 min) CPR • Ischaemic stroke > 3 months ago, ISBN: 978-1-921748-69-1
the patient is action plan and referred to
• Suspected aortic dissection • Recent internal bleeding within 4 weeks dementia or known intracranial
asymptomatic and POS-035 IPM/9/11 comprehensive ongoing
• Any prior intracranial haemorrhage • Active peptic ulcer abnormality (not covered in ‘absolute
haemodynamically prevention and cardiac
• Ischaemic stroke within 3 months • History of chronic, severe, poorly contraindications’) Disclaimer: This document has been produced by the National Heart Foundation of Australia for the information of health professionals. The statements and recommendations it contains are, unless labelled as ‘expert opinion’, based on independent review of the
stable. rehabilitation services.
• Known structural cerebral vascular lesion controlled hypertension • Pregnancy available evidence. Interpretation of this document by those without appropriate medical and/or clinical training is not recommended, other than at the request of, or in consultation with, a relevant health professional. While care has been taken in preparing the content
• Known malignant intracranial neoplasm of this material, the Heart Foundation and its employees cannot accept any liability, including for any loss or damage, resulting from the reliance on the content, or for its accuracy, currency and completeness. The information is obtained and developed from a variety of
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279
2011 National Heart Foundation of Australia, http://www.heartfoundation.org.au/acute-coronary-syndrome.
280 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

of the catheters can damage the blood vessel(s) and alter

FIGURE 10.7 PTCA procedure.28 perfusion to the limb. The sheath used to aid insertion
and maintain access is usually maintained for 1–2 hours
postprocedure for emergency access. Care is as follows:
• Observations: observe access site for haemorrhage
and haematoma; assess perfusion to the lower limb,
including colour, warmth and pulses. This monitoring
needs to be done often in the first few hours, when
complications are most likely to occur.
• ECG monitoring: includes 12-lead ECG on return and
    
ongoing ECG monitoring and chest pain assessment
to detect reocclusion. Patients need to be requested to
inform nursing staff of any chest pain or discomfort.
• Vital signs: are recorded every 15 minutes for the
first hour, half-hourly for one hour and then hourly
according to the patient’s condition.
• Removal of sheath: is usually performed by medical
or specially trained nursing staff.
• Achievement of haemostasis: use either application of
pressure for at least 5 minutes or vascular sealing.35
Pressure application can be by a manual
compression device (such as Femostop, RADI
of the artery by stretching the vessel wall, rupturing the Medical Systems, Uppsala, Sweden) and less often
atheromatous plaque and cracking the intima and media digital, to maintain a pressure of about 20 mmHg.
of the artery (see Figure 10.7). Vascular sealing uses a device such as the Angioseal
PTCA tends to be reserved for patients with single- Vascular Closure Device (St Jude Medical Inc,
or double-vessel disease as assessed on coronary artery St Paul, MN). This includes a collagen plug and a
angiograms. Angioplasty provides better symptom relief small biodegradable plate inside the artery, which
than medication alone, but there is no evidence of survival is held in place by a small suture, tamping tube and
benefits.29 Primary angioplasty results in a higher rate of small spring on the exterior. The tension spring is
patency of the affected artery in AMI (>90%), lower rates removed and the suture trimmed half an hour after
of cerebrovascular accident (CVA) and reinfarction and application. This enables the patient to mobilise and
higher short-term survival than thrombolysis in ACS.30 reduces nursing time.36
PTCA is recommended in all patients presenting with
chest pain who meet the indications for reperfusion when: • Assess: International Normalised Ratio (INR),
prothrombin (PT) and partial thromboplastin
1) facilities are available and it can be achieved within
time (PTT), as bleeding is more likely to occur
60 minutes; 2) there are contraindications to fibrinolytic
if anticoagulants are above the therapeutic range.
therapy described above; 3) ischaemia would result in
Weight-adjusted heparin (100 units/kg) is usually used
large anterior AMI within 4 hours; or 4) haemodynamic
during PTCA to prevent thrombus formation, and
instability or cardiogenic shock is present.
glycoprotein IIb/IIIa inhibitors such as abciximab may
A stent is usually inserted to prevent abrupt closure be used to prevent platelet aggregation and thrombus
and maintain patency for longer.30 The structure of the formation for patients at high risk of occlusion.
stent within the vessel enlarges the lumen and prevents
vessel stricture. Restenosis due to intimal hyperplasia is a • Bedrest (2–6 hours): is used to discourage the patient
relatively common complication, occurring 10–12 weeks from moving the joint of the insertion site to prevent
post-implantation. In response to this problem, drug- clot displacement and haematoma formation. Initially,
eluting stents have been developed. The drug coatings the patient should lie relatively flat if femoral artery
include sirolimus, a macrolide antibiotic that has been access has been used, then progress to sitting. The
demonstrated to effectively decrease hyperplasia and prevent period of rest has been demonstrated to be safely
reduction of flow.31 Paclitaxel has also shown promise in a reduced to 1 hour in low-risk patients (normotensive
series of studies.32 In addition to dactinomycin, these drugs and normal platelet count).35
are undergoing approval processes and, while short-term • Pain relief: is used primarily to promote comfort for
benefits are clear, long-term benefits are not.33,34 patients who find bedrest causes pain and discomfort.
Nursing management of patients post-PTCA includes • Urine output: adequate urine output is essential as
care of the puncture site to prevent bleeding and detect radiographic IV contrast is cleared by the kidneys,
arterial changes (including clot and aneurysm).35 The so it is vital that nurses ensure good hydration and
process used to create and maintain access for insertion monitor initial urine output.
 CHAPTER 10 CARDIOVASCULAR ALTERATIONS AND MANAGEMENT 281

• Oral antiplatelet drugs, such as clopidogrel or ticlopi- the patient recovers. Oxygen saturation levels should be
dine: may be given prior to the procedure to prevent routinely assessed and provision of oxygen by mask or
later reocclusion in the stent. Usually patients will be nasal cannulae provided if levels are reduced. Conventional
discharged on this medication to continue for up to practice was to provide O2 in the first 6 hours to raise SaO2
3 months while endothelium lines the stent/injured levels in the myocardium; however, there is no evidence
area. Unless contraindicated, all patients will take of patient benefit if SaO2 levels are not decreased.10
aspirin for the rest of their lives.36,37 Symptom relief should be provided, including analgesia
for pain. Analgesia management should be conducted by
Many patients find the PTCA procedure and confir- nurses because of their continued contact and thus more
mation of CHD diagnosis stressful.38 It is an important accurate assessment and treatment of pain.20 It is essential
nursing role to provide patients with preparatory infor- to treat pain, not only for the distress it causes patients but
mation about the procedure and care required during also because pain causes stimulation of the sympathetic
recovery. As family members provide valuable support and nervous system (SNS). SNS responses include elevated
reminders about recovery, these people should be included heart rate and potential for arrhythmias, peripheral
in any information sessions. The patient and family need vasoconstriction and increased myocardial contrac-
to be provided with information about the possibility of tility and, therefore, an overall increase in myocardial
restenosis, mobility restrictions at home and the lifestyle oxygen demand. Effective treatments for pain include
changes needed to reduce the risk of worsening CHD. IV morphine and nitrates. The IV route is preferable,
as absorption is predictable and additional punctures in
Practice tip thrombolysed patients are not required. Morphine has
the additional benefit of reducing anxiety in a distress-
Increased hydration can aggravate problems with
ing situation and should be initially provided at a dose
urination when on bedrest, particularly in older men
of 2.5–5 mg at 1 mg/min, followed by 2.5-mg doses as
with prostate enlargement. If a femoral access site is
indicated. While there is little randomised controlled trial
used in these patients, it is easier for the patient to
evidence to support this particular practice, it is generally
urinate while turned on the side, using pillow support
accepted to be appropriate. A standardised method of
to maintain the position.
pain evaluation and charting should be used to ensure
consistent assessment and treatment. An antiemetic such
Practice tip as metoclopramide should be given concurrently to lessen
and prevent nausea. Other drugs, such as beta-blockers
If a femoral access site has been used, bleeding may and nitrates, decrease myocardial workload, contributing
track between the patient’s legs and pool, and this will to pain reduction.
be invisible to a cursory inspection, particularly if the
patient is obese. Always move the patient’s thigh during Nursing care specific to thrombolysis
regular inspections. Patients receiving thrombolytics require constant observa-
tion and regular non-invasive blood pressure measurement
Nursing management of ACS and MI for hypotension. Continuous ECG monitoring for
patients arrhythmias and ST-segment changes is essential. Some
arrhythmias, particularly idioventricular arrhythmias,
The nursing role in patients with ACS and MI includes are associated with reperfusion and tend to be benign.
reducing myocardial workload and maximising cardiac ST-segment monitoring and assessment of pain help
output, provision of treatments, careful monitoring to evaluate the effectiveness of the thrombolysis. Thrombo-
determine the effects of treatment and detect complica- lysis is considered to have failed if the patient is still in
tions, rapid treatment of complications, comfort and pain pain and the ST segment has not resolved within 60–90
control, psychosocial support and teaching and discharge minutes.20 If thrombolysis fails, patients are at high risk
planning. for other interventions, so repeat thrombolysis is often the
Reduction of myocardial workload includes ensuring only treatment option. Salvage or rescue angioplasty may
the patient has bedrest, providing support with activities be undertaken if available at the site.
and limiting stress. A calm, caring manner during
nursing care is essential to lower patient and family Medications
stress levels. Individual evaluation of the patient and the Provision of medications and assessment of the effective-
family is necessary to determine the most appropriate ness of treatment is a major component of the nurse’s
management of visiting. ECG monitoring (preferably role in caring for the cardiac patient. Many of the medi-
including ST monitoring) and evaluation of heart rate, cations are accompanied by side effects and interactions
shortness of breath, chest discomfort and blood pressure with other drugs, which the nurse must monitor. An array
are essential to determine ischaemia, treatment effects, of medications is used to treat AMI patients, including
myocardial workload and complications. This monitoring aspirin, lipid-lowering agents, beta-blockers and organic
should occur hourly during the acute phase, reducing as nitrates (see Table 10.3).
282 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 10.3
Medications used in the treatment of ACS

AGENT ACTION SIDE EFFECTS/CAUTION COMMENTS

A N T I P L AT E L E T A G E N T S

Aspirin Prevents platelet synthesis of Gastrointestinal irritation and Noted to reduce the risk of AMI by
thromboxane A2, a vasoconstrictor bleeding; use enteric-coated tablets 50%,33 although often underutilised.6
and stimulant of platelet aggregation. to minimise Lifelong use is recommended in
May provide benefits from anti- angina patients
inflammatory properties in reducing
plaque rupture34
Clopidogrel Adenosine diphosphate (ADP) Inhibits P450 liver enzyme; care is Clopidogrel produces fewer GI
receptor agonist; prevents the required when delivering with other effects than aspirin and is more
binding of ADP to its platelet drugs and other anticoagulants25 effective in patients with recent
receptor, thus inhibiting platelet stroke, MI and peripheral vascular
aggregation disease37
Ticlopidine As for clopidogrel Severe side effects including
neutropenia
Tirofiban, Glycoprotein IIb/IIIa receptor Bleeding, thrombocytopenia, Early decreases in mortality in ACS
eptifibatide, antagonists prevent the final step nausea, fever and headache;25 doses and MI, particularly when given
lamifiban, of platelet aggregation; used most need to be reduced in renal failure in combination with aspirin and
abciximab37 commonly to inhibit thrombus heparin, have been seen
formation in acute coronary
syndrome angina37
B E TA - B L O C K E R S

Reduce cardiac workload (↓ heart Contraindications include significant Recommended for patients during
rate and force of contraction) by AV block, bradycardia, hypotension, the acute MI phase, reducing risk of
blocking beta-adrenergic receptors, history of asthma or uncontrolled further MI
preventing sympathetic stimulation heart failure
of the heart
N I T R AT E S

Glyceryl Potent peripheral vasodilators, Reflex tachycardia, hypotension, Tolerance to the vasodilator effect
trinitrate (IV, particularly in venous capacitance syncope and migraine-like occurs, so intermittent treatment
sublingual vessels, thereby reducing preload headache; generally occur in first is most effective. In the case of
and spray), and to a lesser extent afterload, to few days of treatment, then subside. transdermal delivery, if treatment is
isosorbide reduce myocardial workload. Blood pressure should be monitored withheld for 8–12 h in every 24 h,
mononitrate Dilate normal and atherosclerotic therapeutic activity is restored
coronary blood vessels to increase
myocardial oxygen supply.
Used to manage unstable angina and
reduce blood pressure in the critical
care setting, where there is some
evidence for symptomatic relief
L I P I D - L O W E R I N G S TAT I N S

Atorvastatin, Inhibit 3-hydroxy-3-methylglutaryl- Headache, gastrointestinal upset, To lower and maintain cholesterol
simvastatin, coenzyme-A (HMG-CoA) reductase, inflammation of voluntary muscles at 5 mmol/L, evidence that statin
fluvastatin, the enzyme that limits the rate of and altered liver function; taking medications can reduce mortality for
pravastatin cholesterol synthesis in the liver, statins with food may reduce GI up to 5 years after AMI.39 Education
thereby reducing plasma cholesterol symptoms needs to include monitoring for
muscle soreness and regular GP
visits for liver function tests

Adapted from Bryant B, Knights K, Saterno E. Pharmacology for health professionals. Sydney: Mosby Elsevier; 2006.

Symptom control for sustained symptom management.21 Beta-blockers

Control of anginal symptoms with medication usually are usually commenced unless contraindicated. Calcium
includes sublingual glyceryl trinitrate (GTN) for immediate channel blockers may be used in patients who do not
symptom control and one or more antianginal medications have cardiac failure or heart block. (These medications are
 CHAPTER 10 CARDIOVASCULAR ALTERATIONS AND MANAGEMENT 283

described in the next section.) The choice of medication the workload of the heart and therefore myocardial
may depend on how acceptable the patient finds the oxygen demand. In an acute cardiac event, these demands
reduction in symptoms and the presence of side effects. occur when perfusion is already poor and may lead to
Patients need to take antianginal agents continuously, worse outcomes, including ventricular arrhythmias and
regardless of symptoms. Patients should also be encouraged increased myocardial ischaemia. Therefore, staff working
to take sublingual GTN prophylactically. in emergency and coronary care should employ strategies
Angina may also be managed by avoiding situations to reduce a patient’s anxiety. Chapter 7 provides a more
that trigger angina. Education needs to be directed at detailed description of psychological care.
awareness of symptoms and management of unstable Increasing a patient’s sense of control, calm and confi-
angina and AMI symptoms, and the need for emergency dence in care reduces the patient’s sense of vulnerability,
care. Although these patients are at low risk of further whether it is realistic or not.42 This can be achieved by:
cardiovascular events in the short term, in the medium to • providing order and predictability in routines,
long term, risk may accumulate. Patients with angina are allowing the patient to make choices, providing
encouraged to attend cardiac rehabilitation programs to information and explanations and including the
learn how to deal with symptom management.39 patient in decision making
Angiotensin-converting enzyme (ACE) inhibitors • using a calm, confident approach
have been recommended for all post-AMI patients while
in hospital, with review of prescription at 4–6 weeks
• communicating with patients and families, while
reducing conversation demands, as excessive
post-discharge. Patients with left ventricular failure should conversation by patients may unnecessarily raise
be maintained on ACE inhibitors. Similarly, diuretics heart rate43
provide the mainstay of the management of left ventricu-
lar failure if it is present (see Chapter 19). Diabetic patients • restricting the number and type of visitors in the
acute phase is customary, but many patients feel safer
have a higher mortality after AMI in both acute and if a family member is present
long-term phases. Provision of an insulin-glucose infusion
for BSL >11 mmol/L during the acute phase, followed • provision of comprehensive information to families,
by subcutaneous injections for at least 3 months, has with more concise information in understandable
been demonstrated to significantly reduce mortality up to language for patients.
3 years post-AMI.40 Nurses need to monitor patients for signs of excessive
Transfer to a step-down unit or general ward usually anxiety, including facial expressions and behavioural
occurs when the patient is pain-free and is haemodynami- changes. However, overt behaviours may be controlled by
cally stable. Stability means that patients are not dependent the patient, so careful conversation and/or use of specific
on IV inotropic or vasoactive support and have no arrhyth- assessments may be necessary to detect anxiety. The move
mias. Discharge home after AMI varies, but usually occurs to the step-down or general ward may also be stressful to
at day 3 for low-risk patients.20 the patient and family.This move needs to be planned and
discussed, and promoted as a sign of recovery.
Emotional responses and patient and
Cardiac rehabilitation
family support
Coronary heart disease is a chronic disease process, which
ACS or AMI is usually accompanied by feelings of acute often presents with acute events such as ACS or AMI.
anxiety and fear, as most patients are aware of the signif- Like all chronic illnesses, it has implications for patients
icant threat posed to their health.18 For many patients in terms of lifestyle change, uncertainty of long-term
it may also be the first experience of acute illness and outcomes, functional changes and social and economic
associated aspects such as ambulance transport, emergency alterations. Cardiac rehabilitation aims to address these
care and hospitalisation, so they may experience shock issues. The World Health Organization describes cardiac
and disbelief as well. Fast-track processes such as prehos- rehabilitation as ‘the sum of activities required to influence
pital triage require patients and their families to process a favourably the underlying cause of the disease, as well as
large amount of information and make decisions quickly, to ensure the patients the best possible physical, mental
and this, added to an alien environment, full of unfamiliar and social conditions so that they may, by their own
technology and personnel, can be quite distressing. efforts, preserve, or resume when lost, as normal a place as
However, the environment can also promote a feeling of possible in the life of the community’.44 Systematic, indi-
security for patients and their families. Patients’ percep- vidualised rehabilitation and secondary prevention need
tions of the CCU environment have been linked to to be offered to all AMI patients and considered for all
recovery, in a study conducted in 1996, which remains patients who have coronary heart disease. Participation
surprisingly relevant today.41 in well-structured, multidisciplinary programs has been
Anxiety is a common response to the stress of an demonstrated to reduce mortality by almost 30% in AMI
acute cardiac event and leads to important physiological and by 13% in other coronary heart disease conditions.45
and psychological changes.42 The sympathetic nervous Additional benefits have been shown for improvements in
system is stimulated, resulting in increased heart rate, exercise tolerance, symptoms, serum lipids, psychological
respiration and blood pressure. These responses increase wellbeing and cessation of smoking.46,47
284 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Cardiac rehabilitation is structured around four effective, rapidly responsive ambulance service, as exempli-
phases, beginning with phase I, during admission.48 The fied in Seattle in the USA.50 Arrhythmias may be generated
components of phase I include: by poorly perfused tissue and electrolyte alterations, and
• information regarding the disease process, the increased sympathetic tone during infarction, but are
prognosis, and an optimal approach to recovery, early more often due to a failing left ventricle. They may also
mobilisation and discharge planning complicate reperfusion after successful revascularisation.51 It
is essential to rapidly and effectively treat arrhythmias in the
• assessment of patients’ understanding of their diagnosis ACS and AMI context.The goal of treatment is to maintain
and treatment as a foundation for self-management
cardiac output while reducing workload. Arrhythmias and
• discharge planning, which incorporates discussions management are described in Chapter 11.
on adaptation to the functional and lifestyle changes
needed for secondary prevention – dietary intake of Pericarditis
lipids, exercise, smoking cessation, stress management Pericarditis is an inflammation of the visceral and parietal
and symptom monitoring, and management of acute layers of the pericardium that cover the heart. This inflam-
symptoms mation occurs in approximately 20% of AMI patients
• early mobilisation as an inpatient to encourage a within the following 2–3 days.13 The patient experi-
positive approach to recovery with monitoring of the ences chest pain, which may be confused with ischaemic
response to activity in heart rate, shortness of breath pain. This confusion with an ischaemic event may be
and chest pain to determine the rate of progress. compounded by the additional presence of ST-segment
(Most hospital units use an activity progress chart for elevation on the ECG. However, pericardial pain increases
this purpose based on metabolic equivalents [METs].) with deep inspiration and a pericardial rub is often present.
The phases that follow, from II to IV, are managed in Electrocardiographically, the elevated ST segments of peri-
the outpatient setting and begin with assessment, liaison carditis are typically concave upwards (saddle-shaped) and
with multidisciplinary professionals and health education. often widespread, contrasting with convex ST-segment
Phase II occurs in the immediate post-discharge period and elevation limited to the distribution of a single coronary
includes liaison with community-based carers and services artery in infarction.52 Pericarditis normally responds to
and further assessment. In phase III, tailored, supervised anti-inflammatory treatment by aspirin, indomethacin and/
exercise programs are usually conducted and there is a or corticosteroids. Approximately 1–5% of AMI patients
range of psychosocial interventions, such as support sessions develop pericarditis as a late complication, 2 weeks to a
and stress management. Finally, in phase IV the focus is on few months post-AMI.21 Usually, this late-onset pericard-
chronic disease management and maintaining risk modi- itis is associated with Dressler’s syndrome and may be an
fication behaviours. All phases require incorporation of autoimmune response to myocardial injury.This is a chronic
the principles of adult learning to maximise learning and condition requiring systemic corticosteroid treatment.
behaviour change. These principles include recognition of
‘readiness to learn’.48 Adults are ready to learn most effec-
Structural defects
tively when they are physically and emotionally stable and Myocardial tissue death may be catastrophic if it is extensive
are aware of the problem or need to learn. Nurses, because or results in rupture of ventricular or papillary muscle.These
of their expertise and continual presence, are best placed to conditions are rare and symptoms develop rapidly. Intra-
assess and provide education at optimal times. ventricular septal rupture is usually associated with anterior
MI. The patient develops progressive dyspnoea, tachy-
Complications of myocardial infarction cardia and pulmonary congestion, as well as a loud systolic
Despite declines in death rates from myocardial murmur associated with a thrill felt in the parasternal area. If
infarction,3–5 many patients will experience complications, a pulmonary artery catheter is present, blood samples from
most of which occur within the first 24 hours. the right atrium and right ventricle will reveal a higher
than usual oxygen content. Diagnosis must be confirmed
Cardiogenic shock by cardiac catheterisation, and urgent surgery is required.
Cardiogenic shock occurs as a complication of MI in Papillary muscle rupture most often occurs 2–7 days
about 5–10% of patients and is the most common cause of after MI. Patients experience a sudden onset of pulmonary
death in hospitals.49 It arises from loss of contractile force, oedema secondary to pulmonary hypertension and
and generally occurs when ventricular damage is more cardiogenic shock. Additional heart sounds and a systolic
than 40% and ejection fraction less than 35%. Cardiogenic murmur will be heard. Urgent surgery is required, as
shock and the related management are described in more the mortality rate for papillary muscle rupture is 95%.53
detail in Chapter 12. Cardiac rupture most often occurs within 5 days of MI
and is commonest in older women. The patient experi-
Arrhythmias ences continuous chest pain, dyspnoea and hypotension as
Arrhythmias often occur in ACS and AMI and are often the tamponade develops. Symptoms may worsen rapidly and
cause of death in the prehospital phase. Management of the result in pulseless electrical activity (PEA) unless surgery is
prehospital phase focuses on community education and an undertaken immediately.
 CHAPTER 10 CARDIOVASCULAR ALTERATIONS AND MANAGEMENT 285

Heart failure to ventricular fibrillation or tachycardia. Valvular disease

causing heart failure usually involves valves on the left
In normal circumstances, the heart is a very effective, side of the heart (mitral and/or aortic valves). Aortic
efficient pump with reserve mechanisms available to allow stenosis results in an increase in afterload and ventricular
output to meet changing demands. These mechanisms hypertrophy develops with reduced diastolic compliance
include: 1) increasing heart rate to increase total cardiac resulting in a reduced ejection fraction. Mitral stenosis is
output, 2) dilation to create muscle stretch and more usually due to rheumatic heart disease.Valvular incompe-
effective contraction, 3) hypertrophy of myocytes over time tence results in a dilated ventricle to accommodate the
to generate more force and 4) increasing stroke volume by regurgitant volume. Stroke volume increases in an attempt
increasing venous return and increased contractility. Heart to empty its contents and ventricular muscle mass increases.
failure is a complex clinical condition that is characterised However, over time the ventricle is unable to maintain
by an underlying structural abnormality or dysfunction the increased workload and heart failure develops.Valvular
that results in the inability of the ventricle to fill with or heart disease and treatment are described in more detail
eject blood.54 The condition is also known as congestive in Chapter 12.
cardiac failure, a term commonly used in the USA but There are several terms used to describe the pathology
not in Australia. Chronic heart failure (CHF) describes and signs and symptoms of heart failure. These include:
the long-term inability of the heart to meet metabolic
demands. • Backward failure: refers to the systemic and
pulmonary congestion that occurs as a result of failure
The burden of disease associated with heart failure is
of the ventricle to expel its volume.
on the rise due to our ageing population, the prevalence
of coronary heart disease and hypertension, the decrease • Forward failure: is due to an inadequate cardiac
in fatality from acute coronary syndrome and improved output and leads to decrease in vital organ perfusion.
methods of diagnosis.54 Survival rates and prognosis for • Acute heart failure: includes the initial hospitalisation
heart failure patients are extremely poor. Approximately for the diagnosis of heart failure and exacerbations of
50% of patients diagnosed with heart failure will die chronic heart failure.
within 5 years of diagnosis.55,56 When compared with • Chronic heart failure: develops over time as a
patients with cancer, heart failure patients have the poorest result of the inability of compensatory mechanisms
5-year survival rate, with the exception of lung cancer.57 to maintain an adequate cardiac output to meet
In Australia during 2007–08, 49,307 patients were hospit- metabolic demands.
alised with a primary diagnosis of CHF (0.6% of all
hospitalisations).58 Internationally, heart failure is the most • Heart failure with reduced ejection fraction (HFrEF)
common cause of hospitalisation in patients aged over or systolic heart failure: refers to the inability of
70 years.59 Approximately 40% of patients admitted to the ventricle to contract adequately during systole
hospital with heart failure will be readmitted or die within resulting in a reduced ejection fraction and an
1 year.59 In the USA approximately 5.1 million people increased end-diastolic volume. This is the most
have been diagnosed with heart failure.60 Approximately, common form of heart failure.
1 million hospital admissions annually have a primary • Heart failure with preserved ejection fraction
diagnosis of heart failure.60 (HFpEF) or diastolic heart failure: indicates normal
Over 50% of patients newly diagnosed with heart failure systolic function with a normal ejection fraction but
have concurrent ischaemic heart disease, hypertension is impaired relaxation so there is a resistance to filling
present in 65% and idiopathic dilated cardiomyopathy in with increased filling pressures. Diastolic dysfunction
5–10% of cases.54 The causes of heart failure can be categor- usually occurs in conjunction with systolic
ised according to: 1) myocardial disease, 2) arrhythmias, dysfunction and is more common in the elderly.
3) valve disease, 4) pericardial disease and 5) congenital heart • Low cardiac output syndrome: this occurs in response
disease.61 Myocardial disease may be caused by myocardial to hypovolaemia and/or hypertension. Severe vaso-
infarction and fibrosis from prolonged ischaemic heart constriction further reduces the cardiac output.
disease, which accounts for approximately two-thirds of
systolic heart failure causing systolic dysfunction and a • High cardiac output syndrome: is the result of an
increase in metabolic demands causing a decrease
reduced ejection fraction. in systemic venous return leading to an increase in
Arrhythmias, including both brady- and tachyarrhyth- stroke volume and cardiac output. Burns and sepsis
mias, may cause heart failure due to changes in filling time
are the main causes.
affecting preload and resultant cardiac output. Myocardial
oxygen demand is increased and, if the heart is poorly • Left-sided heart failure: occurs when there is a
perfused, muscle contraction will be affected. Frequent reduced left ventricular stroke volume resulting in
premature contractions and atrial fibrillation disturb accumulation of blood in the pulmonary system.
mechanical coordination so that the ventricles may not • Right-sided heart failure: is the congestion of blood
be adequately filled for efficient contraction. Heart failure in the systemic system due to the inability of the
patients are also at high risk of sudden cardiac death due right ventricle to expel its blood volume.
286 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Responses to heart failure Figure 10.8).The consequence of this activation is increased

myocardial oxygen demand. Although blood flow to
When heart failure occurs, several adaptive responses are
essential organs is maintained, perfusion to the kidneys,
initiated by the body in an attempt to maintain normal
gastrointestinal system and skin is reduced and peripheral
perfusion (see Figure 10.8). These mechanisms are
resistance increased. Chronic activation of vasoconstrictors
successful in the normal heart, but contribute to decreased contributes to the progression of cardiac failure through
effectiveness in the failing heart. The compensatory increased resistance and effects on cardiac structure, causing
mechanisms include: hypertrophy and fibrosis and downregulation of beta-adren-
• sympathetic nervous system response ergic receptors and endothelial dysfunction. Chronic poor
• renin–angiotensin–aldosterone system (RAAS) perfusion to skeletal muscles may contribute to changes
in muscle metabolism, resulting in further reductions in
• Frank-Starling response exercise tolerance.
• neurohormonal response. The next compensatory mechanism to be activated is
The sympathetic nervous system is the first response to the RAAS. This is stimulated within minutes, in response
be stimulated in heart failure. It occurs within seconds of a to a decrease in kidney perfusion resulting in a decrease in
reduction in cardiac output and the parasympathetic system glomerular filtration rate.Activation of this response results
becomes inhibited. The baroreceptor reflexes are activated in an increase in systemic venous return and sodium and
in response to a reduced arterial pressure. The beta- water reabsorption, which then increases the circulating
adrenergic receptors located in the heart are activated, blood volume, systemic filling pressures and venous return
resulting in an increase in heart rate and contractility to enhancing preload and afterload (see Chapter 9).
increase stroke volume and cardiac output. Sympathetic The Frank-Starling response is also activated. As the
nervous system response in the peripheral vascular system end-diastolic volume increases (preload) in response
results in vasoconstriction, which increases systemic venous to sympathetic nervous system stimulation, ventricular
return and mean systemic filling pressures. This results in dilation occurs stimulating the Frank-Starling response.
an increase in venous return, preload and afterload (see As the myocardial fibres are stretched during diastole the

FIGURE 10.8 Flowchart of the pathophysiology of heart failure.62

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 CHAPTER 10 CARDIOVASCULAR ALTERATIONS AND MANAGEMENT 287

force of contractility also increases to expel the increasing volume by increasing salt and water excretion in the
preload.This is a major mechanism of the heart to maintain kidneys. Plasma ANP is increased in acute heart failure
a normal cardiac output. Optimal contractility occurs but depleted in chronic heart failure.
when the diastolic volume is 12–18 mmHg.63 However, While in the healthy heart these compensatory
when the ventricle is damaged, such as in MI, the sympa- mechanisms would result in an adequate cardiac output,
thetic nervous system increases heart rate and contractility, in heart failure they do not, depending on the aetiology. In
further increasing cardiac workload and exacerbating ischaemic heart failure the damaged myocardium is unable
myocardial dysfunction, which increases end-diastolic to respond adequately to the Frank-Starling response and
volume (preload) and ventricular dilation further, and ventricular remodelling develops. Heart failure caused by
heart failure progresses. As ventricular dilation continues, hypertension or valvular heart disease results in persistent
ventricular hypertrophy results. The myocardium also pressure or volume overload, which is exacerbated by the
increases its muscle mass in an attempt to increase contrac- Frank-Starling response and sympathetic nervous system
tility, called ventricular remodelling. However, over compensatory mechanisms.This causes ventricular remod-
time ventricular hypertrophy results in changes to end- elling and depletion of norepinephrine and a reduction
diastolic compliance and contractility due to the thickened of inotropic response to the cardiac sympathetic nervous
ventricular wall, impaired muscle function and growth of system. These all exacerbate the reduction in circulating
collagen. These result in further impairment of ventricu- blood volume and kidney perfusion. Many patients with
lar function (see Figure 10.9).58 Ventricular hypertrophy heart failure often have a high plasma renin activity due
also has a depressant effect on ventricular compliance, to the continual activation of the RAAS compensatory
heart rate and contractility resulting in an increase in end- mechanism.
diastolic pressure with no associated increase in contractility. In heart failure patients the inadequate cardiac
As the pulmonary artery pressures increase, pulmonary output results in signs and symptoms of hypoperfusion
oedema and cardiogenic shock develop. (oliguria, cognitive impairment and cold peripheries) and
The final compensatory mechanism to be activated congestion of the venous and pulmonary systems (acute
is the neurohormonal response, which takes days to be pulmonary oedema, dyspnoea, hypoxaemia, peripheral
activated. This response involves the activation of vaso- oedema and liver congestion). Classification of signs and
pressin and atrial natriuretic peptide (ANP).Vasopressin is symptoms is usually considered in the context of left or
a potent vasoconstrictor and also an antidiuretic hormone. right ventricular failure.
ANP is important in the regulation of cardiovascu- Left ventricular failure
lar volume homeostasis. It is released from the atria in
response to atrial stretching due to an increased circulating Left ventricular failure (LVF), compared with other
blood volume. ANP blocks the effect of the sympathetic forms of heart failure, is characterised by breathlessness,
nervous system, RAAS and vasopressin. It reduces tachy- orthopnoea and paroxysmal nocturnal dyspnoea, irritating
cardia via the baroreceptors and reduces circulating blood cough and fatigue (see Table 10.4). Left ventricular failure
or HFpEF exists when the ventricle has an ejection
fraction of less than 40%, resulting in increased end-
FIGURE 10.9 Function curves of left ventricular diastolic volume and increased intraventricular pressure.61
pressure during various stages of heart failure.64 The left atrium is unable to empty into the left ventricle
adequately and pressure in the left atrium rises.This pressure
is reflected in the pulmonary veins and causes pulmonary
congestion. When pulmonary venous congestion exceeds
20 mmHg, fluid moves into the pulmonary interstitium.
B Raised pulmonary interstitial pressure reduces pulmonary
compliance, increases the work of breathing and is expe-
rienced by the patient as shortness of breath. Increased
Cardiac Output
Litres/Minute

A
blood volume in the lung also initiates shallow, rapid
5 e breathing and the sensation of breathlessness. Patients
ailur C
rt F also experience orthopnoea (dyspnoea while lying flat)
Hea
d
n

al

ate and paroxysmal nocturnal dyspnoea because, when lying

tio

ns
r
nc

No

pe re down, blood is redistributed from gravity-dependent areas

Failu
rfu

m D
Co ear t
pe

a te dH of the body to the lung. Sitting upright or standing, and

Hy

s
pen
com sleeping with additional pillows, relieves breathlessness
De
at night.63
Acute pulmonary oedema results when pulmonary
12 mmHg 20 mmHg
capillary pressure exceeds approximately 30 mmHg, and
then fluid from the vessels begins to leak into the alveoli (see
Left Ventricular End-Diastolic Filling Pressure
(Wedge Pressure) Figure 10.10).65 This fluid leak decreases the area available
for normal gas exchange and severe shortness of breath
288 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 10.4
Clinical manifestations of failure of right and left sides of the heart

L E F T V E N T R I C U L A R FA I L U R E R I G H T V E N T R I C U L A R FA I L U R E
SIGNS SYMPTOMS SIGNS SYMPTOMS

Tachypnoea Dyspnoea Peripheral oedema Fatigue

Tachycardia Orthopnoea Raised jugular venous pressure Weight gain
Bibasal crackles Paroxysmal nocturnal Raised central venous pressure Anorexia
Haemoptysis dyspnoea Ascites
Cough Fatigue Hepatomegaly
Pulmonary oedema Nocturia
Raised pulmonary artery pressure
S3 heart sound

FIGURE 10.10 Pathophysiology of pulmonary oedema. As pulmonary oedema progresses, it inhibits oxygen and
carbon dioxide exchange at the alveolar–capillary interface. (A) Normal relationship. (B) Increased pulmonary capillary
hydrostatic pressure causes fluid to move from the vascular space into the pulmonary interstitial space. (C) Lymphatic
flow increases and pulls fluid back into the vascular or lymphatic space. (D) Failure of lymphatic flow and worsening of
left-sided heart failure causes further movement of fluid into the interstitial space and then into the alveoli.23

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results, often accompanied by pink, frothy sputum and a cough, cardiomegaly and the presence of pulmonary
noisy respirations.This causes patients to experience severe vessels on chest X-ray.
anxiety and decreased oxygen levels. Pulmonary oedema is
a medical emergency and requires urgent treatment. Right ventricular failure
In addition to pulmonary symptoms, patients with left Right ventricular failure (RVF) does not usually occur
ventricular failure experience signs and symptoms related in isolation, except in the presence of severe lung disease,
to decreased left ventricular output, including weakness, such as chronic obstructive pulmonary disease, pulmonary
fatigue, difficulty in concentrating and decreased exercise hypertension or a massive pulmonary embolus.63 In this
tolerance. These symptoms may be present for some time case, right ventricular failure is due to resistance to outflow.
before an accurate diagnosis of heart failure is made, The right ventricle can adapt to fairly large changes in
because they are non-specific and are consistent with volume; however, when cardiac output decreases, end-
other diagnoses such as depression. Other signs that are diastolic volume increases, and the right atrium is unable to
useful in diagnosis include the presence of S3 (ventricular empty adequately. Right atrial pressure rises and is reflected
gallop), crackles over lung fields that do not clear with into the venous system. Jugular vein distension occurs, and
 CHAPTER 10 CARDIOVASCULAR ALTERATIONS AND MANAGEMENT 289

the veins are usually visible above the clavicle. Symptoms

of right heart failure are not as specific as left ventricular TABLE 10.5
failure, and are mostly related to low cardiac output and New York Heart Association functional classification of
raised venous pressure (see Table 10.4). Ascites and oedema heart failure69
tend to progress insidiously, and dependent oedema in the CLASS DEFINITION
feet and ankles is often most prominent. Weight gain is an
important sign as 1 kilogram of weight gain equals 1 litre I Normal daily activity does not initiate symptoms.
There are no limitations on activity
of excess fluid. Liver congestion may result in tenderness,
ascites and jaundice. Nausea and anorexia may be present II Ordinary activities initiate onset of symptoms,
and are a result of an increased intra-abdominal pressure. but symptoms subside with rest. Slight limitation
Many signs are not readily distinguishable from left ventric- of daily activities
ular failure, including extra heart sounds. III A small amount of activity initiates symptoms;
patients are usually symptom-free at rest.
Patient assessment, diagnostic Marked limitation of activity
procedures and classification IV Any type of activity initiates symptoms, and
Assessment and diagnosis are summarised in a diagnostic symptoms are present at rest
algorithm (see Figure 10.11).51 A full assessment and history
is essential to determine the cause(s) of CHF and to assess
Pulmonary assessment includes chest auscultation for
the severity of the disease. A careful physical assessment is
inspiratory crepitations that do not clear with coughing.
important for initial diagnosis and to evaluate the effective-
They are initially heard in the bases but as congestion
ness of treatments and progress of the disease. The depth
increases they become diffuse. General assessment of the
and time taken to conduct the assessment depend on the
severity of symptoms. The physical examination of the patient includes daily weighing and looking for signs of
patient focuses on cardiovascular and pulmonary assessment. cachexia (usually associated with severe chronic heart
Cardiovascular assessment includes: failure), anaemia and dizziness.
Heart failure is usually classified according to the
• Pulse rate and rhythm: the pulse rate is generally severity of symptoms. In chronic heart failure, the New
elevated due to a low cardiac output. However, if the
York Heart Association (NYHA) Functional Classifica-
patient is prescribed beta-adrenergic blocking agents
tion is commonly used to classify patients on the basis of
and/or angiotensin-converting enzyme inhibitors
the activity level that initiates symptoms (see Table 10.5).65
(ACEIs), the pulse rate may be low.
• Palpation of the precordium and apical impulse: may Diagnostic tests
be displaced laterally and downward to the left due to Tests used to diagnose heart failure include the following:
an increased heart size.
• Auscultation of a third heart sound (S3 gallop): occurs • Trans-thoracic echocardiography is the most useful
investigation to confirm diagnosis. This is the gold
due to a low ejection fraction and diastolic dysfunc-
tion. A fourth heart sound may also be present due to standard diagnostic test for heart failure and should
a decrease in ventricular compliance. always be undertaken when possible.54,66 This test is
vital, as it can distinguish systolic dysfunction
• Assessment of jugular venous pressure (JVP): is (left ventricular ejection fraction [LVEF] <40%) from
performed to estimate the degree of venous volume. If
diastolic dysfunction, and therefore help determine
raised it reflects hypervolaemia, right ventricular failure
treatment.54 Information on left and right ventricular
and reduced right ventricular compliance. It can also
sizes, volumes, left ventricular thrombus and
be raised in the presence of tricuspid valve disease. The
ventricular wall thickness and motion can be
hepatojugular reflex is also assessed by pressing on the
liver and observing an increase in JVP. This results in an provided. Assessment of valve structure and function
increase in blood flow to the right atrium. as well as intracardiac and pulmonary pressures can be
determined, without the need for invasive techniques.
• Blood pressure: lying and standing blood pressure are Pulsed-wave Doppler and tissue Doppler studies can
measured to assess postural hypotension due to a low
be used to determine diastolic dysfunction.
cardiac output and also the prescribing of beta-
adrenergic blocking agents and ACEIs. • Assessment of cardiac function can also be done
by invasive techniques (e.g. coronary angiography)
• Peripheries: look for the presence of cyanosis that and nuclear cardiology tests (e.g. gated radionuclide
may be due to vasoconstriction. Assess the fingers
for clubbing, which indicates long-term cyanosis angiocardiography).
usually as a consequence of congenital heart disease. • ECG should be done as an initial investigation. Most
Also assess the patient for ankle oedema. Peripheral common abnormalities include ST-T wave changes,
oedema up to the midcalves indicates a moderate left bundle branch block, left anterior hemiblock, left
amount of excess fluid and the patient may require ventricular hypertrophy, atrial fibrillation and sinus
a bolus dose of diuretic medication. tachycardia.
290 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

FIGURE 10.11 Diagnostic algorithm for CHF.

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Courtesy National Heart Foundation of Australia and the Cardiac Society of Australia and New Zealand (Chronic Heart Failure
Guidelines Expert Writing Panel). Guidelines for the prevention, detection and management of people with chronic heart failure in
Australia. Updated October 2011. Melbourne: National Heart Foundation of Australia; 2011.
 CHAPTER 10 CARDIOVASCULAR ALTERATIONS AND MANAGEMENT 291

• Chest X-ray shows cardiomegaly and pulmonary over 70 outreach heart failure programs throughout
markings, including evidence of interstitial oedema: Australia that support heart failure patients post-discharge.68
perihilar pulmonary vessels, small basal pleural The main goals of these programs are to reduce symptom
effusions obscuring the costophrenic angles, Kerley B burden, improve functional capacity and minimise hospital
lines (indicating raised left atrial pressure). readmissions. These programs range from in-hospital visits
• Full blood count checks for anaemia and mild to facilitate discharge planning to nurse-led heart failure
thrombocytopenia. Any signs of anaemia should be outpatient clinics, home visit programs and heart failure-
further investigated. specific exercise programs. Several meta-analyses of
home visit programs have shown a reduction in hospital
• Urea, creatinine and electrolytes tests for dilutional
admissions and mortality69,70 and these programs are now
hyponatraemia, hypokalaemia, hyperkalaemia, low
standard care for heart failure patients.54,59,71 Home visit
magnesium and glomerular filtration rate. These should
heart failure programs involve a heart failure nurse visiting
be closely monitored if there are any changes in clinical
the patient at home and providing education to the
status and/or drug therapy such as ACEIs and diuretics. patient and carer, assessing their symptoms and educating
• Liver function tests check for elevated levels of AST, the patients and their carers about self-management
ALT, lactate dehydrogenase (LDH) and serum bilirubin. strategies. Nurse-led outpatient clinics also reduce hospital
• Thyroid function tests are performed particularly in admissions and mortality72,73 and play an important role in
patients with no history of coronary artery disease the management of heart failure patients post-discharge.
and who develop atrial fibrillation. Management of heart failure post the acute phase is
• Urinalysis is conducted to measure specific gravity based on three principles: self-care management, long-term
and proteinuria. lifestyle changes and adherence to pharmacotherapy.
• Myocardial ischemia and viability need to be assessed Management of self-care is the key to non-pharmaco-
in patients with heart failure and coronary artery logical management of heart failure. Self-care refers to
disease.These can be assessed by a stress ECG, stress the decision-making process of patients concerning their
echocardiography or a myocardial perfusion study. choice of healthy behaviour and response to worsening
symptoms when they occur. It involves cognitive decision
Coronary angiography is useful to determine the
making, requiring the recognition of signs and symptoms
contribution of coronary artery disease in these patients.
that indicate a change in condition, which is based on
• Natriuretic peptides include plasma ANP and B-type knowledge and prior experiences of deterioration.74,75
natriuretic peptide (BNP). BNP or N-terminal
proBNP is not recommended to be used as the only Lifestyle modification and self-care
test to diagnose chronic heart failure as an elevated management
BNP may be due to other causes.54 However, it is
Patient education is the key to self-management and must
useful to use it in conjunction with other diagnostic
include family members to be effective. Patient education
tests, particularly to differentiate between dyspnoea should include information on the following:
due to chronic heart failure and dyspnoea due to
chronic obstructive pulmonary disease. • the disease process – this involves discussing what
heart failure is, signs and symptoms and why they
• Endomyocardial biopsy should be conducted if there occur, and strategies to improve their symptoms
is a suspicion of cardiomyopathy.
• lifestyle changes
Patient management • medications and side effects
Treatment of CHF is lifelong and multifactorial, requiring • self-monitoring and acute symptoms
a well-coordinated, multidisciplinary approach. The goals • importance of adherence to the medications and
of heart failure treatment are to identify and eliminate management plan.
the precipitating cause, promote optimal cardiac function, There are numerous resources available for patient and
enhance patient comfort by relieving signs and symptoms carer education. The Heart Foundation has an excellent
and help the patient and family cope with any lifestyle resource titled ‘Living well with chronic heart failure’
changes. Clinical practice guidelines have been developed (http://www.heartfoundation.org.au/SiteCollectionDocu-
to guide the treatment of heart failure on the basis of ments/Living well with chronic heart failure.pdf).Also ‘heart
ventricular dysfunction and grade of symptoms (see online’ (http://www.heartonline.org.au/Pages/default.aspx)
Figures 10.12–10.14).54 is another excellent resource for health professionals
Planning for hospital discharge begins early in the providing information for patients and carers. ‘Heartonline’
admission and aims to promote quality of life for the also provides resources for health professionals regarding
patient and prevent unnecessary admissions. Several heart failure management and tools such as surveys.
healthcare services have been implemented to support the Restriction of fluid to 1.5–2 L/day is one of the most
transition from hospital to home as it is during the first important strategies that patients can adhere to in order to
30 days post-discharge that nearly 35% of heart failure improve their symptoms. Patients are encouraged to weigh
patients are readmitted to hospital.67 There are currently themselves daily and to identify any increase in weight as
292 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

FIGURE 10.12 Pharmacological treatment of systolic heart failure.

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Courtesy National Heart Foundation of Australia and the Cardiac Society of Australia and New Zealand (Chronic Heart Failure
Guidelines Expert Writing Panel). Guidelines for the prevention, detection and management of people with chronic heart failure in
Australia. Updated October 2011. Melbourne: National Heart Foundation of Australia; 2011.

an increase of 1 kg equals 1 litre of excess fluid. National should be advised of early warning signs of excess fluid
guidelines stipulate that, if their weight increases by 2 kg volume and decompensation, such as increasing dyspnoea,
over 2 days, they need to see their local doctor as soon as fatigue and peripheral oedema.
possible.54 Patients who adhere to their management plan Sleep apnoea also occurs commonly in CHF patients.
and closely monitor their daily weight may self-manage There are two types: obstructive sleep apnoea and central
their volume status by using a flexible diuretic action plan sleep apnoea. Obstructive sleep apnoea occurs due to airway
as developed by their cardiologist. In addition, patients collapse and is associated with obesity. It can be treated
 CHAPTER 10 CARDIOVASCULAR ALTERATIONS AND MANAGEMENT 293

FIGURE 10.13 Pharmacological treatment of refractory systolic heart failure.

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HUKKVUV[OH]LHU`JVU[YHPUKPJH[PVU[VIL[HISVJRLYZ

Courtesy National Heart Foundation of Australia and the Cardiac Society of Australia and New Zealand (Chronic Heart Failure
Guidelines Expert Writing Panel). Guidelines for the prevention, detection and management of people with chronic heart failure in
Australia. Updated October 2011. Melbourne: National Heart Foundation of Australia; 2011.

with weight reduction and night-time continuous positive failure and may be treated with CPAP. However, the
airway pressure (CPAP). The use of CPAP for obstructive benefits of oxygen therapy have not been proven. Exercise
sleep apnoea results in an improvement in LVEF due to is equally important, to prevent the deconditioning of
an increase in left ventricular filling and emptying rates, skeletal muscle that occurs in CHF. Exercise training
and a decrease in systolic blood pressure and left ventric- – including walking, exercise bicycle and light resistance –
ular chamber size.76 Central sleep apnoea (Cheyne–Stokes has been shown to improve functional capacity, symptoms,
respiration) occurs due to pulmonary congestion and neurohormonal abnormalities, quality of life and mood in
high sympathetic stimulation in patients with severe heart CHF.65 The Heart Foundation of Australia recommends
294 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

FIGURE 10.14 Management of heart failure with preserved ejection fraction (HFpEF).

Management of HFpEF

Is there fluid overload?* Is there an identifiable cause?

Yes No

Diuretic Treat cause

Hypertension CHD Diabetes** Cardiomyopathy

Anti-hypertensive Investigate Hypertrophic Restrictive

therapy*** suitability for cardiomyopathy— cardiomyopathy
to target revascularisation Investigate family
history

3KDUPDFRORJLFDO 3KDUPDFRORJLFDO Endomyocardial

WUHDWPHQW WUHDWPHQW biopsy for
ACEI**** Beta-blocker infiltrative diseases
Beta-blocker Calcium antagonist e.g. sarcoidosis,
Calcium antagonist amyloidosis

If no specific cause
found, consider
constrictive
pericarditis

Surgical
pericardiectomy

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>
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Courtesy National Heart Foundation of Australia and the Cardiac Society of Australia and New Zealand (Chronic Heart Failure
Guidelines Expert Writing Panel). Guidelines for the prevention, detection and management of people with chronic heart failure in
Australia. Updated October 2011. Melbourne: National Heart Foundation of Australia; 2011.

that all stable CHF patients, regardless of age, should be degree of severity of symptoms. Many CHF patients
considered for referral to a tailored exercise program have comorbidities such as arthritis, which make exercise
(preferably a heart failure-specific exercise program) or programs difficult, but maintaining general activity should
modified cardiac rehabilitation program.54 Heart failure be encouraged.
exercise programs comprise resistance training and have Dietary sodium intake should be reduced to 2 g/day
been shown to improve functional capacity, heart failure for patients with moderate-to-severe heart failure and to
symptoms and survival and reduce hospitalisations.77 In 3 g/day for mild heart failure.54 Reduction in sodium intake
patients with symptomatic heart failure physical activity helps reduce fluid retention, diuretic requirements and
should be undertaken under the supervision of trained potassium excretion. A large proportion of an individual’s
heart failure specialists, e.g. a physiotherapist or exercise sodium intake can come from processed foods, so patients
physiologist, who can tailor the level of exercise to the are encouraged to read nutrition labels and reduce the intake
 CHAPTER 10 CARDIOVASCULAR ALTERATIONS AND MANAGEMENT 295

of these foods. Salt intake can also be reduced by avoiding Pharmacotherapy in patients with heart failure is
adding salt in cooking or to meals. As CHF patients who vital, and includes an array of drugs that require careful
are overweight increase demands on their heart, weight management. Nurse practitioners are authorised to titrate
loss by lowering dietary fat intake may improve symptoms some heart failure medications, including diuretics and
and quality of life. These patients may require referral to beta-adrenergic blocking agents. Pharmacists also provide
a dietician for weight loss management. In patients with essential patient education, and support the optimisation
moderate-to-severe heart failure, cardiac cachexia and of medication treatments and management of complex
anaemia are common, which further exacerbate weakness medication schedules. Some major hospitals have a
and fatigue. These patients will require a referral to a pharmacist outreach program where a pharmacist visits
dietician for nutritional support. Other lifestyle changes the patient at home.
are: cease smoking, ideally cease alcohol intake or otherwise
limit alcohol to less than 2 standard drinks/day (alcohol is a Practice tip
myocardial toxin and reduces contractility), limit caffeinated
drinks to 1–2 drinks/day (to decrease the risk of arrhyth- When considering if a patient is suitable for palliation,
mias), control diabetes and have annual vaccinations for discussion also needs to include deactivation of their
influenza and regular pneumococcal disease vaccinations.54 pacemaker or implantable cardioverter defibrillator (ICD).
Palliative care may be appropriate for patients with
end-stage heart failure who are experiencing significant Medications
symptoms, prescribed maximal pharmacotherapy, frequent Pharmacological management relies on the following cate-
hospital admissions and poor response to treatment. It is gories of drugs: ACEIs, beta-adrenergic blocking agents,
important that all patients have an advanced care plan angiotension receptor blocking agents (ARBs), diuretics,
in place and that this has been discussed with family digoxin and antiarrhythmic drugs. (Beta-adrenergic
members. Advanced care plans should be discussed soon blocking agents and antiarrhythmic drugs are reviewed
after the patient’s first hospital admission for treatment of later in this chapter.) The main actions and adverse effects
decompensated heart failure. of these drugs in heart failure are summarised in Table 10.6.

TABLE 10.6
Common medications for the treatment of heart failure58,69

DRUG/EXAMPLE ACTION MAJOR ADVER SE EF F E CTS

F I R S T- L I N E P H A R M A C O T H E R A P Y
ACE inhibitor Decrease systemic vascular resistance by stopping angiotensin I Symptomatic hypotension
Captopril conversion to II; decreased sodium and water retention Hyperkalaemia
Enalapril Unproductive cough
Renal failure
Rash
Loop diuretics Increase urine volume by decreasing reabsorption of chloride Hypokalaemia
Frusemide and sodium Ototoxicity
Rash
Thiazide diuretics Increase urine volume by decreasing reabsorption of sodium Hypokalaemia
Chlorothiazide Hyperglycaemia
Hydrochlorothiazide Sensitivity: rash
Beta-adrenergic blockers Reduce systemic vascular resistance and heart rate by blocking Hypotension
Bisoprolol adrenoreceptors in arteries and heart Bronchoconstriction
Carvedilol
Metoprolol CR/XL
Potassium-sparing diuretics Increase urine volume by aldosterone blocking and sodium Hyperkalaemia
Spironolactone retention Rash
Gynaecomastia
ARB Block the angiotensin II receptor that responds to angiotensin II Symptomatic hypotension
Candesartan stimulation; decreased sodium and water retention. Alternative Hyperkalaemia
Irbesartan to ACEI Renal failure
SECOND-LINE PHARMACOTHERAPY
Cardiac glycosides Increase myocardial contractility and decrease heart rate by Tachycardia
Digitalis inhibiting sodium pump in myocytes AV block
Nausea and vomiting
Disorientation
Visual disturbances
296 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Angiotensin-converting enzyme inhibitors Beta-adrenergic blocking agents

ACEIs are the cornerstone of CHF treatment, as they have All patients with symptomatic systolic left ventricu-
been demonstrated to prolong survival, improve patient lar dysfunction should be prescribed a beta-adrenergic
symptoms and exercise tolerance, prevent hospitalisation blocking agent. Beta-adrenergic blocking agents (car-
and improve ejection fraction in CHF patients.78,79 All vedilol, metoprolol, bisoprolol) are used in CHF to inhibit
patients with symptomatic systolic LV dysfunction should the adverse effects of chronic activation of the sympa-
be prescribed ACEIs.1,54,59,71 Drugs in this group (captopril, thetic nervous system and improve ventricular function.
enalapril, lisinopril) act on the renin–angiotensin system In heart failure beta-2 receptors predominate with beta-1
by specifically preventing the conversion of angiotensin I receptors being downregulated. In heart failure beta-
to angiotensin II.80 As a result, systemic vascular resistance adrenergic blocking agents reduce this neurohormonal
(afterload) is decreased. This is particularly important in activity. The addition of a beta-adrenergic blocker has
preventing the progression of CHF, because blockade been demonstrated to reduce symptoms, reduce hospi-
of the renin–angiotensin system prevents further devel- talisations and prolong survival in patients.82,83 Similar to
opment of systolic dysfunction. In addition, because ACEIs the dose of beta-adrenergic blocking agents needs
angiotensin II also stimulates the release of aldosterone, to be gradually increased. Once the patient is euro-
sodium and water retention are decreased (preload). This volaemic they should be commenced on low dose and
may also be beneficial when ACEIs are prescribed with gradually increased to maximal dose over several months.
diuretics, as potassium loss is limited. Further, ACEIs In patients with COPD, selective beta-1 blockers are
inhibit the breakdown of bradykinin (a vasodilator), prescribed. Patients will require close monitoring for signs
which also contributes to decreasing vascular resistance. of deterioration of their COPD. Other adverse events are:
The total reduction of systemic vascular resistance reduces symptomatic hypotension, bradycardia and worsening heart
the workload of the heart without affecting heart rate or failure. Also, during the up-titration of beta-adrenergic
cardiac output. blocking agents many patients complain of feeling vague in
Common adverse effects of ACEIs primarily result the morning; this usually disappears after 2–3 weeks.
from hypotension, including dizziness and headache.
Other side effects include hyperkalaemia, deterioration Angiotensin receptor blocking agents
of renal function and an unproductive cough, which may The primary use of angiotensin receptor blocking agents
respond to asthma prophylactic medications. Initial doses (ARBs) is in patients who are intolerant of ACEI symptoms
of ACEIs should be low, as severe – though transient – such as ACEI cough. They have a similar action as ACEIs;
symptomatic hypotension can occur, worsening of renal however, ARBs block the angiotensin II receptor that
function and hyperkalaemia. The dose of ACEIs needs responds to angiotensin II stimulation.ACEIs, on the other
to be gradually increased to maximum dose over 2–3 hand, act on the enzyme that produces angiotensin II.80
months to optimise the survival and functional capacity They have similar benefits as ACEIs, improving survival,
benefits. This group of drugs is contraindicated in patients LVEF and heart failure symptoms and reducing hospit-
with bilateral renal artery stenosis due to the danger of alisations.84,85 Similar to ACEIs, ARBs are commenced
developing renal failure. One important adverse effect of on a low dose and gradually up-titrated to optimal dose
ACEIs is that they cannot be taken in conjunction with over 2 months. Adverse effects are: deterioration in renal
NSAIDs as NSAIDs reduce the action of ACEIs.81 function, hyperkalaemia and symptomatic hypotension.80
Diuretics
Practice tip
Diuretics are one of the mainstays of management of
A dry, non-productive cough is often associated with heart failure, primarily to decrease the sodium and water
the introduction of ACEI medication, but is often retention response to the low cardiac output state. A
mistaken for a symptom of other conditions, so patients combination of diuretics may be used if oedema persists
may not report the symptom as new. The cough usually on one diuretic. Most often, diuretics will be used in
begins within 1–2 days of commencing therapy and combination with ACEIs.
up-titration of dose. • Loop diuretics: (frusemide, ethacrynic acid and
bumetanide) act on the ascending limb of the loop
of Henle of the nephron. They prevent the reab-
Practice tip
sorption of chloride and sodium ions from the loop,
Heart failure is a disease of the elderly. Many elderly so that increased concentrations are present in the
patients have arthritis. However, elderly patients with loop, attracting more water and increasing urine
heart failure must avoid taking NSAID medications, volume. Intravenous administration of frusemide is
especially when taking ACEIs, as NSAIDs counter the often used to manage preload in acute exacerbations.
action of ACEIs. In such cases we usually recommend In fluid-overloaded patients, the aim is to achieve
taking long-acting paracetamol or glycosamine for relief increased urine output and a weight reduction of
from arthritis pain. 0.5–1 kg daily, until clinical euvolaemia is achieved.
Hypokalaemia is a common adverse effect, and
 CHAPTER 10 CARDIOVASCULAR ALTERATIONS AND MANAGEMENT 297

patients on long-term diuretics need regular both inotropic and chronotropic actions, so that cardiac
monitoring and may require potassium supplements. contractility and heart rate are both increased to improve
Hyponatraemia may also occur at high doses, and cardiac output. Continuous ambulatory infusions of
needs careful management in heart failure patients. inotropic agents such as dobutamine are administered to
Ototoxicity, presenting as tinnitus, vertigo and patients with severe heart failure as a bridge to transplan-
deafness, can occur at high doses, so IV delivery of tation, which allows these patients to be discharged home
frusemide should be no faster than 4 mg/min. with support from a home visit nurse.
• Thiazide and thiazide-like diuretics: (chlorothiazide, Cardiac glycosides
hydrochlorothiazide, chlorthalidone) act on the
Cardiac glycosides such as digitalis inhibit the sodium
ascending loop of the nephron and decrease sodium
pump such that the exchange between sodium and calcium
reabsorption. As a result, the fluid in the collecting ducts
is impaired. This results in calcium stores being released
is more concentrated and attracts more water.Thiazides
and intracellular calcium levels rising. As more calcium is
also cause peripheral arteriole vasodilation, which may
available for contraction, contractility and cardiac output
be beneficial in hypertensive patients. Adverse effects
increase. These changes in ion movement and additional
are similar to loop diuretics due to potassium and
effects, which enhance parasympathetic stimulation, result
sodium loss, and supplementation may be necessary.
in decreased impulse generation by the sinoatrial (SA)
When ACEIs are prescribed concurrently, there is less
node. This is known as a negative chronotropic effect.
potassium loss (details below). Hyperglycaemia can
Conduction is also slowed through the atrioventricular
occur, so diabetics need monitoring. Impotence may
(AV) node and ventricles, allowing more filling time, and
also occur, as well as sensitivity due to the presence of therefore having a positive effect on cardiac output. The
sulfonamide in the drug structure. negative chronotropic effects are particularly beneficial in
• Aldosterone antagonists: are potassium-sparing patients with the atrial fibrillation that is so common in
diuretics and include spironolactone.54 Aldosterone CHF. Digitalis may also affect cardiopulmonary barorecep-
acts on the distal convoluted tubule of the nephron tors to reduce sympathetic tone, which may be a valuable
to cause sodium retention and thus water retention, offset to excessive sympathetic stimulation in CHF.
although potassium is lost. Antagonists stop this action, The most important adverse effects of digoxin are
so potassium is not lost and not as much sodium caused by changes in conduction: tachycardia, fibrilla-
retained, thus there is minor diuresis. Spironolactone tion and AV block. Digoxin may also cause nausea and
is particularly useful in chronic heart failure because vomiting due to direct brain effects and gastrointestinal
there is excessive aldosterone production, causing irritation. Digitalis has a narrow margin of safety, a long
oedema. There is the potential that spironolactone, half-life and side effects that can be fatal, so assay of plasma
by blocking aldosterone systemically, may prevent the drug levels must be conducted regularly and at initiation
negative effects of aldosterone on the heart, such as and change of treatment. Excessive digoxin causes disori-
fibrosis, hypertrophy and arrhythmogenesis. Adverse entation, hallucinations and visual disturbances. Potassium
effects include hyperkalaemia, which may occur more levels directly alter the effect of digoxin, so that low levels
readily in CHF patients because of renal failure, and enhance effects and high levels reduce effects.
because of its potentially lethal effects spironolactone Arrhythmias are common in heart failure and need to
requires regular monitoring. Other effects include be treated. The agent must be carefully selected, as chronic
hyponatraemia and feminisation effects such as heart failure patients often have complex medication
gynaecomastia. In patients with HFpEF, spironolactone regimens and interactions may occur. Also, some ventricu-
has been shown to reduce heart failure-related lar antiarrhythmics, such as class 1 agents (e.g. flecainide), are
hospitalisations.86 Spironolactone is recommended associated with sudden death in CHF. Implantable cardio-
for use in patients with severe symptomatic (NYHA verter-defibrillator (ICD) therapy may be more effective
class III–IV) systolic heart failure in addition to in treating ventricular arrhythmias. ICDs reduce mortality
other pharmacotherapy such as ACEIs. Aldosterone by 20–30%89 and are first-line therapy in patients with a
antagonists have additional survival benefits and reduce history of VF or sustained VT, LVEF ≤30% with NYHA
hospital readmission.87,88 class II–III, at least 40 days post-myocardial infarction, and
prescribed optimal pharmacotherapy or NYHA class I with
Inotropic agents LVEF ≤35% and prescribed optimal pharmacotherapy.66
This category of drugs increases cardiac contractility. The Cardiac resynchronisation therapy (CRT) (also known as
group includes cardiac glycosides (digoxin) and dopamine biventricular pacing) is also indicated in patients with symp-
agonists (dopamine, dobutamine), sympathomimetics tomatic heart failure to reduce asynchronous pacing of the
(adrenaline, noradrenaline) and calcium sensitising agents left ventricle (QRS duration >150 ms).71 Systolic function
(levosimendan). Inotropes are used as IV infusions in is improved when the left and right ventricles are paced
severe heart failure, acute exacerbations of chronic heart simultaneously. Often patients with a prolonged QRS will
failure and for palliative care or bridging to transplant have a combination of an ICD with CRT therapy. ICDs
in very severe chronic heart failure. These drugs have and CRT are discussed in more detail in Chapter 11.
298 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

In severe heart failure, when patients do not respond to when filling pressures are increased due to the recumbent
pharmacological treatment, mechanical measures such as position of sleeping.54 Diuretics should be administered
cardiopulmonary bypass and left ventricular assist devices intravenously to optimise the excretion of intra- and extra-
may be used. In appropriate candidates, cardiac transplant vascular cellular fluid to reduce circulating blood volume
may also be an option. These procedures are covered to reduce cardiac workload. Fluid restriction, usually to
under cardiac surgery. 1–1.5 L in 24 hours, is begun. A urinary catheter may
need to be inserted so that accurate, continuous measures
Acute exacerbations of heart failure of urine output can be gained and an accurate fluid
Acute exacerbations of CHF usually occur as episodes balance calculated. This is necessary, along with consistent
of decompensation due to progression of the disease or daily weighing, to determine the effectiveness of diuretic
non-adherence to the management plan.90 Acute episodes therapy and renal status.Various positive inotropes may be
usually present as congestive heart failure with associated administered (e.g. IV dobutamine causes vasodilatation; IV
pulmonary oedema, cardiogenic shock (see Chapter 21) dopamine improves renal function) to improve contractil-
or decompensated CHF.54 Patients with severe dyspnoea ity and reduce systemic venous return.Various mechanical
due to pulmonary congestion should be administered devices are also available, e.g. intra-aortic balloon pump,
oxygen therapy. If their hypoxaemia does not improve, LVAD (discussed in Chapter 12). CRT with or without an
they may benefit from bilevel positive airway pressure ICD may be implanted. CRT is recommended in NYHA
(BiPAP) to support ventilation and gas exchange. The use class II–III or ambulatory class IV patients on optimal
of continuous positive airway pressure ventilation (CPAP) pharmacological therapy, LVEF ≤35%, left bundle branch
or BiPAP in acute pulmonary oedema will reduce the block with a QRS duration >150 ms, and sinus rhythm.71
need for intubation and mechanical ventilation. All of these criteria must be fulfilled. Criteria for implant-
The mainstay of treatment of an acute exacerbation ation of an ICD include: symptomatic patients (NYHA
is pharmacological, so a combination of the medications class II–IV) and LVEF ≤35%, LVEF <30% at least 40 days
is given, usually comprising diuretics, morphine and post AMI.71 If a patient is to have an ICD implanted,
nitrates. The nitrates and morphine cause vasodilatation. extensive counselling pre- and post-implantation must
Morphine also reduces the respiratory drive and respi- be undertaken with the patient and carer to ensure they
ratory workload. Nitrates also cause epicardial artery are aware of the painful and unexpected shocks that may
dilatation and reduce preload, which also helps to relieve be delivered.54,71 Figure 10.15 provides an overview of the
symptoms of pulmonary congestion particularly at night escalation of treatment for acute heart failure.54

FIGURE 10.15 Emergency therapy of acute heart failure.

Ventricular assist devices

Intra-aortic balloon counterpulsation

Assisted ventilation

CPAP

Positive inotropes

Morphine

Vasodilators

Diuretics

Oxygen

Courtesy National Heart Foundation of Australia and the Cardiac Society of Australia and New Zealand (Chronic Heart Failure
Guidelines Expert Writing Panel). Guidelines for the prevention, detection and management of people with chronic heart failure in
Australia. Updated October 2011. Melbourne: National Heart Foundation of Australia; 2011.
 CHAPTER 10 CARDIOVASCULAR ALTERATIONS AND MANAGEMENT 299

Most patients in acute heart failure have poor diuretics and antiarrhythmic therapy where indicated
perfusion of the gastrointestinal system and, combined or, if necessary, an ICD for recurrent haemodynamically
with dyspnoea, a resultant limited appetite. Small, easily significant ventricular arrhythmias.91 The use of cardiac
ingested meals are best. While the patient is on bedrest, resynchronisation therapy (CRT) has produced significant
nursing care to prevent problems related to immobility is clinical improvements and is recommended for DCM
important. Skin care is particularly important, as poor skin patients with NYHA functional class II–III or ambulatory
perfusion and oedema place the CHF patient at higher class IV, optimal medical therapy, LVEF ≤35% and sinus
risk of skin breakdown. rhythm with left bundle branch block with a QRS >150
ms.71 Cardiac transplantation is considered when standard
Selected cases therapies fail to influence clinical progression and left
ventricular assist devices and ICDs may be used as a bridge
Cardiomyopathy to transplantation.
As the term implies, the cardiomyopathies are primary
disorders of the myocardium in which there are systolic,
Hypertrophic cardiomyopathy
diastolic or combined abnormalities. Classification of Hypertrophic cardiomyopathy (HCM) is a genetic
the most common forms of cardiomyopathy is made on abnormality that gives rise to inappropriate hypertrophy
the basis of the dominant abnormality, which may be especially in the intraventricular septum with preserved
dilation, hypertrophy or restricted filling. However, each or hyperdynamic systolic function. The main abnormality
has different haemodynamic effects and therefore requires with HCM is diastolic rather than systolic as in DCM.The
different treatment. hypertrophy is not a compensatory response to excessive
load, such as in aortic stenosis or hypertension. Left
Dilated cardiomyopathy ventricular hypertrophy of variable patterns is seen, occa-
Dilated cardiomyopathy (DCM) is the most common sionally with disproportionate septal hypertrophy, which
form of cardiomyopathy and is characterised by ventric- causes left ventricular outflow tract obstruction in which
ular and atrial dilation and systolic dysfunction.91 All four HCM progresses to hypertrophic obstructive cardiomy-
chambers become enlarged, which is not in proportion opathy, or HOCM. In HCM the muscle mass is large and
to the degree of hypertrophy. It presents as heart failure hypercontractile, but the left ventricular cavity is small.
of variable severity, sometimes complicated by thrombo- The increase in left ventricular systolic pressure and the
embolism, at least partly due to atrial fibrillation, which altered relaxation cause diastolic dysfunction and impaired
is common. Conduction abnormalities are common in ventricular filling. Mitral regurgitation is common. These
DCM further exacerbating AV dyssynchrony and left abnormalities combine to produce pulmonary congestion
ventricular dysfunction. DCM is the most common cause and dyspnoea due to raised end-diastolic pressure. Sudden
of sudden cardiac death due to ventricular arrhythmias. cardiac death, often after exertion or other increases in
Annual mortality from DCM ranges from 10–50%.91 contractility, is sometimes seen in HCM and is thought
Idiopathic DCM is the most common cause of heart to be partly attributable to outflow obstruction.71 It is the
failure in young people. Aetiology of DCM includes most common cause of death in athletes.71
coronary heart disease, myocarditis, cardiotoxins, genetics
and alcohol misuse.
Diagnosis
Echocardiography will confirm the presence and pattern
Diagnosis of hypertrophy and the presence (or absence) of an outflow
Many of the features of DCM are non-specific. Heart tract gradient. Examination findings include cardiomegaly
failure, as mentioned, is present with typical symptoms of and pulmonary congestion. An S4 heart sound is common,
dyspnoea, fatigue, peripheral oedema and cardiomegaly. and the ECG shows left ventricular hypertrophy and
S3 and S4 heart sounds may be present on auscultation. often ventricular arrhythmias. When the obstructive form
Atrial and ventricular arrhythmias are common, particu- hypertrophic obstructive cardiomyopathy (HOCM) is
larly atrial fibrillation, ventricular tachycardia, ventricular present, a systolic murmur, mitral regurgitation murmur
fibrillation and torsades de pointes. Left bundle branch and deep narrow Q waves on ECG may be present.91 The
block (LBBB) is often present, which worsens systolic majority of patients are asymptomatic and, when they
performance and shortens survival, especially when the present to hospital, it will be with severe symptoms of
QRS interval is markedly prolonged.91 Echocardiogra- dyspnoea, angina and syncope. Angina is the result of an
phy demonstrates the defining abnormalities and may be imbalance between oxygen supply and demand due to the
useful in revealing atrial thrombus. Occasionally, endocar- increased myocardial mass and not due to atherosclerosis.
dial biopsy is undertaken to differentiate from myocarditis
or rarer causes of cardiomyopathy. Patient management
Treatment for HCM is aimed at the prevention of sudden
Patient management cardiac death and pharmacotherapy to increase diastolic
Treatment for DCM is similar to that of heart failure filling and to reduce the left ventricular outflow tract
and includes beta-adrenergic blocker therapy, ACEIs, obstruction. Pharmacotherapy includes beta-adrenergic
300 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

blocker or calcium channel blocker therapy, as these Patient management

decrease contractility and lessen outflow tract obstruction. There is no treatment for RCM so the aim of therapy is to
Care is necessary with medication selection, as vasodila- relieve symptoms. This includes diuretics, corticosteroids
tion may worsen obstruction, causing haemodynamics and pacing. The use of nitrates should be initiated with
to suffer.91 The impact of atrial fibrillation, by worsening caution as the filling defect can be worsened by decreased
the ventricular filling defect, can be dramatic in HCM venous return or hypovolaemia. Generally, prognosis is
patients and will require antiarrhythmics and anticoagu- poor with many dying within 1–2 years of diagnosis.91
lation. If ventricular arrhythmias are present, or there is
a family history of sudden cardiac death, treatment with Hypertensive emergencies
an ICD should be considered.92 For severely symptom- Acute, uncontrolled hypertension is often divided into
atic patients or those worsening despite maximal drug two categories: hypertensive emergencies and hyperten-
treatment, surgical myectomy to reduce the size of the sive urgencies. In hypertensive emergencies blood pressure
septum and lessen obstruction may be necessary and can needs to be reduced within 1 hour to prevent end-organ
result in a marked improvement of symptoms.92 Septal damage, such as hypertensive encephalopathy, papill-
ablation with alcohol injected into the first septal branch oedema or aortic dissection.93 Immediate blood pressure
of the left anterior descending artery is a less invasive reduction with IV agents under critical care monitoring
alternative, a procedure that is usually undertaken with is needed. By contrast, hypertensive urgencies are those in
pacemaker insertion as AV block is produced. Although which end-organ damage is not occurring and, although
surgical myectomy remains the gold standard, both prompt management is required, this can be approached
treatments provide effective symptom relief and improve- more gradually with oral antihypertensive agents under
ment in heart failure severity.92 If the patient with HCM close supervision, without necessarily requiring admission
deteriorates and is hospitalised, positive inotropes, chro- to a critical care unit.93 Previous hypertension is not always
notropes and nitrates worsen left ventricular outflow present, but because of chronic adaptive vascular changes
tract obstruction and should be avoided. However, beta- may provide some level of protection against acute
adrenergic blockers, amiodarone and calcium antagonists tissue injury. Symptoms may not develop until the blood
such as verapramil are indicated.91 Due to the familial pressure exceeds 220/110 mmHg, whereas in patients
nature of HCM, relatives aged 12–18 years also need to be without previous hypertension, hypertensive emergencies
screened for HCM. may occur at levels of even 160/100 mmHg.94 When the
diastolic pressure is persistently above 130 mmHg, there is
Restrictive cardiomyopathy risk of vascular damage and it must be treated.
Restrictive cardiomyopathies (RCMs) limit diastolic
distensibility or compliance of the ventricles. The stiff Diagnosis
ventricular walls produce diastolic dysfunction and there A thorough history is taken, including any hyper-
is impaired ventricular filling. Infiltrates into the inter- tension management, known renal or cerebrovascular
stitium and the replacement of normal myocardium with disease, eclampsia in previous pregnancies if gravid or
abnormal tissue hamper this relaxation.91 Initially, systolic use of stimulants or illicit drugs such as cocaine. Patient
function and wall thickness are normal. However, as the assessment should include evidence of: end-organ damage,
disease progresses systolic dysfunction occurs. RCM is such as back pain (aortic dissection); neurological damage,
commonly caused by myocardial infiltration, as in amyloid- such as headache, altered consciousness, confusion, visual
osis, sarcoidosis, fibrosis or cardiac metastases, or may be loss, stupor or seizure activity (encephalopathy); cardiac
idiopathic. Endomyocardial disease is more common in damage, such as chest pain, ST-segment changes, cardiac
tropical countries, but in the Western world, RCMs are enlargement or the development of heart failure or
the least common form of cardiomyopathy.91 pulmonary oedema; and renal damage, such as oliguria and
azotaemia.93 Serum urea, creatinine, electrolytes, urinalysis,
Diagnosis ECG and chest X-ray should be performed.
Clinically, there is heart failure (increase in JVP, dyspnoea,
S3 and S4 heart sounds and oedema), particularly right Patient management
ventricular, and infiltration of the conduction system may More severe, or malignant, hypertension may cause retinal
cause conduction defects and heart block. Low-voltage haemorrhage or papilloedema, and emergency treatment
ECGs are commonly seen. Patients commonly present with should immediately be instituted. Other contexts in which
decreased exercise tolerance due to the impaired ability to there is a need for rapid treatment of severe hypertension
increase heart rate and cardiac output because of reduced include intracranial bleeding, acute myocardial infarction,
ventricular filling. RCM must be distinguished from phaeochromocytoma, recovery from cardiac surgery and
constrictive pericarditis (which it may closely resemble), bleeding from vascular procedure sites. Hypertensive
as pericarditis may be easily managed.91 If echocardiogra- emergencies in pregnancy threaten both the mother and
phy demonstrates a restrictive pattern, a myocardial biopsy the fetus.95
may be undertaken to determine its aetiology, especially in The aim of treatment is to acutely lower the blood
the case of systemic infiltrative disease. pressure, but neither too quickly nor too dramatically.
 CHAPTER 10 CARDIOVASCULAR ALTERATIONS AND MANAGEMENT 301

Recommendations vary, but an initial aim of 150/110– valve structures), producing valvular stenosis or regurgi-
160/100 mmHg within 2–6 hours, or a 25% reduction tation.100 The mitral valve is more commonly affected,
in mean arterial pressure within 2 hours, has been but aortic valve involvement carries a worse prognosis.98
described.96,97 Continuous direct arterial pressure Conduction system involvement manifests as arrhyth-
monitoring should be in place during treatment. Intra- mias and conduction defects. Embolic complications
venous sodium nitroprusside, a rapidly acting arterial are relatively common and multifactorial. Septic emboli,
and venous dilator, is most frequently used, at doses of embolisation of atrial thrombi when atrial fibrillation
0.25–10 mcg/kg/min.97 Weaning of nitroprusside is is present and fragmentation of vegetations may all give
undertaken after the later introduction of oral antihyper- rise to pulmonary and systemic emboli. These most often
tensives. Care is required to avoid hypotension during present as splenic infarction, stroke, peripheral vascular
treatment, as well as rebound hypertension as nitroprus- occlusion and renal failure.98
side is withdrawn. Rapidly acting beta-adrenergic blocking
agents with short half-lives, such as IV esmolol, may be Diagnosis
used at doses of 50–100 mcg/kg/min (or higher) in Diagnosis of infective endocarditis is based on the modified
patients without standard contraindications to beta-adren- Duke criteria.100 These are based on the presence of micro-
ergic blockers (asthma, heart failure).97 Glyceryl trinitrate organisms (identified in blood cultures), pathological
infusions at 10–100 mcg/min or higher are used for lesions (vegetation or abscess present) and clinical criteria.
combined venous and arterial dilation, especially if there is The clinical criteria are based on two major criteria or
angina.97 Intravenous frusemide may be introduced during one major and three minor criteria or five minor criteria.
the acute phase. After intravenous therapies have been Major clinical criteria are:
established and progress towards target pressures is made, • positive blood culture
oral agents are introduced.These include oral beta-adrener-
gic blockers, calcium channel blockers, ACEIs and diuretics. • evidence of endocardial involvement (positive
echocardiography, abscess, partial dehiscence of a
Infective endocarditis prosthetic valve or new valvular vegetation).
Infective endocarditis remains a potentially life-threatening Minor clinical criteria include:
disorder, with mortality remaining as high as 20–25%98 even • fever with body temperature ≥38°C
in this era of relative rheumatic fever control. This same
era, however, sees other means of developing endocarditis,
• predisposing heart condition or intravenous drug use
with factors such as longer life, IV drug use, prosthetic • vascular signs: arterial emboli, intracranial haemor-
valves, greater rates of cannulation during hospitalisation, rhage, Janeway lesions (erythematous spots on the
cardiac surgery, resistant organisms and increased numbers palms and feet) or conjunctival haemorrhages
of immunocompromised patients from immunosuppres- • immunological signs: Osler nodes (painful,
sant drugs and human immunodeficiency virus/acquired reddened nodules on the fingers and the feet)
immune deficiency syndrome HIV/AIDS.99,100 or glomerulonephritis.98
Infection of the endocardium, often with involve- Echocardiography may reveal vegetations, abscess and
ment of the cardiac valves, occurs most commonly due valvular abnormalities, but endocarditis is more a clinical
to staphylococcal, streptococcal and enterococcal bacte- diagnosis based on the appearance of febrile illness, positive
raemia.99,100 The definition of infective endocarditis now blood cultures with organisms known to cause endocard-
also includes an infection of any structure within the itis, new murmur and vascular features.
heart such as prosthetic valves, implanted devices and
chordae tendineae.101 Infective endocarditis can be acute Patient management
or subacute. Acute infective endocarditis progresses over Prosthetic valve endocarditis must be aggressively
days to weeks with destruction of valves and metastatic managed, as mortality may be as high as 65%.100 Impaired
infection. Subacute infective endocarditis occurs over valvular opening, even obstruction, may occur or the
weeks to months and is milder than acute infective prosthetic valve may become unseated. Reoperation to
endocarditis. Endothelial damage occurs in the endocar- replace the affected valve should be undertaken when
dium. Platelet-fibrin deposits form and a lesion develops. valvular dysfunction is present. Antibiotic therapy is
Bacterial colonisation then occurs and vegetation adheres provided empirically until blood culture and sensitiv-
to the endocardial lesion. Many of the signs and symptoms ities are established. Cardiac failure, if present, is managed
of infective endocarditis are due to the immune response along standard lines (see section on nursing management
to the microorganism. The patient presents with fever, of acute heart failure). Observations during endocarditis
and general features of febrile illness, which may include should be directed at detecting embolic complications
septic shock. Joint pain is common and septic arthritis involving the brain, kidneys, or spleen; development and
is sometimes seen. Cardiac symptoms develop when progress of heart failure; progress of the febrile illness,
there is valvular involvement, which may manifest as including hydration and dietary status.
erosion through valve leaflets producing regurgitation, Prophylactic antibiotic coverage should be undertaken
fusing of valve leaflets or vegetations (outgrowths from for at-risk patients 1 hour before dental procedures are
302 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

to be performed, in particular for those with previous particularly susceptible to aneurysm formation because of
rheumatic fever or endocarditis, or prosthetic valves.101 constant stress on the vessel wall and the absence of pene-
Antibiotic prophylaxis for genitourinary and gastrointesti- trating vasa vasorum that normally provide perfusion to
nal procedures is no longer recommended.101 the adventitia. As the blood flows through the aneurysm
it becomes turbulent and some blood may stagnate along
Aortic aneurysm the walls, allowing a thrombus to form. This thrombus
The aorta is the major blood vessel leaving the heart. An in addition to atherosclerotic debris may embolise
aneurysm is a local dilation or outpouching of a vessel into the distal arteries compromising their circulation.
wall and comes in several forms (see Figure 10.16).28 Most Atherosclerosis is the commonest cause of aneurysm,
aortic aneurysms are fusiform and saccular, and occur in because plaque formation erodes the vessel wall. Other
the abdominal aorta. A fusiform aneurysm is uniform in causes include syphilis, infection, inflammatory diseases
shape with symmetrical dilation that involves the whole and trauma. Aneurysms occur most often in men and in
circumference of the aorta.102 A saccular aneurysm has people with the risk factors of hypertension or smoking.
dilation of part of the aortic wall so the dilation is very Approximately 80% of aortic aneurysms rupture into
localised.102 A dissecting aneurysm occurs when the layers the left retroperitoneum, which may contain the rupture.
of the wall of the aorta continue to separate and fill with However, the other 20% rupture into the peritoneal cavity
blood, resulting in obstructed blood flow. The aorta is and uncontrolled haemorrhage results.102
Patients often experience no symptoms until the
FIGURE 10.16 Aneurysm. Major types of aneurysm: aneurysm is extensive or ruptures. Clinical presentation
(A) fusiform aneurysm has an entire section of an artery varies and depends on the location and expansion rate.
dilated, occurring most often in the abdominal aorta due Aneurysms of the ascending aorta tend to affect the aortic
to atherosclerosis; (B) sacculated aneurysm affects one root and cause valve regurgitation. Expansion of the
side of an artery, usually in the ascending aorta; aneurysm may also compress the vena cavae, leading to
(C) dissecting aneurysm results from a tear in the intima, engorged neck and superficial veins, or compress the large
causing blood to shunt between the intima and media;
airways, causing respiratory distress. The first symptom
(D) pseudoaneurysm usually results from arterial trauma,
such as intra-aortic balloon pump catheter or an arterial
most patients experience is pain, which may be steady
introducer; the opening does not heal properly and is and continuous from local compression or sudden and
covered by a clot that can burst at any time.28 severe in the case of dissection or rupture, usually in the
lower back. In this case, the pain is usually associated with
syncope and is an acute emergency. Depending on the site
$UWHU\
of the aneurysm, there is usually an absence or decrease in
the pulses below the site of the aneurysm, most commonly
in the limbs. The renal arteries may be affected, resulting
in decreased urine output and renal failure. The spinal
blood flow may also be affected, resulting in paraplegia
$ )XVLIRUPDUHD and, if the carotid arteries are affected, there may be altered
$UWHU\ consciousness. Infrarenal aneurysms are the most common
form of aortic aneurysm and are located below the renal
arteries. Bruits can also be heard over the aneurysm.
Diagnosis
A chest X-ray is usually the first investigation, and may
% 6DFFXODWHGDUHD reveal a widened mediastinum or enlarged aortic knob.
Some aneurysms will be hidden, so normal chest X-ray
7RUQLQWLPD does not exclude the diagnosis. If available, a CT scan,
)DOVH using contrast dye, provides accurate information on the
%ORRG FKDQQHO location and size of the aneurysm.Transoesophageal echo-
IORZ FUHDWHG cardiography (TOE) provides an accurate diagnosis and is
the preferred investigation in dissecting aneurysms. TOE
& can clearly identify the tear/flap, to enable classification of
5XSWXUHGDUHDZLWK the aneurysm. There are some limitations in viewing the
FORWFRYHULQJWKH ascending aorta, and patients with respiratory dysfunction
RSHQLQJ may have difficulty with lying flat for the procedure and
%ORRG
having a light anaesthetic.
IORZ
Patient management
' Management of asymptomatic aneurysms is conservative,
unless the size of the aneurysm is >1.5 times the normal
 CHAPTER 10 CARDIOVASCULAR ALTERATIONS AND MANAGEMENT 303

size of the aortic segment102 or the situation is acute. The Ventricular aneurysm
primary aim is to lower hypertension and prevent increases
Less than 5% of patients post-STEMI, particularly a
in thrombus size and emboli through the administration
transmural anterior infarction, develop a left ventricular
of aspirin. Usually, the patient has regular monitoring to
aneurysm.103 Post-STEMI, dyskinetic or akinetic areas of
assess the aneurysm and to determine the timing and need
the left ventricle are common and known as regional wall
for surgical repair.
motion abnormalities. It is in these areas that there is a
Acute and dissecting aortic aneurysms are life-threat-
risk of an aneurysm developing.Ventricular aneurysms are
ening emergencies, and surgery is often the only option.
more likely to develop post-anterior STEMI with a totally
The development of new or worsening lower back pain
occluded LAD with poor collateral circulation.
may indicate impending rupture and there may be a
Aneurysms form when the intraventricular tension
palpable pulsatile abdominal mass. The faster treatment is
stretches the dyskinetic area and a thin, weak layer of
initiated, the higher the chances of survival with optimal
necrotic muscle and fibrous tissue develops and bulges with
recovery. The primary goal is to control blood pressure. If
each contraction of the ventricle resulting in a reduction in
hypertensive, beta-adrenergic blockers or sodium nitro-
stroke volume. Aneurysms range from 1–8 cm in diameter
prusside is used to reduce further arterial wall stress. If
and are four times more likely to occur at the apex and
the patient is hypotensive, IV fluid and inotropes may be
anterior wall rather than the inferoposterior wall.103 Large
necessary.
ventricular aneurysms may result in a reduction in stroke
Nursing management of dissecting aortic aneurysm
volume causing an increase in myocardial oxygen demand
involves the following:
resulting in angina and heart failure. The mortality rate in
• support during the diagnostic phase people with ventricular aneurysms is four times higher
• assessment of pain and provision of analgesia than those with no aneurysm due to a higher risk of
• stabilising and monitoring the clinical condition tachyarrhythmias and sudden cardiac death. Unlike
aortic aneurysms these aneurysms rarely rupture so their
• providing psychological support to patient and management is usually conservative.
family
• preparation for surgery and long-term care. Diagnosis
Assessment of the patient’s symptoms and effects of Diagnosis of a ventricular aneurysm is by echocardi-
the aneurysm is essential.This includes careful assessment ography. Ventricular aneurysm should be considered
and recording of symptoms, including pain level and when ST-segment elevation persists beyond 1 week after
intensity, peripheral pulses, oxygen saturation levels, myocardial infarction.
blood pressure in both arms and neurological symptoms
to assist with diagnosis and detect progression. Intra- Patient management
venous analgesia is essential to control the severe pain, Management of a left ventricular aneurysm consists of
and an antiemetic is useful to prevent opiate side effects. aggressive management of STEMI and reperfusion therapy.
Opiates may also contribute to a sedative effect and Long-term anti-coagulation therapy with warfarin is
slight vasodilation, which are both beneficial. Oxygen required. A complication of a ventricular aneurysm
therapy via mask should be administered as indicated by includes the development of an intraventricular thrombus
oxygen saturation levels. Blood pressure control is vital, within the aneurysmal pocket which, if mobilised,
and usually IV medications are titrated to a narrow MAP becomes arterial emboli. Also due to the high risk of
range of 60–75 mmHg. Close observation of fluid balance tachyarrhythmias, antiarrhythmic therapy is indicated. An
to detect changes in renal perfusion and maintain appro- ICD may also be necessary if antiarrhythmic therapy is
priate blood volume is also essential. Finally, preparation unsuccessful in suppressing tachyarrhythmias. Surgical
for surgery is necessary, and must include the patient aneurysmectomy may also be required, if heart failure and
and family. angina become severe, and is usually successful.

Summary
Compromise of the cardiovascular system, as either a primary or secondary condition, is a common problem that necessi-
tates admission of patients to a critical care area. Prompt and appropriate assessment and treatment are required to ensure
adequate oxygen supply to the tissues throughout the body. The most common cardiovascular problems experienced by
patients include coronary heart disease, arrhythmias and cardiogenic shock; however, heart failure and selected conditions
such as cardiomyopathies, hypertensive emergencies, endocarditis and aortic aneurysm also occur. Appropriate assessment
and management are essential to prevent secondary complications arising. Important principles covered in this chapter
are summarised below.
• Coronary heart disease:
Incorporates myocardial ischaemia, angina and acute coronary syndrome.
Early patient assessment and diagnosis are essential to facilitate prompt intervention.
304 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Initial diagnosis is based on history, clinical assessment, electrocardiographic and biochemical examination, with
coronary angiography, exercise testing and chest radiography available to provide later detail.
Early restoration of blood flow – including reperfusion therapy and coronary angioplasty – to reduce myocardial
damage is a core component of treatment.
Other goals of care include reducing plaque and clot formation in coronary arteries, reducing the workload of
the heart, controlling symptoms, providing psychosocial support to the patient and family and educating the
patient about the disease process, lifestyle and future responses to illness.
• Heart failure:
May affect either the left, right or both ventricles, resulting in different symptoms being displayed by the patient.
Diagnosis is usually made on the basis of echocardiography, ECG, chest X-ray, full blood count, electrolytes, liver
function tests and urinalysis.
In acute heart failure, CPAP or BiPAP may be necessary to improve hypoxaemia.
Pharmacological therapy of acute heart failure consists of morphine, nitrates and diuretics. Positive inotropes may
also be used, such as IV dopamine and dobutamine, to improve renal perfusion and contractility.
Many patients with heart failure will also have a pacemaker with cardiac resynchronisation therapy and/or a
defibrillator to improve cardiac function and reduce the incidence of sudden death.
Patient care must be lifelong and coordinated between all members of the healthcare team. Broad interventions,
including medications, diet and lifestyle modification, may be appropriate for some patients, while palliative care
might be more appropriate for other patients.

Case study
Ms Patel is a 60-year-old woman who presented to the emergency department with intermittent chest
pain. She presented to her general practitioner (GP) 2 days ago complaining of intermittent chest pain over
a 2–3 hour period. An ECG was done showing old Q waves anteriorly and ST depression in V5 and V6.
A troponin-I was done by her GP that was 0.16 mcg/L.
Her past medical history included: diabetes mellitus type 2, infrarenal abdominal aortic aneurysm, asthma/
COPD, peripheral vascular disease, hypercholesterolaemia and hypertension. Her medications consisted
of: diamicron 60 mg daily, glargine 26 units nocte, perindopril 5 mg daily, seretide and ventolin puffers and
lipitor 20 mg daily.
One day after visiting her GP, she presented to the emergency department with further intermittent chest
pain and upper abdominal pain. Initial 12-lead ECG showed ST elevation in leads II, III and aVF. She was
also feeling very tired and nauseated at times. She denied any chest pain. She was afebrile, BP 143/96
mmHg, pulse 120 bpm and regular, respiratory rate 33 bpm and O2 sat 91% on room air. Her respiration
was laboured and her skin was cool and clammy. On chest auscultation there were bibasal crackles to
mid-zones. Her jugular venous pressure was +5 and she had peripheral oedema to lower calves. She had
dual heart sounds (S1, S2) and a third heart sound (S3). U&E blood test results included: Na 134 mmol/L,
K 5.1 mmol/L, urea 5.2 mmol/L, creatinine 86 mcmol/L, ctroponin-I 2.0 mcg/L, CK 590 U/L and random
glucose 9.2 mmol/L. Her FBE and LFTs were normal. Fast-track treatment was commenced, including
administering aspirin 300 mg orally, oxygen via mask 6 L/min, glyceryl trinitrate patch, morphine 2.5 mg IV,
metoclopramide 10 mg IV and frusemide 40 mg IV. Chest X-ray showed horizontal linear interstitial
opacities at both bases, which were not present on a previous X-ray taken 6 months ago, which
was consistent with the clinical impression of pulmonary oedema. There was also a marked increase
in the size of the heart, which also had a slightly globular configuration. There was no evidence of a
pericardial effusion.
Within a short time her acute pulmonary oedema was stabilised and so she was considered for a primary
PTCA. Coagulation profiles and a brief history of, and contraindications to, fibrinolytic treatment were
collected. Preparation for PTCA included locating, assessing and marking peripheral pulses in both right
leg and right arm. The coronary angiogram report stated: moderate-to-severe reduction in left ventricular
function, ejection fraction 30%; intact left circumflex artery, intact left main coronary artery with minor
irregularities (30%) in left anterior descending artery; and severe localised 70–80% stenosis within the
proximal third of the right coronary artery and collaterals from the left coronary artery. Her right coronary
artery was the dominant vessel. The stenosis was dilated by PTCA with resulting TIMI 3 flow, and a paclitaxel
drug-eluting stent was placed.
 CHAPTER 10 CARDIOVASCULAR ALTERATIONS AND MANAGEMENT 305

Post-PTCA, Ms Patel was admitted to CCU with oxygen via mask, PTCA access site and sheath in her
right groin. Her observations included: BP 100/60 mmHg, HR 80 beats/min, RR 20/min. She was free of
pain. Her ECG was normal except for T inversion in lead III with a generalised widened QRS (200 ms).
Post-PTCA she experienced short runs of ventricular tachycardia. These were initially thought to be due
to reperfusion arrhythmias. However, the short intermittent runs of ventricular tachycardia continued.
Her blood test results were: Na 137 mmol/L, K 4.6 mmol/L, urea 8.8 mmol/L, creatinine 99 mcmol/L,
calcium 2.37 mmol/L, magnesium 0.96 mmol/L. Fasting cholesterol profile: total cholesterol 4.3 mmol/L,
HDL-C 1.91 mmol/L, LDL-C 2.1 mmol/L, triglycerides 0.7 mmol/L, cholesterol/HDL-C 2.3 mmol/L. Her liver
function and full blood examination tests were normal. She was commenced on an intravenous amiodarone
infusion and considered for an ICD with CRT, in light of her newly diagnosed heart failure (evident on
coronary angiogram) and NYHA class III symptoms.
Post-ICD-implantation, her hospital stay was uneventful. Her fluids were restricted to 1.5 L/day, and she
was weighed daily, commenced a beta-adrenergic blocking agent and diuretic and was provided with
education concerning heart failure and coronary artery disease. Her husband was also included in the
education sessions. She was transferred from CCU to the ward and then a few days later discharged
home. On discharge her medications were: bisoprolol 5 mg daily, perindopril 5 mg daily, spironolactone
25 mg daily, co-plavix 100/75 mg daily, spirivia 18 mcg daily, seretide 250/25 mg BD, lantus 36 units nocte,
amiodarone 200 mg BD, gliclazide MR 60 mg mane, frusemide 80 mg mane and midi and GTN spray. She
was also referred to a heart failure management program and a cardiac rehabilitation program.

CASE STUDY QUESTIONS

1 Identify the key indicators of ST-elevation myocardial infarction (STEMI).
2 Discuss the use of oxygen in acute myocardial infarction.
3 Identify the common complications of myocardial infarction in the early recovery period.
4 What is the significance of an S3 heart sound in the clinical setting of heart failure?
5 What criteria might have been considered when deciding to implant an ICD with CRT in Ms Patel?
6 When the patient was discharged from hospital, why was she prescribed perindopril, bisoprolol,
spironolactone and frusemide? Include in your answer the reason for prescribing these medications
and their actions and major side effects.

RESEARCH VIGNETTE

Dizon JM, Brener SJ, Maehara A, Witzenbichler B, Biviano A, Godlewski J et al. Relationship between ST-segment
resolution and anterior infarct size after primary percutaneous coronary intervention: analysis from the
INFUSE-AMI trial. Eur H J Acute Cardiovasc Care 2014;3:78–83

Abstract
Objective: ST-segment resolution after reperfusion therapy has been shown to correlate with prognosis in patients
with ST-segment elevation myocardial infarction (STEMI). We investigated whether acute ECG measurements also
correlate with ultimate infarct size.

Methods: The INFUSE-AMI trial randomized 452 patients with anterior STEMI to intracoronary bolus abciximab
vs. no abciximab, and to thrombus aspiration vs. no aspiration. Infarct size as percentage of total LV mass was
calculated by cardiac magnetic resonance imaging (MRI) 30 days post intervention. Five ECG methods were
analysed for their ability to predict MRI infarct mass: 1) summed ST resolution across all infarct-related ECG leads
(ΣSTR); 2) STR in the single lead with maximum baseline ST-segment elevation (maxSTR); 3) summed residual
ST-segment elevation across all infarct-related leads at 60 min post intervention (ΣST residual); 4) maximum
residual ST-segment elevation in the worst single lead at 60 min post intervention (maxSTresidual); 5) number of
new significant Q-waves (Qwave) at 60 min.

Results: All ECG methods strongly correlated with 30-day MRI infarct mass (all p<0.003). Simpler ECG measure-
ments such as maxSTresidual and Qwave were as predictive as more complex measurements. A subset analysis of
306 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

158 patients who had microvascular obstruction (MVO) determined by MRI 5 days post intervention also showed
strong correlations of MVO with the ECG measures.

Conclusions: ST-segment and Q-wave changes after primary PCI in anterior STEMI strongly correlated with 30-day
infarct size by MRI. In particular, maxSTresidual and Qwave at 60 min are simple ECG parameters that offer rapid
analysis for prognostication.

Critique
This study investigated the relative importance of ECG measures at the end of the angioplasty procedure for
determining cardiac tissue viability after STEMI, an important indicator of prognosis including mortality. International
guidelines recommend the use of 12-lead ECG to monitor myocardial ischaemia after STEMI and primary angioplasty,
but a variety of ECG markers, including ST-segment markers, are available for this purpose and TIMI flow post
procedure is often considered before ECG evidence.

The study was a multicentre study and enrolled patients who had proximal or mid-left anterior descending artery
occlusion indicated by STEMI. Participants were then entered into a four-arm randomized controlled trial to receive
intracoronary abciximab or not and manual aspiration thrombectomy or not. ECG interpretation was blinded and
conducted by two staff at independent laboratories. Both the random allocation to group and the blinding of ECG
interpretation are important strengths of the study. Five ECG measurements were used to determine residual ischaemia
and/or infarction at varying levels of complexity, for instance, determining change from pre to post intervention from
all affected leads (ΣSTR) to percentage ST-segment residual elevation in a single maximally affected lead (maxSTR) or
number of new significant Q waves (Qwave). MRI was performed at 30 days to measure infarct size and in a subgroup
at 5 days to measure microvascular obstruction.

Of the 482 patients enrolled 91% were alive at 30 days and MRI was performed and assessable in 80% of these
participants and paired ECGs available for 73%. All ECG measures correlated well with MRI infarct size, with simpler
measures (MaxSTR and Qwave) performing as well as complex measures. Only one ECG measure correlated
significantly with mortality at 30 days and this was Qwave.

Several limitations are relevant to the study including that the sample was restricted to patients with anterior
infarcts due to proximal or LAD occlusion so the results may not apply to other MI. Loss to follow-up and unusable
assessments were low; however, the loss of these participants may limit generalisability. Regardless, the results
confirm that in STEMI patients straightforward ECG measures following angioplasty, such as new Q waves and level
of ST-segment elevation of the most affected lead, are good indicators of myocardial tissue damage, and therefore of
the potential for complications in the early recovery phase. Considerations before changing clinical practice include
whether nursing staff are skilled at ECG interpretation, particularly determining the presence and size of Q waves.
Also, many other clinical factors aside from the size of the infarction are likely to influence mortality, such as pre-
existing cardiovascular fitness and/or ejection fraction as well as the presence of comorbid conditions, and need to
be taken into account in determining prognosis.

Lear ning a c t iv it ie s
1 Follow two patient journeys, one each for early triage primary PTCA and elective PTCA, and compare the
patient experiences from the two pathways.
2 Describe the key nursing care requirements of a patient immediately following stent placement in an abdominal
aortic aneurysm.
3 Discuss the compensatory mechanisms that are activated in heart failure and their effects on the cardiovascular
system.
4 Observe an echocardiograph and ask the sonographer to explain what is visualised on the screen, particularly
in Doppler mode. Ask them to identify areas of hypokinesis or akinesis and any evidence of dyssynchrony
between the ventricles.
 CHAPTER 10 CARDIOVASCULAR ALTERATIONS AND MANAGEMENT 307

Online resources
American Heart Association, www.heart.org/HEARTORG/
Australian Institute of Health and Welfare, www.aihw.gov.au
Cardiac Society of Australia and New Zealand, www.csanz.edu.au
Heart Education Assessment and Rehabilitation Toolkit (HEART), www.heartonline.org.au
National Heart Foundation of Australia, www.heartfoundation.com.au
National Heart Foundation of New Zealand, www.heartfoundation.org.nz
Patient information on living with heart failure, www.heartfoundation.org.au/SiteCollectionDocuments/Living well with
chronic heart failure.pdf

Further reading
Woods SL, Froelicher ESS, Motzer SU, Bridges EJ, eds. Cardiac nursing. 6th ed. Baltimore: Lippincott, Williams & Wilkins; 2010.
Zipes DP, Libby P, Bonow RO, Braunwald E, eds. Braunwald’s heart disease: a textbook of cardiovascular medicine. 7th ed.
Philadelphia: Elsevier Saunders; 2008.

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64 Michaelson CR. Congestive heart failure. St Louis: Mosby; 1983.
65 Gould M. Chronic heart failure. In: Hatchett R, Thompson D, eds. Cardiac nursing: a comprehensive guide. Edinburgh: Churchill Livingstone
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66 Krum H, Driscoll A. Management of heart failure. Med J Aust 2013;199(5):174-178.
67 Ezekowitz JA, Bakal JA, Kaul P, Westerhout CM, Armstrong PW. Acute heart failure in the emergency department: short and long-term
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68 Driscoll A, Worrall-Carter L, Hare DL, Davidson PM, Riegel B, Tonkin A et al. Evidence-based chronic heart failure management programs:
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69 McAlister FA, Stewart S, Ferrua S, McMurray JJ. Multidisciplinary strategies for the management of heart failure patients at high risk for
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70 Whellan DJ, Hasselblad V, Peterson E, O’Connor CM, Schulman KA. Meta-analysis and review of heart failure disease management randomised
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71 Yancy CW, Jessup M, Bozkurt B, Butler J, Casey DE Jr, Drazner MH et al. 2013 ACCF/AHA Guideline for the Management of Heart Failure:
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72 Phillips CO, Singa RM, Rubin HR, Jaarsma T. Complexity of program and clinical outcomes of heart failure disease management incorporating
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73 Driscoll A, Toia D, Gibcus J, Srivastava PM, Hare DL. Heart failure nurse practitioner clinic: an innovative approach for optimisation of beta-
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74 Driscoll A, Davidson P, Clark R, Huang N, Aho Z on behalf of National Heart Foundation Consumer Resource Working Group. Tailoring
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75 Riegel B, Carlson VV. A situation-specific theory of heart failure self-care. J Cardiovasc Nurs 2008;23(3):190–6.
76 Kaneko Y, Floras JS, Usui K, Plante J, Tkacova R, Kubo T et al. Cardiovascular effects of continuous positive airway pressure in patients with
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77 Piepoli MF, Davos C, Francis DP, Coats AJ for the ExTraMATCH Collaborative. Exercise training meta-analysis of trials in patients with chronic
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78 CONSENSUS Trial Study Group. Effects of enalapril on mortality in severe congestive cardiac failure. Results of the Cooperative North
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79 SOLVD Investigators. Effect of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure.
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80 Opie LH, Pfeffer MA. Inhibitors of angiotensin-converting enzyme, angiotesin II receptor, aldosterone and renin. In: Opie LH, Gersh BJ, eds.
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81 Ailabouni W, Eknoyan G. Nonsteroidal anti-inflammatory drugs and acute renal failure in the elderly. A risk–benefit assessment. Drugs Aging
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82 Hjalmarson A, Goldstein S, Fagerberg B, Wedel H, Waagstein F, Kjekshus J et al. Effects of controlled-release metoprolol on total mortality,
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83 Packer M, Fowler MB, Roecker EB, Coats AJ, Katus HA, Krum H et al. Effect of carvedilol on the morbidity of patients with severe chronic
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84 McMurray JJ, Ostergren J, Swedberg K, Granger CB, Held P, Michelson EL et al. Effects of candesartan in patients with chronic heart
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85 Cohn JN, Tognoni G, for the Valsartan Heart Failure Trial Investigators. A randomized trial of the angiotensin receptor blocker valsartan in
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86 Pitt B, Pfeffer MA, Assmann SF, Boineau R, Anand IS, Claggett B et al. for the TOPCAT Investigators. Spironolactone for heart failure with
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87 Pitt B, Zannad F, Remme WJ, Cody R, Castaigne A, Petez A et al. The effect of spironolactone on morbidity and mortality in patients with
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88 Pitt B, Remme W, Zannad F, Neaton J, Martinez F, Roniker B et al. Eplerenone, a selective aldosterone blocker, in patients with left ventricular
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89 Bokhari F, Newman D, Greene M, Korley V, Mangat I, Dorian P. Long-term comparison of the implantable cardioverter defibrillator versus
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90 Moser D, Mann D. Improving outcomes in heart failure: it’s not unusual beyond usual care (Editorial). Circulation 2002;105:2810–2.
91 Wynne JA, Braunwald E. The cardiomyopathies and myocarditides. In: Zipes DP, Libby P, Bonow RO, Braunwald E, eds. Braunwald’s heart
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95 Vidaeff AC, Carroll MA, Ramin SM. Acute hypertensive emergencies in pregnancy. Crit Care Med 2005;33(Suppl 10):S307–12.
96 Shapiro S. Cardiac problems in critical care. In: Bongard FS, Sue DY, eds. Current critical care: Diagnosis and treatment. 2nd ed. New York:
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100 Nakagawa T, Wada H, Sakakura K, Yamada Y, Ishida K, Ibe T et al. Clinical features of infective endocarditis: comparison between the 1990s
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102 Isselbacher EM, Eagle KA, Descanctis RW. Diseases of the aorta. In: Zipes DP, Libby P, Bonow RO, Braunwald E, eds. Braunwald’s heart
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a textbook of cardiovascular medicine. 7th ed. Philadelphia: Elsevier Saunders; 2008. p 1215.
 Chapter 11

Cardiac rhythm assessment

and management
Malcolm Dennis, David Glanville

KEY WORDS Learning objectives

ablation After reading this chapter, you should be able to:
antiarrhythmic • describe the various arrhythmogenic mechanisms implicated in the
development and propagation of cardiac arrhythmias
antitachycardia
pacing • recognise the features of the various commonly observed arrhythmias
and discuss the aetiological factors that predispose to the development
arrhythmia
of each
atrial
• discuss the actual or potential haemodynamic consequences and
atrioventricular prognostic implications of each of the commonly observed arrhythmia
bradycardia types
cardiac • describe the general and specific assessment and treatment strategies
resynchronisation applicable to each of the various arrhythmia types
therapy • discuss the principles and indications for pacemaker therapy
cardioversion • recognise abnormal pacemaker activity on the ECG and discuss the
failure to capture causes and corrective actions for complications during temporary pacing
failure to pace • describe the principles and benefits of cardiac resynchronisation therapy
failure to sense (CRT), including the factors that limit the effectiveness of the therapy
implantable • discuss the principles and indications for treatment of arrhythmias
cardioverter
including ablation therapies, permanent pacing, cardioverter defibrillators,
cardioversion and defibrillation.
defibrillator
junctional
oversensing Introduction
pacemaker Cardiac arrhythmias occur as primary diagnoses or as a complication of cardiac,
sinoatrial other organ or systemic abnormalities. In broad terms most arrhythmias occur
tachycardia with greater frequency and with greater impact in the critically ill patient.
Early detection and interpretation of arrhythmias and their impacts are essential
threshold
with initiation of appropriate arrhythmia management that takes into account
ventricular biochemical and metabolic variation and pharmacological interventions in
critical illness.
The clinical impact of arrhythmia is highly variable and depends upon the
type and rate of the arrhythmia and the presence of any underlying cardiac
disease.When occurring in the critically ill patient, the impact is likely worsened
due to coexistent circulatory, metabolic or biochemical abnormalities and the
high oxygen demand states of many critical illnesses. Symptomatic impact
312 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

ranges from lethargy, exercise intolerance, dyspnoea, The cardiac conduction system
lightheadedness and palpitations, to marked haemody-
namic instability and syncope. Arrhythmias may present The normal heartbeat sequence occurs through rhythmic
as, or progress to, cardiac arrest. Physiological effects of stimulation of the heart via its specialised conduction
tachyarrhythmias include increased myocardial oxygen system. Through inherent automaticity, the sinus node
demand at the same time that reduced oxygen delivery is spontaneously generates an activation current that
occurring, with scope for resultant myocardial ischaemia. conducts across preferential atrial pathways (producing a
The metabolic impact of compromising arrhythmias is P wave on the surface ECG) and then to the atrioventricu-
effectively the same as the outcomes of shock from other lar node. After a brief physiological slowing, this wavefront
aetiologies, with escalating stress responses, along with conducts to the bundle of His and then to the ventricles
reduced oxygen delivery and consumption, increased via the right and left bundle branches. These terminate
oxygen extraction and lactic acidosis. distally as branching Purkinje fibres, which activate the
ventricles. This ventricular activation (or depolarisation)
Practice tip sequence produces a QRS complex on the surface ECG
and subsequent repolarisation gives rise to the T wave.
Morbid obesity (BMI ≥40 kg/m2) is associated with The ability to spontaneously generate a cardiac rhythm
discrete ECG alterations including low chest lead is termed automaticity and, in health, automaticity is tightly
voltages, leftward QRS, T wave and P wave axis shifts, controlled by neurohormonal inputs to match heart rate to
left atrial abnormalities and T wave flattening in the metabolic rate. Excitatory influences increase automaticity,
inferior and lateral leads. However, the mean resting accelerating the heart rate, while automaticity depressant
heart rate and incidence of conduction abnormalities influences slow the heart rate. Arrhythmias may thus arise
do not differ from those with a normal BMI and any from alterations in automaticity (increased or decreased),
alteration in these parameters in obese patients failure of the conduction pathways described above or via
should be considered abnormal. Similarly, a localised reentry or triggered mechanisms (described below).7,8
T wave inversion pattern should always be considered
abnormal in persons with significant obesity. Arrhythmogenic mechanisms
Arrhythmias result from three primary electrophysiologi-
Arrhythmia incidence in critical care units is far cal mechanisms: abnormal automaticity, triggered activity
greater than in the general community.The most common and reentry.
compromising arrhythmia is atrial fibrillation (AF). Its
community incidence is 8–9% over the age of 80,1,2 Abnormal automaticity
but it occurs in 20% of critically ill patients.3 Subgroup The action potentials of sinus and atrioventricular (AV)
incidence is even greater with half of septic shock patients4 conducting tissues differ from that of the myocardium in
and 30–40% of post cardiac surgical patients3,5 developing that phase 4 of their action potentials undergo spontan-
atrial fibrillation. Ventricular arrhythmias occur in less eous depolarisation (automaticity). This property allows
than 2% of critically ill patients.6 these tissues to assume the role of electrophysiological
The arrhythmia landscape continues to change for pacemaker dominance. However, in some circumstances,
the critical care nurse. The increasing multiculturalism such as myocardial ischaemia or under cardiostimulatory
of most populations increases the chances of encounter- influences, regional levels of spontaneous automaticity can
ing arrhythmic syndromes previously only encountered be abnormally accelerated, stimulating ectopic locations
in certain countries, such as the Brugada syndrome and (foci) within the atria, ventricles or AV node to discharge
arrhythmogenic right ventricular dysplasia. In addition, more rapidly.9,10 Conversely, depressed automaticity gives
the increased survival of children to adulthood with rise to bradyarrhythmias and accompanies myocardial and
congenital structural and arrhythmic diseases (e.g. long conduction system disease, pharmacological and biochem-
QT syndromes) further adds to the complexity of ical influence and often, strikingly, vagal (parasympathetic)
arrhythmias with which critical care nurses must be stimulation.
familiar.
Triggered activity
Practice tip
Arrhythmias may occur through the occurrence of
Reduced amplitude of ECG complexes may occur abnormal oscillations within the early and late repolar-
in critical illness (e.g. severe sepsis, renal failure). It isation stages of the cardiac action potential. Normally,
is important to adjust the bedside cardiac monitor all areas of the myocardium repolarise in a uniform
‘gain’ size in response to this phenomenon and to be manner. However, when adjacent areas of myocardium
mindful of the potential ‘masking’ effect it may have on show different rates of repolarisation, voltage differences
underlying 12-lead ECG cardiac hypertrophic voltage between these areas at the critical ‘superexcitable’ phase in
enlargement criteria and the possible suppression of the relative refractory period can be sufficient to re-excite
ST segment changes. tissues, generating premature ectopic beats or acceler-
ated ectopic rhythms. Such variations in repolarisation
 CHAPTER 11 CARDIAC RHYTHM ASSESSMENT AND MANAGEMENT 313

and the consequent ‘self-triggering’ of depolarisation at arrest and require treatment according to advanced life
least partially explain the arrhythmias accompanying long support algorithms (see Chapter 25).
QT intervals. Bradyarrhythmias may be due to failure of sinus node
Voltage oscillations are classified as either ‘early after discharge (sinus bradycardia, pause, arrest or exit block) or
depolarisations’, which occur during phases 2 and 3 of the to failure of AV conduction (AV block). Unless junctional
action potential, or ‘late after depolarisations’, which occur or ventricular escape rhythms emerge asystole or ventric-
during phase 4. Digitalis toxicity, ischaemia, hypokalaemia, ular standstill results.
hypomagnesaemia and elevated catecholamine levels are
the more common causes of triggered activity.11 Excessive Arrhythmias of the sinoatrial node
prolongation of the action potential duration enhances the and atria
risk of triggered activity and, as such, these mechanisms The sinus node controls the heart rate according to
are implicated in the development of certain subtypes metabolic demand, responding to autonomic, adrenal and
of ventricular tachyarrhythmias, in particular torsade de other inputs, which vary according to exertion or other
pointes (refer to description later in this chapter). stressors. In response to needs, the sinus node discharge
Reentry rate typically varies from as low as 50 beats/min to as high
as 160 beats/min. In the conditioned heart (e.g. athletes),
The most common cause of tachyarrhythmias is reentry, this range extends down as low as 40 beats/min and as
in which current can continue to circulate through the high as 180 beats/min. Peak activity in the elite athlete
heart because of different rates of conduction and repol- may even achieve sinus rates of 200/min, though this
arisation in different areas of the heart. Slow conduction represents the extreme end of the sinus rate (see Figure
through a region of the heart may allow enough time for 11.1 for an illustration of sinus rhythm). An individual’s
other tissues that have already been depolarised to recover, maximal sinus rate is approximately 220 beats/min minus
and then to be re-excited by the arrival of this slowly their age. The ECG rhythm criteria for arrhythmias of the
conducting wavefront. Once this pattern of out-of-phase sinoatrial node and atria are summarised in Table 11.1.
conduction and repolarisation is established, a current Sinus node disease predominantly manifests as inappro-
may continue to circulate continuously around a reentry priately slow rather than fast sinus rates. Sinus tachycardia
circuit. Each ‘lap’ of the circuit gives rise to another depol- is therefore not generally an expression of sinus node
arisation (P wave or QRS complex).10,12 The ultimate dysfunction but a physiological response to some stressor
rate of the tachycardia depends on the size of the circuit (see below). A rare exception to this is ‘inappropriate
(micro versus macro reentry) and the conduction velocity
sinus tachycardia’ that appears most commonly in young
around the circuit.
women,13 in whom the resting daytime heart rate chron-
ically exceeds 100/min. Treatment includes beta-blockers,
Arrhythmias and arrhythmia calcium channel blockers or the novel selective sinus node
inhibitor agent ivabradine.14
management
Arrhythmias may arise from myocardial or conduction Sinus tachycardia
system tissue, appearing as inappropriate excitation or In adults, a sinus rate above 100/min is termed sinus
depression of automaticity, impaired conduction or altered tachycardia and may occur with normal exertion15,16 (see
refractoriness.9 Figure 11.2). When sinus tachycardia occurs in the patient
The clinical impact of tachyarrhythmias is highly at rest, reasons other than exertion must be sought and
variable and is influenced by the rate and duration of the include compensatory responses to mental or physiological
arrhythmia, the site of origin (ventricular vs supraventric- stress, hypotension, anaemia, hypoxaemia, hypoglycae-
ular) and the presence or absence of underlying cardiac mia or pain, in which there is increased neurohormonal
disease. As a result, arrhythmias may require no treatment, drive. Inotropes and sympathomimetics also accelerate
at least in the short term, or at worst may present as cardiac the sinus rate. Sinus tachycardia should therefore be

FIGURE 11.1 Sinus rhythm, rate 78/min. All P waves are followed by QRS complexes of normal duration after a
P–R interval of around 0.16 s.
314 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 11.1
ECG rhythm criteria for arrhythmias of the sinoatrial node and atria

RHYTHM ECG CRITERIA

Sinus rhythm (SR) Upright P waves in inferior leads. Rate 60–100/min. Regular
Sinus tachycardia (ST) Upright P waves in inferior leads. Rate 100–180/min. Regular
Sinus bradycardia (SB) Upright P waves in inferior leads. Rate <60/min. Regular
Sinus arrhythmia Upright P waves in inferior leads but they are irregular, with gradual increase and decrease
in rate. Usually in phase with respiration
Sinus pause Abrupt drop in P wave rate, absent P waves (usually <3 s duration)
Sinus exit block Abrupt drop in P wave rate
P–P interval spanning the pause is a multiple of the preceding P–P interval
Sinus arrest Abrupt cessation in P wave rate (>3 s duration)
Atrial ectopic beats (AEs) Premature ventricular complexes of normal morphology
Also: premature atrial contractions P’ waves of altered morphology precede premature ventricular complexes
(PACs) Compensatory pause may occur after premature ventricular complex
Atrial tachycardia Atrial rate regular 140–230/min
AV conduction may be 1:1, 2:1 or less
P waves may be hidden in T waves
P wave when visible usually different morphology to sinus P wave
Ventricular rate usually regular
May show ‘warm up’ in rate at onset
Atrial flutter (AFl) Atrial rate 220–430/min, commonly close to 300/min. Regular atrial rhythm
Flutter waves appear as sawtooth baseline in II, III, aVF, but more like discrete P waves in
V1/MCL1, and as fibrillatory waves in I and aVL
1:1 uncommon in adults, unless flutter rate is slow
2:1, 3:1, 4:1 AV block more common (therefore ventricular rate often close to 150, 100, 75/min)
Atrial fibrillation (AF) Atrial rate 300–500/min. Ventricular rate rarely >180/min
Discrete P waves not seen – irregular fibrillatory baseline
Ventricular rhythm markedly irregular (irregularly irregular)
Ventricular rate >100/min = ‘uncontrolled’ AF
If ventricular rhythm regular – escape or complete heart block

FIGURE 11.2 Sinus tachycardia. The rhythm is slightly irregular and varies between 105/min and 115/min.

regarded as a response to a physiological stimulus rather Sinus bradycardia

than an arrhythmia arising from sinus node dysfunction, A sinus rate of less than 60 beats/min is termed sinus brady-
with treatment directed at the trigger for the tachycardia, cardia15,16 (see Figure 11.3). In general terms the slower
not the tachycardia itself. As sinus tachycardia may point the rate, the more likely it is to produce symptoms related
to covert events such as internal bleeding or pulmonary to low cardiac output. Slowing of the rate to less than
embolism, there should be a thorough investigation for 50/min is common during sleep, especially in the athletic
unexplained sinus tachycardia. heart, but is otherwise uncommon. Bradycardia may
 CHAPTER 11 CARDIAC RHYTHM ASSESSMENT AND MANAGEMENT 315

FIGURE 11.3 Sinus bradycardia. The rhythm is regular and at a rate of 50/min. Borderline first-degree AV block: the
P–R interval is 0.20 s.

accompany myocardial ischaemia (especially when due to the abrupt prematurity with which atrial ectopic beats
right coronary artery disease), conduction system disease, make their appearance, or the abrupt slowing of the sinus
hypoxaemia and vagal stimulation (e.g. nausea, vomiting or rate seen in sinus pause and sinus arrest. Sinus arrhythmia
painful procedures). As vagal stimulation may also produce may accompany sinus node dysfunction but is seen also
vasodilation, hypotension may be more marked during in the normal heart. Of itself, sinus arrhythmia does not
vagally mediated bradycardia. Bradycardia also accompanies require treatment.
beta-blocker, digitalis, antiarrhythmic or calcium channel
blocker treatment.17 Treatment of sinus bradycardia reflects Sinus pause and sinus arrest
the treatment of AV block and is covered below under the Abrupt interruption to the sinus discharge rate has
management of atrioventricular block. spawned a variety of descriptive terms, based partly on
Although sinus bradycardia strictly is defined as less than physiology and partly on severity. Sinus pause is self-
60 beats/min, many people have sinus rates that may be descriptive: during a period of sinus rhythm, there is a
normal but that are inappropriately slow for a given level of sudden pause during which the sinus node does not
activity. This behaviour is usually described as chronotropic discharge.17 The heart rate abruptly drops, during which
incompetence18 and, if it causes activity limitation, can be an time there may be bradycardic symptoms. Sinus arrest tends
indication for pacemaker implantation. to be used as a descriptor when the pause is longer rather
than shorter (usually greater than 3 seconds, while less than
Sinus arrhythmia 3 seconds might be called sinus pause) (see Figure 11.5).
When the rhythm is clearly sinus in origin but is irregular, The longer the period of sinus arrest, the greater the
then the term sinus arrhythmia is used (see Figure 11.4). likelihood of symptoms, and syncope is possible.17
Generally, a gradual rise and fall in rate can be appreciated Sinus pause may be indistinguishable from sinus exit block
in synchrony with respiration. The gradual rise and fall in (in which there are sinus discharges that fail to excite the
rate is important: it distinguishes sinus arrhythmia from atria), as both result in missing P waves. The distinction

FIGURE 11.4 Sinus arrhythmia with marked rate variation in synchrony with respiration. The rhythm is clearly sinus
but is irregular, accelerating from 75 to 120/min before slowing back to 75/min by the end of the strip.

FIGURE 11.5 Sinus pause and sinus arrest. Sinus rhythm at 60/min followed by an abrupt rate drop. Using 3 s as a
cut off between sinus pause and sinus arrest, the first long interval of 2.5 s would qualify as sinus pause whereas the
next interval (3.2 s) would be classified as sinus arrest.
316 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

FIGURE 11.6 Sinus exit block. An abrupt rate drop follows the first three sinus beats. As the P–P interval spanning
the pause is exactly twice the P–P interval of the preceding beats, the pause here could be due to sinus exit block.
It could equally simply be a sinus pause.

is academic, however, as both arrhythmias arise from the Arrhythmias of the atria and
same groups of causes, and are significant only when they
cause symptomatic bradycardia. Pauses in which the P–P atrioventricular node
intervals spanning the pause are multiples of the pre-pause The term supraventricular tachycardia (SVT) is often used
P–P interval favour the diagnosis of exit block (Figure to group the tachyarrhythmias that arise from tissues above
11.6).11 Recurrent syncopal pauses may require acute the ventricles. In its more common usage, SVT is thus an
responses for symptomatic bradyarrhythmias. If episodes umbrella term, and includes any of the tachyarrhythmias
continue, consideration should be given to permanent arising from the sinus node, the atria or the atrioventric-
pacemaker implantation. ular node.21 However, when a specific arrhythmia can be
classified, the specific term is used rather than the more
Special contexts for reducing the rate general term SVT. On occasion the electrocardiographic
during sinus rhythm distinction between atrial flutter, atrial tachycardia and
In general, treatment of tachycardia is directed at the cause atrioventricular nodal reentry tachycardia may be difficult
of the rhythm disturbance and will be considered when to make, and it may be useful in that context to use the
physiological instability is experienced. In select situations, more general term SVT. Supraventricular arrhythmias
however, elevated sinus rates (not necessarily reaching may occur as single-beat ectopics arising from atrial or
tachycardia) may be counterproductive and heart rate junctional tissue or runs of consecutive premature beats,
reduction may commence earlier. This is particularly the and thus be termed supraventricular tachycardias. SVTs
case in patients with angina or moderate-to-severe heart may be self-limiting (paroxysmal) or sustained (until
failure, where sinus rate reduction confers a mortality and treatment), recurrent or incessant (sustained despite
morbidity benefit.19 In the ischaemic population, heart rate treatment). The ECG rhythm criteria for arrhythmias of
reduction reduces myocardial oxygen demand and prolongs the atria and atrioventricular node are summarised in
diastole, during which coronary perfusion occurs. In the Tables 11.1 and 11.2 (later).
heart failure population, in addition to these effects, heart Atrial ectopy
rate reduction increases diastolic ventricular filling time. In
the recent landmark SHIFT study,20 use of a novel selective Impulses arising from atrial sites away from the sinus
sinus node inhibitor (ivabradine) to lower the sinus rate node (atrial foci) conduct through the atria in different
in moderate-to-severe heart failure patients significantly patterns to sinus beats, and so generate P waves of different
lowered composite end points of cardiovascular death or morphologies. These altered P waves define atrial ectopy,
heart failure-related rehospitalisation compared to placebo and their prematurity, or faster discharge rate, sees them
(see Chapter 10 for related information). more completely described as premature atrial beats. A
characteristic P wave morphology cannot be provided,
Practice tip as ectopy may arise anywhere within the atria, causing
upright, inverted or biphasic P waves. However a P wave
Sinus tachycardia is usually the compensatory morphology different to the prevailing sinus P wave is
response to raised metabolic needs; however about the norm. Ectopic P waves are often so premature that
1% of the population experience a syndrome known as they become hidden within the preceding T wave. At
‘inappropriate sinus tachycardia’, which is characterised such times evidence of their presence can be concluded
by the presence of a high resting heart rate (average only because they deform the T wave, and because
HR >90 bpm over a 24-hour period) coupled with an premature QRS complexes of normal morphology
excessive heart rate response to minimal physical follow, suggesting a supraventricular origin of those beats.
effort. This exaggerated chronotropic response – which Premature atrial beats may conduct normally, aberrantly
is unrelated to structural heart disease, underlying or not at all, depending on their degree of prematurity and
pathological processes or lack of physical conditioning the state of AV nodal and intraventricular conduction (see
– is usually asymptomatic and benign but may Figure 11.7).
uncommonly result in palpitations.
 CHAPTER 11 CARDIAC RHYTHM ASSESSMENT AND MANAGEMENT 317

FIGURE 11.7 Sinus rhythm with frequent atrial ectopics. The notched P waves at a rate of 75–80/min are the Ps of the
dominant sinus rhythm, while the more rapidly firing P waves with peaked configurations are the atrial ectopic beats.
Note that the ectopic P waves have some variability in their shapes and firing rate. They should therefore be described
as multifocal atrial ectopics.

Atrial tachycardia nodal reentry tachycardia). When the atrial rate exceeds
A rapidly discharging atrial focus or the presence of an the conduction capability of the AV node, some degree
atrial reentry circuit may give rise to a rapid rate, which of AV block occurs. Atrial tachycardia may be paroxysmal,
is termed atrial tachycardia. Rates range from 140–230 sustained or incessant (see Figure 11.8). Symptoms vary
beats/min and the rhythm is typically very regular once and are partly dependent on the rate of the arrhythmia,
established.11 Onset is usually abrupt but, when the cause and the presence or absence of myocardial dysfunction.
is increased automaticity, a short ‘warm up’ phase occurs
during which the rate gradually accelerates up to the final
Multifocal atrial tachycardia
tachycardia rate. During atrial tachycardia P waves may When multiple atrial sites participate in generating atrial
be difficult to identify, as they become hidden in T waves. ectopic beats at a rapid rate, the term multifocal atrial tachy-
At such times, the presence of narrow QRS complexes cardia is used (see Figure 11.9). The different foci produce
confirms supraventricular conduction and aids discrimina- P waves of varying morphology, and the strict regularity
tion from ventricular tachycardia. Distinction from other of normal atrial tachycardia is not seen.17 Multifocal atrial
supraventricular arrhythmias may rely on the absence of tachycardia is something of a signature arrhythmia for
characteristic features of other SVTs (e.g. the sawtooth pulmonary disease as it in particular complicates chronic
baseline of flutter, the irregularity of fibrillation or the obstructive pulmonary disease (COPD), as well as other
pseudo-R waves and onset pattern of atrioventricular pulmonary diseases as part of the cor pulmonale spectrum.22

FIGURE 11.8 Atrial tachycardia. In this narrow complex tachycardia the rhythm is very regular and the rate close to
210/min. It is not possible to clearly identify P waves within the T waves.

FIGURE 11.9 Multifocal atrial tachycardia. After three beats of sinus rhythm, the rate abruptly rises during a paroxysm
of multifocal atrial tachycardia, which spontaneously reverts. The resultant tachycardia is irregular, and P waves of
varying shapes can sometimes be clearly seen while others can be gleaned only by the deformity of T waves.
318 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

AV conduction during supraventricular waves. The atrial rate of close to 300/min rarely conducts
tachyarrhythmias on a 1:1 basis to the ventricles in adults. Rather, 2:1, 3:1,
4:1 or variable levels of AV block intervene to limit the
The rapid atrial rates associated with atrial arrhythmias may ventricular response rate, often to between 75 and 150/
exceed the conduction capability of the AV node, with the min.9 When the AV block is variable, beats at 3:1, 4:1
result that not all of the atrial impulses can be conducted or other ratios are seen together in a single strip. When
(see Figures 11.10 and 11.11). This usually occurs when there is 2:1 block, the flutter waves are often concealed
the atrial rate exceeds 200/min. Thus, during atrial flutter, within the QRS and/or T wave, and so definite identifi-
or rapid atrial tachycardia, it is common to see 2:1 block or cation may be difficult (see Figure 11.12). At such times,
greater. During atrial fibrillation the ventricular response the presence of a narrow QRS tachycardia at a fixed rate
rate rarely exceeds 180/min unless there is an accessory close to 150/min is particularly suggestive of atrial flutter
pathway of the Wolff-Parkinson-White syndrome linking with 2:1 block. The tendency for flutter waves to appear
the atria and ventricles. Using these pathways the ventric- as discrete P waves in lead V1 can be useful in identify-
ular rate may reach 300/min or more. ing atrial flutter with 2:1 block as the flutter waves are
more easily visualised in this lead. Where there is uncer-
Atrial flutter tainty about the diagnosis, vagal manoeuvres, or adenosine
Atrial flutter is a rapid, organised atrial tachyarrhyth- administration, may increase the degree of block and so
mia (see Figure 11.11). The atrial rate may be anywhere reveal the flutter waves (Figure 11.12).15,16
between 240 and 430/min, but most commonly the rate is
close to 300/min.17 At these rates the atrial depolarisation Atrial fibrillation
waves (flutter waves) run together to produce the char- Atrial fibrillation is a chaotic atrial rhythm in which
acteristic ECG feature of this arrhythmia: the so-called multiple separate foci either discharge rapidly or participate
‘sawtooth’ baseline, because of its resemblance to the teeth in reentry circuits, resulting in rapid and irregular depolari-
of a saw. This sawtooth baseline is generally best shown in sations. None of these gain complete control of the atria.15,17
the inferior leads. By contrast, in lead V1 the flutter waves Discrete P waves (representing the coordinated depolar-
usually appear more like discrete P waves, while in leads isation of the atria) are therefore not seen; rather, there is
I and aVL they have more the appearance of fibrillatory a continuous undulation of the ECG baseline (fibrillatory

FIGURE 11.10 Atrial tachycardia with high-degree block (many consecutive P waves do not conduct). The atrial rate is
around 190/min but, because there is variable AV block (3:1 to 4:1), the resultant ventricular rate is between 50 and 60/min.
This patient had digitalis toxicity, which should always be considered with atrial tachycardia and high-degree AV block.

FIGURE 11.11 Atrial flutter with variable block. Note the sawtooth baseline, which characterises atrial flutter. The atrial rate
is regular and is a little faster than 300/min, while the ventricular rate is irregular because of the variable block. At times the
ventricular rate is close to 150/min (when there is 2:1 block) and at other times close to 100/min (when there is 3:1 block).
 CHAPTER 11 CARDIAC RHYTHM ASSESSMENT AND MANAGEMENT 319

FIGURE 11.12 A regular narrow complex tachycardia at a rate of 165/min could be any number of supraventricular
rhythms, among them atrial flutter with 2:1 block. Administration of IV adenosine produces momentary high-degree
AV block, during which flutter waves at a rate of 330/min become apparent. Carotid sinus massage or other vagal
manoeuvres may produce the same diagnostic impact via transient AV block.

waves at a rate between 300 and 500/min), reflecting the the atria enhance the risk of thrombus formation and
continuous erratic electrical activity within the atria. This embolic stroke. When atrial fibrillation becomes chronic,
erratic, uncoordinated electrical activity results in uncoor- lifelong antithrombotic prophylaxis is usually necessary.
dinated contraction, and the atria can be seen not so much In addition, the incomplete atrial emptying results in
to contract but to quiver continuously. It is this quivering congestion of first the atria and then the pulmonary
(fibrillatory) motion that gives atrial fibrillation its name. circulation, and contributes to dyspnoea, increased work
The irregularity of the atrial rate results in an irregular of breathing and hypoxaemia. Patients with left ventric-
arrival of impulses at the AV node and, as a result, ular failure rely more heavily on atrial kick, and so
conduction to the ventricles at irregular intervals.15 Thus, symptoms and the severity of their heart failure typically
a hallmark of atrial fibrillation is the marked irregularity worsen during atrial fibrillation. At times, atrial fibrilla-
of the ventricular rhythm.The ventricular response rate to tion is debilitating in this group, and shock and/or acute
the rapid atrial rate is determined by the state of AV nodal pulmonary oedema may develop.
conduction and, in patients with normal AV conduction, Antiarrhythmic therapy aims at reverting atrial fibrilla-
is often in the range of 140–180/min (rapid, or uncon- tion, or limiting the ventricular rate (rate control) even if
trolled, atrial fibrillation) (see Figure 11.13). Alternatively, fibrillation persists.23 For patients with chronic atrial fibril-
when AV conduction is impaired, or limited by drug effect, lation in whom adequate rate control cannot be achieved
slower ventricular rates are seen. When atrial fibrillation pharmacologically, it is sometimes necessary to perform
is accompanied by a ventricular rate less than 100/min, radiofrequency ablation of the AV node itself, thereby
it may be termed controlled atrial fibrillation. Excessive inducing complete heart block. Permanent pacemaker
antiarrhythmic treatment or AV conduction disease may implantation is therefore also necessary.
result in more pronounced AV block and genuinely slow Common causes of atrial fibrillation are left atrial
(but still irregular) ventricular rates. enlargement (secondary to heart failure), hyperthyroidism,
Atrial fibrillation is the most common signifi- low serum potassium or magnesium and physiologi-
cant arrhythmia23 and, while not usually immediately cal stress.2 More recently, it has been identified that the
life-threatening, it contributes significantly to morbidity, pulmonary veins, at sites near their entry to the left atrium,
especially in patients with existing cardiac failure. The may give rise to electrical impulses that communicate with
loss of organised atrial contraction (atrial kick), as well the atria and give rise to atrial fibrillation.24 Circumferen-
as the rapid rates, deprive the ventricles of adequate tial ablation of the pulmonary veins, known as pulmonary
filling, and so hypotension and low cardiac output may vein isolation, can isolate these electrical foci and cure
result. The congestion and altered flow patterns through atrial fibrillation from this cause.

FIGURE 11.13 Atrial fibrillation with a rapid (uncontrolled) ventricular response. The rate is around 170/min and
the rhythm clearly irregular. Because of the rapid rate there is little opportunity to identify the fibrillatory baseline,
but enough can be seen for confirmation.
320 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Extremely rapid atrial fibrillation in Wolff-Parkinson- has longer refractoriness. Conduction into the AV node
White syndrome and to the ventricles is still possible by the slow AV nodal
The usual maximal ventricular response rate to atrial fibril- pathway, but the resultant P–R interval will be quite
lation is around 180/min, representing peak conduction long (AV delay plus slow conduction into the AV node).
capability of the AV node. However, in patients with Following this atrial ectopic with its long P–R interval is
Wolff-Parkinson-White (WPW) syndrome, an accessory the onset of the tachycardia.25
pathway links the atria to the ventricles. These pathways The tachycardia develops because the initiating
can conduct more rapidly than the AV node and so it impulse, the atrial ectopic, is delayed in reaching the AV
is possible for the ventricular response rate to reach or node. Once it does reach the AV node it conducts to the
even exceed 300/min during atrial fibrillation.16,17 This ventricles, but also now finds the previously refractory fast
will present as a wide complex tachycardia that is largely pathway recovered and able to conduct retrogradely back
monomorphic but with an irregular rhythm. At such rates to the atria. There is now a functional circuit for reentry
syncope may occur and the rhythm may degenerate into between the atria and the AV node. Impulses conduct
ventricular fibrillation. Flecainide is an effective drug in slowly into the AV node, lengthening the P–R interval,
this context, but digoxin should be avoided as it acceler- but on reaching the AV node conduct just as quickly to
ates conduction across accessory pathways.11 atria as to the ventricles. As a result, the P waves appear at
Atrioventricular nodal reentry much the same time as the QRS.25 In some instances of
AVNRT it is not possible to identify P waves because they
tachycardia are hidden within the QRS. Often, however, the P waves
Atrioventricular nodal reentry tachycardia (AVNRT) is can be seen distorting the final part of the QRS complex,
the most common type of paroxysmal supraventricular appearing as small R waves in V1 and small S waves in
tachycardia, accounting for greater than 50% of cases of lead II. Because they are P waves rather than part of the
paraoxysmal SVT.11 (Note that the term paraoxysmal SVT
QRS, this ECG appearance has been dubbed ‘pseudo-R
as used here does not include atrial flutter or fibrillation.)
AVNRT is more common in women (75% of cases), more waves’ in V1 and ‘pseudo-S waves’ in lead II11,25 (Figure
often occurs in younger than older patients, and in some 11.14). AVNRT is regular, and most commonly at rates
individuals there is an identifiable link to stress, anxiety between 170 and 240/min but may be slower.The QRS is
or stimulants. As the name suggests the arrhythmia arises narrow unless there is concomitant bundle branch block.
because of reentry involving the AV node. Normally, atrial AVNRTs sometimes respond well to vagal manoeuvres,
impulses reach the AV node via both slow and fast AV including coughing, bearing down and carotid sinus
nodal pathways that link the atria to the AV node proper. massage. Adenosine may interrupt the arrhythmia, and
The resultant P–R interval is <0.20 s and represents other AV blocking drugs or antiarrhythmics may be
conduction across the fast AV nodal pathway. In AVNRT, necessary to prevent recurrence. Elective cardioversion is
the trigger mechanism is a premature atrial ectopic that sometimes necessary and, if the arrhythmia is chronically
is blocked by the fast pathway because it (paradoxically) troublesome, slow pathway ablation may be undertaken.11,13

TABLE 11.2
ECG rhythm criteria for arrhythmias of the atrioventricular node

RHYTHM ECG CRITERIA

Junctional ectopic Premature QRS complexes of normal morphology

beats P waves inverted in inferior leads. They may precede QRSs with short P–R intervals or may be (partially)
concealed within the QRS or ST segment
Junctional escape Normal QRS following a pause in the rhythm, escape rate 40–60/min
beat P waves may precede the QRS with short P–R intervals or may be (partially) concealed within the QRS or
ST segment. P waves inverted in inferior leads
Junctional escape Regular rhythm with normal QRS, rate 40–60/min
rhythm P waves inverted inferiorly and may precede QRS with short P–R interval, or may be (partially) concealed
within the QRS or ST segment
Accelerated junctional Regular rhythm with normal QRS, rate 60–100/min
rhythm P wave behaviour as per junctional escape rhythms
Junctional tachycardia Regular rhythm with normal QRS, rate >100/min
P wave behaviour as per junctional rhythms
Atrioventricular nodal Narrow QRS tachycardia. Rate 170–230/min (sometimes slower)
reentry tachycardia P waves may be absent or seen to distort terminal part of QRS (‘pseudo R wave’ in V1, ‘pseudo S wave’ in II)
AVNRT) Typical onset is via premature atrial ectopic with long P–R (>0.30 s) ahead of onset of tachycardia
 CHAPTER 11 CARDIAC RHYTHM ASSESSMENT AND MANAGEMENT 321

FIGURE 11.14 Atrioventricular nodal reentry tachycardia (AVNRT). Lead V1. There is sinus rhythm initially.
A premature atrial ectopic conducts with a long P–R interval (0.36 s), initiating onset of AVNRT at a rate of 140/min.
Note the P waves during the tachycardia can be seen distorting the end of the QRS (the ‘pseudo R wave in V1’ of
AVNRT), which is not present before the tachycardia.

Management of patients with atrial Bradyarrhythmias and

arrhythmias atrioventricular block
General symptoms of atrial tachyarrhythmias include: Bradycardia, a slowing of the ventricular rate to less than
palpitations, dyspnoea/tachypnoea, fullness in the 60 beats/min, may occur in the form of slowing of the sinus
throat/neck, fatigue, lightheadedness, syncope, chest
node rate or failure of conduction at the level of the AV
pain and angina symptoms and nausea and/or vomiting.
node. As the rate slows, escape rhythms should intervene,
Management of atrial tachyarrhythmias includes: 1)
searching for and correction of the cause; 2) rate control limiting the severity of the bradycardia. However, these
limiting the ventricular response, even if the arrhythmias may also fail, rendering the patient asystolic or with cata-
cannot be suppressed;2,26,27 3) reversion of the arrhyth- strophic bradycardia.30–32 The ECG rhythm criteria for
mias by vagal manoeuvres, medication, cardioversion or atrioventricular block are summarised in Table 11.3.
overdrive pacing; 4) ablation;26,28 5) prophylactic antico-
agulation; and 6) prevention of recurrence using cardiac Bradycardic influences
resynchronisation therapies such as biventricular pacing Conduction system depression may occur with abnormal
if necessary.29 autonomic balance (increased vagal or decreased sympathetic

TABLE 11.3
ECG rhythm criteria for atrioventricular (AV) block

RHYTHM ECG CRITERIA

First-degree AV block (1° AVB) 1:1 AV conduction. P–R interval >0.20 s

Second-degree AV block Mobitz Intermittent non-conducted P waves
type I (Wenckebach) P–R intervals show progressive P–R interval prolongation until ‘dropped’ beat
Second-degree AV block Mobitz Intermittent non-conducted P waves
type II P–R intervals of conducted beats show constant P–R interval (i.e., not the progressive
increase in P–R interval in advance of dropped beats)
Third-degree AV block (3° AVB) No P waves conduct. No uniform P–R intervals or P–R relationships
Also: complete heart block (CHB) Bradycardia, appearing as:
Junctional escape rhythm – normal QRS, regular, rate 40–60/min
Ventricular escape rhythm – wide QRS, regular, rate 20–40/min
High-degree AV block Intermittent non-conducted P waves
Some P waves conduct but unlike 2° block there are consecutive non-conducted P waves
(2 or more at a time)
Ventricular standstill Absence of QRS complexes. The term is perhaps more often applied when there are P
waves but no QRSs
322 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

tone), decreased endocrine stimulation (reduced catechol- may not be evident and are inverted because of retrograde
amine or thyroid hormone secretion) or from pathological conduction, as atrial activation spreads from the AV node
influences such as conduction system disease or congestive, and upwards through the atria.These P waves may at times
ischaemic, valvular or cardiomyopathic heart diseases. Many be seen in advance of the QRS (at shorter than normal
biochemical and pharmacological factors cause conduction P–R intervals), within the ST segment, or may be hidden
system depression with resultant bradycardia.18 The causes within the QRS complexes (see Figure 11.15).
of bradycardia and AV block include:30
Ventricular escape rhythms
• drugs – virtually all antiarrhythmics, calcium channel When either the sinus or AV node fails and stimulation of
or beta-blockers and digitalis preparations may
contribute to bradycardia and AV conduction the ventricles does not occur, the ventricles can autoexcite
disturbance to a greater or lesser extent themselves, usually at a rate of 20–40 beats/min (Figure
11.16). Symptoms of bradycardia commonly accompany
• decreased sympathetic activity or blockade of neural these idioventricular rates, and acute rate restoration may
transmission (e.g. spinal injury, anaesthetic or receptor
blockade) be necessary. However, true cardiac arrest requiring cardio-
pulmonary resuscitation is less common, with the escape
• increased parasympathetic activity – vagal rhythm providing sufficient cardiac output to sustain vital
stimulation such as nausea, vomiting, carotid sinus functions in the short term. ECG features of idioventric-
pressure, increased abdominal pressure, femoral ular escape beats include:
manipulation or instrumentation
• single ventricular ectopic beats occurring after a
• hypoxaemia – the respiratory or ventilated patient pause in the dominant rhythm, or as groups of beats
with acute disturbance of oxygenation may develop at the slow escape rate
sudden and marked bradycardia; in this situation
increased oxygen administration is first-line and • QRS >0.12 s, often notched, larger in amplitude and
often definitive treatment. bizarre
In the absence of stimulation by the SA node, other • ST segment and T wave displacement in the opposite
tissues within the conduction system and myocardium direction to the major QRS direction.
can generate cardiac rhythms at rates slower than the When these beats occur at a rate of 20–40/min the
normal sinus rate. Thus, sinus node failure need not rhythm is termed ventricular escape, or idioventricu-
severely compromise the patient, as the inherent automa- lar rhythm. Under excitatory influences the ventricular
ticity of the AV node can generate a (junctional or nodal) pacemaker cells may increase their firing rate to between
rhythm at a rate of 40–60 beats/min. Similarly, should the 60 and 100/min (accelerated idioventricular rhythm) or
AV node fail and the ventricles receive no stimuli, there to faster than 100/min (ventricular tachycardia).33
is an additional layer of protection, as the ventricles
themselves can generate (ventricular) rhythms at rates of Accelerated idioventricular rhythm
20–40 beats/min.15 Accelerated idioventricular rhythm (AIVR) has assumed a
special place in cardiology because of its relatively common
Junctional escape rhythms appearance during postinfarction reperfusion, thus often
When sinus bradycardia falls to a rate slower than the indicating successful revascularisation following percuta-
inherent automatic rate of the AV node, then the junctional neous coronary intervention or thrombolytic therapy.33,34
tissues discharge.15,17 Typical rates are 40–60/min but may It may therefore imply therapeutic success rather than
be slower, as the cause of the primary bradycardia may mishap, and usually needs no treatment. The arrhythmia is
also suppress the firing of escape foci. Intraventricular commonly due to increased automaticity and, as with other
conduction may be normal or aberrant. P waves may or automaticity, arrhythmias may show a ‘warm-up’ in rate, i.e.

FIGURE 11.15 Sinus bradycardia followed by onset of junctional escape rhythm. Note that the sinus rate is
initially around 37/min. It then slows into the escape rate range of the AV node, which then discharges at 35/min.
The junctional beats are not preceded by P waves: the more slowly discharging sinus node probably has its P waves
hidden first in the QRS of the second-last beat and then distorts the ST segment of the last beat.
 CHAPTER 11 CARDIAC RHYTHM ASSESSMENT AND MANAGEMENT 323

FIGURE 11.16 Ventricular escape rhythm (idioventricular rhythm). Note that after the first sinus beat, the slow rate
allows the ventricular escape rhythm to emerge. The resultant rhythm is at a rate of 35/min, with wide QRS complexes
and absent P waves.

it may commence and then gradually accelerate and settle antiarrhythmics).33 It may occur abruptly following vagal
at a faster rate. This behaviour can be useful in differenti- stimulation. When accompanying myocardial infarction, it
ating arrhythmias from reentry, which typically display an is more likely to be transient following inferior infarction,
abrupt change in rate at onset. When it occurs outside of whereas its appearance following anterior infarction is
the context of reperfusion, AIVR should be regarded as more likely to be permanent.
inappropriate ventricular excitation (Figure 11.17).
Degrees of atrioventricular block
Atrioventricular conduction First-degree AV block
disturbances All atrial impulses are conducted to the ventricles but
Atrioventricular conduction disturbances make their conduction occurs slowly, with a P–R interval >0.20 s. 1:1
appearance as delayed or blocked conduction from atria AV conduction is maintained (see Figure 11.18). First-
to ventricles, and thus appear as altered P–QRS (or P–R) degree AV block by itself may be a benign occurrence.
relationships. The conventional classifications for AV It is more concerning when the P–R interval lengthens
block are based purely on the patterns of conduction. The over time as this may precede the development of higher
classification as first-, second- and third-degree partially degrees of AV block. If this occurs with the introduction
represents the severity of AV node or His-bundle dysfunc- of digoxin or antiarrhythmic therapy, drug cessation or
tion.15,17 AV block may complicate heart disease and dose modification should be considered. If the P–R is
is also seen commonly with drug therapy (e.g. digitalis, so long that P waves coincide with the T wave of the
calcium channel blockers, beta-blockers and other previous beat, effective loss of atrial kick develops due

FIGURE 11.17 Accelerated idioventricular rhythm (AIVR) following reperfusion in myocardial infarction. An
accelerated ventricular focus emerges at 65/min, taking over from the slower sinus rate of 60/min. It then accelerates
gradually until settling at a rate of 85/min by the end of the second strip. This display of rate ‘warm-up’ at onset is a
characteristic of arrhythmias due to increased automaticity. The distortion of the ST segment from the third beat of
AIVR onwards is due to retrograde conduction to the atria, and explains the absence of the sinus P waves.
324 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

FIGURE 11.18 Sinus rhythm with first-degree AV block. Rhythm is regular, rate 100/min, 1 : 1 AV conduction, with a
P–R interval of 0.24 s.

to the atria contracting while the mitral and tricuspid • Second-degree AV block Mobitz type II: dropped
valves are closed. Remember that ventricular systole lasts beats (non-conducted P waves) are also present,
roughly until the latter part of the T wave. Hypotension but the conducted beats show a uniform P–R
or reduced cardiac output and cannon a waves, caused by interval rather than any progressive lengthening17
contraction of the atria against closed AV valves, become (Figure 11.20). The dropping of beats may be
visible in the jugular veins and CVP waveforms. regular, e.g. every fourth P wave (termed 4:1 block),
Second-degree AV block progressing to 3:1, or even 2:1 block as AV nodal,
This is an intermediate level of block in which some or His bundle conduction, worsens. Alternatively,
P waves conduct to the ventricles while others do not. the dropping of beats may be more irregular
Thus there are periodic non-conducted P waves, or (variable block), with combinations of 2:1, 3:1,
‘dropped’ beats. A further distinction is made into either 4:1 or other levels of block evident in a given strip.
type I or type II second-degree AV block: The more frequent the dropped beats, the slower
the ventricular rate and the greater the likelihood
• Second-degree AV block Mobitz type I of symptoms. Second-degree type II AV
(Wenckebach): a cyclical pattern of AV conduction is
block is often associated with intraventricular
seen in which the conducted P waves show a
conduction delay, with corresponding widening
progressive lengthening of the P–R interval until
of QRS complexes. When this is seen it represents
one fails altogether to be conducted (blocked, or
conduction impairment not just of the AV node but
dropped, P wave). Cycles begin with a normal or
prolonged P–R interval, which then extends over of intraventricular conduction as well. Progression to
succeeding beats until there is a dropped beat. After complete AV block is more common.17
the dropped beat the cycle recurs, commencing A final form of second-degree block is ‘high-degree’
with a P–R interval equivalent to that commencing AV block, in which some conducted P waves can be
previous cycles17 (Figure 11.19). The frequency of seen, and these conducted P waves show a uniform P–R
dropped beats partially represents the severity of interval. However, rather than single periodic dropped
AV block. When, for example, every fifth P wave is beats, multiple consecutive non-conducted P waves can
not conducted, 5:4 conduction is said to be present. be seen (Figure 11.21). The impact on ventricular rate
If AV conduction deteriorates further, more frequent and therefore haemodynamic status is typically more
P waves fail to be conducted (4:3, 3:2 conduction). severe.

FIGURE 11.19 Sinus rhythm with second-degree AV block type I. Every third P wave is not conducted (3 : 2
conduction). The P–R interval can be seen to lengthen before the dropped beats(*). After the dropped beats the cycle
starts with a P–R interval of 0.18 s. It then extends to 0.25 s before again dropping a beat.

PR prolonged dropped
 CHAPTER 11 CARDIAC RHYTHM ASSESSMENT AND MANAGEMENT 325

FIGURE 11.20 Second-degree AV block type II. A non-conducted beat confirms the second-degree block. There is
no progressive prolongation of the P–R interval before the dropped beat (*), rather, the uniformity of all P–R intervals
distinguishes this as type II.

FIGURE 11.21 Sinus rhythm with high-degree AV block. At the beginning and end of the strip there is second-degree
block (2:1). Alternate P waves fail to conduct, qualifying as at least second-degree AV block. The appearance
of consecutive non-conducted P waves in the middle of the strip (5 in a row), however, escalates the classification
to ‘high-degree’ block.

Third-degree (complete) AV block and, where the P–R interval becomes prolonged, there
None of the atrial impulses are conducted to the ventricles, should be an increase in vigilance directed towards further
resulting in a loss of any relationship between P waves prolongation or the development of dropped beats, to
and QRS complexes (AV dissociation). Usually, a slower identify advancing AV block. Treatment of AV block and
pacemaker assumes control of the ventricular rate, and this bradycardia includes assessment of cardiovascular status or
focus may be either junctional (narrow QRS, at a rate of other symptoms, including chest pain, dyspnoea, conscious
40–60/min) or ventricular (wide QRS, at a rate of 20–40/ state and nausea.The cause should be identified and treated
min). These escape rhythms will typically be regular where possible. Patients need to rest in bed, provided with
(Figure 11.22).17 Symptom severity depends on the rate reassurance and oxygen by mask or nasal prongs. If the
of the escape rhythm and the presence of underlying patient is hypotensive, IV fluids should be administered
ventricular dysfunction. and the patient laid flat. Standardised protocols for brady-
Patient management during AV block cardia should be applied if the patient is symptomatic, and
these usually include:30
AV block may be progressive in nature, worsening with
advancing heart disease or after introduction, or dose modi- • atropine sulfate 0.5–1.0 mg IV37
fication, of drugs that depress AV conduction.35–37 Thus, • isoprenaline38hydrochloride in 20–40 mcg
monitoring should include P–R interval measurement increments, with an infusion at 1–10 mcg/min

FIGURE 11.22 Sinus rhythm with third-degree AV block. Note the P waves (*) at a rate of 90–100/min and the ventricular
rate of 40/min. The P waves bear no relationship to the QRS complexes – they are dissociated. (The seventh asterisked
P wave is premature and different in morphology from the others, and is therefore possibly an atrial ectopic P wave.)
326 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

• transthoracic pacing (usually with sedation) • excess sympathetic stimulation

• possibly low-dose adrenaline infusion. • biochemistry: hypokalaemia, hypomagnesaemia,
If the patient is pulseless or unconscious, standard pH derangements
advanced life support should be administered (see Chapter • hypoxaemia, hypoglycaemia
25). Persistent or recurrent symptomatic bradycardia or • shock, hypotension
AV block may require permanent pacemaker implanta-
tion.30,31 • excitatory pharmacology (positive chronotropes or
inotropes)
Ventricular arrhythmias • adrenaline, isoprenaline, dobutamine, dopamine,
Ventricular ectopic rhythms may either occur as a levosimendan, atropine
response to slowing of the dominant cardiac rhythm • arrhythmic syndromes, Brugada syndrome, long
(escape beats or escape rhythms) or emerge at faster rates QT syndromes, arrhythmogenic right ventricular
than the dominant rhythm (as premature ectopic beats, dysplasia.
couplets or ‘runs’ of ventricular tachycardia).17 Escape
rhythms (occurring after a pause) should be regarded as Patterns of ectopy
physiological, as they protect against otherwise severe Some patterns of ectopic frequency and morphology may
bradycardia (see Figure 11.16), whereas premature beats warn of increasing risk for the development of serious
(occurring in advance of the dominant rhythm) and rapid arrhythmias such as ventricular tachycardia or fibrillation,
ventricular ectopic rhythms occur when pathology gives and therefore earn a particular mention in monitoring.
rise to increased automaticity, or reentrant or triggered Historically, ectopic patterns have been graded according
behaviours (Figure 11.23).15,17 Single ectopic beats may to their pre-emptive risk of serious arrhythmia develop-
be benign occurrences, often seen in the absence of heart ment or 2-year mortality.40 Studies undertaken in 2003
disease. However, their new appearance accompanying and 2005 did, however, call into question the predictive
cardiac or systemic disease may precede the development status of certain ‘high-risk’ ectopic patterns (such as ‘R on
of more serious arrhythmias, such as ventricular tachy- T’ ectopy), instead postulating that other factors such as
cardia or fibrillation, and thus warrant close monitoring. a patient’s underlying left ventricular function and level
Ectopic beats, whether premature or late (escape), show of autonomic responsiveness may play a more signifi-
characteristic features as follows: cant role in the generation of life-threatening ventricular
• wide QRS complexes (>0.12 s) that are39of different tachyarrhythmias, independent of the prior presence or
morphology (large and bizarre in shape) pattern of ectopy present.41,42 However, in the critical
care context it is reasonable to respond to certain patterns
• commonly, notching of the QRS (as shown in Box 11.1) by investigating and managing
• ST segments and T waves in the opposite direction to potential contributing causes. If the patient can be seen
the major QRS deflection.
to be advancing through stages of increased arrhythmic
Ectopic beats may occur as single or coupled beats, complexity, consideration for antiarrhythmic therapy
or in runs of consecutive beats. Ventricular tachycardia should be given. The ECG rhythm criteria for ventricular
is defined as more than 3 consecutive ventricular beats arrhythmias are summarised in Table 11.4.
occurring at a rate greater than 100/min.11,39
Causes of ventricular tachyarrhythmias include:9,16 Ventricular tachycardia
• myocardial disease Ventricular tachycardia (VT) is described as a ‘run’ of
three or more consecutive ventricular ectopic beats,
• myocardial ischaemia, infarction at a rate greater than 100/min (Figure 11.24).23 The
• cardiomyopathies/cardiac failure arrhythmia varies in its clinical impact, but when sustained
• hypertrophy is typically symptomatic with some degree of haemody-
• myocarditis namic compromise. Ventricular tachycardia often presents

FIGURE 11.23 Sinus rhythm with premature ventricular ectopic beats occurring bigeminally. The second, fourth and
sixth beats arise prematurely, appearing in advance of the dominant rhythm, and are clearly wider than the intervening
supraventricular beats.
 CHAPTER 11 CARDIAC RHYTHM ASSESSMENT AND MANAGEMENT 327

TABLE 11.4
ECG rhythm criteria for ventricular arrhythmias

RHYTHM ECG CRITERIA

Ventricular ectopic beats (VEs) Broad complex QRS (>0.12 s duration), often notched
Also: premature ventricular ST-T waves in opposite direction to major QRS deflection
contractions (PVCs) Occur prematurely – earlier than the prevailing rhythm
Compensatory pause post ectopic usually seen
Ventricular escape rhythm Broad complex QRS (as above) rhythm during slowing of sinus rate or AV block
(idioventricular rhythm) Rate 20–40/min. Regular
Accelerated idioventricular rhythm Broad complex QRS rhythm (as above) but at rates of 40–100/min.
(AIVR) P waves may be absent, retrogradely conducted, or dissociated from ventricular rhythm
Ventricular tachycardia (VT) 3 or more consecutive wide QRS beats (>0.12 s), at rate >100/min
Rate range 100–240/min
P waves may be absent, dissociated or retrogradely conducted after each QRS
Usually regular, sometimes irregular at onset of rhythm and prior to reversion
Ventricular fibrillation (VF) No recognisable/organised QRS. Irregular baseline deflections of variable amplitude at
300–500/min. P waves not discernible
Ventricular flutter (VFl) Very regular. Ventricular rate 270–330/min. ‘Zig-zag’ deflections where it is difficult to
identify which is QRS and which is T wave
Torsades de pointes (TdP) Broad complex tachycardia. Some irregularity. Rate 220–330/min
Obvious polymorphism of QRS with ‘sinusoidal twisting’ around the baseline and
transitions between polarity of QRS complexes – first positive then negative. Baseline ECG
shows QT prolongation
May appear monomorphic in some leads
Asystole Absence of QRS complexes. ECG baseline may show some slow undulation
Agonal rhythm Extremely slow ventricular rate (<20/min). Usually with markedly wide QRS complexes.
The wide QRS and T wave amalgam often referred to as a ‘sine wave’ rhythm. Commonly
a terminal rhythm

longer), incessant (persisting until or despite treatment)

BOX 11.1
or intermittent. Additional defining terminology includes
Patterns suggesting higher risk of arrhythmia monomorphic (all beats of the same morphology) or
• Increasing frequency of ectopy polymorphic (in which the rhythm conforms to the other
features of VT but there is variability in the QRS shapes).
• Trigeminy, bigeminy
ECG features of ventricular tachycardia include:11,39,43
• Polymorphic ectopics (multiple QRS shapes),
regarded as more important than monomorphic • Three or more ventricular beats occur at a rate
>100/min, uncommonly >240/min.
ectopics (single QRS shape)
• Two ectopic beats in a row (couplets) • Rhythm typically regular; there may be minor
irregularity, especially on commencement and
• Three or more beats in a row (defined as ventricular sometimes preceding self-termination.
tachycardia)
• R-on-T ectopics
• P waves may be absent. Atrial activity, whether
dissociated or retrograde, is usually difficult to
• Bradycardia-dependent ectopics when the identify electrocardiographically.
Q-T interval is long
• Morphology: QRS is wide (>0.12 s). QRS often
notched or bizarre in shape.
as cardiac arrest, with the patient pulseless and uncon- • Any axis is possible (normal axis, left or right axis
scious, and is one of the major mechanisms of sudden deviation). An axis in the range of −90 to −180°
cardiac death. The severity of symptoms depends partly (‘no man’s land’) provides strong support for the
on the rate (which may be 100–250/min), the duration diagnosis of ventricular tachycardia, as it implies the
of the arrhythmia, the presence of cardiac disease and QRS originates at the left ventricular apex and spreads
the presence of comorbidities.17,33 When it develops, VT through the ventricles upwards and to the right.
may be categorised as self-limiting (terminating without • ST-segment and T-wave displacement is in the
treatment), sustained for some period of time (minutes or opposite direction to the major QRS direction.
328 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

FIGURE 11.24 Sinus rhythm at 65/min before the onset of ventricular tachycardia. Note a ventricular ectopic
emerges from the T wave of the third sinus beat (R-on-T ventricular ectopic), precipitating ventricular tachycardia
(VT). The VT is then sustained at a regular rate of 220/min, with the characteristic wide QRS and ST/T in the opposite
direction to the QRS.

If VT is not self-limiting, treatment depends on the Ventricular flutter

severity of the symptoms. If the patient becomes pulseless This uncommon arrhythmia is most likely just a subset
and unconscious, advanced life support is initiated (see of ventricular tachycardia, but because of its rapid rate
Chapter 25). If the patient is conscious and has a pulse, (at times up to 300/min or more) and the appearance of
therapy can be undertaken less aggressively. Occasionally, QRS complexes that are largely indistinguishable from the
robust coughing may revert VT in the cooperative patient. T waves, ventricular flutter has earned its own classifica-
Antiarrhythmic therapy (at slower administration rates tion.17,43 It is typically very regular and monomorphic. An
than during cardiac arrest) is usually undertaken first, along example is shown in Figure 11.25 in which it is difficult
with biochemical normalisation. If unsuccessful, sedation to say which deflection is the QRS and which is the
and elective cardioversion may be necessary. Consideration T wave. The diagnostic separation from other types of
for internal cardioverter defibrillator (ICD) implantation VT is clinically unimportant, and treatment should follow
should be given to patients surviving ventricular tachycardia normal guidelines for VT.
or fibrillation.31,44,45
Ventricular fibrillation
Practice tip During ventricular fibrillation (VF) there are no recog-
Initial tolerance of VT may be evident, only to be followed
nisable QRS complexes. Instead, there is an irregular
by abrupt deterioration when reserves or compensatory
and wholly disorganised undulation or erratic deflec-
mechanisms are exhausted. Emergency responses
tions about the baseline.11,17 There are deflections, which
should always be activated on initial identification.
at times approach rates of 300–500/min, but these
are typically of low amplitude and none convincingly

FIGURE 11.25 Probable ventricular flutter. The complexes are broad, regular and monomorphic (one shape), but it is
difficult to know which is the QRS deflection and which is the T wave. This feature plus the very fast rate of 300/min or
more are the typical defining characteristics of this uncommon but serious arrhythmia, recorded during recovery from
tricyclic antidepressant overdose in a 16-year-old female.
 CHAPTER 11 CARDIAC RHYTHM ASSESSMENT AND MANAGEMENT 329

FIGURE 11.26 Ventricular fibrillation. Rapid, irregular and wholly disorganised deflections from the baseline are
present, and produce nothing resembling QRS complexes.

resemble QRS complexes (Figure 11.26). In the absence direction), which is first positive and then negative, usually
of organised QRS complexes the patient becomes imme- with an ill-defined transition between the two. In addition
diately pulseless, and unconsciousness follows within to the changing directions there is a gradual rise and fall
seconds. Immediate defibrillation is required. If VF in amplitude, giving an overall appearance sometimes
persists treatment occurs according to standing basic and described as a ‘sinusoidal twisting’ (Figure 11.27).47,48
advanced life support guidelines.Ventricular fibrillation is ECG features of torsades de pointes are:47,48
the leading cause of sudden cardiac death worldwide. For • broad complex rhythm
survivors of sudden cardiac death an implantable cardio-
verter defibrillator (ICD) is generally indicated unless
• QRS polymorphic, with the transitions between
polarity as described above
there are reversible or transient causes, e.g. primary VF in
the acute phase of myocardial infarction.46 • in some leads the QRS complexes may appear
monomorphic
Polymorphic ventricular tachycardias • rate often very rapid, in the range of 300/min
These forms of VT do not have a single QRS morphology. • regularity: the evident complexes are often regular
Rather, the QRS complexes during the rhythm vary from but, particularly within the transition between
one shape to another, either alternating between two QRS directions, there may be irregularity
discrete morphologies on a beat-to-beat basis (seen most • often self-limiting but recurrent
commonly in digitalis intoxication) or switching between
groups of beats, with first one morphology and then another • Q–T prolongation evident during normal rhythm
(bidirectional VT).17 The more common form of polymor- • commonly pause-dependent, with bradycardia or
phic VT is torsades de pointes (TdP), in which the QRS single beat pauses precipitating onset
undergoes a gradual transition from one QRS pattern to • ventricular bigeminy common in advance of onset of
another. The descriptive French term, literally ‘twisting of torsades de pointes
the points’, refers to the appearance of the ‘points’ (QRS • onset commonly via R-on-T ectopic beats.

FIGURE 11.27 Torsades de pointes polymorphic ventricular tachycardia. After three beats of sinus rhythm a
ventricular ectopic beat emerges from the T wave and precipitates onset of a rapid and sustained polymorphic
ventricular rhythm. The characteristic sinusoidal twisting around the baseline and changing direction of the QRS are
clearly apparent and, along with the rate of 300/min, define this as torsades de pointes.
330 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Because of the very rapid rate, syncope and cardiac • immediate CPR and cardioversion/defibrillation for
arrest are common, and advanced life support is required.A pulseless, unconscious ventricular arrhythmias (cardiac
thorough search for possible causes of Q–T prolongation arrest).50 In conscious patients, initial treatment is
should be undertaken. Causes include: class IA (procain- usually pharmacological and, if necessary, cardioversion
amide, quinidine, disopyramide) or class III (amiodarone, is applied under the influence of short-acting
sotalol) antiarrhythmics,11,17 erythromycin, antidepressants, anaesthetics (e.g. propofol)
hypocalcaemia, hypokalaemia and hypomagnesaemia.49 • antiarrhythmic therapy
Congenital long Q–T syndromes also exist.47,49 Apart from immediately: IV amiodarone, lignocaine, sotalol50
the general ventricular arrhythmia management principles ongoing: oral amiodarone, sotalol, procainamide,
listed below, the treatment of torsades de pointes includes flecainide, beta-blockers53
cessation of Q–T prolonging agents, a greater emphasis on • heart failure management, which needs to be
IV magnesium and the use of isoprenaline and/or pacing aggressive if contributory
to shorten the Q–T interval and prevent bradycardia.50 • electrophysiological testing, which should be
Bradycardia in patients with long Q–T requires special performed for serious arrhythmias to identify foci or
mention as torsades de pointes is so often bradycardia pathways and confirm effectiveness of treatment53
or pause dependent. Bradycardia and pauses prolong the • pacing strategies
Q–T interval further and favour ectopy, which more cardiac resynchronisation therapy using biventricular
easily finds the T wave, triggering torsades de pointes. pacemaker, providing benefit for the heart failure
The roles of pacing and isoprenaline are to both prevent patient at greater risk for ventricular arrhythmias54
pauses and shorten the Q–T interval47,51 Pacing rates of overdrive pacing therapy: antitachycardia pacing
90 to 120 may be necessary to prevent torsades de pointes strategies via implantable cardioverter defibrillator44,45
recurrence. Overdrive pacing (pacing at a rate greater • implantable cardioverter defibrillator therapy, which
than the tachycardia) is an effective treatment to terminate should be considered for all survivors of sudden
monomorphic forms of ventricular tachycardia, but is not cardiac death not due to transient or reversible
effective in terminating torsades de pointes episodes. factors,44,45 especially those with low ejection fraction
and recurrent sustained ventricular arrhythmias55
Rapid differential diagnosis of
extremely fast ventricular rates
• where a myocardial scar can be confirmed as the
arrhythmic focus, surgical resection may sometimes
For broad complex tachycardias approaching rates of 300/ be undertaken.
min in an adult, differential diagnosis becomes relatively
straightforward using the following approach: Arrhythmia identification and analysis
• if perfectly regular and with one morphology – likely Arrhythmia differentiation requires knowledge of ECG
ventricular flutter criteria and a systematic approach to interpretation. The
flow diagram in Figure 11.28 aids identification of the site
• if largely regular but with obvious polymorphism – of origin of rhythms or location of conduction disturbances.
likely torsades de pointes
• if irregular, and with largely one morphology – likely Antiarrhythmic medications
atrial fibrillation with WPW. Antiarrhythmic drugs are classified partly on the basis
of beta-receptor or membrane channel activity, and
Management of patients with partly by their physiological effects on the cardiac action
ventricular arrhythmias potential. This is represented by the Vaughan Williams
The emergency management algorithm for life-threat- classification system (see Table 11.5).51 However, as action
ening ventricular arrhythmias is described in the chapter potential abnormalities cannot be expediently identified
on resuscitation. In general terms, the management of at the bedside, matching antiarrhythmic agents to cellu-
ventricular arrhythmias should include the following:50 lar physiology cannot realistically be undertaken. Instead,
antiarrhythmics are chosen partly on the basis of their
• a search for and correction of causes, including known efficacy, by their effectiveness on atrial or ventric-
ischaemia: ECG, cardiac enzymes ular arrhythmias and after consideration of the side effects
biochemical: potassium derangement, and contraindications to known comorbidities in a given
hypomagnesaemia patient.53,56
metabolic: shock, hypoxaemia, pH derangement, The classification of the major acute antiarrhythmics in
hypoglycaemia use, along with doses, arrhythmic indications, precautions
drug effect: inotrope, chronotrope, recreational and side effects, are depicted in Table 11.6. Class I agents all
drugs slow phase 1 (depolarisation) and so may slow conduction
pulmonary artery or intracardiac catheters52 and prolong the QRS. The subgroups of class I agents
cardiomyopathy, hypertrophy, myocarditis denote strength (A = weakest, C = strongest) and affect
long Q–T interval and Q–T prolonging influences repolarisation, with class IA (prolonging), IB (shortening)
proarrhythmia from antiarrhythmic drugs and IC (not affecting) repolarisation duration. Class II
 CHAPTER 11 CARDIAC RHYTHM ASSESSMENT AND MANAGEMENT 331

FIGURE 11.28 Stepwise approach to arrhythmia identification.

Obvious P waves present on rhythm strip?

Same number
of P waves to No QRS
YES complexes NO
QRS complexes

More QRS More P Ventricular QRS present?

complexes waves than standstill
than P QRS
waves complexes
YES NO

Asytole
Sinus, or VF
junctional or
atrial rhythm,
(+/– 1st degree Regular Irregular
AV block)

Junctional or Atrial fibrillation

ventricular or
rhythm supraventricular
Junctional or (consider rhythm with
ventricular concealed P variable block
ectopic rhythm waves
suggesting SVT
or atrial flutter)

AV block

TABLE 11.5
Antiarrhythmic classifications43

CLASS ACTION DRUGS

IA Sodium channel blockers: action potential prolongation quinidine

procainamide
disopyramide
IB Sodium channel blockers: accelerate repolarisation; shorten action potential lignocaine
duration mexiletine
IC Potent sodium channel blockers: little effect on repolarisation flecainide
II Beta-blockers: depress automaticity (prolong phase 4); indirect prolongation metoprolol
phase 2 propanolol
esmolol
III Potassium (outward) channel blockers: prolong duration of action potential amiodarone
(prolonged repolarisation) sotalol (beta-blocker with class II actions)
IV Calcium channel blockers verapamil
diltiazem
332 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 11.6
Acute antiarrhythmic characteristics41,44,45

ARRHYTHMIC
AGENT DOSE I N D I C AT I O N C O N S I D E R AT I O N S SIDE EFFECTS

quinidine (class IA) Oral treatment only Supraventricular Avoid hypokalaemia QRS prolongation
WPW Increased risk torsades Q-T prolongation
following elective Hypotension
cardioversion GI intolerance

procainamide (class IA) 50 mg increments Supraventricular Potentiates class IA and QRS prolongation
per minute IV (up to Ventricular class III Hypotension
10 mg/kg) WPW Q-T prolongation
AVB

lignocaine (class IB) 1 mg/kg over 2 min; Ventricular If hepatic/renal Hypotension,

1–4 mg/min infusion dysfunction: dose bradycardia, AVB
24 h modification necessary CNS disturbance
to avert toxicity
Avoid hypokalaemia

flecainide (class IC) IV 1–2 mg/kg over Supraventricular Proarrhythmia more Hypotension
10 min; infusion Ventricular marked in structural Bradycardia, AVB
0.150–0.025 mg/kg/min WPW heart disease Proarrhythmia
QRS prolongation

esmolol (class II) 0.5 mg/kg/min over Supraventricular Hypotension

1 min, followed by Bradycardia, AVB
decremental infusion Symptom provocation
protocol in asthma, COAD,
diabetes, peripheral
metoprolol (class II) Supraventricular
vascular disease
sotalol (class III + beta- 5 mg increments per Supraventricular Potentiation of class IA Q-T prolongation
blocker, class II) min up to 80 mg total; Ventricular and III agents ++ (sotalol)
maintenance
160–280 mg/day

amiodarone (class III, 150–300 mg (over Supraventricular Slow GI absorption Hypotension

also strong class I, with 2 min in cardiac arrest, Ventricular Long half-life Bradycardia, AVB
some class II and IV otherwise over 20 min); 25–110 days Q-T prolongation
activity) maintenance Potentiation of digoxin, Thyroid, hepatic
400–800 mg/day warfarin, class IA, dysfunction
class III effects Pulmonary fibrosis
Photosensitivity

verapamil (class IV) 5–10 mg IVI Supraventricular Potentiates digoxin Hypotension

Selected use in Bradycardia
ventricular AVB

adenosine (class IV-like) 6–12 mg rapid IVI Supraventricular Experience may be Transient AVB/
bolus followed by flush disturbing. Consider ventricular standstill
(repeatable) pre-sedation.
Half-life 10 s

ivabradine Oral 5–7.5 mg twice Modest selective Selective sinus node Bradycardia
(If channel inhibitor) daily slowing of sinus rate inhibitor Hypotension
Heart failure or ischaemic Visual disturbances
heart disease where rate
reduction required

AVB = atrioventricular block; CNS = central nervous system; COAD = chronic obstructive airway disease; GI = gastrointestinal;
If = sinoatrial funny channel; WPW = Wolff-Parkinson-White syndrome.
 CHAPTER 11 CARDIAC RHYTHM ASSESSMENT AND MANAGEMENT 333

agents (beta-blockers) depress automaticity, slowing the ventricular rate.66 Temporary transvenous pacing is almost
heart rate and prolonging the action potential. The class III always undertaken as ventricular pacing only. While there
agents notably prolong repolarisation, action potential are transvenous leads available for temporary atrial pacing,
duration and the Q–T interval. Class IV drugs are calcium they are more difficult to position, and their use is very
channel blockers, decreasing automaticity and prolonging infrequent. By contrast, in the cardiac surgical patient,
the action potential.48 where direct lead attachment is straightforward, pacing
Amiodarone ranks as the most effective agent in may be undertaken as single chamber (atrial or ventricu-
converting tachyarrhythmias, but its use must be weighed lar) or dual chamber (atrial and ventricular).
against its considerable side effects.57,58 As with other class Temporary transvenous wires are particularly vulnerable
III drugs (e.g. sotalol) and class IA agents, there is a risk of to movement.65 Unlike permanent pacing leads, which are
Q–T interval prolongation and the development of torsades ‘fixed’ in some manner to the myocardium,55,67 temporary
de pointes.47,49,59,60 Although sotalol carries the greatest risk leads are simply blunt-ended leads that rely on lodging
of this arrhythmia, it may be selected when amiodarone in muscular folds (trabeculae) near the apex of the right
side effects need to be avoided, or when combined antiar- ventricle to hold the lead in position. Activity limitation
rhythmic–beta-blocker therapy is desired, (e.g. arrhythmias and strict rest in bed are therefore recommended for
postinfarction or in the setting of heart failure). Lignocaine, the patient with temporary transvenous pacing who is
the front-line ventricular antiarrhythmic for many years, pacemaker-dependent.
lacks the efficacy of amiodarone, but is well tolerated The details and descriptions of pacing in this section
and effective in the setting of ischaemic myocardium.61 apply equally to temporary and permanent pacing.
Whatever the choice of antiarrhythmic, attention should However, the strategies for the correction of problems
also be directed to biochemical correction, in particular are oriented more towards temporary pacing. Additional
serum magnesium, potassium and pH.50 features and issues related to permanent pacing are
provided at the end of this section.
Cardiac pacing
Artificial cardiac pacing is most commonly used to provide
Major pacemaker controls
protection against bradycardia and/or AV block. Slow All temporary pacemakers give the operator control over
heart rates can be sustained at more physiological rates by pacing rate, pacemaker output (strength of the applied
repetitive electrical stimulation, delivered by a pacemaker at electrical stimulus), sensitivity (to intrinsic rhythm) and
a programmed rate. Temporary pacing may be provided in (in dual-chamber modes) the AV interval. Additional
an emergency, providing rhythm protection while reversible controls such as mode selection, output pulse width, upper
factors are overcome (biochemical or drug influence, tracking rate and the post ventricular atrial refractory
myocardial ischaemia) or as a bridge to permanent period (for DDD mode) are available on some temporary
pacemaker implantation.62 Separate from such bradycardia and all permanent devices. Table 11.7 describes the
protection, pacing may be undertaken to improve haemo- major parameters that can be directly controlled on most
dynamic status, or to treat or suppress tachyarrhythmias. temporary devices.

Principles of pacing Pacing terminology

A paced rhythm can be achieved by delivering To aid in communication when discussing pacing
electrical stimuli through pacing leads connected to the functions, international agreement on terminology has
myocardium. Electrical impulses are delivered to the been reached (see Table 11.8). A 5-letter code68 describes
heart via the negative electrode of the circuit, while the the pacing (and/or defibrillation) capabilities of any given
positive electrode completes the electrical circuit and device in terms of chambers involved in pacing, sensing or
enables sensing (detection) of the patient’s intrinsic cardiac other functions such as rate responsive pacing capabilities.
rhythm.63,64 Electrical impulses of sufficient strength A pacemaker designated as VVIR, for example, is capable
stimulate the myocardium to depolarise (and then to of Ventricular pacing, sensing of Ventricular activity,
contract) at a selected rate. Inhibiting pacing in response to sensing of ventricular
Pacing leads (electrodes) may be positioned in contact activity, as well as possessing Rate responsiveness. While
with the endocardium via transvenous access, or attached the first three positions in the terminology relate to all
to the epicardium at the time of cardiac surgery.65 For types of pacing, the fourth and fifth letters relate only to
epicardial pacing, two separate leads or ‘wires’ are usually permanent pacing and have not been used in this chapter.
attached to each chamber paced, with one wire connected
to each of the negative and positive terminals of the pulse Capture
generator (pacemaker). For transvenous pacing, a single A pacing stimulus that successfully generates a P wave
lead is advanced to the apex of the right ventricle. These or QRS complex is said to have ‘captured’ the atria or
leads have a pacing electrode at their tip and a circum- ventricles, respectively. If pacing stimuli are not followed
ferential (or ‘ring’) sensing electrode slightly proximal to by a P wave or a QRS complex, ‘failure to capture’ is said
this. In an emergency, these transvenous ventricular pacing to be occurring and requires immediate corrective action
wires can be inserted promptly and establish a supportive (Figure 11.29).
334 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 11.7
Pacemaker controls and settings

CONTROL FUNCTION

Base rate Sets the rate at which the pacemaker will discharge: pacing occurs at this rate unless the patient’s
own rate is faster and is sensed by the pacemaker. Typically set at 60–100/min
Ventricular output The size, or strength, of the stimulus delivered to the ventricles. In temporary devices this is an
adjustable current (measured in milliamperes [mA]). Output is increased until capture (successful
stimulation) is achieved. The minimum current required to achieve capture is termed the output
threshold. Impulses delivered below the threshold value will not capture the myocardium.
Temporary pacemakers have an adjustable output range of 0.1–25 mA
Atrial output The size or strength of the stimulus delivered to the atria. Range 0.1–20 mA
Atrial and ventricular pulse Only adjustable on some devices. Allows adjustment of the duration for which the pacemaker
width output is applied to the myocardium. Selectable range typically 1.0–2.0 milliseconds (ms) in 0.25-ms
increments. Increasing the pulse width enhances ability to gain capture
Atrioventricular delay The interval between the delivery of the atrial and ventricular pacing stimuli. Normally this is set in
the same range as normal P–R intervals (between 0.12 and 0.20 s)
Sensitivity Affects the ability of the pacemaker to detect the presence of spontaneous cardiac activity.
Sensitivity settings can be adjusted between 1.0 and 20 millivolts (mV). Set at 1.0 mV the device is
very sensitive (able to sense small electrical signals from the heart). Set at higher values, the device
becomes less sensitive (higher voltage signals required to be detected), with the risk that QRS
complexes or P waves will not be sensed

TABLE 11.8
Pacemaker terminology56

RESPONSE TO PROGRAMMABLE A N T I TA C H YA R R H Y T H M I A
C H A M B E R PA C E D CHAMBER SENSED SENSING FUNCTIONS FUNCTIONS

O, none O, none O, none O, none O, none

A, atrium A, atrium T, triggered P, simple P, pacing
V, ventricle V, ventricle I, inhibited programmable S, shock
D, dual (A & V) D, dual (A & V) D, dual (T & I) M, multi-programmable D, dual (P & S)
C, communicating
R, rate modulation

FIGURE 11.29 Ventricular pacing at 86/min. There is capture on the first five beats but none of the remaining pacing
spikes are followed by the expected wide QRS of capture. Note that, while there is capture, the patient’s own rhythm is
suppressed. When capture is lost, the patient’s slower rate emerges. Consistent capture needs to be re-established, by
either increasing the pacemaker output or correcting factors that depress myocardial responsiveness.

Output and threshold first establishing pacing, the output is typically increased
The strength of the pacing stimulus applied is termed gradually until 100% capture is achieved. The minimum
the pacing ‘output’, and is adjustable by the operator. For output required to achieve capture is termed the output
temporary pacing this is more often an adjustable current, threshold. This pacing threshold may vary significantly
and with permanent pacing is an adjustable voltage.When with changes in biochemistry, arterial pH, myocardial
 CHAPTER 11 CARDIAC RHYTHM ASSESSMENT AND MANAGEMENT 335

perfusion, drugs and other factors.65,69–71 To accommo- Ventricular pacing delivered at the time of the T wave
date potential threshold changes, output settings on the may induce ventricular tachyarrhythmias72 (Figure 11.31),
pulse generator are set with a ‘safety margin’, i.e. the pulse while atrial pacing during atrial repolarisation (shortly
generator is set to deliver outputs that are at least double after the P wave) may precipitate atrial tachyarrhythmias.60
the threshold value.70
Asynchronous pacing
Practice tip Pacing may be delivered in an asynchronous mode, that
is, without the capability of sensing the heart’s inherent
Thresholds for stimulation are more volatile in the rhythm. When in an asynchronous mode, the pulse
temporary pacemaker patient in whom ischaemia or generator will pace perpetually at the set rate, irrespec-
postoperative biochemical, pH and haemodynamic tive of whether the patient is generating his/her own
changes are common. Monitoring should be focused rhythm. The main applications of non-sensing (asynchro-
on confirming capture and low heart rate limits should nous) modes are: 1) when there is oversensing, or risk of
be set to 5 or 10 beats below the base pacing rate. oversensing, such as in environments with strong electro-
magnetic fields and 2) when patients would otherwise
Demand versus asynchronous pacing be asystolic or critically bradycardic if pacing were inter-
Pacing can be configured in either demand (sensing) or rupted (pacemaker-dependent).63,73,74 In demand modes
asynchronous (non-sensing) modes. of pacing, false sensing of electromagnetic interference is
able to inappropriately inhibit pacing, returning patients
Demand pacing to their own unreliable rhythm.73 Temporary repro-
The most common approaches to pacing are the so-called gramming to non-sensing modes (AOO, VOO, DOO)
‘demand’ modes. In these modes, pacing is provided only is commonly undertaken during surgery to prevent false
on demand: that is, when the heart rate falls below a pacemaker inhibition by electrocautery. For permanent
nominated level (demand rate) (Figure 11.30). Demand pacing this is achieved by reprogramming, or by magnet
pacing requires pacemaker detection of the patient’s application over the device causing asynchronous pacing
intrinsic cardiac rhythm. If an intrinsic rhythm is sensed, it at elevated rates (90–100/min) while the magnet is in
‘inhibits’ the pacemaker from delivering a pacing stimulus. place. The appropriateness of continuing in an asynchro-
The demand modes ensure that pacing is provided only nous mode should always be reconsidered if the patient’s
when needed, and also protect against pacing during rate re-emerges in competition with the pacing due to the
arrhythmically vulnerable moments in the cardiac cycle. risk of precipitating arrhythmias.

FIGURE 11.30 Demand ventricular pacing at a rate of 60/min. The patient’s rate increases after the first two paced
beats and inhibits the pacemaker. It then slows to below 60/min and the pacemaker recommences ‘on demand’.

FIGURE 11.31 Intermittent asynchronous pacing due to incomplete sensing. Set pacing rate 66/min. The 1st, 3rd
and fourth beats are sensed and appropriately inhibit pacing. However, a pacing spike can be seen at the apex of the
T wave of the second beat, which does not cause arrhythmia. The next pacing spike, just after the apex of the T wave
of the fifth beat, arrives during the period of increased excitability in the action potential and precipitates ventricular
tachycardia.
336 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Ventricular pacing The characteristic arrhythmias of such patients are sympto-

Stimulation of just the ventricles results in the generation of matic sinus bradycardia and/or sinus pause/arrest that may
a ventricular ectopic rhythm. Functionally this will be no be syncopal. For atrial-only pacing to be undertaken, there
different from an intrinsic ventricular rhythm. There will needs to be confidence that AV conduction is intact, and that
be loss of atrioventricular synchrony, and the loss of atrial it will remain intact in the future76 as the annual incidence
kick may cause low cardiac output and hypotension. To of progression to AV block is 1% in these patients.77 If there
offset the loss of atrial kick, ventricular pacing is sometimes is AV block, atrial pacing alone is unsuitable, and dual-
undertaken at slightly higher rates than normally seen in the chamber pacing should be considered.62,74,76 In permanent
resting patient (e.g. 70–80/min, rather than 50–60/min). pacing the reliability of AV conduction is sometimes
The delivered pacing stimulus should be followed assessed by pacing the atria rapidly (e.g. at rates of up to 120
immediately by a QRS complex that is wide (>0.12 s) to 150/min). If AV block does not develop at these faster
and often notched, resembling a ventricular ectopic rates there can be confidence that AV conduction is reliable.
rhythm. Pacing from near the apex will produce an The advantage of atrial pacing over ventricular pacing is the
ECG that closely resembles left bundle branch block provision of atrial kick, which may contribute substantially
morphology, with left axis deviation. ST segments and to cardiac output and blood pressure. In this respect atrial
T waves will appear in the opposite direction to the major pacing is superior to ventricular-only pacing.
QRS direction in all leads.69 Atrial pacing tends to produce low-amplitude P waves,
Ventricular pacing provides protection against brady- which vary from the typical P waves seen during sinus
cardia or AV block by stimulating the ventricles at a set rhythm (Figure 11.33). They may at times be difficult
rate (Figure 11.32).Temporary ventricular pacing may also to identify on the ECG. Appropriate lead selection is
be undertaken to prevent bradycardia-dependent tachy- important to reveal the atrial depolarisation and confirm
arrhythmias such as torsades de pointes.75 In this context, atrial capture. It is common for the AV interval (P–R
pacing at faster rates provides protection by reducing the interval) to extend slightly (e.g. to 0.20–0.22 s) during atrial
QT interval, as well as preventing pauses that give rise to pacing compared with sinus rhythm, as the time taken for
ectopy and onset of torsades de pointes.75 atrial impulses to traverse the atria from the pacing focus
is longer than the sinus-to-AV node conduction interval.
Practice tip
Atrial pacing and AV block
If haemodynamic status is suboptimal during ventricular Any degree of AV block is possible during atrial pacing and
pacing (low blood pressure and/or cardiac output), it must be remembered that AV block is rate dependent.76,77
consider changing the pacing rate. A faster pacing rate Thus, the severity of AV block may be worsened not only
may offset the loss of atrial kick and so restore cardiac by AV node dysfunction but also by changes in the atrial
output despite low stroke volume. Alternatively, turning pacing rate. A patient with first-degree block may develop
down the pacing rate may reveal an underlying (slower) second-degree block if the atrial pacing rate is increased,
sinus rhythm that produces improved cardiac output without this implying worsening AV node function.
due to the inclusion of atrial kick. Conversely, AV block developing during atrial pacing may
be lessened or overcome by reducing the atrial pacing rate.
Atrial pacing An example of such rate-dependent AV block behaviour
Atrial pacing alone is indicated when there is sinus node is demonstrated in Figures 11.34 to 11.36, which are
dysfunction in the presence of reliable AV conduction.62,74 sequential strips from the same patient.

FIGURE 11.32 Onset of ventricular pacing. At the start of the strip the patient’s heart rate is around 70/min. The
pacemaker is then turned on with the rate set at 80/min. Capture is achieved immediately and, because the pacing rate
is faster, there is suppression of the patient’s own rhythm. Note the wide QRS and ST elevation during pacing. This is
the expected appearance.
 CHAPTER 11 CARDIAC RHYTHM ASSESSMENT AND MANAGEMENT 337

FIGURE 11.33 Commencement of atrial pacing. The patient’s own sinus rhythm is around 65/min at the start of the
strip. Pacing is turned on at a rate of around 70/min, and causes suppression of the slower sinus rhythm. Note that the
commonly seen changes during pacing compared with sinus rhythm are present here – paced P waves are lower in
amplitude than the sinus beats, and the P–R interval prolongs slightly during pacing.

FIGURE 11.34 Atrial pacing at 70/min with first-degree AV block. Note the long P–R interval, at almost 0.4 s;
particular caution is warranted in increasing the rate as, although AV conduction is 1:1, it is already very slow. See
Figures 11.35 and 11.36 for worsening of AV block as the atrial rate is increased.

FIGURE 11.35 Second-degree AV block type I with 3:2 conduction. The same patient as above, with worsening
AV block after increasing the atrial pacing rate to 80/min. Note the 1:1 conduction has been lost and there are dropped
beats. After each of the dropped beats the P–R is 0.30 s, which extends to 0.46 s on the next beat, before dropping of
the third beat of each cycle.

PR longer dropped PR longer dropped PR longer dropped

FIGURE 11.36 The same patient again, now with the atrial pacing at 86/min. At the faster atrial rate, AV conduction
has worsened further. There is now a 2:1 block yielding a ventricular rate of 43/min.
338 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

delay as described above, or may operate as simply atrial

Practice tip
pacing if normal AV node conduction occurs before the
If AV block is encountered during atrial pacing and is programmed AV delay has elapsed. Deliberately prolonging
causing significant bradycardia, consideration should the programmed AV delay provides greater opportunity
be given to reducing the atrial pacing rate to see for patients to conduct to the ventricles by themselves. In
whether the severity of the AV block can be reduced. some patients intrinsic ventricular conduction produces a
contractile pattern that is superior to the contraction from
Dual-chamber pacing ventricular pacing; however the difference will be minor.
There has been increasing interest in permitting native
Pacing of both the atria and ventricles offers the benefit of AV conduction because of the above reasons, and also
atrial kick as well as a guarantee of a ventricular response. on the basis of recent data from the DAVID trial, which
Thus, it provides protection against bradycardia and AV revealed that chronic ventricular pacing induces negative
block. As with either atrial or ventricular pacing, demand ventricular remodelling and worsening of heart failure.78
modes have been preferred in dual-chamber pacing, unless Prolonging AV delays to permit native conduction has
oversensing and pacemaker dependence warrant asynchro- become commonplace in permanent pacemakers, but
nous pacing. Particular features of the DDD pacing mode carries some slight arrhythmic risk79 (Figure 11.38).
have made it the predominant mode in both permanent
and postsurgical temporary pacing. DDD pacing: the ‘universal’ pacing mode
Pacing stimuli are delivered to the atria and ventricles The introduction of the DDD mode of pacing (Dual
at a selected rate. After delivery of the atrial stimulus there chamber pacing, Dual chamber sensing and Dual responses
is a delay of usually 0.16–0.24 seconds (equivalent to a [inhibition and triggered ventricular pacing]) added an
P–R interval) before delivery of the ventricular pacing important new dimension to dual-chamber pacing: the
stimulus (Figure 11.37). If the patient is able to conduct ability to synchronise ventricular pacing to spontaneous
the atrial depolarisation to the ventricles themselves before atrial activity in patients with AV block.74 In addition
the ventricular pacing is due, then the pacemaker senses to the normal bradycardia and AV block protection,
the resultant QRS and inhibits ventricular pacing. the DDD mode features a ‘triggered’ function. If the
A dual-chamber pacemaker may demonstrate atrial pacemaker detects a P wave but a QRS does not follow
and ventricular pacing at the set rate and at the set AV within the preset AV interval (AV block), the pacemaker

FIGURE 11.37 Dual-chamber pacing at a rate of 72/min. Note the atrial spikes are followed by P waves (atrial capture),
then after an AV interval of 0.20 s there is a ventricular spike, followed by a QRS complex (ventricular capture).

FIGURE 11.38 AV pacing with prolongation of the AV delay to permit native conduction. There is initially AV pacing at
a rate of 75/min, with an AV delay of 0.16 s. The AV delay is then increased to 0.30 s, during which the patient can be
seen to conduct spontaneously through to the ventricles to produce spontaneous narrow QRS. These are sensed by
the pacemaker and inhibit the ventricular pacing.
 CHAPTER 11 CARDIAC RHYTHM ASSESSMENT AND MANAGEMENT 339

will be triggered to provide ventricular pacing at the end This triggering of ventricular pacing in response to
of the programmed AV interval. In short, the pacemaker sensed P waves is intended to mimic the behaviour of
paces the ventricles after any P wave. This means that the the AV node. It ensures that a QRS follows each P wave
ventricular rate can be brought back under control of the and brings the ventricular rate back under the control of
sinus node, even though there is AV block. Consequently, the sinus node (see Figures 11.39 and 11.40). Ventricu-
in a DDD pacemaker it is common to see ventricular lar pacing will thus be seen at a wide range of rates, as
pacing at a range of different rates as it responds to sinus the ventricular pacing follows the normal speeding and
activity. This triggered behaviour of the DDD device is slowing of the sinus rate in response to activity or illness.
sometimes called ‘P-synchronous ventricular pacing’, If the atrial rate exceeds the upper rate for tracking, then
although ‘atrial tracking’ is a more practical term as the it is no longer possible for all of the atrial beats to be
ventricular pacing ‘tracks’ the atrial rate. tracked. DDD pacemakers will start ‘dropping’ beats when
Atrial tracking allows the pacemaker to pace the the atrial rate exceeds the upper tracking rate in a manner
ventricles in response to the atrial rate sensed by analogous to the behaviour of the AV node.
the pacemaker. This is desirable when the atrial rate is External (‘transcutaneous’) pacing
controlled by the sinus node, but is inappropriate during Emergency pacing may be undertaken noninvasively
atrial arrhythmias. For example, in the patient with AV via external pacing electrodes, and is termed ‘external’
block it is beneficial to pace the ventricles after each sinus or ‘transthoracic’ pacing. Adhesive defibrillation pads
P wave. In contrast, atrial tracking at a 1:1 rate during are applied in either the anteroposterior (preferred) or
atrial flutter would produce an intolerable ventricu- standard apicobasal positions as per defibrillation. These
lar rate, and during atrial fibrillation the tracking rate are connected to a defibrillator with additional pacing
could be even higher. For this reason, an ‘upper rate’ for capability. Pacing stimuli of large current (10–200 mA) are
atrial tracking is programmed in the DDD pacemaker. necessary to achieve myocardial capture, and frequently
The upper rate controls the maximal rate at which also cause uncomfortable or painful skeletal muscle stim-
ventricular pacing can be provided (how fast it may track ulation. Its use is therefore usually reserved for highly
the atria at a 1:1 ratio). This is typically set to around symptomatic/life-threatening bradyarrhythmias, and only
120–130 per minute. In younger patients it may be set as a short-term bridge to invasive pacing. Sedation is
higher, e.g. 140–170/min. typically required in the conscious patient.

FIGURE 11.39 ECG excerpt from a patient with sinus rhythm and 2:1 AV block. The non-conducted P waves are
partially concealed but can be seen distorting the T waves (arrows). Although the sinus node can generate a rate of
75/min, the patient is rendered bradycardic by the AV block.

III aVF V3 V6

FIGURE 11.40 The same patient as above, 2 hours later. A DDD pacemaker has been inserted and, although some
of the pacing spikes are difficult to see, all QRSs are paced beats. The sinus rate is again close to 75/min, and atrial
tracking ensures that a paced QRS follows each P wave. The ventricular rate has been brought back under control
of the sinus node. Note that, although set to a backup rate of 60/min, the pacemaker is pacing much faster than this
because of the triggered behaviour of DDD.

III aVF V3 V6
340 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

External/transthoracic cardiac pacing provides ventric- be unacceptably slow. Failure to capture may be complete
ular pacing only, and the patient should be assessed not only (all spikes not capturing) or intermittent (with only some
for reliable capture, but also for an adequate pulse and blood spikes achieving capture). Even if there are only occasional
pressure during pacing. Pacing may be in either demand spikes that fail to capture, immediate attention is required,
or asynchronous mode, usually at rates of 40–80 beats as complete failure to capture may ensue. Causes and
per minute. management of failure to capture63,70,71,80,81 are listed in
Table 11.9.
Complications of pacing
Effective pacing may be disturbed by problems related
to pacing leads, myocardial responsiveness, programmed TABLE 11.9
values, the pulse generator itself (including power sources), Failure to capture: causes and management
and interactions between these factors.68–72 Four major
CAUSES MANAGEMENT
disturbances to pacing are described below. These provide
the bulk of pacing problems encountered and, because • Output too low • Increase output
they may either interrupt pacing or precipitate serious • Increase pulse width if feature
arrhythmias, critical care nurses need to be competent in is available
their recognition and management. • Changing capture • Check for and treat ischaemia,
threshold hyperkalaemia, acidosis or
Failure to capture alkalosis
When pacing spikes do not successfully stimulate the • Lead maturation
heart this is termed ‘failure to capture’. Pacing spikes • Antiarrhythmic • Consider cessation or dose
are evident on the ECG but are not followed by either drugs reduction
QRS complexes (in ventricular pacing) or P waves (in
• Lead migration/ • Reposition lead if able
atrial pacing) (see Figures 11.41 and 11.42). Failure to dislodgement • Reverse polarity of leads
capture may occur when the myocardial responsiveness (for epicardial wires)
(threshold) worsens, or when impulses do not reach • Position patient on left side
responsive myocardium. Note that dislodgement of a lead (if transvenous lead)
from the myocardium will still show pacing spikes on the • Consider unipolar pacing via
ECG as long as the lead is in contact with body fluids or application of a skin suture
tissue. Repositioning of leads must therefore be included • Treat the resultant rhythm
in considerations during management. (e.g. atropine, isoprenaline)
Failure to capture may present as a clinical emergency • Place another lead
and requires immediate attention. With failure to capture, • Consider external pacing
patients are left to generate their own rhythm, which may

FIGURE 11.41 Intermittent failure to capture. The 1st, 2nd, 6th and 7th spikes gain ventricular capture but the
rest do not. Note the significant pause during failure to capture, in which there is atrial but not ventricular activity.
Symptoms during failure to capture depend on the rate of any underlying rhythm.

FIGURE 11.42 Atrial pacing with intermittent failure to capture (output set at 14 mA). Note that capture is evident
following the 1st, 3rd, 5th, 7th and 8th pacing spikes, but not the others. Fortunately, here the patient has an underlying
sinus rhythm, so that the impact of failure to capture is of no great consequence.

1 2 3 4 5 6 7 8
 CHAPTER 11 CARDIAC RHYTHM ASSESSMENT AND MANAGEMENT 341

Failure to sense
BOX 11.2
Sensing of the intrinsic cardiac rhythm is necessary to
achieve demand pacing. If rhythms are not sensed, pacing Failure to sense: causes and management
will proceed at a fixed rate and in competition with the Causes:
native rhythm (Figures 11.43 and 11.44). Pacing spikes • Sensitivity set too low (too high a number)
may thus be delivered during the excitable period of
• Set in asynchronous mode (AOO, VOO or DOO)
the action potential and trigger tachyarrhythmias (see
Figure 11.31). The risk of arrhythmias is greatest when • Altered sensing threshold (lead maturation)
ventricular pacing spikes are delivered just after the peak of • Decreased myocardial voltages
the T wave, especially when there is myocardial ischaemia • Lead movement/dislodgement
or infarction, or hypokalaemia. Immediate restoration
Management:
of appropriate sensing needs to be undertaken. Causes
and management of failure to sense72,80,82 are detailed in • Increase sensitivity (to a lower number)
Box 11.2. Remember, however, that sensing controls are • Check/tighten connections
inverse: lowering numerical settings (e.g. from 5 to 2 mV) • If epicardial leads, reverse the polarity of the
increases the sensitivity while increasing the value (from electrodes (reverse connections of positive and
1 to 4 mV) makes the pacemaker less sensitive. negative electrodes)
Failure to pace • Increase the pacing rate to overdrive the competing
rhythm
Failure to pace is an imperfect term that is used to
describe the event when the pacemaker does discharge • If underlying rhythm satisfactory, consider turning
but the impulse fails to reach the patient. In this sense it pacemaker off
may be useful to regard failure to pace as resulting from an • Consider placement of an alternative sensing
incomplete electrical circuit. The flashing pace indicators electrode (skin suture) to create unipolar pacing
on temporary pacemakers confirm that pacing has

FIGURE 11.43 Ventricular pacing with failure to sense. At the start of the strip there is ventricular pacing. A junctional
rhythm appears at a slightly faster rate than the ventricular pacing, but despite this the pacemaker continues to fire,
delivering the spikes into the ST segment and T wave. Appropriate sensing of the last three beats of the strip would
have caused inhibition of these pacing spikes.

FIGURE 11.44 Atrial failure to sense. The first three beats show atrial pacing. Then there are two spontaneous
P waves (fourth and fifth beats). These P waves should have inhibited the atrial pacing, but pacing spikes can be
seen at the start of the QRS of the fourth beat and in the ST segment of the fifth beat.
342 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

FIGURE 11.45 At the start of the strip there is ventricular pacing at a rate of around 85/min. However, the pacing
spikes abruptly cease and the patient is left to generate his/her own slower rate. Spikes do reappear but these are
at a slower than the programmed rate. This could be either failure to pace or oversensing during ventricular pacing,
and differentiation cannot be made absolutely from this strip. Rather, pacing indicators need to be examined to aid
this differentiation. This was a case of ventricular failure to pace due to a poor connection of the pacing leads to the
bridging cable.

FIGURE 11.46 Atrial pacing with failure to pace. There is sudden disappearance of the pacing spikes after the first
three beats. From this strip alone, failure to pace or oversensing cannot be separated as possibilities. However, the
pacing indicator was flashing through such pauses, rather than the sensitivity indicator, confirming failure to pace. The
connection between the pacing wires and the bridging cable needed tightening and immediately corrected the problem.

occurred but the spikes fail to appear on the ECG. Most

BOX 11.3
commonly, failure to pace is due to a loose connection in
the lead system or a fractured lead or bridging cable, and Failure to pace: causes and management
may involve either the negative or positive limb of the Causes:
circuit. Electrocardiographically, failure to pace appears as
failure of the pacing spikes to appear when expected. As • Disconnected lead/loose connections – commonest
with failure to capture, this leaves patients with whatever cause
rhythm they can generate themselves, which may or may • Pacemaker turned off or dysfunctional
not be adequate. Failure to pace (also termed ‘failure to • Output turned off
output’ in some literature) may present as complete loss • Battery depleted
of pacing, or just pacing at a slower rate than set (see
Figures 11.45 and 11.46). If the patient’s rhythm is very • Fractured lead (may be internally fractured but
slow, failure to pace can be a clinical emergency. Even outwardly intact)
if there is an adequate rhythm, the situation requires Management:
immediate attention. Causes and management of failure • Check that pacemaker is turned on
to pace36,63,80,81 are detailed in Box 11.3. • Check all connections and leads, and tighten/
replace if necessary
Practice tip • Change battery
The ECG usually does not help to distinguish between • Replace the bridging cable between the pacemaker
oversensing and failure to pace, and instead – at least and the pacing leads
with temporary pacing – the distinction is made from • Ensure output is turned on
inspection of the flashing pacing indicators. If the
• Complete circuit with skin suture to positive
pacing indicator continues to flash during periods where
terminal of the pacemaker, and try each of the
the spikes do not appear, then the problem is failure to
existing wires in the negative terminal
pace (an interrupted electrical circuit). Alternatively, if
the sense indicator is flashing during a period where the • Differentiate from oversensing
spikes do not appear, then the problem is oversensing. • Assess and support rhythm and haemodynamics
 CHAPTER 11 CARDIAC RHYTHM ASSESSMENT AND MANAGEMENT 343

Oversensing
Practice tip
As in failure to pace, pacing spikes fail to appear when
oversensing occurs. Rather than sensing intrinsic cardiac A ring magnet placed over a permanent pacemaker
activity, the pacemaker may sense electrical signals (electro- causes a permanent pacemaker to revert to an
magnetic interference) from other sources. The device asynchronous mode (VOO or DOO). It is thus a
will respond as if these are genuine signals and inhibit management strategy for symptomatic oversensing
pacing. Oversensing is a common event during temporary or for contexts where there is risk of oversensing
pacing and electrocardiographically may be indistin- (e.g. the pacemaker-dependent patient receiving
guishable from failure to pace, as both appear as missing diathermy). The magnet may need to be taped in
pacing spikes. place while the oversensing risk persists. To avoid
Oversensing may result in momentary interruptions possible undersensing of an emerging cardiac rhythm,
to pacing (pauses) or complete cessation of pacing. The asynchronous pacing under magnet influence is applied
clinical impact depends on the duration of oversensing, at an elevated rate (e.g. 90–100 beats per minute).
and on the patient’s ability to generate an underlying
rhythm. Electromagnetic interference resulting in over- Patient nursing practice
sensing may arise from a variety of causes, originating Monitoring and management of the patient and pacing
from the patient (muscle movement) or external sources largely fall to the nursing staff of critical care units. Nurses
(devices). The sources of oversensing36,63,82 may be difficult monitor pacing performance and the detection of pacing
to establish clinically but should be sought and corrected abnormalities, the integrity of the pacing system, the
where possible. Causes and management of oversensing avoidance of clinical situations or physical changes that
are detailed in Box 11.4. may alter pacing effectiveness, patient safety and the
An important distinction must be made between prevention of complications.
failure to pace and oversensing as both appear electro- Nursing responsibilities in the care of the patient with
cardiographically as missing spikes. Examination of the a pacemaker include:
pacemaker indicator lights is most useful: during failure • pacemaker site inspection for inflammation/swelling/
to pace, the pace indicator will flash during the periods of haematoma
missing spikes whereas in oversensing the sense indicator
will flash. • avoidance of hip flexion and rest in bed if femoral
insertion
• vital signs, circulatory observations etc, at intervals
BOX 11.4 appropriate to the overall patient context

Oversensing: causes and management

• confirmation of capture and sensing
Causes:
• identification of return of spontaneous rhythm
• Muscle potentials other than QRS complexes:
• assessment of haemodynamic adequacy during both
paced and spontaneous rhythms (BP, CO, perfusion,
Cardiac: T waves, U waves, P waves symptoms)
Non-cardiac: shivering, fasciculations, • strip documentation of rhythm 6-hourly and daily
seizure activity, any skeletal muscle 12-lead ECG
movement
• chest X-ray to confirm the position of the wire/
• External electrical interference: absence of complications
Electrocautery, TENS machines • checking and tightening of all connections (leads to
Electrical devices (rare) bridging cable, bridging cable to pulse generator) at
• Movement of the connecting pins at the commencement of the shift and during all pacing
connection to the pulse generator (common) adverse events
Management: • confirmation of battery status each shift
• Reduce sensitivity (turn sensitivity to higher • performance of pacemaker threshold assessment each
number) shift or daily.
• Consider disabling the sensitivity altogether Protection against microshock
(i.e. asynchronous, VOO, AOO, DOO mode)
Normally, small electrical stimuli (even static electricity
• Consider reversing the polarity of the wires applied to the body) dissipate through body tissues and
(positive to negative) never reach sufficient current density at the heart to produce
• Remove the source of interference where it can arrhythmias. However, pacing wires provide a direct route
be identified to the heart, so that even minor electrical sources may
achieve sufficient current density at the heart to precipitate
344 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

arrhythmias. Protection strategies include nursing patients that temporary pacemakers carry a small stored charge
in body- and cardiac-protected areas, insulating lead that is enough to sustain pacing for about 10 seconds. If
connector pins when pacing is not in use and using rubber a well-rehearsed procedure is undertaken, battery change
gloves at all times when handling pacing wires.82 can be performed without interrupting pacing for even
a single beat. An understanding of the behaviour of the
Battery depletion in a temporary device in use should be established before undertaking
pacemaker battery replacement.
A standard 9V battery powers a temporary pacemaker for
up to a week, although this is variable depending on the Pacemaker function testing
device and settings. It is prudent to commence treatment Routine pacemaker performance checks should be
with a new battery to avoid unexpected power failure undertaken regularly in the patient with a temporary
during use. pacemaker. Temporary pacing leads and wires are prone to
Indicators of declining battery status are usually movement and other causes of sensing and capture threshold
displayed when less than 24 hours of battery life remains: variation. Variations may also be marked when there is
flashing battery icons appear on the digital screens of myocardial, biochemical and haemodynamic volatility as
newer generation devices while, on both new and older often seen in the critically ill patient. Pacemaker tests are
non-digital screen devices, pacemakers will stop supplying performed to reveal the return of underlying rhythm,
power to the flashing sense/pace LEDs while pacing which may be being concealed by pacing, and to measure
continues. Battery replacement should be undertaken thresholds for both capture and sensing as these values
as soon as reasonably possible as these indicators are not typically change with time and in response to changing
obvious until looked for, so some time may have elapsed myocardial responsiveness.66,70,74,80 Regular checking allows
before detection by staff. detection of threshold changes, and setting of sensing and
Changing the battery on a temporary device carries output safety margins, in order to minimise the develop-
the risk of interrupting pacing, which may be disastrous ment of acute failure to capture or failure to sense.
in the pacemaker-dependent patient. Although the The practices employed to test temporary pacemakers
time taken to change a battery may be brief, additional vary widely, as do attitudes to whether this may or may
significant time may be lost if the device ‘powers down’ not be undertaken by nurses. The sample protocol shown
during the battery change. It is worth noting, however, in Figure 11.47 provides an organised approach to testing

FIGURE 11.47 Routine temporary pacemaker testing protocol: underlying rhythm, output and sensitivity threshold test.

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 CHAPTER 11 CARDIAC RHYTHM ASSESSMENT AND MANAGEMENT 345

during which safety has been emphasised. Because of the so decrease the rate gradually and only to reasonable levels
varying attitudes to nursing responsibilities, the use of (sinus rates of less than 50 are unlikely to be beneficial).
this approach should be ratified at individual institutions Be sure to gain participation of the multidisciplinary team
before use. before undertaking testing in this context.
Testing pacemaker thresholds is performed daily or on Threshold testing in the pacemaker-dependent patient
each shift, but not if the patient is unstable, using the steps is also contentious as loss of capture during testing may be
described in Figure 11.47. The test should be carried out poorly tolerated. If the capture threshold is not measured,
promptly, with attention to avoiding undue bradycardia however, a rising threshold and loss of safety margins
or periods of asynchronous pacing. The patient should be cannot be identified, and may only become apparent upon
advised that pacemaker assessment is being undertaken development of acute failure to capture, possibly with
and to report any sensations of lightheadedness, dyspnoea outputs already set to maximum and, therefore, no scope
or other discomfort. for recovering capture. An alternative approach to testing
thresholds in this context is useful. Rather than formally
Pacemaker testing in the unstable pacemaker- measuring threshold by creating loss of capture, the output
dependent patient may be decreased to a value that confirms safety margins
Greater caution must be applied in the testing of pacemaker are still possible, but without having lost capture at any
functions if the patient has marked haemodynamic instabil- point, e.g. decreasing output to 10 mA on a device with
ity or has little or no underlying rhythm. It is common for an output capability of 20 mA. If there is still capture
pacemaker testing to be avoided altogether in such circum- at 10 mA, further reductions can be avoided because a
stances although this may be misguided. Routine testing of 10 mA safety margin has been demonstrated.
pacemaker function as described in Figure 11.47 may not
be suitable, but testing for underlying rhythm and some Permanent pacing
level of testing of capture threshold so as to be confident For bradyarrhythmias that are not due to temporary,
of safety margins are beneficial. For the patient with reversible factors or that are likely to be sustained or
haemodynamic instability and/or inotrope use, testing for recurrent, permanent pacemaker implantation may be
underlying rhythm becomes of even greater importance undertaken. Indications vary, but syncopal events, symp-
as pacing may either prevent or conceal the return of tomatic bradycardia, pauses greater than 3 seconds and
sinus rhythm capability, and cardiac output may be as bradycardia-dependent tachyarrhythmias are general indi-
much as 50% greater with the atrial kick of sinus rhythm cations for permanent pacing.75 Dual chamber pacing is
than during pacing (see Figure 11.48). It may take several usually provided83 unless the patient has chronic atrial
seconds for the sinus node to ‘warm up’ and express itself, fibrillation as it is not possible to capture the atria during

FIGURE 11.48 Unveiling haemodynamically superior underlying rhythm (strips are continuous). Initially there is
ventricular pacing at a rate of 68/min. No atrial activity can be seen and the blood pressure is 85/50 mmHg with
noradrenaline support at 8 mcg/min. Across the top strip the paced rate is reduced, allowing P waves to emerge at a
rate of 60/min (arrow) and then accelerate to around 70/min across the lower strip. Note the impressive BP increase to
125/65 mmHg allowing discontinuation of noradrenaline infusion. (Note also: cardiac index recorded during V pace
1.7 L/min/m2, during sinus rhythm 2.3 L/min/m2.) Importantly, there was no suggestion of sinus capability until the
pacing rate was reduced.

68 60

85/50

70

125/65
346 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

fibrillation. For such patients rate responsive ventricular Passage of leads into the heart during insertion may
pacing (VVIR) is the most common mode.83,84 A dual result in endocardial contact, causing AV block or bundle
chamber pacemaker may still sometimes be implanted if branch block. Therefore, a femoral temporary pacing wire
there is anticipation of possible future reversion of atrial may be inserted before progressing to placement of the
fibrillation, and the device programmed to DDI or VVI permanent pacing leads, particularly to ensure reliable
in the interim. Alternatively, the device may be implanted ventricular rhythm during the insertion procedure.
in DDD mode, which allows the device to automatically Ventricular lead placement is most commonly in the right
mode switch to DDI or VVI while the patient is in atrial ventricular outflow tract (RVOT) or against the ventri-
fibrillation and then automatically switch back to DDD if cular septum,78,85 to produce a more normal contractile
atrial fibrillation reverts. pattern than from the previously used apex and to prevent
The most common mode of pacing with dual chamber the ventricular remodelling seen in chronic RV apical
devices is DDD, unless the patient has recurrent atrial pacing.78,85 Atrial lead insertion is most commonly at the
tachyarrhythmias in which case a non-tracking mode right atrial appendage, i.e. in the roof of the right atrium.
(e.g. DDI) may be selected.83,84 Patients with sinus node Both ventricular and atrial leads are tested for performance
dysfunction are more likely to have rate responsive pacing following placement. Leads are then secured within the
enabled so that the pacemaker can adjust pacing rates to pacemaker pocket and the pulse generator is attached to
activity and exercise. the leads and secured in the pocket. The pocket is closed
A pulse generator is positioned in a pre-pectoral and testing is repeated to confirm secure connections
pocket and leads advanced into the heart either through of the leads to the pacemaker. Device and lead testing is
subclavian vein puncture (from within the pocket) or via repeated on day 1, weeks 6–8 and then every 12 months
cephalic vein cut-down. The cephalic approach avoids to confirm operation and to fine tune programming to
intrathoracic complications such as pneumothorax or patient status.50
haemothorax, which may accompany subclavian puncture.
Typical pacemaker longevity is 8–12 years. Pacemaker parameters: programming
Permanent pacing leads differ from temporary pacing and status reports
wires in that, for chronic stability over a lifetime of Knowing how a patient’s pacemaker is programmed
activity, the leads must be ‘fixed’ in some manner to the is crucial to interpreting pacemaker behaviour in the
myocardium. ‘Active fixation’ leads have an extendable clinical setting. This has become increasingly important to
helix that is screwed into the myocardium at the time enable determination of whether a change in behaviour
of implantation, much like a corkscrew. ‘Passive fixation’ represents a pacing problem or is simply an automated
leads in contrast are not directly secured to myocardium behaviour. Device printouts are available whenever a
but have soft tines similar to the barbs of a spear, near device is interrogated or reprogrammed. The following
the lead tip.67 The lead is positioned where these tines section is a guide to how to interpret device printouts
can embed within muscle infoldings (trabeculae) at the to access key information about pacemaker program-
ventricular apex or in the right atrial appendage. Both ming, highlighting some of the features of the modern
types of leads have good chronic performance in terms of permanent pacemaker, as well as some of the clinical and
sensing and stimulation thresholds.67 However, an inflam- diagnostic value of the information provided. Device
matory response does develop at the lead–tissue interface printouts contain an enormous amount of information,
and contributes to an increase in capture thresholds. This but of immediate importance are the summary pages that
is most marked in the first month (acute threshold phase) outline all of the operating parameters, active automated
during which the threshold may double or triple, before features, results from recent tests and battery status (see
settling at a lower chronic threshold.67 Steroid-tipped Figure 11.49 for an example). Important elements include
leads are now universal and limit the local inflammatory the following:
response, reducing the magnitude of the acute threshold
increase.67 Because of the expected threshold change • Patient/device details: patient name, type of device,
date and time of the printout.
during the first month or so, output safety margins need
to be set more generously and patients are typically sent • Battery information: a bar graph displays the progress
home with outputs set high (e.g. 3.5–5 V) even when of the battery towards the elective replacement
thresholds at implantation may have been only 0.5–1 V. indicator (ERI); the magnet rate (i.e. the rate that
Chronic output settings will then be established at the first asynchronous pacing will occur at if a magnet is
postoperative visit to the doctor in 6–8 weeks.48 placed over the device); the longevity (indicating the
minimum remaining longevity of the device if the
Implantation activities patient were to be paced 100% of the time at the
Devices are inserted under light conscious sedation and current settings).
local anaesthesia. Analgesia may also be administered at the • Current parameters: basic pacemaker set-up including
outset of the case, and antibiotics are commenced before base rate, maximum rate at which the atrial rhythm
skin incision. An anaesthetist is usually only present if will be tracked, AV delay, output settings and pulse
judged necessary by the implanting doctor. widths for both chambers.
 CHAPTER 11 CARDIAC RHYTHM ASSESSMENT AND MANAGEMENT 347

• Episodes: summary of any arrhythmia episodes that • Lead impedance: the results of impedance
have been recorded since the last interrogation and measurements from the current interrogation and
any automatic mode switching events that have the last session; this provides information about the
occurred. integrity of the pacing leads, connections and their
interface with the myocardium. Impedance is the
• Events: an event in pacing terms is a beat, rather than
resistance to current provided by the electrical circuit.
a clinical event; every atrial beat (sensed or paced) and
every ventricular beat (sensed or paced) is recorded Variations in impedance may be seen if the pacing
allowing the calculation of the percentage of atrial lead insulation is being degraded, the pacing circuit
and ventricular pacing since the last interrogation; is interrupted or not properly connected or the
this can be compared to previous reports to assess pacing lead becomes dislodged. Generally, measured
whether pacemaker dependence is increasing or impedances do not vary by more than 100 ohms
decreasing. between sessions.

• Test results: the results of device and lead testing Cardiac resynchronisation therapy
performed during the current interrogation as well
Cardiac resynchronisation therapy (CRT) involves the use
as testing from the last session performed, including
of pacing to improve the performance of the left ventricle
graphic trends of all test results over time shown in
in heart failure patients. Initially, CRT was undertaken
a separate section of the report. only in patients with severe heart failure (New York Heart
• Sense results: the results of the sensing tests carried Association Class III–IV with ejection fraction <30%) due
out in the current interrogation, the last session’s to dilated cardiomyopathy and with left bundle branch
values are also shown, and graphic trends of sensing block (LBBB),86,87 but its proven efficacy in all major
over time can be viewed in a separate section of the randomised controlled studies88–92 has seen the range of
report. indications expand to include patients with less severe

FIGURE 11.49 FastPath Summary from a St Jude Medical Accent™ dual chamber pacemaker (St Jude Medical
Sylmar CA), highlighting basic parameters, events and test results recorded during pacemaker interrogation. Any test
results or settings followed by an ‘A’ in a circle denote automated features. Thus, this device will automatically test
capture thresholds and set outputs according to these tests every 8 hours or if ever there is non-capture. Similarly,
sensing is automatically tested and automatic sensitivity algorithms allow for changing myocardial voltages. Lead
impedance measurements are automatically tested daily, and the pacemaker can automatically switch from bipolar
to unipolar to maintain normal capture and sensing if impedance measurements violate alarm limits. See text for
additional details.

page 1 of 3
AccentTM DR RF 2210 (DEMO prB.E.60) FastPathTM Summary 9 Nov 2010. 17:35
Alerts Note Current Paramenters
Mode DDDR
Base Rate 60 min–1
Max Track Rate 130 min–1
Paced/Sensed AV Delay 200/150 ms
A/V Pulse Amp 2.0/1.25 V
Battery Information A/V Pulse Width 0.4/0.4 ms
Longevity: 11.1–12.2 yrs
Episodes
Voltage: 3.13 V
New EGMs: 3
~ERI Most Recent: Entry Into AMS

Magnet Rate 100.0 ppm

Battery Current 9 uA Events

Text Results (Last Session: 8 Sep 2010) AP: 11% VP: 24%
100
A Automatic

Atrium Ventricle %
Time
Capture Today: 1.0 V A Today: 1.0 V A
Last Session: 1.0 V Last Session: 1.0 V
AS-VP AS-VS AP-VP AP-VS PVC
Sense Today: 4.2 mV A Today: >12.0 mV A 21% 68% 3.0% 8.0% 0%
Last Session: 4.2 mV Last Session: >12.0 mV

Lead Today: 530 Ω A Today: 530 Ω A

Impedance Last Session: 530 Ω Last Session: 530 Ω
Mode Switch
Mode Switch: 2%
AMS Episodes: 5
348 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

heart failure (New York Heart Association Class I and

II).93 CRT is typically only undertaken after demonstrat- Practice tip
ing failure to respond to optimal pharmacological therapy. For the patient with a CRT device whose heart failure is
Optimum systolic performance requires all segments worsening, investigate whether there are device-related
of the ventricles to contract more or less synchronously. factors that may be correctable:
However, in LBBB septal depolarisation occurs well
in advance of the delayed conduction to the postero- • Is the patient being ventricularly paced >90% of the
lateral left ventricular wall. The impact on contraction time? If not, they will be losing the potential benefit
of resynchronisation.
is to create ventricular dyssynchrony, with the septum
contracting before the lateral wall.94 Similarly, ventricular • Can you determine whether there is capture from
both the LV and RV leads? Compare with old ECGs
relaxation becomes dyssynchronous, which may lessen
where available.
myocardial perfusion and limit ventricular filling, both
of which contribute to the severity of heart failure.94
The majority of patients with LBBB have dyssnchrony Non-responders to CRT
and systolic dysfunction, and the impact of this becomes Disappointingly, up to 25 % of patients who receive
more pronounced when there is existing myocardial CRT devices fail to gain the expected benefits of
disease and/or heart failure.26,81 With very wide LBBB improved heart function and are termed non-respond-
(e.g. >0.14 s) the impact is greater, as the dyssynchrony ers.90,92,101 Failure to respond may be due to device- or
between the septal and free wall contraction is exagger- lead-related factors, or because of cardiac factors that
ated.87, 94– 96 contribute to worsening heart failure, especially
In CRT, pacing leads on both the right ventricular (RV) myocardial ischaemia, atrial fibrillation98 and diminish-
septum and the left ventricular (LV) posterolateral wall are ing responses to adjunctive pharmacological therapy. It
used to stimulate both muscle masses at the same time, should be noted that the preference in CRT is to see
with the aim of improving heart failure in patients with paced ventricular rhythms rather than the patient’s own
significant dyssynchrony.97 LV and RV pacing stimuli may QRS complexes as pacing produces a synchronised
be delivered simultaneously, although programming of LV contraction of the LV compared to the patient’s native,
stimulation prior to RV pacing by 10–60 milliseconds is dyssynchronous contraction. The aim is for >90% of
more common with the aim to reduce QRS duration to ventricular beats to be paced to achieve the desired
normal duration (<0.12 s).97 Expected outcomes of CRT benefit from CRT. Amongst device/lead-related factors
include:88–98 is loss of capture by either the LV or RV lead, resulting
in loss of resynchronisation. Recognition of this can
• improvement in New York Heart Association be difficult because loss of capture by only one of the
functional class
ventricular leads will still appear as capture from the
• improvement in quality of life remaining ventricular lead (see below). Atrial fibrillation
• improvement in physical function is a particularly problematic event for CRT patients as
• improvement in ejection fraction and reduction in they are generally more dependent on atrial kick and the
ventricular size faster rates reduce ventricular filling times. Additionally,
because they conduct with their own LBBB rather than
• reduced hospitalisations for heart failure receiving biventricular pacing they lose the benefit of
• cardiovascular mortality reduction. resynchronisation.
The right ventricular lead is implanted in standard
fashion, positioned either at the RV apex or outflow Optimisation of device programming
tract. Most commonly, the left ventricular lead is also Optimum device programming can have a significant
positioned transvenously, with the lead advanced through impact on the benefit conferred by CRT.101 It is not
the coronary sinus into a coronary vein on the lateral or practical for all patients to undergo regular echocardio-
posterolateral LV wall. In a minority of cases a separate graphy for programming optimisation and so alternative
mini-thoracotomy may be necessary for secure position- approaches to optimisation have been developed. The
ing of an epicardial LV lead when access to the coronary critical timing factors that should be optimised are
sinus cannot be achieved or where the patient lacks the atrioventricular (AV) delay and the delay between
suitable coronary veins. stimulation of the left and right ventricles (V–V
Two types of devices currently exist: CRT-P delay). Recent developments allow ‘electronic optimi-
(pacemaker), which is a pacemaker achieving resyn- sation’ whereby CRT devices themselves can calculate
chronisation, and CRT-D (defibrillator), which adds optimum settings based on automated measurements
resynchronisation to an implantable cardioverter defibril- of intracardiac conduction,102,103 but these are not
lator. The latter devices are more commonly implanted available on all devices. The impact of effective optimi-
as the combination of severe heart failure and ventricular sation may be sufficient to convert non-responders to
tachyarrhythmias is frequently present.99,100 responders.
 CHAPTER 11 CARDIAC RHYTHM ASSESSMENT AND MANAGEMENT 349

Recognising failure to capture in a R wave, or less commonly as an rSR. QRS in lead I

CRT device will be a negative complex, either as a QS or rS
complex104 (see Figure 11.50).
Recognising failure to capture in CRT is made difficult
by the fact that both ventricles are paced. Failure of pacing • Bi-ventricular capture: the ECG is less predictable
to produce QRS complexes will only occur if there is depending upon the timing of the left and right
failure to capture from both LV and RV leads.103 The ECG, ventricular stimuli. If LV stimulation occurs well
during failure to capture by just the LV lead, will still show ahead of RV, the ECG will look more like LV capture
capture from the RV lead, and vice versa. Instead of loss only whereas, if RV stimulation occurs well ahead of
of the QRS, to identify loss of capture it is necessary to LV, the ECG will look more like RV capture only.
look more closely at QRS morphology and vectors to Nevertheless, the expectation is that, when both
confirm capture or loss of capture from either the left or leads are capturing, the QRS will become narrower
right ventricular lead.103 A 12-lead ECG is helpful but, if (usually <0.12 s)98,104 with the axis deviated most
not available, lead V1 (or MCL1) and lead I are the most commonly to the right. Morphologies are usually
helpful in confirming RV, LV or bi-ventricular (Bi-V) somewhere between those seen with RV-only or
capture. Specific changes include: LV-only pacing. A uniform ECG pattern cannot
be described, but in a given patient there should be
• RV capture only (loss of LV capture): the QRS will consistency between serial ECGs (see Figure 11.50).
be wide (>0.12 s) with left-axis deviation; lead V1 (or
MCL1) will be a negative complex, most commonly Phrenic nerve stimulation in CRT patients
as a QS complex. QRS in lead I will be upright, as an The phrenic nerve courses inferiorly behind the
R wave or sometimes rSR104 (see Figure 11.50). left ventricle and it is possible for left ventricular pacing
• LV capture only (loss of RV capture): the QRS will to directly stimulate the phrenic nerve producing
be wide (>0.12 s) with right-axis deviation; lead V1 repetitive diaphragmatic contraction of varying intensities.
(or MCL1) will be an upright complex, either as an These may be continuous and uncomfortable or painful.

FIGURE 11.50 The appearance of lead V1 during alternation of pacing sites with a CRT system. In the top strip
there is Bi-V pacing with a narrow QRS, which is negative in V1. In the same strip, loss of LV capture results in RV-
only pacing. The QRS widens to beyond 0.12 s and becomes more deeply negative in V1. In the second strip RV-only
becomes Bi-V pacing after re-establishing LV capture. The QRS returns to its initial morphology as in strip 1. In the
3rd strip Bi-V pacing is present initially followed by loss of RV capture, resulting in LV-only pacing. Note that the QRS
becomes upright in V1 and again widens to well beyond 0.12 s. In the lower strip LV-only pacing precedes the return to
the previous Bi-V morphology as RV capture is restored.

Bi-V RV only

RV Bi-V

Bi-V LV only

LV Bi-V
350 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Programming may overcome the problem but, if unsuccess- defibrillator may be necessary. Emergency defibrillation,
ful, reoperation to reposition the left ventricular lead may electrical principles and equipment management are
be necessary, or resynchronisation therapy may need to be discussed more completely in Chapter 24.
abandoned altogether. More recent developments with
‘quadripolar’ left ventricular leads, featuring four separate Elective cardioversion
pacing electrodes, permit programming to use an alternative Elective direct current reversion (DCR, or cardioversion)
electrode rather than the one causing phrenic stimulation applied under short-acting sedation or anaesthesia is
and have been successful. Quadripolar leads also provide undertaken for non-cardiac arrest arrhythmias.108 These
the ability to program to an electrode (or vector) that has include atrial fibrillation, tachycardia or flutter, conscious
the lowest capture threshold, improving battery longevity. ventricular tachycardia, AV nodal reentry tachycardia
and conscious tachyarrhythmias complicating Wolff-
Multipoint biventricular pacing Parkinson-White syndrome. The time available for prepa-
The new quadripolar leads mentioned above have also led ration is variable and depends on the haemodynamic
to newer generation devices that now permit pacing from impact of the arrhythmia. Patients admitted for reversion
two separate electrodes on the quadripolar lead.101 So-called of atrial fibrillation or flutter may be stable throughout
multi-point pacing further improves left ventricular resyn- their hospitalisation, whereas patients with conscious VT
chronisation beyond single site pacing and has been shown may initially demonstrate stability, only to decompensate
to improve haemodynamics and patient response rates over later without warning.
conventional CRT configurations.101,105,106 Unlike emergency defibrillation, cardioversion shocks
are synchronised to the cardiac cycle so that they are
Cardioversion delivered into the QRS complex. Unsynchronised shocks,
if delivered into the T wave, can cause immediate degen-
Electrical cardioversion can be applied as an alternative or eration into ventricular fibrillation.When synchronisation
adjunct to pharmacological therapy in the management is selected (‘ON’) on the defibrillator control panel, a
of tachyarrhythmias. By far the most common cause of marker is inscribed on each detected QRS complex on
tachyarrhythmias is reentry, in which current can continue the monitor screen to confirm successful synchronisation.
to circulate through the heart because of different rates When time permits the patient should be thoroughly
of conduction and recovery in different areas of the investigated, including physical examination, neurological
heart (temporal dispersion). Conduction through reentry assessment, palpation of peripheral pulses, electrocardio-
circuits can continue as long as the circulating stimulus graph, biochemistry and serum drug levels where necessary.
encounters non-refractory tissue.The aim of cardioversion Fasting should be ensured.108,109 If atrial fibrillation is
is to excite all myocardial cells at the same time with present transthoracic echocardiography is undertaken to
the result that all of the heart will also be refractory at the rule out atrial thrombus, as restoration of atrial contraction
same time. If this is achieved, the circulating stimulus dies may cause pulmonary or systemic arterial embolisation.
out for lack of non-refractory tissue to conduct through. If The patient should be fully informed of the rationale for
the applied shock does not depolarise the greater bulk of and nature of the procedure and have all necessary prepa-
myocardium, then non-depolarised cells are still available ratory tasks explained to them.
for conduction and the arrhythmia may persist. External The cardioversion team should include a minimum
shocks of 100–200 joules (biphasic) are required for of one medical officer, skilled in emergency rhythm
sufficient current density to reach the myocardium and management and airway management including intubation,
depolarise the greater bulk of cells, thus extinguishing and two critical care nurses, who usually prepare the patient
available pathways.107 Drugs or biochemical correction and equipment, assist in sedation, perform the cardiover-
may be necessary to prevent recurrence. Success rates sion, document events and manage aftercare. Usually, there
from cardioversion range from 70–95%, depending on the is a cardiologist and anaesthetist present for the separate
rhythm.107 Arrhythmias due to increased automaticity are roles. All team members should confirm readiness and
less amenable to cardioversion, as there is a higher chance confirm synchronisation selection and correct defibrilla-
of early arrhythmia recurrence; and for arrhythmias tor energy settings (in joules). The patient is sedated (e.g.
occurring as a complication of digitalis toxicity, cardio- midazolam) or anaesthetised (e.g. propofol), preoxygenated
version (but not defibrillation) is contraindicated.107 on 100% oxygen delivered by bag and mask and cardio-
Early defibrillation increases survival from ventricu- verted under ECG and oximetry monitoring. Electrical
lar fibrillation. The success of public-access defibrillator safety, and ensuring that all personnel are clear of the bed, is
schemes has warranted their increased availability.108 Auto- the primary responsibility of the nurse delivering cardiover-
matic external defibrillators (AEDs) in the home or sion, whether via paddles or hands-free electrodes.
community simplify the task of applying defibrillation by After the procedure the patient should be closely
non-healthcare responders and increase access to definitive monitored for return to wakefulness, airway protection
electrical management for patients suffering ventricu- capability, effective respiration and gas exchange, rhythm
lar arrhythmias. For patients who have survived previous stability, blood pressure and for any changes in neurolog-
arrhythmic cardiac arrest, an implantable cardioverter ical status or peripheral pulses. Pain and inflammation at
 CHAPTER 11 CARDIAC RHYTHM ASSESSMENT AND MANAGEMENT 351

cardioversion discharge sites may be lessened by applica- failure the antibradycardia arm may be provided as biven-
tion of topical ibuprofen 5% cream 2 hours before elective tricular pacing (to achieve cardiac resynchronisation).
DCR, where this is feasible.110 Energy requirements for Antitachycardia features are those therapies provided to
reversion of atrial tachycardia or flutter may be as little as treat ventricular tachyarrhythmias and include antitachy-
50 J.110,111 The 2010 recommendations of the European cardia pacing (ATP), also termed overdrive pacing, as well
Resuscitation Council are for initial shocks at 70–120 J as cardioversion (for VT) and defibrillation (for very fast
(biphasic) for atrial flutter, and 120–150 J for cardiover- VT or VF). Refer to Figure 11.51 for examples of these
sion of atrial fibrillation and ventricular tachycardia.58 If therapeutic modes.
initial shocks are unsuccessful, repeat attempts at higher Devices are inserted in a similar fashion to the
energy settings (up to 360 J) may be undertaken. Prior to pacemaker (see the above section Permanent pacing).
discharge, patients and their families should be informed However, ICDs are most commonly positioned in the
of the potential for post-procedural chest wall discomfort left subclavian/pectoral location, leaving the right side of
and topical and oral analgesic advice provided. the chest available for conventional placement of external
Implantable cardioverter defibrillators defibrillator paddles should they ever become necessary.
Atrial and ventricular leads are placed transvenously via
Implantable cardioverter defibrillators (ICDs) may the left subclavian vein. Atrial leads are normal atrial
be implanted for survivors of sudden cardiac death
pacing leads, but the ventricular ICD leads are slightly
(SCD) or haemodynamically significant, potentially
larger than pacing leads and carry the normal ventricular
lethal, ventricular arrhythmias.112 They have been
pacing circuitry, as well as coils encircling the lead that
repeatedly demonstrated in large clinical trials to provide
emit the high energy shock discharges. Single coil systems
significantly improved survival compared with pharma-
cological treatment.113–115 This ‘secondary prevention’ have one coil positioned on the lead at the level of the
application of ICDs dominated the early indications for right ventricular cavity, and shocks travel from this coil
devices, with trial meta-analysis demonstrating a mean to the metal casing of the ICD. Dual coil leads feature
27% mortality reduction compared to antiarrhythmics.55 this same right ventricular coil as well as a second coil
However, more recently indications have expanded to in the superior vena cava. In these systems, shocks can
‘primary prevention’ in patients without prior cardiac be configured to travel from the RV coil to the superior
arrest, as it has become clear that heart failure patients vena cava coil, from the RV coil to the ICD, or from the
with ejection fractions <30% (including both ischaemic RV coil to both the superior vena cava coil and the ICD.
and non-ischaemic cardiomyopathies) have a high risk Configurations can impact significantly on the defibril-
of sudden cardiac death due to ventricular arrhyth- lation threshold, and changes to the shock vector may be
mias, including patients with and without documented undertaken for patients with high defibrillation thresholds.
non-sustained VT.116,117 In these contexts patients may All modern ICDs provide biphasic shock waveforms
receive pure ICDs, or ICDs coupled with cardiac resyn- only. Arrhythmia detection and classification usually
chronisation therapy capabilities to also combat their require only a few seconds, and charging to maximum
heart failure (CRT-D devices). joules in a new device takes up to 10 seconds. As the
The modern ICD features both antibradycardia and battery declines charge time may increase to 15–20 seconds
antitachycardia capabilities. As antibradycardia devices or longer. Maximum energy delivery capabilities vary
they possess all the characteristics of standard pacemakers, between manufacturers but are all in the range of 30–40 J.
increasingly in the DDD mode. However, if there is no Typically, shocks for ventricular fibrillation are provided
history of bradycardia, they may be programmed at low at the maximum available capability of the device, but for
base pacing rates (e.g. 40/min). If there is significant heart ventricular tachycardia, lower ‘cardioversion’ shocks may

FIGURE 11.51 Successful antitachycardia pacing delivered by an implantable cardioverter defibrillator. Three
simultaneous strips show the presence of sustained ventricular tachycardia (VT). After the first eight beats, pacing is
applied at a rate slightly faster than the tachycardia. Entrainment, or capture, by the pacemaker is best seen in lead II,
where the QRS morphology clearly changes. After 11 paced beats, ATP is ceased, revealing interruption of the VT.

403400 11/11/02 13:20:12 BASELINE 25 mm/sec 0.40

I

II

III
352 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

be attempted first (e.g. 15–25 joules). If initial shocks are sudden or gradual onset, similar or different morphology
unsuccessful, devices are usually programmed to increase to the previous sinus rhythm and atrioventricular
to maximum joules for subsequent shocks.112 relationships. If these discriminators indicate that a tachy-
Defibrillation thresholds may be measured at the time arrhythmia is supraventricular, therapy can be withheld,
of implantation of the ICD. It is desirable that a 10-J avoiding inappropriate therapy. The major device capabil-
safety margin exists, i.e. for a device that can deliver 30 J, ities and programming options of an ICD are shown in
it is preferred that successful defibrillation can be demon- Figure 11.52.
strated at 20 J or less so that there can be confidence that Patients receiving ICDs require particular education
the device will revert clinical arrhythmias, and to cover and support, as the experience of shocks can be painful
any defibrillation threshold increases in the future.118 and disturbing. Anticipation of shocks can cause anxiety
Intraoperative defibrillation testing, in which ventric- and/or depression,120 especially in patients who have expe-
ular fibrillation is induced and then defibrillated, has rienced shocks while conscious. Inappropriate therapy
become less common with time, partly because of the delivery remains a significant problem, and as many as
risks associated with inducing ventricular fibrillation, and 25% of ICD therapies have been reported as inappropri-
partly because of evidence that spontaneous ventricular ate, delivered due either to supraventricular arrhythmias
fibrillation has different characteristics to induced fibril- or oversensing of electromagnetic interference.120,121
lation.119 However,VF induction and defibrillation testing Refinement of rhythm discrimination behaviours has
remains the only way to demonstrate whether a device has seen the incidence of inappropriate shocks reduced in
successfully interrupted VF. If testing is to be performed recent years. The avoidance of strong electrical fields
the patient is prepared for external defibrillation with all (welding, magnetic resonance imaging, generators) should
safety precautions and subsequent care as outlined above be stressed, as well as direct contact with devices such
in the section on cardioversion. as transcutaneous electrical nerve stimulation (TENS)
ICDs are usually programmed to deliver up to six machines or electrocautery devices.73 If surgery requiring
‘therapies’ during a tachyarrhythmia episode. For VF, diathermy becomes necessary, antitachycardia therapies
this usually means six attempts at defibrillation at maximum are usually programmed to ‘OFF’ to avoid inappropriate
joules after which further antitachycardia therapies are detection and treatment.
aborted. No more shocks will be delivered. Antibradycar- Patients should be encouraged to rest after any therapy
dia pacing operation will continue. If the tachyarrhythmia delivery and, where multiple discharges occur, they should
is interrupted at any point and then recurs, the six-ther- report to a healthcare facility for assessment.122 Most doctors
apy counter will recommence. For ventricular tachycardia, advise contact with their rooms if any shocks are received
attempts may first be made to overdrive pace. So-called by the patient. If repeated inappropriate therapy continues
antitachycardia pacing (ATP) aims to interrupt VT by (shocks delivered despite the patient not being in VT or
pacing the ventricles slightly faster than the VT rate VF), further shocks may be suspended by the placement of
so as to interrupt reentry, the major cause of VT (see a ring magnet over the device.123 This suspends the anti-
Figure 11.50 for example of reversion). A number of tachycardia features of the device while the magnet is in
attempts at ATP may be programmed, often with slightly place – no therapy will be delivered by the device. Cardiac
faster rates at each successive attempt. This is especially monitoring is imperative while a magnet is in place to
true if the patient is known to tolerate their VT reasonably detect any development of genuine ventricular arrhyth-
well. Persistence of VT after ATP attempts will see the mias as these would not be treated by the device. Removal
device first attempt low energy cardioversion (15–25 J) of the magnet will immediately reactivate antitachycardia
and then progress to 30–40 J if unsuccessful. The same therapies. Back-up (antibradycardia) pacing functions
limit of six therapies usually applies for an episode. remain active and unaffected during magnet application.
In the event of unsuccessful reversion of a ventricular
Tachyarrhythmia detection and arrhythmia by ICD therapy, standard advanced life support
classification protocols should be applied. External defibrillation can
ICDs are configured to classify and treat arrhythmias be undertaken with paddles in normal apicobasal or
first on the basis of rate. Defibrillation algorithms using anteroposterior positions, taking care to avoid positioning
high-energy settings (30–40 J) are followed when the rate paddles over the ICD.122 External chest compressions can
is very fast (e.g. >200/min), as syncope is likely even if safely be undertaken by rescuers, including during device
the rhythm is not ventricular fibrillation (e.g. very fast therapy.124
VT). At slower rates, other antitachycardia options may
first be attempted as described above. Additionally, at Practice tip
slower rates of tachycardia, attempts are made to discrim- If cardiac arrest occurs in a patient with an ICD in
inate between ventricular and supraventricular (including place, all standard therapies should be undertaken,
sinus) tachycardias (SVTs) using a variety of criteria. SVT including CPR, drug administration, and immediate
discrimination by a device uses similar criteria to those preparation for external defibrillation. If device shocks
by which a clinician would differentiate between VT and are unsuccessful, proceed to external defibrillation.
SVT and includes regularity or irregularity of the rhythm,
 CHAPTER 11 CARDIAC RHYTHM ASSESSMENT AND MANAGEMENT 353

FIGURE 11.52 Implantable cardioverter defibrillator (ICD) programmed parameter summary report from St Jude
Medical ICD Ellipse™ dual chamber ICD model 2277-36 (St Jude Medical, Sylmar CA). Similar to the report shown
earlier for a pacemaker, the report includes battery status and test results for lead impedances, sensing and capture
thresholds for the atrial and ventricular lead. The battery status section also displays the most recent time (in seconds)
taken for the device to charge to a maximum joule shock and the date. In the parameters section are the programmed
settings for pacing and defibrillation behaviours. The tachyarrhythmia treatments are shown at the right of the
parameters section and show the device behaviour for tachycardias occurring at different rates. In the so-called ‘VF
zone’, the ICD will respond to any arrhythmia faster than 214 beats per minute (whether it is VF or fast VT). As rhythms
at this rate are likely to be syncopal ICDs are usually programmed to proceed directly to delivering shocks rather than
spending time delivering antitachycardia pacing (ATP) unless, as here, a single attempt at ATP is selected to be delivered
while the device is charging (and therefore not delaying the time to first shock delivery). Shocks in the VF zone are
more commonly at maximum joules although 1st shocks may be of lesser strength with subsequent escalation. In the
VT-2 zone, a different strategy has been programmed for VT between 181 and 214/min. Three attempts at delivering
ATP have been programmed and, if unsuccessful, the ICD will progress to increasing energy levels (20, 30, 36 joules) if
reversion is not achieved. An additional strategy has been included for slower forms of VT (150–181/min) (VT-1 zone). As
VT at these rates is more likely to be tolerated greater use of ATP is often programmed so as to avoid shocks if possible.
Two different ATP regimes have been set, with the second set of 6 pacing attempts more aggressive than the first set
of 6. If ATP is unsuccessful, the device progresses to escalating shocks. Details of how the device is set to discriminate
between VT and SVT, as well as the set-up of the pacing strategies, are given in separate sections of these reports. Also
shown on the summary are any VT/VF episodes since the last device check. In this case there had been two episodes of
VT and two of VF. Recordings of these arrhythmias and treatments are recorded elsewhere in the report.

DEMO PATIENT 25 Jul 2014

ST. JUDE MEDICAL* Ellipse TM DR 2277-36 ICD DEMO 13:53
MORE CONTROL. LESS RISK.
In-Clinic

FastPathTM Summary ! 6 Alerts Page 1 of 2

Battery Implant Date: 31 Jan 2013

Longevity: 5.4–5.8 yrs
Last Max Charge 10.0 sec (20 May 2014)
Battery Current 14 μA
~ERI > 5 yrs Remaining Capacity to ERI 83%
Test Results 25 Jul 2014 A Automatic

Capture Sense Lead Impedance

A 1.0V @ 0.5ms (Bi) A 4.0mV (Bi) A 600 ⍀ (Bi) A
0.875V @ 0.5ms (Bi) 26 May 2014 4.0mV (Bi) 26 May 2014 580 ⍀ (Bi) 25 Jun 2014
V 1.0V @ 0.5ms (Bi) A >12.0mV (Bi) A 580 ⍀ (Bi) A
1.0V @ 0.5ms (Bi) 26 May 2014 >12.0mV (Bi) 26 May 2014 580 ⍀ (Bi) 25 Jun 2014
HV 42 ⍀ (RV to SVC & Can) A
41 ⍀ (RV to SVC & Can) 25 Jun 2014
Parameters
Mode DDDR Zone Configuration VT-1 VT-2 VF
Base Rate 65 min-1 Detection Criteria 150 min–1 181 min–1 214 min–1
Max Track Rate 110 min-1 Therapy (ENABLED) ATP x6 ATP x6 ATP x1
Paced AV Delay 200 ms ATP x6 20.0 J 30.0 J
Sensed AV Delay 150 ms 30.0 J 30.0 J 35.0 J
36.0 J x2 36.0 J x2 36.0 J x4
Capture & Sense A V
ACapTM Confirm/V AutoCapture On On
Pulse Amplitude 2.0 V A 1.25 V A
Pulse Width 0.5 ms 0.5 ms
AutoSense On On
Sensitivity Auto A Auto A
Diagnostics Summary Since 30 July 2013 VT/VF Episodes: 4 Since 26 May 2014
AP 3.5% VT-1 VT-2 VF
VP 14% Episodes 0 2 2
ATP Delivered 0 0
AMS Episodes 6 Shocks Delivered 2 0
Mode Switch <1%
AT/AF Burden <1% SVT Episodes: 0
Non-sustained Episodes: 0

End-of-life care in the patient with the ICD, and there is often sufficient time to incorpo-
an ICD rate this step into palliative planning. Alternatively, when
ICDs often create uncertainty amongst healthcare workers active treatment is being withdrawn as a patient progresses
as to how death may occur. In the palliative patient, more rapidly towards an unexpected (acute) death, there
where active resuscitation for cardiac death is not to be may be a need to disable therapy before the availability
pursued, the decision to disable antitachycardia therapies of personnel to reprogram the device. In this context,
is often taken. This can be achieved by reprogramming securing a ring magnet over the ICD (tape it in place)
354 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

will disable tachycardia therapies so that, if the terminal The use of percutaneous catheter ablation therapies
rhythm is VT or VF, therapies will not be delivered. has expanded rapidly as technology and familiarity have
Other than by disabling therapy, cardiac death may developed, and they have been used to treat atrial, ventric-
occur by normal mechanisms. However, cardiac depressive ular and AV nodal reentry tachyarrhythmias, as well as
factors will not cause bradycardia or asystole because of the the abnormal atrioventricular connections of Wolff-
pacemaker function. What would otherwise be a brady- Parkinson-White syndrome. For incessant atrial fibrillation,
arrhythmic death will instead become eventual failure to it is sometimes necessary to ablate the AV node to control
capture by the pacemaker. Similarly, if the cardiac impact of the ventricular rate. Since this causes complete heart block,
acute or terminal illness produces tachyarrhythmias, these a pacemaker must first be implanted. Identification of the
same influences will increase the defibrillation threshold and pulmonary veins as the culprit arrhythmic foci for many
antitachycardia therapies will become unsuccessful. Devices patients with atrial fibrillation has seen the development
offer no protection against pulseless electrical activity. of ablation techniques to prevent conduction from the
pulmonary veins to the atria (pulmonary vein isolation).
Ablation For arrhythmia ablation, electrophysiological studies
are undertaken to closely map the location of abnormal
Ablation therapies are aimed at destroying tissues that foci, reentry circuits or accessory pathways, and radio-
1) generate or sustain haemodynamically significant or frequency catheters are then guided to these sites to deliver
potentially lethal arrhythmias (arrhythmic foci or reentry therapy. Studies are well tolerated as long as patients can
pathways) or 2) permit uncontrollable atrial arrhythmias remain supine for the sometimes extended periods. The
to conduct at rapid rates to the ventricles (the accessory application of radiofrequency and the consequent tissue
pathways of the Wolff-Parkinson-White syndrome, or at injury is painless in most cases.124,125
times the AV node itself).125 Tissue destruction is achieved Success rates for ablation therapies have been reported
by the application of radiofrequency energy or cold as 82–92% for accessory pathway ablation (depending on
(cryoablation) to very localised areas of the endocard- pathway location), 90–96% for AV nodal reentry tachycardia
ium, which results in tissue damage and eventual tissue and 75% for atrial tachycardia and flutter.126 Complication
death.125 Unlike preventive or episode-terminating phar- rates, mostly AV block, have been reported as 2.1–4.4%,
macological or electrical arrhythmia therapies, successful with procedure-related mortality below 0.2%.125,126 When
ablation is curative and can therefore spare patients a applied to patients with idiopathic ventricular tachycar-
lifetime of careful medication compliance, self-monitor- dia, procedural success has been reported as 85–100%.127
ing for complications and living under the uncertainty of Complications, including death from ventricular wall
arrhythmic threat and/or the delivery of therapy from an perforation,126 have occurred, but major complication
implantable cardioverter defibrillator. rates of less than 1% are generally seen.127

Summary
Alteration to the electrophysiological function of the heart is very common in patients admitted to critical care settings.
Arrhythmia detection is largely the responsibility of the critical care nurse, who must maintain accurate monitoring,
constantly observe for the development of arrhythmias, assess their clinical impact and assist in identifying causative
factors.The critical care nurse must also deliver the care and management of arrhythmias, including pharmacological and
electrical therapies, being aware of complications and management of complications of these treatments.

Case study
In 1997 Mr Thomas suffered an anterolateral AMI at the age of 37. He subsequently had a prolonged
cardiac arrest and was resuscitated from ventricular fibrillation. Prior to this Mr Thomas was a very active
windsurfer and competitive solo yachtsman, as well as running his own business as a yacht restorer, and
he maintained all these activities after his AMI.
A single chamber implantable cardioverter defibrillator (ICD) was implanted in 1997, with a dual coil ICD
lead placed at the apex of the right ventricle. He has subsequently undergone three ICD replacements
with each device lasting approximately 4 years before battery depletion. It would normally be anticipated
that ICD batteries provide 6 or more years of service; however, frequent shocks diminish battery longevity.
In addition to the ICD, Mr Thomas was discharged on oral sotalol 40 mg bd for antiarrhythmic cover.
Between 1997 and 2008 Mr Thomas received repeated shocks for VT at rates of 185 per minute (further
details not available due to a change in doctor). In 2008 and 2009 Mr Thomas experienced 10–50 episodes
 CHAPTER 11 CARDIAC RHYTHM ASSESSMENT AND MANAGEMENT 355

of VT per month, at rates of 185–200/min. While antitachycardia pacing (ATP) reverted many episodes
without major symptoms, he regularly received shocks. Sotalol was increased incrementally to 80 mg tds
and then 160 mg, although at these doses it began to cause chronic fatigue. In 1999 Mr Thomas suffered
a pulmonary embolism and remains on life-long warfarin.
In June of 2009 a new, slower form of sustained VT emerged (175/min) that was recurrent and
produced dizziness (systolic blood pressure: 70 mmHg). Mr Thomas’ ICD was previously programmed to
treat VT above 180/min; therefore this VT did not qualify for ICD treatment – reprogramming of the ICD
to treat VT above 160/min was consequently undertaken. A similar scenario, although with VT of 125/min,
occurred 3 months later and the ICD was again reprogrammed, this time to treat VT above 120/min.
Mr Thomas continued to receive multiple shocks, often while undertaking his normal activities. One shock
was delivered while completing an acrobatic loop on his wind surfer, another while 10 meters under water
after having been dumped by a wave while surfing and a third while competing in a solo yacht race.
On each occasion he paddled or sailed slowly back to shore and attended ED. Throughout this period
Mr Thomas was also experiencing intolerable fatigue from his sotalol treatment. Agreement was reached
to undergo VT ablation.
In December 2009 electrophysiological (EP) study revealed Mr Thomas had three separate VT patterns with
rates of 150, 180 and 250/min (ventricular flutter), all emerging from different borders of his anteroapical
AMI scar. Pace-mapping identified three target sites and radiofrequency ablation was applied to these.
After his ablation Mr Thomas’ sotalol dose was reduced to 80 mg bd.
Mr Thomas had a review in February 2010 when it was identified that his VT had not decreased significantly
with 61 episodes in 2 months that were all terminatd by ATP.
As Mr Thomas’ ICD was set to treat VT >120/min, the risk of inappropriate shocks was high and this
became reality in October 2010 when Mr Thomas presented to ED after sinus tachycardia and atrial
fibrillation accounted for 50 episodes diagnosed as VT with multiple inappropriate shocks. The ICD was
reprogrammed with tighter parameters for discriminating between SVT and VT and this proved effective in
preventing further inappropriate shocks. Sotalol was also increased back to 160 mg bd.
Six months later Mr Thomas had a routine review that revealed 17 episodes of VT and 5 shocks throughout
that period. The argument for amiodarone had become compelling, though not without reservation as
warfarin had been commenced some years earlier. Amiodarone inhibits enzymes that degrade warfarin
and so International Normalised Ratio (INR) volatility accompanies amiodarone addition. The long half-life
of amiodarone and variable rise to peak plasma levels make the management of warfarin more complex. In
addition, photosensitivity had weighed against amiodarone use previously given Mr Thomas’ outdoor work
and leisure activities. Although a beta-blocker was still required because of the original AMI, sotalol was
replaced by metoprolol to avoid lengthening the QT interval due to the combined effects of amiodarone
and sotalol. The combination of metoprolol and digoxin was used to limit further atrial arrhythmias and for
rate control.
After amiodarone (200 mg bd) was commenced there was only one episode of VT in the next 3 years. Digoxin
levels were intermittently high (remember amiodarone and digoxin compete for excretion) and digoxin was
ultimately withdrawn. Annual thyroid function testing and chest X-ray revealed no complications of amiodarone
therapy. After 12 arrhythmia-free months amiodarone was reduced to 200 mg mane, 100 mg nocte.
In 2014 Mr Thomas attended ED after receiving a vibratory notification from his ICD. The ICD was vibrating
in his chest as an instruction to seek attention. Device interrogation revealed an out-of-range automatic
daily impedance measurement. His ICD lead was now 17 years old and the alert suggested one of the
conductors to the shock coils was wearing out. With reprogramming to shock via a different vector
the device was able to continue operating normally.
Living with an ICD and the associated threat of unexpected shocks, as well as the side effects of medications
and arrhythmias, can be challenging. Both anxiety and depression are experienced by some ICD recipients.
Mr Thomas has proven remarkably resilient and demonstrates that it is possible to live life relatively normally.
As critical care nurses it is important to recognise the pharmacological and technical challenges in caring
for patients with lifelong arrhythmic conditions and ongoing vigilance is required.

CASE STUDY QUESTIONS

1 Sotalol rather than amiodarone was chosen as the first antiarrhythmic agent used for Mr Thomas. What
reasons might have prompted this decision?
2 Mr Thomas’ ICD was eventually programmed to treat ventricular tachycardia at a rate of 120/min when
slower VTs (125/min) developed. What particular risk does this programming change now bring into play?
356 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

RESEARCH VIGNETTE

Graham K, Cvach M. Monitor alarm fatigue: standardising the use of physiological monitors
and decreasing nuisance alarms. Am J Crit Care 2010;19:28–34

Abstract
Background and purpose: Reliance on physiological monitors to continuously ‘watch’ patients and to alert the
nurse when a serious rhythm problem occurs is standard practice on monitored units. Alarms are intended to alert
clinicians to deviations from a predetermined ‘normal’ status. However, alarm fatigue may occur when the sheer
number of monitor alarms overwhelms clinicians, possibly leading to alarms being disabled, silenced, or ignored.
Excessive numbers of monitor alarms and fear that nurses have become desensitized to these alarms was the
impetus for a unit-based quality improvement project.
Methods: Small tests of change to improve alarm management were conducted on a medical progressive care unit.
The types and frequency of monitor alarms in the unit were assessed. Nurses were trained to individualize patients’
alarm parameter limits and levels. Monitor software was modified to promote audibility of critical alarms.
Results: Critical monitor alarms were reduced 43% from baseline data. The reduction of alarms could be attributed
to adjustment of monitor alarm defaults, careful assessment and customization of monitor alarm parameter limits and
levels, and implementation of an interdisciplinary monitor policy.
Discussion: Although alarms are important and sometimes life-saving, they can compromise patients’ safety
if ignored. This unit-based quality improvement initiative was beneficial as a starting point for revamping alarm
management throughout the institution.

Critique
This study evaluated the pre- and post-intervention effects of a series of alarm management quality improvement
measures in a 16-bed mixed medical progressive care unit in Baltimore, USA over a 12-month period. The study’s pre-
evaluation process included measurement of the quantity and type of alarms occurring in the unit over a consecutive
18-day period, along with a survey that explored the existing alarm setting practices of 30 of the unit’s nursing staff.
The investigation team then implemented a series of interventions designed to improve staff alarm setting practices
including education on troubleshooting practices, the need to individualise patient alarm assignment and revision of
the unit’s default ‘patient’ and monitor ‘crisis level’ settings. These included reduction in lower heart rate level and
elevation of upper rate limit, premature ventricular contraction upper limit rise and re-setting of allocated default alarm
warning levels within the unit’s monitoring system (for example, the re-assignment of heart rate high and low alarms
to a ‘message’ level alert while changing bradycardia and tachycardia from ‘advisory’ to ‘warning’ level).

Postintervention evaluation revealed a 43% overall reduction in unit alarm frequency (with heart rate low and high
alerts being decreased the most) and improved bedside alarm evaluation and adjustment compliance by staff.
Environmental noise levels were also perceived by staff to be lower following the initiatives.

As the authors state, modern physiological monitors are ‘set for high sensitivity at the expense of specificity’ and the
results of this quality improvement initiative demonstrate the potential reduction in ‘false positive’ alarm events that
can be achieved through a program that specifically reviews staff and alarm knowledge and default setting practices.

The issue of excessive ‘inappropriate’ or ‘nuisance’ bedside alarms in acute healthcare settings has become a topic of
raised emphasis over recent years. Of particular concern is the development of alarm ‘fatigue’ by staff, with resulting
auditory alert desensitisation and reactive alarm silencing and even disablement enhancing the risk of missed critical
physiological events, including cardiac arrhythmias. In addition, excessive nuisance alarms disrupt patient care and
rest and add significantly to the ambient noise of high acuity care settings. As some previous studies have shown that
fewer than 1% of clinical alarms actually result in a change to patient management, it’s therefore necessary to explore
strategies that reduce the incidence of inappropriate clinical alarm events in order to optimise the clinical relevance
and safety of patient bedside monitoring.
 CHAPTER 11 CARDIAC RHYTHM ASSESSMENT AND MANAGEMENT 357

The authors have not stated whether the actual or missed ‘true positive’ critical alarm incidence was monitored during
the evaluation periods and this would be vital to ensuring the clinical safety of a clinical monitoring change initiative.
The study was also confined to a single clinical setting and staff training and experience levels were not detailed,
therefore making it difficult to ascertain whether low technical knowledge or limited clinical exposure significantly
influenced the baseline findings.

However, the study’s outcomes highlight the significant ‘inappropriate’ alarm reductions that can be achieved
through a focused alarm education and system configuration review and, as such, provide renewed awareness
of the important need for individual clinicians and critical care departments to give more detailed attention to the
management of bedside and system based alarm settings.

Lear ning a c t iv it ie s
1 Utilise the flowchart in Figure 11.28 to assist in refining your final interpretation of a selection of the ECG rhythm strips
presented in pages 314–329 of this chapter.
2 Draw a series of simple diagrams of the heart’s conducting system, then sketch and label the differing sequences
of sinoatrial, AV junctional and ventricular conduction events that occur with second degree AV block types I and
II and third degree AV block. Compare and contrast the relative conduction events occurring with each AV block
type and their relationship to the surface ECG rhythm patterns that are typically observed in each.
3 When next at the bedside, take the time to review the number of higher level ’warning’ and ‘crisis’ level alarms
that have been stored over the previous 24 hours of monitoring on your allocated patient. Determine the
incidence and types of ‘false positive’ ECG alarm events that have occurred and, with consideration of the
patient’s current clinical state, readjust the monitor settings to more individually appropriate (yet clinically safe)
settings. Which particular ECG monitoring settings would most likely require adjusting?
4 You are caring for a 68-year-old patient with chronic atrial fibrillation who develops intermittent non-sustained
runs of ventricular tachycardia. The patient has been admitted to critical care for the management of acute
renal failure and has a history of coronary artery disease and chronic obstructive pulmonary disease. With
reference to antiarrhythmic classifications (Table 11.5) and with further reading, consider the relative benefits
and risks of administering flecainide, sotolol or amiodarone for the treatment of this man’s ventricular
tachycardia.

Online resources
Arrhythmia and cardiac device presentations, manuals, and learning resources, www.hrsonline.org
ECG quizzes and teaching materials: http://library.med.utah.edu/kw/ecg/, http://ekgreview.com/, http://biotel.ws/quizzes/
ekgs/ekgs.htm, www.ecglibrary.com/ecghome.html, http://en.ecgpedia.org, www.learntheheart.com/ecg-review/ecg-quiz
ECRI Institute Alarm Safety Resource site, www.ecri.org/forms/pages/Alarm_Safety_Resource.aspx
European Heart Rhythm Association (EHRA), www.escardio.org/communities/EHRA/Pages/welcome.aspx
European Resuscitation Council, www.erc.edu/index.php/mainpage/en/ECG
Pacing resources, www.sjmprofessional.com, www.medtronic.com/for-healthcare-professionals/education-training

Further reading
Brignole M, Auricchio A, Baron-Esquivias G, Bordachar P, Boriani G, Breithardt OA et al. 2013 ESC Guidelines on cardiac
pacing and cardiac resynchronization therapy: the Task Force on cardiac pacing and resynchronization therapy of
the European Society of Cardiology (ESC). Developed in collaboration with the European HeartRhythm Association (EHRA).
Eur Heart J 2013; 34(29):2281–329. doi:10.1093/eurheartj/eht150. Epub 2013 Jun 24. PubMed PMID: 23801822.
358 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Drew B, Ackerman M, Funk M, Gibler B, Kligfield P, Menon V et al. Prevention of torsades de pointes in hospital settings: a
scientific statement from The American Heart Association and The American College of Cardiology Foundation. J Am Coll
Cardiol 2010;55(9):934–47.
Epstein A, DiMarco J, Ellenbogen K, Estes NA 3rd, Freedman R, Gettes LS et al. American College of Cardiology Foundation;
American Heart Association Task Force on Practice Guidelines; Heart Rhythm Society. 2012 ACCF/AHA/HRS focused
update incorporated into the ACCF/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a
report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and
the Heart Rhythm Society. J Am Coll Cardiol 2013;22:61(3):e6–75. doi: 10.1016/j.jacc.2012.11.007.

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 CHAPTER 11 CARDIAC RHYTHM ASSESSMENT AND MANAGEMENT 359

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60 Ahmad K, Dorian P. Drug induced QT prolongation and proarrhythmia: an inevitable link? Europace 2007:iv16–iv22.
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62 Ryan TJ, Anderson JL, Antman EM, Braniff BA, Brooks NH, Califf RM et al. ACC/AHA guidelines for the management of patients with
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63 Mattingly E. AANA Journal course: update for nurse anesthetists – arrhythmia management devices and electromagnetic interference.
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64 Swerdlow CD, Gillberg JM, Olson WH. Sensing and detection. In: Ellenbogen KA, Kay GN, Lau CP, Wilkoff BL, eds. Clinical cardiac pacing,
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65 Hayes DL, Friedman PA. Cardiac pacing, defibrillation and resynchronization. 2nd ed. Singapore: Wiley-Blackwell; 2008.
66 Laczika K, Thalhammer F, Locker G, Apsner R, Losert H, Kofler J et al. Safe and efficient emergency transvenous ventricular pacing via the right
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67 Kay GN, Shepard RB. Cardiac electrical stimulation. In: Ellenbogen KA, Kay GN, Lau CP, Wilkoff BL, eds. Clinical cardiac pacing, defibrillation,
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68 Bernstein AD, Camm AJ, Fletcher RD, Gold RD, Rickards AF, Smyth NP et al. The NASPE/BPEG generic pacemaker code for
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69 Sgarbossa EB, Pinski SL, Gates KB, Wagner GS. Early diagnosis of acute myocardial infarction in the presence of ventricular paced rhythm.
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70 Schuchert A, Frese J, Stammwitz E, Novák M, Schleich A, Wagner SM et al. Low settings of the ventricular pacing output in patients dependent
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71 Ellenbogen KA, Wood MA. Cardiac pacing and ICDs. 4th ed. Oxford: Blackwell Publishing; 2005.
72 Tommaso C, Belic N, Brandfonbrener M. Asynchronous ventricular pacing: a rare cause of ventricular tachycardia. PACE 1982;5(4):561–3.
73 Ahmed FZ, Morris GM, Allen S, Khattar R, Mamas M, Zaidi A. Not all pacemakers are created equal: MRI conditional pacemaker and lead
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74 Hayes DL, Zipes DP. Cardiac pacemakers and cardioverter-defibrillators. In: Braunwald E, Dipes DP, Libby P, eds. Heart disease: a textbook of
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75 Vardas PE, Auricchio A, Blanc JJ, Daubert J-C, Drexler H, Ector H et al. Guidelines for cardiac pacing and cardiac resynchronization therapy.
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76 Kristensen L, Nielsen JC, Pedersen AK, Mortensen PT, Andersen HR. AV block and changes in pacing mode during long-term follow-up of
399 consecutive patients with sick sinus syndrome treated with an AAI/AAIR pacemaker. Pacing Clin Electrophysiol 2001;24(3):358–65.
77 Brandt J, Anderson H, Fahraeus T, Schüller H. Natural history of sinus node disease treated with atrial pacing in 213 patients: implications for
selection of stimulation mode. J Am Coll Cardiol 1992;20(3):633–9.
78 Wilkoff BL, Cook JR, Epstein AE, Greene HL, Hallstrom AP, Hsia H et al. Dual chamber pacing or ventricular backup pacing in patients with an
implantable defribrillator: The Dual Chamber and VVI Implantable Defibrillator (DAVID) trial. JAMA 2002;288:3115–23.
79 Dennis MJ, Sparks PB. Pacemaker mediated tachycardia as a complication of the autointrinsic conduction search function. PACE
2004;27(6Pt1):824–6.
80 Finkelmeier BA. Cardiothoracic surgical nursing. 2nd ed. Philadelphia: Lippincott, Williams & Wilkins; 2000.
81 Elmi F, Tullo N, Khalighi K. Natural history and predictors of temporary epicardial pacemaker wire function in patients after open heart surgery.
Cardiol 2002: 98(4):175–80.
82 Chen LK, Teerlink JR, Goldschlager N. Pacing emergencies. In: Brown DL, ed. Cardiac intensive care. Philadelphia: WB Saunders; 1998.
83 Connolly SJ, Kerr CR, Gent M. Roberts RS, Yusuf S, Gillis AM et al. Effects of physiologic pacing versus ventricular pacing on the risk of stroke
and death due to cardiovascular causes. N Engl J Med 2000;342(19):1385–91.
84 Lamas GA, Lee KL, Sweeney MO, Silverman R, Leon A, Yee R et al. For the Mode Selection Trial in Sinus-Node Dysfunction. Ventricular pacing
or dual-chamber pacing for sinus node dysfunction. N Engl J Med 2002;346(2):1854–62.
85 Mond HG, Hikkock RJ, Stevenson IH, McGavigan, AD. The right ventricular outflow tract: the road to septal pacing. Pacing Clin Electrophysiol
2007;30:482–91.
86 Bakker P, Meijburg H, De Vries JW, Mower MM, Thomas AC, Hull ML et al. Biventricular pacing in end-stage heart failure improves functional
capacity and left ventricular function. J Interv Card Electrophysiol 2000;4(2):395–404.
87 Hawkins NM, Petrie MC, MacDonald MR, Hogg KJ, McMurray JJ. Selecting patients for cardiac resynchronization therapy: electrical or
mechanical dyssynchrony? Eur Heart J 2006;27:1270–81.
88 Linde C, Leclerq C, Rex S, Garrigue S, Lavergne T, Cazeau S et al. Long-term benefits of biventricular pacing in congestive heart failure: results
from the MUSTIC study. J Am Coll Cardiol 2002;40:433–40.
89 Cleland JGF, Subert JC, Erdmann E, Freemantle N, Gras D, Kappenberger L et al. Longer-term effects of cardiac resynchronization therapy on
mortality in heart failure [The Cardiac Resynchronisation-Heart Failure (CARE-HF) trial extension phase]. Eur Heart J 2006;27:1928–32.
90 Auricchio A, Stellbrink C, Sack S, Block M, Vogt J, Bakker P et al. Pacing Therapies in Congestive Heart Failure (PATH-CHF) Study Group.
Long-term clinical effect of hamodynamically optimized cardiac resynchronisation therapy in patients with heart failure and ventricular
conduction delay. J Am Coll Cardiol 2002;39:2026–33.
91 Young JB, Abraham WT, Smithe AL, Leon AR, Lieberman R, Wilkoff B et al. Combined cardiac resynchronization and implantable cardioverter
defibrillation in advanced chronic heart failure: the MIRACLE ICD trial. JAMA 2003;289:2685–94.
92 Bristow MR, Saxon LA, Boehmer J, Krueger S, Kass, DA, De Marco T et al. Comparison of Medical Therapy, Pacing, Defibrillation in Heart
Failure (COMPANION) Investigators. Cardiac resynchronization therapy with or without an implantable defibrillator in advanced chronic heart
failure. N Engl J Med 2004;350:2140–50.
93 Ghi S, Constantin C, Klersy C, Serio A, Fontana A, Campana C et al. Interventricular and intraventricular dyssynchrony are common in heart
failure patients, regardless of QRS duration. Eur Heart J 2004;25:571–8.
94 Littmann L, Symanski JD. Hemodynamic implications of left bundle branch block. J Electrocardiol 2000;33(Suppl1):115–21.
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95 Verrnooy K, Verbeek XA, Peschar M, Crijns HJ, Arts T, Cornelussen RN et al. Left bundle branch block induces ventricular remodelling and
functional septal hypoperfusion. Eur Heart J 2005;26:91–8.
96 Sundell J, Engblom E, Koistinen J, Ylitalo A, Naum A, Stolen KQ et al. The effects of cardiac resynchronization therapy on left ventricular
function, myocardial energetics and metabolic reserve in patients with dilated cardiomyopathy and heart failure. J Am Coll Cardiol
2004;43:1027–33.
97 Peichl P, Kautzner J, Cihak R, Bytesník J. The spectrum of inter- and intraventricular conduction abnormalities in patients eligible for cardiac
resynchronization therapy. Pacing Clin Electrophysiol 2004;27(8):1105–12.
98 Alonso C, Leclercq C, Victor F, Mansour H, de Place C, Pavin D et al. Electrocardiographic predictive factors of long-term clinical improvement
with multisite biventricular pacing in advanced heart failure. Am J Cardiol 1998;84:1417–21.
99 Abraham WT, Fisher WG, Smith AL, Delurgio DB, Leon AR, Loh E et al. MIRACLE Study Group. Multicenter InSync Randomized Clinical
Evaluation: cardiac resynchronization in chronic heart failure. N Engl J Med 2002;13(346):1845–53.
100 Daubert JC. Atrial fibrillation and heart failure: a mutually noxious association. Europace 2004;5:S1–S4.
101 Pappone C, Ćalović Ž, Vicedomini G, Cuko A, McSpadden LC, Ryu K et al. Multipoint left ventricular pacing improves acute hemodynamic
response assessed with pressure-volume loops in cardiac resynchronization therapy patients. Heart Rhythm 2013;11(3)394-401.
102 Meine TJ. An intracardiac EGM method for VV optimization during cardiac resynchronization therapy. Heart Rhythm J 2006;3:AB30–35.
103 Kenny T. The nuts and bolts of cardiac resynchronization therapy. Massachusetts: Blackwell Futura; 2007.
104 Barold SS, Herweg B. Usefulness of the 12-lead electrocardiogram in the follow-up of patients with cardiac resynchronizaiton devices. Part I.
Cardiol J 2011;18(5):476-86.
105 Thibault B, Dubuc M, Khairy P, Guerra PG, Macle L, Rivard L et al. Acute haemodynamic comparison of multisite and biventricular pacing with
a quadripolar left ventricular lead. Europace 2013;15(7):984-991.
106 Rinaldi CA, Kranig W, Leclercq C, Kacet S, Betts T, Bordachar P et al. Acute hemodynamic benefits of multisite left ventricular pacing in CRT
recipients. J Am Coll Cardiol 2012;59(13s1):E972
107 Miller JM, Zipes DP. Management of the patient with cardiac arrhythmias. In: Braunwald E, Zipes DP, Libby P, eds. Heart disease: a textbook
of cardiovascular medicine. 6th ed. Philadelphia: WB Saunders; 2001.
108 Deakin C, Nolan J, Sunde, K, Koster R. European Resuscitation Council Guidelines for Resuscitation 2010 Section 3. Electrical therapies:
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109 Valenzuela TD, Bjerke HS, Clark LL, Hardman R, Spaite DW, Nichol G. Rapid defibrillation by nontraditional responders: the Casino Project.
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110 Ambler JJ, Zideman DA, Deakin CD. The effect of topical non-steroidal anti-inflammatory cream on the incidence and severity of cutaneous
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111 Pinski SL, Sgarbossa EB, Ching E, Trohman RG. A comparison of 50-J versus 100-J shock for direct current cardioversion of atrial flutter.
Am Heart J 1999;137:439–42.
112 Pinski KL, Fahy GJ. Implantable cardioverter defibrillators. Am J Med 1999;106:446–58.
113 The Antiarrhythmics versus Implantable Defibrillators (AVID) Investigators. A comparison of antiarrhythmic-drug therapy with implantable
defibrillators in patients resuscitated from near-fatal ventricular arrhythmias. N Engl J Med 1997;337:1576–83.
114 Conolly SJ, Gent M, Roberts RS, Dorian P, Roy D, Sheldon RS et al. Canadian Implantable Defibrillator Study (CIDS): a randomized trial of the
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115 Kuck KH, Cappato R, Siebels J, Rüppel, R. Randomized comparison of antiarrhythmic drug therapy with implantable defibrillators in patients
resuscitated from cardiac arrest. The Cardiac Arrest Study Hamburg (CASH). Circulation 2000;102:748–54.
116 Moss AJ, Hall WJ, Cannom D, Daubert JP, Higgins SL, Klein H et al. Multicentre Automatic Defibrillator Implantation Trial Investigators.
Improved survival with an implanted defibrillator in patients with coronary artery disease at high risk for ventricular arrhythmias. N Engl J Med
1996;335(26):1933–40.
117 Mark DB, Nelson CL, Anstrom KJ, Al-Khatib SM, Tsiatis AA, Cowper PA et al. Cost-effectiveness of ICD therapy in the sudden cardiac death
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118 Swerdlow MD, Kalyanam Shivkumar MD, Jianxin Zhang MS. Determination of the upper limit of vulnerability using implantable cardioverter
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119 Viskin S, Rosso R. The top 10 reasons to avoid defibrillation threshold testing during ICD implantation. Heart Rhythm 2008;5(3):391–3.
120 Sola CL, Bostwick JM. Implantable cardioverter-defibrillators, induced anxiety, and quality of life. Mayo Clinic Proc 2005;80(2):232–7.
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Chapter 12

Cardiac surgery and transplantation

Judy Currey, Sher Michael Graan

Learning objectives KEY WORDS

After reading this chapter, you should be able to: arrhythmia

• outline cardiac surgical procedures including coronary artery bypass graft cardiac surgery
surgery and valve repair and replacement
cardiopulmonary
• describe the indications, advantages and disadvantages of using bypass
cardiopulmonary bypass
denervation
• outline methods of myocardial preservation during cardiac surgery heart transplant
• outline immediate postoperative management of cardiac surgical patients intra-aortic balloon
including haemodynamic, rhythm monitoring, ventilatory support, pump
postoperative bleeding including pericardial tamponade, postoperative
pain, fluid and electrolyte and emotional and family support ischaemic
reperfusion injury
• outline the principles of counterpulsation in intra-aortic balloon pumping (IABP)
valve replacement,
• outline the benefits and timing of balloon inflation and deflation, including repair
conventional and real timing, management and assessment of timing and
timing errors
• describe the nursing management of IABP complications, including limb
perfusion, bleeding and immobility-related complications
• discuss methods of weaning IABP and management of intra-aortic balloon
catheter removal
• discuss the immediate postoperative care of heart transplant recipients
• describe the clinical manifestations of postoperative complications in heart
transplant recipients
• identify signs and symptoms of rejection in heart transplant recipients
• evaluate the effectiveness of nursing interventions in the postoperative
management of heart transplant recipients.

Introduction
Many critically ill patients experience compromised cardiac function, as either
a primary or secondary condition. This chapter follows on from those situations
examined in Chapter 10, and reviews patients with conditions that tend to be
cared for in specialised critical care units. The burden of cardiovascular disease
estimated by the World Health Organization of years of life lost has increased
from 14.9% in 2000 to 18.5% in 2012, and ischaemic heart diseases have become
 CHAPTER 12 CARDIAC SURGERY AND TRANSPLANTATION 363

the leading cause of years of life lost in 2012.1 In Europe, and dilation of the affected chamber(s) as a compensa-
cardiovascular diseases account for 47% of all deaths; just tory mechanism. The second valvular abnormality is valve
less than half of mortality is due to coronary heart diseases.2 regurgitation, which is also called incompetence or insuf-
Cardiovascular diseases in Australia affect one in six Austra- ficiency. In this condition the incomplete closure of the
lians and accounted for 31% of all deaths in 2011,3 with valve leaflets results in backflow of blood into the chamber
acute coronary syndrome affecting 69,500 Australians increasing its end-diastolic volume, which may cause
and contributing to 15% of all deaths in 2011.4 Currently, chamber hypertrophy and dilation.
cardiovascular diseases are the second most common health In both of these conditions heart failure may result
issue, with the level of burden in Australia slightly lower as the pressure in the ventricles and atria grows and this
than other developed nations (25.8% versus 33.7%).3 pressure is reflected back into the pulmonary or venous
In this chapter three topics will be discussed. First, the system. Although the heart contains four valves, the
management of a patient who requires cardiac surgery majority of disorders affect the mitral and aortic valves in
for coronary artery disease or valvular disease will be the left side of the heart.
discussed, including the use of cardiopulmonary bypass.
Second, the use and management of intra-aortic balloon Aortic valve disease
counterpulsation in cardiac surgical and medical patients The aortic valve is located between the left ventricle and
will be outlined. Finally, the management of patients the aorta with a normal surface area of 2–3 cm2. Mild aortic
following heart transplantation will be described including stenosis is a narrowing of the opening of the valve area to
the prevention and management of immediate postoper- less than 1.5 cm2 and a pressure gradient between the left
ative complications. ventricle and aorta of more than 25 mmHg; severe aortic
stenosis is defined as a valve area of less than 1.0 cm2 and
a pressure gradient of more than 55 mmHg (Figure 12.1).
Cardiac surgery Aortic stenosis often results from degenerative changes or
The focus of this section is on cardiac surgery, for repair congenital abnormalities such as a bicuspid aortic valve
of structural abnormalities and repair or replacement (with a prevalence of 0.5% in the general population),
of stenotic or regurgitant valves, and bypass grafting of which may also cause regurgitation. Aortic stenosis
coronary artery lesions. The structural abnormalities increases left ventricle afterload, causing impedance to left
resulting from myocardial infarction have been described ventricle ejection. This increases left ventricle end-systolic
in Chapter 10. In this chapter, structural and functional volume and left ventricle systolic pressure, resulting in left
abnormalities that are causing valvular disease (mitral, ventricle hypertrophy and dilation. Increased myocardial
aortic, tricuspid or pulmonic valves) and ventricular oxygen demands from the hypertrophied muscle also
defects will be discussed. mean that angina is common.
Clinical manifestations of aortic stenosis include low
Valvular disease cardiac output, increased left ventricle workload, angina,
The incidence and types of valvular disease have changed dyspnoea, syncope and fatigue. On auscultation, additional
over the past 50 years.3 Valvular disorders, such as mitral heart sounds are heard as a systolic ejection murmur and
stenosis and aortic regurgitation, often arise from a loud S4. Left heart failure with pulmonary congestion
infectious diseases such as rheumatic fever (β-haemolytic is usually a late sign. The ECG may show left ventricular
streptococcal pharyngitis) and syphilis, which are much hypertrophy with strain patterns.
less common today. Conversely, there has been a rise in Aortic regurgitation may occur acutely when the
the rate of valvular diseases due to degenerative changes aortic valve is damaged by endocarditis, trauma or aortic
including leaflet degeneration and/or annulus calcifica- dissection, and presents as a life-threatening emergency.
tion, which are common in ageing. In contrast to these Chronic aortic regurgitation usually results from
trends, the prevalence of rheumatic fever and rheumatic rheumatic heart disease, syphilis or congenital conditions.
valvular disorders among Aboriginal people (one of the In aortic regurgitation reflux of blood to the left ventricle
highest in the world) and Pacific Islanders living in New during diastole, due to incomplete closure of the valve,
Zealand is six times higher than the general population.3 increases left ventricle end diastolic pressure and volume.
Other causes of valvular diseases are congenital valve This results in left ventricle dilation and hypertrophy and
diseases (common in the younger population, with respect left heart failure. When left heart failure occurs, left atrial
to e.g. bicuspid valves) and endocarditis. pressure rises and may cause pulmonary congestion and
Two valvular abnormalities that alter the blood pulmonary hypertension.
flow across the valve are common. Stenotic valves have In acute aortic regurgitation, the patient presents
a tightened, restricted orifice causing the valve to not with signs and symptoms of acute left ventricle failure,
fully open. There is a restriction to forward flow of cardiogenic shock and acute pulmonary oedema.6 Patients
blood, which must be forced through the valve at higher with chronic aortic regurgitation may remain asympto-
pressure (Figure 12.1). The high pressure combined with matic for years, finally presenting with signs of left heart
incomplete emptying of the chamber may increase the failure including fatigue, palpitation, syncope, angina and
end-systolic volume, which will result in hypertrophy dyspnoea. On auscultation, a diastolic murmur can be
364 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

FIGURE 12.1 Valvular stenosis and regurgitation: (A) normal position of valve leaflets (cusps) when the valve is
open and closed; (B) open position of a stenosed valve (left) and closed position of a regurgitant valve (right);
(C) haemodynamic effect of mitral stenosis shows the mitral valve is unable to open completely during left atrial systole,
limiting left ventricular filling; (D) haemodynamic effect of mitral regurgitation shows the mitral valve does not close
completely during left ventricular systole, allowing blood to re-enter the left atrium.5

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adult cardiac surgery safely improves outcomes and lowers costs. J Thorac Cardiovasc Surg 2014;148(6):3101-9.e1, with permission.

heard. The ECG may show left ventricular hypertrophy failure, but left ventricular function is usually intact.5 Lung
due to volume overload and a chest X-ray may reveal compliance is reduced, causing dyspnoea, orthopnoea and
cardiomegaly and features of acute pulmonary oedema. nocturnal paroxysmal dyspnoea. Patients may complain
of fatigue, low exercise tolerance, cough and haemopty-
Mitral valve disease sis. On auscultation a low-pitched diastolic murmur and
Mitral stenosis is a chronic and progressive narrowing an opening snap can be heard. The ECG may show left
of the mitral valve orifice (normally 4–6 cm2), restrict- atrial enlargement and possibly atrial fibrillation (AF), and
ing blood flow from the left atrium to the left ventricle. a chest X-ray may reveal right ventricular hypertrophy, left
Patients may exhibit symptoms when the valve area is atrium enlargement and features of pulmonary oedema.
<2 cm2 and they will have symptoms at rest when the In mitral valve regurgitation, the mitral valve is not
valve area is <1 cm2. closing during left ventricular systole, causing backflow
Mitral valve stenosis often occurs as a result of rheumatic of blood into the left atrium, which creates elevated
heart disease, degenerative valve diseases and, less often, atrial and pulmonary pressures, and possibly pulmonary
from systemic lupus erythematosus. These diseases cause oedema.5Acute mitral regurgitation is often caused by
damage to the leaflets and chordae tendineae, so that acute myocardial infarction (AMI) resulting in papillary
during healing the scars contract and seal, restricting the muscle rupture, trauma or infectious endocarditis, and
aperture. The incomplete emptying of the left atrium patients may present with signs and symptoms of acute left
causes increased left atrial pressure and left atrial enlarge- ventricular failure, acute pulmonary oedema and cardio-
ment, and results in pulmonary congestion and pulmonary genic shock. The causes of chronic mitral regurgitation
hypertension. In chronic conditions, this pressure may are rheumatic diseases, congenital mitral valve prolapse
also affect the right ventricle, causing right ventricular or degenerative changes. The patient may complain of
 CHAPTER 12 CARDIAC SURGERY AND TRANSPLANTATION 365

weakness, fatigue, exertional dyspnoea, palpitation and patients with a left main coronary artery lesion, multiple
symptoms of pulmonary congestion and right ventric- (double- or triple-vessel) disease, longer lesions and failed
ular failure such as cough, dyspnoea, orthopnoea and angioplasty may need CABG surgery.6
lower extremity oedema. On auscultation, a third heart In CABG a section of vein or artery is used to bypass
sound and a pansystolic murmur can be heard. ECG may a blockage in the patient’s coronary artery. The vessels
show left atrial enlargement, left ventricular hypertrophy, used for grafting arise from arteries (internal mammary
P mitrale and possibly AF, and a chest X-ray may reveal artery or radial artery and, less commonly, gastroepiploic
left ventricular hypertrophy, left atrium enlargement and artery) or veins (saphenous vein). Saphenous veins are
features of pulmonary oedema. harvested from the legs, and the radial artery from the
Tricuspid valve disease forearm, and each is used as a free graft with anastomo-
ses at the ascending aorta and distal to lesions to one
Tricuspid stenosis (normal area is 7 cm2) is often seen or more coronary arteries. When saphenous veins are
with aortic or mitral valve diseases, and rarely in isolation. used as grafts (SVG), they often develop diffuse intimal
The restriction of blood flow from the right atrium to
hyperplasia, which ultimately contributes to re-stenosis.
the right ventricle causes systemic venous congestion.
Patency rates are lowest in saphenous vein grafts attached
On auscultation, a diastolic murmur can be heard.
to small coronary arteries or coronary arteries supplying
Tricuspid regurgitation is most commonly a functional
disorder due to annulus dilation as a result of increased myocardial scars. Consequently, arterial grafts are used
right ventricle pressure and hypertrophy, mitral stenosis, more often, as they are more resistant to intimal hyper-
pulmonary embolism, cor pulmonale or right ventricle plasia. Internal mammary arteries (IMAs) and radial artery
AMI. The backflow of blood from the right ventricle to grafts may be used.7 The IMA remains attached to the
the right atrium causes systemic venous congestion. On subclavian artery and is mobilised from the chest wall and
auscultation, a pansystolic murmur can be heard. In both anastomosed to the coronary artery distal to the occlusion
stenosis and regurgitation of the tricuspid valve patients (Figure 12.2). If the radial artery is being harvested for
present with a high central venous pressure (CVP) and grafting, the collateral circulation in the forearm is
jugular venous pressure ( JVP), hepatomegaly, ascites and
peripheral oedema, and their ECG may show P pulmonale
and possibly AF, and a chest X-ray may reveal prominent FIGURE 12.2 Coronary artery bypass grafts.
right heart border. CX = circumflex artery; LAD = left anterior descending;
LIMA = left internal mammary artery; LM = left main;
Pulmonic valve disease RCA = right coronary artery; SVG = saphenous vein graft.
Pulmonic valve stenosis is rare in isolation and is often
due to a congenital defect. The restriction to blood flow /HIWVXEFODYLDQDUWHU\
from the right ventricle to the pulmonary arteries causes
right ventricular hypertrophy and dilation, and the patient
presents with exertional dyspnoea, syncope, cyanosis and a
systolic murmur, and a split S2 heart sound.The ECG may 69*WR5&$
show right ventricular hypertrophy. /,0$WR
Pulmonic valve regurgitation is also a rare condition /$'
that is usually caused by a congenital defect or pulmonary
hypertension or is iatrogenic (e.g. post balloon valvulo-
plasty). Patients might be asymptomatic, but in severe 5&$
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ventricular failure. WR&;
Surgical procedures
/0
The most common cardiac surgical procedures include &;
coronary artery bypass graft (CABG) surgery, to bypass
lesions within the coronary arteries, and repair or replace- /$'
ment of stenotic or regurgitant valves. During these
procedures preservation of systemic circulation, ventilation
and perfusion of the myocardium is required and is often
achieved with the aid of cardiopulmonary bypass (CPB).
Coronary artery bypass graft surgery
The pathophysiology and implications of ischaemic
heart disease are explained in detail in Chapter 10. Single &RURQDU\DUWHU\OHVLRQV
lesions can be treated by angioplasty and stent; however,
366 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

assessed. Echo colour Doppler provides the best accuracy is primarily based on the clinical state of the patient
in assessing forearm circulation, although the clinical Allen using the New York Heart Association (NYHA) classifi-
test is quite commonly used.The disadvantage of the Allen cation system and echocardiographic findings.6 The type
test is that it gives false patency results around 5% of the of surgery used will depend on the valves involved, the
time.8 A selection of IMA, SVG and radial artery grafts may valvular pathology, the severity of the condition and the
be necessary over time as repeat procedures are needed or patient’s clinical condition. Often valve surgery is not a
in patients with extensive disease requiring multiple grafts. single procedure, and it may involve multiple valves, CABG
For single-vessel disease, particularly of the left anterior and an implantable cardioverter defibrillator (ICD). Valve
descending (LAD) artery, a new approach to CABG – surgery is palliative, not curative, and patients will require
minimally invasive direct coronary artery bypass grafting lifelong health care.
(MIDCABG) – has been used. This procedure uses inter- Valve repair may involve resecting and/or suturing
costal incisions and a thorascope instead of a sternotomy prolapsed or torn leaflets (valvuloplasty) and repairing
to access the heart and coronary arteries. MIDCABG is the ring of collagen the valve sits in (annuloplasty), and
also often performed without cardiopulmonary bypass is commonly used for mitral and tricuspid regurgitation.
(off-pump coronary artery bypass, OPCAB); instead, the Commissurotomy (incising valve leaflets and debriding
heart is slowed with beta-blockers to allow the surgery to calcification) is the treatment of choice for mitral stenosis.
be performed on a beating heart.9 OPCAB procedures Both repair processes have demonstrated lower operative
may also be performed using full or partial sternotomy mortality than replacement, although complete valve
to provide access for multiple vessel grafting. Both competence may not be achievable. Open procedures are
procedures have been successful responses to the drive to preferred because thrombi and calcification can thereby
reduce the need for transfusion, recovery times, patient be removed.
stays in hospital and costs.9,10 Valve replacement may be necessary, but could be
In the last decade robotically-assisted cardiac surgery associated with higher risks due to the long-term disease
has evolved in America and Europe and has been intro- process and poor underlying left ventricular function. The
duced at a small number of Australian hospitals for CABG most common indication for valve replacement is aortic
and mitral valve surgery.This technique has further reduced stenosis, which accounts for around 60% of valve surgery.15
the invasiveness of cardiac surgery, as little more than stab Prosthetic valves may be mechanical or biological.
wounds are required in the right chest for thoracoscopy Mechanical valves are made of metal alloys, pyrolite
and the robotic instruments. Avoiding true thoracotomy carbon and Dacron (Figure 12.3). Biological valves are
or sternotomy improves postoperative pain experience, constructed from porcine, bovine or human cardiac tissue.
is associated with quicker recovery and shortens length Mechanical valves are more durable but have an increased
of stay.11,12 risk of thromboembolism, so lifelong anticoagulation is
Although CABG is the most common cardiac surgical required. Biological valves suffer from the same problems
procedure undertaken in Australia, the incidence has as the patient’s valve (i.e. calcification and degeneration).
declined since 2000/01 from 87 to 61 procedures/100,000 The choice of valve depends on the age of the patient and
population in 2007–08.3,13 The decline in surgery rates is potential difficulties with taking anticoagulants.
due to changes in the treatment of CHD, including the For elderly patients with high risk of open heart
advent of percutaneous coronary intervention (PCI). surgery and higher comorbidity, trans-catheter aortic
More procedures are now being performed in older valve implantation (TAVI) of commercial artificial valves
patients, with 73% of current patients aged over 60 (for example Medtronic CORE Valve or Edwards Sapein)
years.3 CABG is used to relieve the symptoms of angina has been used. This procedure is usually performed in a
by increasing coronary blood flow distal to occlusive catheter laboratory, via femoral artery approach, similar
coronary lesions. It is a palliative, not curative, treatment to angiography procedure and light anaesthesia. This
as the underlying disease process continues. CABG is procedure carries higher risks of all-cause 1-year mortality
more effective than percutaneous transluminal coronary of 13.9–16.3%, major vascular complications of 9.3–12.3%
angioplasty (PTCA) in patients with extensive, multivessel and 2.6% incidence of stroke.16,17
disease with improved survival over a 3–5-year period by Mortality is higher for valvular surgery than for CABG,
5%, and a 4–7-fold reduction in the need for reinterven- reflecting the underlying loss of ventricular function and
tion.14 CABG is also used in left main vessel lesions due additional procedures that are common. Risk stratifica-
to the high risk of extensive infarction associated with tion models have been developed to help determine the
PTCA in this area. CABG surgery is commonplace, and patients that are most likely to have poor recovery and
many cardiothoracic centres have highly efficient, effective outcomes.18 The major factors that contribute to poor
systems in place with mortality rates as low as 2%. outcomes are worse left ventricular function and age over
70 years.15
Valve repair and replacement
Valve surgery is usually undertaken to repair the patient’s Cardiopulmonary bypass
valve or, more often, to replace the valve with a mechanical CPB was developed to enable surgery to be performed
or tissue prosthesis. The clinical decision for valve surgery on a still, relatively bloodless heart, while preserving
 CHAPTER 12 CARDIAC SURGERY AND TRANSPLANTATION 367

FIGURE 12.3 Prosthetic valves: (A) the Bjork-Shiley valve, with a pyrolyte-carbon disc that opens to 60°; (B) the
Starr-Edwards caged-ball valve model 6320, with satellite ball; (C) the St Jude Medical mechanical heart valve, with a
mechano-central flow disc; (D) the Hancock II porcine aortic valve, with stent and sewing ring covered in Dacron cloth 5
(published with permission).

A B

C D

the patient’s circulation. CPB temporarily performs the increases capillary leakage, and lung deflation during
functions of the heart in circulating blood and of the surgery leading to postoperative atelectasis
lungs by enabling gas exchange with the blood. Silicone • cardiovascular effects due to volume changes, fluid
cannulae are inserted into the venae cavae or right atrium, shifts and decreased myocardial contractility, which
and venous blood is circulated through a circuit outside decreases cardiac output; this is most severe during
the body. In this circuit the blood is oxygenated, carbon the first 6 hours, but usually resolves within
dioxide removed and blood temperature controlled. Drugs 48–72 hours
and anaesthetics may be added. A roller pump is generally • neurological effects due to poor cerebral perfusion
used to provide the pressure to create blood flow in the and generation of thromboemboli from aortic
circuit and back to the patient’s aorta. cannulation, which can lead to cerebrovascular
Adverse effects of CPB are diverse, and include the accidents
following (Table 12.1):19
• renal effects due to decreases in cardiac output during
• haematological effects due to exposure of the blood initiation of CPB, which decreases renal perfusion
to tubing and gas exchange surfaces, which initiates • post-pump delirium or psychosis, which occurs in
surface activation of the clotting cycle; also blood 32% of CPB patients although the cause has not been
component damage due to shear stress from the roller identified; symptoms include short-term memory
action of the pump, which reduces haematocrit, deficit, decreased attention and inability to respond to
leucocyte and platelet count. and integrate sensory information
• pulmonary effects due to activation of systemic • activation of a systemic inflammatory response, which
inflammatory response syndrome (SIRS), which may cause vasodilation and increased cardiac output.
368 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

be protected from ischaemia during the cardiac surgical

TABLE 12.1 procedure. This protection is achieved through several
Summary of the impact and side effects of CPB mechanisms directed towards reducing oxygen demand:
first, oxygen demand is reduced by mild-to-moderate
BODY SYSTEM C P B I M PA C T SIDE EFFECTS
hypothermia (28–32°C); second, myocardial tempera-
Haematology Surface activation ↓ WBC, ↓ HcT, ture is reduced (0–4°C) by infusing cold fluids directly
of clotting cascade ↓ platelets
into the coronary arteries; and third, normal conduction
Thromboembolism
is prevented by arresting the heart during diastole, by
formation
infusing a concentrated potassium solution into the
Pulmonary SIRS activation ↑ Capillary coronary arteries. Return to normal rhythm is usually
(CPB circuit) permeability and achieved by circulation of warm blood, though defibrilla-
leakage tion may be necessary.
Pulmonary
congestion Patient management
↓ Surfactant
The often-rapid turnaround from complete dependence in
production
intensive care to discharge in post-cardiothoracic surgery
Lung deflation Atelectasis
patients can provide particularly rewarding nursing experi-
(during surgery) Impaired gas
exchange
ences. However, this rapid progression is also often marked
by haemodynamic instability, arrhythmias and biochemi-
Cardiovascular Volume changes Fluid shift cal and haematological changes. The increased emphasis
SIRS activation ↓ Myocardial
on rapid weaning and extubation, often occurring during
contractility and CO
turbulent anaesthetic recovery, presents one of the more
Vasodilation and ↓
volatile periods in ventilatory support, requiring know-
SVR
ledgeable and skilled nursing and medical management.
Neurological Poor cerebral ↑ Risk of CVA In addition to the management of ventilation, temporary
perfusion pacemaker therapies and mechanical circulatory assist
Thromboembolism
(intra-aortic balloon pumping and ventricular assist)
Post pump delirium Short-term memory
devices provide opportunity for the development of broad
or psychosis deficit
and detailed expertise.
↓ Attention
Sensory deficit
Patients are usually admitted to the intensive care
unit for 1–2 days although, when early extubation is
Renal ↓ CO and renal ↓ Urine output, and
undertaken, they may spend only hours in a recovery unit
perfusion ↑ risk of ARF
before progressing to a cardiothoracic high-dependency
ARF = acute renal failure; CO = cardiac output; area, where nurse-to-patient ratios may be 1:2 to 1:3.
CPB = cardiopulmonary bypass; CVA = cardiovascular
accident; HcT = haematocrit; SIRS = systemic inflammatory The immediate postoperative period
response syndrome; SVR = systemic vascular resistance;
Patients should be transported to intensive care accompa-
WBC = white blood cells.
nied by at least an anaesthetist, an appropriately qualified
nurse and transport personnel under continuous cardiac
These effects are well documented, and routine monitoring and assisted ventilation. It is a requirement to
CPB management and postoperative care are designed include capnography during patient transport to detect
to minimise and treat the complications. Heparin is ventilator disconnection, dysfunction or endotracheal
added at the commencement of CPB and is reversed tube migration. Intensive care or theatre nursing staff may
with protamine (1 mg of protamine for every 100 U of be a component of the transport team. The admission to
heparin) when CPB ceases; activated clotting times are intensive care requires a team approach, with the parti-
monitored throughout and after CPB. Blood returning to cipation of intensive care nursing and medical staff and/
the circulation is filtered, and surgical procedures proceed or technician input.The immediate postoperative decision
carefully to reduce microemboli. Monitoring and mainte- making on patient management is influenced by handover
nance of adequate arterial flow rates are used to prevent from anaesthetists, settling in procedures and collegial
low perfusion. Temperature gradients and a rewarming assistance.20,21 Admission activities are commonly divided
process are instituted slowly so that cardiac output can between nurses, with one nurse taking responsibility for
meet metabolic demands. establishing monitoring and haemodynamic assessment
and management, and a second nurse managing ventila-
Myocardial preservation tion and endotracheal tube security, as well as managing
One of the processes involved in CPB is that the aorta chest drains, gastric tube and urinary catheter. If staffing
is clamped where a cannula is inserted to return blood permits, additional nurses may take responsibility for
to the circulation. This clamp prevents blood flow into documentation, performing arterial blood gases, 12-lead
the coronary arteries; therefore, the myocardium must ECG and providing assistance as required.
 CHAPTER 12 CARDIAC SURGERY AND TRANSPLANTATION 369

The objectives of immediate postoperative manage- Hypertension

ment of cardiac surgical patients may include: Hypertension is present in up to 30% of patients
• optimisation of cardiovascular performance initially,24 as hypothermia, stress responses, pain and hypo-
• reestablishment and/or maintenance of normothermia volaemia contribute to vasoconstriction.21,24 When the
systemic vascular resistance is excessive, the high afterload
• promotion of haemostasis may contribute to low cardiac output.24 Rewarming
• ventilatory support and management to normothermia with space blankets or heated air
• prevention and management of arrhythmias blankets, fluid administration, administration of sedation
• optimisation of organ perfusion. or analgesics and infusion of IV vasodilators (glyceryl
trinitrate or sodium nitroprusside) are all commonly
Haemodynamic monitoring and used to overcome vasoconstriction when contribut-
support ing to hypertension.21,24 Occasionally, beta-blockers are
Typical haemodynamic monitoring includes an intra- used. Hypertension increases myocardial workload and
arterial catheter for continuous blood pressure monitoring contributes to bleeding.
and arterial blood sampling. Cardiac output and preload Hypotension
measurement are achieved most commonly with either a
Transient hypotension requiring treatment is common
pulmonary artery or central venous catheter configured
at some stage during the postoperative period. Contrib-
for pulse contour cardiac output (PiCCO) monitoring
uting factors to hypotension include hypovolaemia and
(see Chapter 9).
decreased venous return (from polyuria, bleeding, venti-
Preload measures provided by the pulmonary artery
lation and positive end-expiratory pressure and excess
catheter include right atrial pressure (RAP) to approx-
vasodilation), contractile impairment (from ischaemia or
imate right ventricular filling and pulmonary artery
infarction, hypothermia and negative inotropic influences),
pressure (PAP) to approximate right ventricular systole
pericardial tamponade and vasodilation (from excess vaso-
and provide insight into pulmonary vascular resistance
dilator therapy, or as part of an inflammatory response to
and left heart function. The pulmonary capillary wedge
cardiopulmonary bypass).21,25
pressure (PCWP) is available to approximate left ventricu-
Hypotension may present with reduced or elevated
lar filling and left heart function. Alternatively, the PiCCO
preload, reduced or elevated cardiac output and reduced or
monitoring system represents preload by intrathoracic
elevated systemic vascular resistance (SVR). When hypo-
blood volume index (ITBVI) and global end-diastolic
volaemia is present, cardiac output will be low and SVR
volume index (GEDVI). In addition, the extravascular
usually high. Hypovolaemia is diagnosed by measuring
lung water index (EVLWI) can demonstrate the accumu-
preload indicators, as pressure (RAP, PAP, PCWP) or
lation of interstitial lung water.22
volume (ITBVI, GEDVI).22,26 Choice of colloids or crys-
Cardiac output is measured by either intermittent
talloid fluids for volume restoration in the postoperative
or continuous thermodilution via pulmonary artery
period has no effect on mortality,27 but colloids affect clot
catheters, or measured intermittently and then approxi-
formation and strength and also produce greater haemo-
mated continuously on a beat-to-beat interpretation of
dilution, which is associated with more blood product
pulse contour by the PiCCO monitoring system. Cardiac
transfusion.23,28 Blood returned from the cardiopulmonary
output measurement can be combined with other
bypass circuit (‘pump blood’) usually accompanies the
pressure variables to calculate systemic and pulmonary
patient to ICU, and this should be readministered at a rate
vascular resistance, stroke volume and measures of
suitable to filling indices and blood pressure.
ventricular work.
Hypotension accompanied by elevated preload and
Certain common haemodynamic patterns are seen
low cardiac output usually represents cardiac dysfunction
in the early postoperative phase. These must be detected
or pericardial tamponade, and the distinction should be
through thorough monitoring and interpretation of
quickly sought.29,30 When such left ventricular dysfunction
variables, and managed according to specific needs. During
is present, there is usually compensatory vasoconstriction
the initial 2 hours of recovery period, 95% of patients will
and tachycardia, although heart rate responses may be
experience haemodynamic instability.19,23
unreliable due to cardioplegia, cold, conduction disease21
and preoperative beta-blocking agents. Inotropic agents,
Practice tip including milrinone hydrochloride, adrenaline, dopamine
The choice of inotropes and vasoactive drugs or dobutamine, may become necessary (these are covered
should be based on the haemodynamic findings, for more completely in Table 21.7 and its accompanying text).
example: a patient with low SVR and low contractility When the profile of severe left ventricular dysfunction is
(low CO and BP) will need an ino-constrictor such persistent (either at the time of coming off bypass or later
as adrenaline or dopamine; a patient with high SVR in intensive care), intra-aortic balloon pumping may be
and low contractility will need an ino-dilator such as instituted. ECG assessment for new ischaemia or infarction
milrinone or dobutamine. should be made, which if of significant size, may warrant
surgical re-exploration or angiographic investigation.
370 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Pericardial tamponade is also a cause of hypotension Rhythm monitoring and postoperative

(covered later in this chapter). arrhythmias
A fourth common postoperative profile is hypo- Continuous rhythm monitoring is necessary while the
tension with normal or elevated cardiac output in the patient is in intensive care, and telemetry monitoring
presence of low SVR. This may occur with excess vaso-
is usually continued until discharge from hospital. Lead
dilator administration, the use of postoperative epidural
selection is often haphazard, but a chest lead in the V1
infusions and vasodilation from a systemic inflammatory
position (or lead MCL1) generally provides the best infor-
response to cardiopulmonary bypass and other factors
mation on atrial and ventricular activity.35 Unlike many
such as reinfusion of collected operative site blood.31
leads, these two leads reliably demonstrate normal rhythms,
The inotrope milrinone hydrochloride is popular in
bundle branch block and ventricular rhythms,35 and
the postoperative phase because of its dilating effect on
radial artery grafts,32 but often contributes to hypoten- may be useful in confirming pulmonary artery catheter
sion through its systemic vasodilator properties. When irritation as the cause of ventricular arrhythmias.36
hypotension is attributable to vasodilation, metaraminol A 12-lead ECG is performed on admission to the ICU
or noradrenaline may be used.26 Arginine vasopressin, and should be compared with the preoperative ECG. It
by infusion, could be used as an effective alternative should be assessed for signs of new ischaemia or infarction,
vasoconstrictor for cardiac surgical patients, but early new bundle branch block and arrhythmias or conduction
introduction of vasopressin demonstrated improved disturbances. Pericarditis, a frequent complication of
haemodynamic response.33,34 surgery, appears as ST-segment elevation (often, but not
A mean arterial pressure of 70–80 mmHg is always, in many leads), and may mask or mimic myocardial
generally targeted in the postoperative period.21 This can infarction. The nurse should look for the classic concave
sometimes be reduced if there has been ventriculotomy upward, or ‘saddle-shaped’ ST segment, to distinguish
or if there is concern about the status of the aorta. The pericardial changes from the more convex upward ST
cardiac index should be maintained above 2.2 L/min/m2, segment of infarction. Worsening of pain on inspiration
as hypoperfusion develops below these values. When at and a pericardial rub help to confirm pericarditis.35
these levels, additional assessments are often undertaken, Atrial fibrillation is the most common postoperative
such as mixed venous oxygen saturation measurement arrhythmia and contributes significantly to postoperative
(to assess oxygen delivery deficits) and arterial pH and morbidity and hospital length of stay.37 It occurs in up
lactate measurements (to detect metabolic acidosis from to 30–50% of patients, most often on days 2–3 post-
anaerobic metabolism). operatively.30,37 Many patients revert without treatment,
In addition to assessment of preload, contractility and but when treatment becomes necessary beta-blockers and
afterload, heart rate and rhythm should be assessed for amiodarone appear to be the most successful agents for
their input to cardiac output and blood pressure. Extremes correction.37,38 Digitalis is effective for rate control and IV
of rate and arrhythmias alter ventricular filling and may magnesium is often used, although further evidence for
need correction. If temporary pacing wires are present, its use is needed. Atrial pacing to prevent atrial fibrillation
pacing strategies for haemodynamic improvement include is being increasingly explored but a clear recommenda-
rate rises (even if already in the normal range)21 and the tion on pacing sites and protocols has yet to emerge. In
provision of dual-chamber or atrial pacing as alternatives contrast, atrial overdrive pacing can be an effective means
to ventricular pacing only in order to maximise atrio- to immediately and safely interrupt atrial flutter.37,38
ventricular synchrony and the contribution of atrial kick Ventricular ectopic beats are common and by them-
to blood pressure. Alternatively, if ventricular pacing is selves do not require treatment unless they accompany
present, reducing the rate to permit expression of a slower ischaemia or biochemical disturbance,39 in which case
sinus rhythm may, with the provision of atrial kick, improve they may progress to more complex arrhythmias. Consid-
cardiac output and blood pressure (refer to Chapter 11 for eration should always be given to the pulmonary artery
more information on pacing). catheter as the cause (including both correctly and incor-
rectly positioned catheters),36 as this is an easily corrected
Practice tip influence. Ventricular tachycardia and fibrillation are
uncommon and usually denote myocardial distur-
Be aware of an apparent paradox: hypertension may
bance such as ischaemia or infarction, shock, electrolyte
occur even if there is hypovolaemia. The intense
disturbance, hypoxia or increased excitation due to high
vasoconstriction often seen postoperatively not only
circulating catecholamine levels.39 Standard approaches to
raises blood pressure but aids venous return so that
resuscitation according to protocols in Chapter 24 apply,
right atrial pressure is normal. It may not be until the
including standard CPR over the recent sternotomy.When
patient has warmed and dilated that the true filling status
ventricular fibrillation cannot be corrected, consideration
is revealed. When the patient is cold and has normal
is often given to re-exploration of the chest to examine
filling pressures, be prepared for possible hypotension,
graft patency and/or provide internal cardiac massage.The
and the need for significant fluid resuscitation, on
cardiac surgical intensive care unit should be equipped to
rewarming.
enable emergency re-exploration for such purposes.
 CHAPTER 12 CARDIAC SURGERY AND TRANSPLANTATION 371

For many patients, ventilation is provided purely

Practice tip for initial airway and apnoea protection rather than
Appropriate patient management should be based on for treatment of pulmonary deficits. In the absence of
frequent assessment and evaluation of their condition, pulmonary disease, many centres provide fairly uniform
especially during the immediate postoperative period, approaches to parameter settings that aim at sustaining
to achieve: ventilation and oxygenation, while limiting traumatic
risk to the lungs (see Table 12.2). However, approaches
• optimal preload to ventilation will need to be tailored in the presence of
• optimal contractility operative complications or coexisting lung disease.
• optimal afterload. Ventilation challenges specific to the postoperative
cardiac setting include:
Ventilatory support • atelectasis due to operative access
Ventilation should be approached according to the general • pneumothorax (pleural opening for grafts, or
principles described in Chapter 15. As anaesthesia is not ventilation-induced trauma)
typically reversed at the end of the operation, patients are
generally admitted apnoeic, and within 1–3 hours return
• pulmonary hypertension from cardiac failure or valve
disease
to wakefulness and spontaneous breathing.
Ensuring a secure airway is an initial priority; the • cardiogenic shock/post-pump failure
following should be undertaken: • systemic inflammatory response syndrome due to
cardiopulmonary bypass
• Confirmation of endotracheal tube (ETT) position
and its security immediately on admission: • early or rapid weaning that is undertaken before
auscultation for equal bilateral air entry to rule out complete readiness, leading to failure at weaning attempt
right main bronchus intubation • surgical pain limiting spontaneous effort and poten-
recording of the ETT insertion length to detect tially leading to atelectasis or sputum retention.
ETT migration
postoperative chest X-ray, taken within 30 minutes, Approaches to weaning
should also be examined for ETT positioning As patients often have no underlying pulmonary path-
ology, and have been ventilated for brief periods only,
• Initial ETT care:
rapid weaning phases have become the norm in most
assessment for air leak around the cuff (via
performance of minimal occlusive volume or centres. In many instances, as soon as the patient wakes
pressure tests) and auscultation of the neck and begins spontaneous breathing activity, he/she may
ensure ETT is adequately secured and positioned so be suitable for at least a trial of spontaneous breathing in
as not to apply undue pressure against soft tissues of CPAP mode, usually with some modest level of pressure
the mouth and lips. support (e.g. 5–10 cmH2O). If tolerated and the patient
maintains an adequate minute volume, SpO2 and PaCO2,
There has been a general trend to more rapid venti- extubation may be considered within as little as another
latory weaning in recent years, and in some centres 30 minutes. Normal demonstrations of airway protection
‘fast-track’ cardiac surgical recovery includes extubation capability (e.g. neuromuscular control, gag, swallow, cough
at the end of the operation before transfer to a recovery and patient strength) should be sought before extubation
unit for suitable patients. Indices of respiration show no (see Chapter 15 for details).
improvement when intubation is maintained for longer These short ventilation times and rapid weaning carry
compared with early extubation,40 and pooled results a greater risk of weaning failure. Patients may initially wake
from randomised early extubation trials show earlier ICU and appear to sustain spontaneous ventilation well for
discharge and shorter lengths of stay (by 1 day) when early some time, only to lapse back under anaesthetic influence.
extubation is undertaken.40,41 A return to greater ventilatory support may be necessary.
Apart from these fast-track approaches, ventilation is Failure to wean carries greater significance in the cardiac
commonly employed for 2–6 hours in the uncomplicated surgical patient with existing pulmonary hypertension, as
patient. Reasons for continuing ventilation beyond this respiratory acidosis causes pulmonary vasoconstriction,
time frame may include: abruptly worsening pulmonary hypertension and the risk
• intraoperative neurological event of pulmonary oedema and/or right ventricular failure.
• gas exchange deficit with unresolved hypoxaemia When ventilation has been more prolonged due to
postoperative pulmonary problems, weaning may be
• ventilatory inadequacy approached more cautiously, as might be applied to the
• significant haemodynamic insufficiency general longer term ventilated patient. Gradual mandatory
• patients returning from theatre late in the evening rate reduction or increasing periods of spontaneous venti-
may sometimes continue ventilation overnight to lation interspersed with periods of greater assistance have
optimise postextubation breathing ability. been employed.40,42
372 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 12.2
Postoperative ventilation settings

N O M I N A L O R G E N E R A L LY
A C C E P TA B L E S E T T I N G S A LT E R N AT I V E S T O N O M I N A L S E T T I N G S A N D R E A S O N S F O R VA R I AT I O N

SIMV with volume control Pressure control suitable. Generally used only if there is significant hypoxaemia or the need
ventilation to exert greater control on pulmonary pressure. Hybrid modes such as Autoflow, pressure-
regulated volume control or volume control plus (VC+) are also suitable, generally for the
same indications as pressure control
Tidal volume 8–10 mL/kg Lower tidal volumes (6–8 mL/kg) when there is known compliance disorder (atelectasis,
pulmonary oedema, fibrosis) or unexplained high plateau pressures
Mandatory rate 10 L/min Faster rates may be necessary if low tidal volume strategies become necessary. Lower rates
if gas trapping risk due to airways disease
Adjust according to PaCO2 level
Inspiratory flow 30–50 L/min Slower flows to prolong the inspiratory time may be necessary if there is atelectasis and
to provide I: E ratio of 1 : 2 to hypoxaemia, or if there is a desire to lessen inspiratory pressures. Faster flows to enhance
1 : 4 acceptable expiratory time necessary only if gas-trapping risk
PEEP minimum levels of Higher levels of PEEP according to severity of hypoxaemia
5 cmH2O
Pressure support 5–10 cmH2O Automated pressure support modes such as automatic tube compensation (autoadjusted
pressure support to overcome flow resistance of tracheal tubes) or volume support
(autoadjusted pressure support to achieve target tidal volume on spontaneous breaths) exist.
There is no pressing indication for their use in uncomplicated cardiac surgical patients
Permissive hypercapnoea rarely Particularly important to avoid if existing pulmonary hypertension, as may worsen acutely with
necessary respiratory acidosis
FiO2 initially 0.8–1.0 then wean According to PaO2/SaO2
down according to PaO2/SaO2

FiO2 = fraction of inspired oxygen; PEEP = positive end expiratory pressure; SIMV = synchronised intermittent mandatory ventilation
mode.

Postoperative bleeding retrosternal/anterior mediastinal drain, as the sternum is

The harvest sites for radial arteries or saphenous veins generally the major source of bleeding in the absence of
are uncommon sources of significant blood loss and are complications. Additional drains may be inserted in the
generally easily managed with dressings or compression. pericardial or pleural spaces. Pericardial drains are more
likely to be inserted following aortic valve surgery, whereas
Intrathoracic bleeding, however, may be torrential and
pleural drains become necessary following mammary
threaten life. Occasionally, surgical bleeding from the
artery harvesting or when the pleura is opened for any
aorta, arterial grafts or myomectomy sites may exceed
other reason. Pleural drains may be anterior, posterior
replacement capabilities, and at times patients succumb or ‘wrap-around’ configurations in which they project
to overwhelming haemorrhage. Maintenance of drain over the anterior lung, following the pleural space first
patency and strict recording of losses and total fluid balance from midline to lateral and then, finally, the posterior
are paramount, and fluid balance assessments over shorter pleural space.
intervals, even every 5–10 minutes, become necessary Reportable postoperative blood losses vary, but greater
during active bleeding. Because of the potential rates of than 100 mL/h, or greater than 400 mL in the first 4 hours,
bleeding, the cardiac surgical unit must be equipped to would generally be regarded as excessive and worthy of
institute rapid volume replacement, and have access to surgeon notification. Importantly, excessive bleeding does
adequate blood and blood product stores, blood warmers not always represent a surgical defect that reoperation
and all necessary procoagulant therapies. In addition, might correct, as there are many contributors to impaired
dedicated equipment should be available to facilitate haemostatic capability in the cardiac surgical patient (see
emergency resternotomy to control haemorrhage. below).
One or more chest drains are inserted to remove Chest drainage should be monitored closely and,
and monitor blood loss, but the positioning of drains is while bleeding is active, volumes should be assessed every
variable, depending in part on the procedure performed, 5 minutes and patency of drains ensured to avert tamponade.
the surgical route taken and surgeon preference. Sudden cessation of drainage should always raise the possi-
Regardless of these considerations there will always be a bility of the loss of tube patency and risk of tamponade,
 CHAPTER 12 CARDIAC SURGERY AND TRANSPLANTATION 373

but tamponade may also occur while drainage continues, protamine or other agents.45,46 Treatable levels vary from
as collections and compressions may occur at sites isolated greater than 120 s to greater than 150 s among different
from drains, or losses may simply be occurring faster than centres.
that able to be removed by patent drains. A limitation of ACT measurements is that they provide
Chest drains should also be observed for bubbling, to no information about clotting processes beyond initial
assess for air leaks originating from either system faults fibrin formation, so clotting deficits such as impaired
or patient leaks. When bubbling can be attributed to clot strength or the presence of significant fibrinolysis as
the patient, the patency of tubes becomes additionally contributors to bleeding are not revealed by this test.47
important to avert tension pneumothorax, which may By contrast, the thromboelastograph (TEG) measures the
accumulate rapidly, even over the course of a few breaths clotting process as it proceeds over time.47 TEG monitoring
in the ventilated patient. not only reveals abnormalities early in the clot process
Blood transfusions are not aimed at restoring haemo- (time to fibrin formation, as would be demonstrated by
globin to normal levels and, despite variations in acceptable the ACT) but also the subsequent development of clot
levels, relative anaemia is almost universally tolerated. strength, clot retraction and, finally, fibrinolytic activity for
Haemoglobin levels are thus not routinely treated unless each of their contributions in the bleeding patient.47 TEG
below 80 g/L, except in the elderly or when there are monitoring, although considerably more expensive than
significant comorbidities.43,44 From these levels patients the ACT, is now available as a bedside or operating room
return to normal haemoglobin status within 1 month technology and offers better insight into bleeding causes.
postoperatively.43,44 In addition, because TEG monitoring identifies deficien-
cies at the various stages of clot formation, development
Contributors to impaired haemostatic capability
of clot strength and the presence of undue fibrinolytic
Many factors may contribute to postoperative bleeding activity, it may permit better matching of procoagulant,
by their influence on coagulation and haemostatic ability. blood product or antifibrinolytic therapy to needs.47
CPB is used in the majority of cardiac surgical cases and No matter which of the above technologies is used at
exerts many influences on coagulation, as do additional the bedside, the patient with significant bleeding should
factors such as preoperative medications, anaemia or coag- be evaluated more fully as soon as bleeding develops.
ulopathies. Contributing factors include: Blood should be drawn and sent for laboratory assessment,
• cardiopulmonary bypass influences: including full blood examination, clotting profile and
heparinisation, haemodilution, platelet damage and measures of fibrinolytic activity.
altered function
disseminated intravascular coagulation (DIC) Heparin reversal
following activation of the systemic inflammatory Cardiopulmonary bypass requires full heparinisation (ini-
response syndrome post-CPB tially 300 IU/kg), which is reversed at end-operation.45,47
The specific antidote, protamine sulfate, is administered
• preoperative anticoagulant/antiplatelet medications
as bypass is ceased, at a dose of 1 mg per 100 IU heparin
commonly encountered
used (i.e. 3 mg/kg).45 If reversal is less than complete,
• aspirin, warfarin, clopidogrel as evidenced by a prolonged ACT, further protamine
• preoperative anaemia due to aortic valve disease, sulfate (at doses of 25–50 mg over 5–10 minutes) may be
autologous blood donation or the various chronic necessary.
anaemias
Management of bleeding
• clotting factor deficiency
Treatment approaches to bleeding once the patient is in
• hypothermia intensive care include further protamine administration
• coexisting coagulopathies if the ACT remains prolonged, blood and blood product
• increased fibrinolytic activity administration (platelets, clotting factors, fresh frozen
• surgical defects such as failure of access site closure, or plasma), procoagulants (desmopressin acetate [DDAVP])
vascular anastomosis defects. and antifibrinolytic agents (see Table 12.3 for more details).
Other general measures such as rewarming the patient and
Bedside assessment of bleeding preventing or treating hypertension should be undertaken.
The activated clotting time (ACT) is the most commonly
used assessment of coagulation and heparin activity during Autotransfusion
cardiac surgery and subsequently in intensive care. It Chest drain systems used in cardiothoracic surgery can
measures the time to onset of fibrin formation (initial clot be configured for retransfusion of collected blood during
development). The ACT has been valuable because it can rapid blood loss. If losses are fresh, and are collected with
be inexpensively and efficiently performed at the bedside, reliable sterility, they can be transfused back into the
providing prompt results and requiring only modest patient. Blood that has been collected and left standing
personnel training. Bleeding patients with a prolonged in the drain receptacle rapidly becomes unsuitable for
ACT come under consideration for administration of retransfusion, and so autotransfusion is generally limited
374 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 12.3
Management of the bleeding patient post cardiac surgery21,33,43,44,48
THERAPY DOSE COMMENTS / ISSUES
Protamine sulfate 25–50 mg slow IV (<10 mg/min); Specific antidote to heparin. May cause
may be repeated if ACT prolonged hypotension. Contraindicated in patient with
seafood allergy
Aprotinin (Trasylol) Continuous infusion of 2 million Antifibrinolytic. Proteinaceous. Anaphylaxis risk on
units over 30 min, then 500,000 re-exposure. Alert should be posted on history
units per hour
Desmopressin acetate (DDAVP) 0.4 mcg/kg IV Promotes factor VIII release; limited evidence for
use
‘Pump blood’ (blood retrieved from Often 400–800 mL This is the remaining blood in bypass circuit;
bypass circuit at end-operation) usually centrifuged before returning to patient
Note: this blood contains heparin from CPB
Whole blood/packed cells As necessary to achieve Hb >80 g/L Autologous blood sometimes available when
or more, according to needs patients have donated blood preoperatively
Fresh frozen plasma As necessary ‘Broad-spectrum’ factor replacement; contains
most factors. Useful adjunct to massive blood
transfusion
Platelet concentrates As necessary Generally ABO and Rh compatible preferred
Epsilon-aminocaproic acid (Amicar) 100 mg/kg IV followed by 1–2 g/h Antifibrinolytic. Inhibits plasminogen activation
Cryoprecipitate 10 units IV Contains factor VIII and fibrinogen (factor I)
Calcium chloride or gluconate 10 mL 10% solution Used to offset citrate binding of calcium in stored
blood
Prothrombinex 20–50 IU/kg IV Contains factors II, IX and X

ACT = activated clotting time; CPB = cardiopulmonary bypass.

Adapted from (with permission):
St Andre AC, DelRossi A. Hemodynamic management of patients in the first 24 hours after cardiac surgery. Crit Care Med
2005;33(9):2082–93.
Albright TN, Zimmerman MA, Selzman CH. Vasopressin in the cardiac surgery intensive care unit. Am J Crit Care 2002;11(4):326–30.
Galas F, Almeida JP, Fukushima JT, Osawa EA, Nakamura RE, Silva C et al. Blood transfusion in cardiac surgery is a risk factor for
increased hospital length of stay in adult patients. J Cardiothorac Surg 2013;8(54):1–7.
Hajjar LA, Vincent J, Galas FRBG, Nakamura RE, Silva CMP, Santos MH et al. TRACS randomized controlled trial transfusion
requirements after cardiac surgery. JAMA 2010;304(14):1559–67.
Bryant B, Knights K, Salerno E. Pharmacology for health professionals. Sydney: Mosby; 2003.

to blood that has collected over 1–2 hours, rarely longer. tachycardia and marked vasoconstriction, elevating the
Blood filters should always be used for protection against systemic vascular resistance. As in cardiogenic shock,
clots that may have developed in the drain receptacle. there is usually elevation of the filling pressures (right
atrial, pulmonary artery and pulmonary capillary wedge
Pericardial tamponade
pressures), sometimes with a particularly suggestive
Postoperative pericardial tamponade results from the merging of the pulmonary artery diastolic, right atrial
accumulation of blood or effusion fluid within the peri- and pulmonary artery wedge pressures.29,49 Additional
cardium. An increasing volume within the pericardial
features that may be present include muffled heart sounds,
space eventually compresses cardiac chambers, impeding
decreased QRS voltage, electrical alternans, narrowing
venous return and therefore causing low cardiac output
and hypotension. Pericardial tamponade is an emergency, pulse pressure and pulsus paradoxus, along with features of
and varies in severity from shock to pulseless electrical increasing anxiety and/or dyspnoea in the awake patient.
activity.29,49 Echocardiography is the definitive assessment tool to
Described as one of the extra-cardiac obstructive reveal the presence of pericardial collections as well as
shocks, pericardial tamponade often resembles cardiogenic identifying the impact on relaxation, filling and contrac-
shock. The low cardiac output and hypotension result in tion of each cardiac chamber.The chest X-ray is of limited
oliguria, altered mentation, peripheral hypoperfusion and use and may show little, even with significant pericardial
development of lactic acidosis. Compensation includes collections.
 CHAPTER 12 CARDIAC SURGERY AND TRANSPLANTATION 375

Importantly, the ‘classic’ or typical haemody- to provide uncertainty and opportunities for nursing
namic profile described above is not uniformly seen in clinicians and researchers. Principles are similar to those
tamponade, and tamponade should never be excluded outlined in Chapter 7. Surgical pain is often compli-
because the haemodynamic status does not match this cated by pericardial inflammation and pain management
profile. This may be because classic tamponade implies must be balanced against the promotion of spontaneous
uniform compression of the entire heart, which may not breathing, chest physiotherapy, mobilisation and partici-
be the case with haemorrhagic tamponade. A clot may pation in education and lifestyle modification programs.
develop over just one chamber rather than occupying the Analgesic options for pain control include intravenous,
entire pericardium, and so there may be compromise to oral or rectal analgesics, non-steroidal anti-inflammatory
only a single chamber rather than the whole heart.29,49 medications and, less commonly, epidural therapies and
nerve blocks. Intravenous opiates and codeine/para-
Management of pericardial tamponade cetamol preparations provide the mainstay of postoperative
The management of pericardial tamponade includes analgesia. When insufficient, or when clinical and electro-
limiting further losses into the pericardium, relief of peri- cardiographic features suggest pericarditis, non-steroidal
cardial pressure through evacuation of blood or clots and anti-inflammatory drugs such as rectal indomethacin are
management of the haemodynamic impact of tamponade. appropriate, except in patients with renal impairment due
Steps to control bleeding and blood pressure as to their renal side effects of reducing glomerular filtration
described above may limit further losses into the pericar- rate and acute deterioration of renal function.50 The place of
dium. All steps should be taken to maintain or re-establish IV COX-2 inhibitors such as parecoxib appears uncertain,
chest tube patency (crushing clots within tubing, ‘milking’ as analgesic efficacy now must be weighed against emerging
when it is truly necessary) and to ensure free flow of blood data suggesting increased thrombotic complications.51
from the chest by avoiding dependent tubing loops or by
instigating side-to-side rolling of the patient to possibly Fluid and electrolyte management
bring collections into proximity of drain tubes.When tube Fluid therapy in the postoperative period is aimed at main-
patency is in doubt, the surgeon may even pass a suction taining blood volume, replacing recorded and insensible
catheter through the chest drain under aseptic conditions losses and providing adequate preload to sustain haemody-
in an attempt to remove clots at the drain tip.29,49 If the namic status. Isotonic dextrose solutions (5%) or dextrose
above measures do not relieve tamponade, consider- 4% + saline 0.18% are commonly used at approximately
ation is given to re-exploring the pericardium, either by 1.5 L/day as maintenance fluids.21,23
returning to the operating theatre or, in an emergency, to Potassium replenishment is generally necessary accord-
the intensive care unit, although this is less preferable. ing to measured serum potassium. Polyuria is usually
Emergency opening of the sternotomy and media- evident in the early postoperative period due to deliberate
stinal re-exploration requires a coordinated team response haemodilution while on cardiopulmonary bypass. With
and, where possible, operating room staff should be polyuria comes potassium loss, which must be treated to
included to manage the sterile field and assist the surgeon. avert atrial or ventricular ectopy and tachyarrhythmias.
Equipment and disposable materials should be counted Because of these predictable potassium losses, proto-
and documented in the manner normally applied in cols for potassium replacement may be instituted, with
theatre. When the situation has been stabilised, consid- standing orders for potassium replacement (e.g. 10 mmol
eration should be given to returning to theatre for final over 1 hour if the serum potassium is <4.5 mmol/L, or
assessment and chest closure.29,49 20 mmol over 2 hours if <4.0 mmol/L). Main line hydra-
tion infusions may also have added potassium to avoid
Practice tip hypokalaemia. Hypomagnesaemia may also develop due
to polyuria, and is likewise proarrhythmic. Supplemen-
Given the variability of presentation of cardiogenic tation (magnesium chloride) is often used for arrhythmia
shock, and the importance of accurate identification, management postoperatively, but its effectiveness has been
clinicians should search for tamponade whenever there questioned in many trials.52
is haemodynamic instability postoperatively, especially Hyperkalaemia occurs less often but is seen particu-
when the haemodynamic status does not match classic larly when there is impaired renal function. Additional
patterns for the major shock states. The management contributors to a rising potassium level include acidosis,
of postoperative cardiac arrest accompanying any administration of stored blood, haemolysis, inotrope use
arrhythmia, as well as pulseless electrical activity, and any postoperative use of depolarising muscle relaxants
should include consideration of tamponade. such as suxamethonium.
Emotional responses and family support
Assessment and management of The experience of being diagnosed with a cardiac disorder,
postoperative pain waiting for surgery, the surgical experience and recovery
As much an art as a science, pain control in the cardiac is an emotional journey for patients and their families.
surgical patient remains a major challenge and continues Regardless of low mortality rates, the possibility of death
376 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

and painful wounds can concern patients. Consequently, take care to consider this aspect. Printed information
patients undergoing cardiac surgery often experience regarding the surgery, recovery and emotions will be
anxiety and depression,53,54 and women appear to be useful for the patient and family (for further information
more vulnerable to these emotions in relation to cardiac refer to Chapter 7, Psychological care, and Chapter 8, Family
surgery than men.55 In addition, the same levels of anxiety, and cultural care of the critically ill patient).
depression and stress have been experienced by patients’
spouses but significantly reduce over time in both patients
and their families. It has been suggested that providing
Intra-aortic balloon pumping
appropriate information about the procedures to both Intra-aortic balloon pumping (IABP) is a widely-used
patients and their spouses will assist them to deal better circulatory assist therapy that has become straightforward
with their psychological state in the recovery period.56 in application and relatively free of complications.59–61
Similarly, adequate preparation of the patient and The primary aim of IABP is to assist repairing an
their family in the preoperative period will assist them existing imbalance between myocardial oxygen supply
with their stress and anxiety coping strategies as well as and demand. The main indications are for cardiogenic
reduce their work stress after their return to work.57 The shock, myocardial infarction or ischaemia, haemodynamic
preoperative preparation is usually provided by nurses support for PCI and weaning from cardiopulmonary
and should incorporate information and support about bypass. The combined effects of increasing cardiac output
the procedures and recovery period, so that patients and mean arterial pressure (increasing oxygen supply)
and their families are better equipped during their and decreasing myocardial workload (reducing oxygen
recovery. Emphasis should be on identifying the intra- demand) make IABP therapy ideal for the management of
personal stressors, such as pain and discomfort, invasive infarct-related cardiogenic shock,62,63 for which it should
lines and surgical procedures, for individual patients to be regarded as standard management.
assist them coping with their perioperative and rehabil- IABP therapy involves placement of a balloon catheter
itation period.58 However, patients who have had their in the descending thoracic aorta. This catheter is most
surgery postponed or who have been operated on in an commonly advanced from a percutaneous femoral artery
emergency setting may need additional support. Also, access until the tip of the catheter is situated just below
critical pathways for cardiac surgery do not include the left subclavian artery (Figure 12.4). A chest X-ray or
assessing the patient’s psychological state, so nurses must fluoroscopy should reveal the catheter tip just below the

FIGURE 12.4 Intra-aortic balloon catheter. On the left the inflated catheter can be seen behind the heart, with its tip
below the arch of the aorta and the left subclavian artery. The balloon cycles between inflated (during diastole), and
deflated (during systole) as on the right. Blood fills the aorta while the balloon is deflated, and with inflation the balloon
almost fills the descending aorta, displacing 40 mL blood from the aorta to the coronary and systemic circulation.

Published with permission from Datascope Corporation, Fairfield, NJ, USA.

 CHAPTER 12 CARDIAC SURGERY AND TRANSPLANTATION 377

FIGURE 12.5 IABP catheter position in CXR; the tip is Principles of counterpulsation
located in the 2nd intercostal space anterior ribs or 5th When intra-aortic balloon pumping is initiated, the
intercostal space posterior ribs. balloon will be inflated rapidly at the onset of diastole
of each cardiac cycle and then deflated immediately
just before the onset of the next systole; this sequence is
referred to as counterpulsation.
Balloon inflation
At the onset of diastole, the balloon is rapidly inflated with
(most commonly) 40 mL of helium. This inflation causes
a sudden rise in pressure in the aortic root during diastole,
raising mean arterial pressure and, importantly, coronary
perfusion pressure. The blood displaced by the balloon
expansion improves blood flow into the coronary circu-
lation (which fills largely during diastole), as well as to
the brain and systemic circulation. Thus there is improved
myocardial oxygen supply and increased mean arterial
pressure, as well as improved systemic perfusion.6,64 The
balloon remains inflated for the duration of diastole. The
arterial pressure wave should reveal a sharp rise in pressure
at the dicrotic notch, with a second pressure peak now
appearing on the waveform, described as the ‘augmented
diastolic’ or ‘balloon-assisted peak diastolic’ pressure. This
peak is usually at least 10 mmHg higher than the systolic
pressure (Figure 12.6).
Balloon deflation
aortic arch, or at the level of the second anterior intercostal
As the inflated balloon largely obstructs the aorta, it must
space or fifth posterior intercostal space (Figure 12.5). be deflated to permit systolic emptying of the left ventricle.
The catheter has two lumens: a monitoring lumen, which Two separate approaches to the timing of balloon deflation
opens at the catheter tip from which the aortic pressure have emerged: ‘conventional timing’ and ‘real timing’.
waveform is monitored; and a helium drive lumen, through
which the helium is shuttled from the pumping console to Conventional timing
the catheter balloon. Balloon volumes range from 25 mL In conventional timing, the balloon is deflated immedi-
(paediatric use) to 34–50 mL in adults (most commonly ately prior to systole. Rapid deflation induces a precipitous
used is a 40-mL balloon) and are selected according to drop in aortic pressure at the end of diastole (a reduced
patient height (e.g. a 40-mL balloon is used for a patient aortic end-diastolic pressure). This reduces the duration
height of 162–183 cm). of the left ventricle isovolumetric contraction phase of

FIGURE 12.6 IABP during 1:1 assist (counterpulsation on every beat). Balloon inflation at the start of diastole and
deflation just before the next systole. IABP during 1:2 assist (counterpulsation on every second beat). Inflation of
the balloon rapidly at the inflation point (IP) raises diastolic pressure, producing a peak diastolic pressure (PDP) that
exceeds the peak systolic pressure (PSP). The balloon remains inflated during diastole. With balloon deflation just prior
to the next systole there is a rapid decline in pressure to the balloon assisted end-diastolic pressure (BAEDP), which is
lower than normal non-assisted end-diastolic pressure (EDP), reducing afterload. The ensuing systole is achieved with
a reduced systolic pressure (the assisted peak systolic pressure, APSP).

1:2 assist PSP APSP PDP

IP BAEDP EDP
378 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

the cardiac cycle (most oxygen-consuming phase of the Complications of intra-aortic

cardiac cycle), reduces the left ventricular afterload and
improves left ventricular emptying, improving stroke balloon pumping
volume and cardiac output.6,64 In addition, less pressure Serious complications are uncommon during IABP
is required for left ventricular emptying, so systolic work treatment and continued to decrease in frequency during
and oxygen demands on the myocardium are reduced.6 the past decade with advances in pump technology and the
Thus, deflation during conventional timing should see advent of smaller catheter sizes.66 Limb ischaemia remains
the aortic pressure drop to below normal at end-diastole, the most common serious complication, especially in
just in advance of the subsequent systole. Systolic pressure patients with existing vasculopathy,67 providing impetus
should also be lower than during a non-assisted beat. to the development of smaller catheters, which have
now reached 7.5 French gauge. Additional complications,
Real timing such as bleeding, catheter migration, thromboembolism,
In contrast to conventional timing, during real timing (also insertion-site vascular damage, thrombocytopenia and
referred to as R wave deflate) the balloon remains inflated device-related problems such as timing inaccuracy, device
for slightly longer, and is deflated not before but at the failure and gas leaks, also occur but are less common.These
same time as systole. The reduction in aortic end-diastolic are described below.
pressure is therefore not seen, but deflating simultane- Patient management
ously with left ventricular contraction still favourably
affects left ventricular emptying.65 Thus, there is improved Prevention of complications, as well as optimisation of the
stroke volume, systolic pressure reduction and decreased impact of counterpulsation, form the major components
ventricular work and oxygen demand as seen during of nursing care of a patient being treated with IABP.
conventional timing.6,65 Box 12.1 summarises the impact Thorough understanding of the impact of the presence
of balloon inflation and deflation on haemodynamic status of the balloon, as well as the beneficial and detrimental
and the oxygen supply/demand balance. effects of counterpulsation, is essential.
The arterial pressure wave reveals the impact of IABP Maintenance of limb perfusion
therapy on haemodynamic status. Placing the pump into
The use of smaller-gauge catheters has reduced the
1:2 assist (balloon pumping on only every second beat)
potential for obstruction of arterial flow past the catheter
is useful to highlight balloon pump impact and how
to the lower limbs, as has the trend to sheathless insertion.
assisted beats vary from the normal pressure cycle during
Nevertheless, the threat of limb ischaemia remains an
systole and diastole. Figure 12.6 depicts the impact of important issue in patient care, as IABP is most commonly
IABP on haemodynamic status and the arterial pressure undertaken in patients with atherosclerosis, potentially
waveform. involving the lower limbs, even in the absence of overt
peripheral vascular deficits. Identification of patients
BOX 12.1 at risk (known claudication, chronically cold feet and
peripheral vascular diseases) may be useful to ensure
Effects of intra-aortic balloon counterpulsation appropriate vigilance and prompt intervention where
• Balloon inflation: necessary. Peripheral perfusion may also be compromised
increased aortic diastolic pressure (augmented, by arterial embolisation should thrombi develop on the
or balloon-assisted peak diastolic pressure, catheter. Although catheter materials are non-throm-
balloon aortic end diastolic pressure [BAEDP]) bogenic, the risk of thrombi formation remains and
is heightened if periods of catheter stasis (interrupted
increased mean arterial pressure
pumping) are encountered. Systemic heparinisation is not
increased myocardial perfusion and oxygen recommended routinely for thromboembolic prevention
supply as it increases the risk of bleeding except for specific
increased cerebral and systemic perfusion indications.68
• Balloon deflation: Hourly assessments of peripheral perfusion (colour,
warmth, movement, sensation) should be performed to
decreased afterload
identify potential deficits. Dorsalis pedis and posterior
increased stroke volume and cardiac output tibialis pulses should be palpated and may sometimes
decreased LV congestion, decreased PCWP, require examination with a Doppler probe. Deficits
decreased pulmonary congestion should be promptly reported and consideration given
decreased left ventricular workload to catheter removal or reinsertion on the contralateral
decreased systolic pressure
limb. When pulses cannot be demonstrated, the limb
should be assessed for the development of compart-
decreased myocardial oxygen demand ment syndrome. At times, the viability of a limb must be
decreased duration of isovolumetric contraction weighed against the potential survival benefit of IABP
to the patient.
 CHAPTER 12 CARDIAC SURGERY AND TRANSPLANTATION 379

Prevention and treatment of bleeding gradual reductions in balloon inflation volume (volume
51
Significant bleeding is uncommon, but blood loss may weaning) or gradual reductions in assist frequency from
occur from the femoral arterial access site. In addition to 1:1 through 1:2 and 1:4 (ratio weaning). Hybrids of the
physical factors at the insertion site, contributors to bleeding two approaches are sometimes used. Support is reduced at
include heparinisation, thrombocytopenia from the physical intervals while the patient is observed for haemodynamic
effect of the pump on platelets and/or other anticoag- deterioration, pulmonary congestion and the return of
ulants or antiplatelet agents used for the primary disease. ischaemic signs and symptoms.
Regular observation should be made of the insertion site
for bruising or external bleeding, as well as other possible
Assessment of timing and timing errors
sites of bleeding due to heparinisation. Treatment includes Accurate timing of inflation and deflation in relation to
manual pressure at the insertion site or use of compression the cardiac cycle is required to maximise IABP benefit.
devices such as FemoStop, reinforcement of dressings and/ Errors in timing may lessen the potential benefit, or in
or topical procoagulant agents. Monitoring of coagulation some cases may worsen cardiac performance and increase
status and haemoglobin should be undertaken and blood or demands on the myocardium. Nurses are required to
blood products may (uncommonly) be required. continually assess the haemodynamic impact of balloon
pumping and the accuracy of timing via inspection of
Prevention of immobility-related the arterial pressure waveform, and to adjust timing to
complications optimise the impact of balloon pumping. The develop-
The need for immobilisation of the patient, and in particu- ment of automated IABP counterpulsation has reduced
lar the leg, is often overemphasised, and may heighten the timing errors by automatic trigger signal recognition
risk of atelectasis, pressure area development and venous and selection, accuracy of automatic setting for optimal
stasis and thrombosis. Sensible limitation of leg movement inflation and deflation timing and automatic adjustment
is advised, but patients can generally still move in bed, and to changing patient conditions. Therefore the automated
should still be turned 2-hourly for pressure relief as long mode of counterpulsation is recommended.70,71
as the insertion site is adequately protected and supported.
Early inflation
The femoral access limits flexion at the hip beyond 30°,
which may also hamper effective chest physiotherapy and Early inflation will at times be difficult to differentiate from
increase the risk of atelectasis and pneumonia. correct inflation timing but is recognised by the onset of
Migration of the balloon catheter towards the aortic inflation soon after the peak systolic pressure, before the
arch or towards the abdominal aorta may cause compro- pressure has declined to the level of the dicrotic notch
mised perfusion to the left arm (occlusion of left subclavian (Figure 12.7). Early inflation may limit the stroke volume
artery), kidneys (renal arteries) or abdominal viscera and cardiac output, as terminal systole is impeded, and may
(superior mesenteric artery). Therefore, neurovascular result in increased myocardial oxygen demands, increased
observation of the upper limbs, urine output and bowel left ventricle workload and premature valve closure. The
sounds are part of nursing management of the patient inflation point should be adjusted (to later) until the inflation
with IABP in situ. upstroke emerges smoothly out of the dicrotic notch.
Weaning of IABP Late inflation
Weaning of intra-aortic balloon pumping therapy is The arterial pressure waveform reveals the onset of diastole
generally undertaken once the patient has stabilised, is free (the dicrotic notch) before balloon inflation commences
of ischaemic signs and symptoms and is on minimum or (Figure 12.8). This generally results in a lower augmented
no inotropic support. Algorithms have been offered for diastolic pressure than could otherwise be achieved. As the
approaches to weaning therapy, with no haemodynamic duration of balloon inflation is lessened, the desired rise
or mortality benefit.69 Weaning is carried out by either in mean arterial pressure and coronary perfusion will not

FIGURE 12.7 IABP during 1:2 assist. Early inflation. The inflation point (IP) can be seen high in the downstroke of
systole, in this case well before the dicrotic notch (DN).

1:2 assist
380 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

FIGURE 12.8 IABP during 1:2 assist. Late inflation. Note that the inflation point (IP) occurs well after the dicrotic
notch (DN). Late inflation is also obvious in 1:1 assist with balloon inflation well after the dicrotic notch.

1:2assist
1:2 assist DN

1:1 assist

be achieved. The inflation marker should be set to ‘earlier’ exceed the normal end-diastolic pressure, increasing
until the inflation upstroke emerges smoothly out of the the duration of the isovolumetric phase, worsening left
dicrotic notch. ventricular afterload and increasing myocardial oxygen
demand (Figure 12.9). Correction is achieved by setting
Early deflation deflation to later until the pressure drop of deflation
Deflating the balloon earlier than necessary shortens occurs just in advance of the succeeding systole.
the duration for which the balloon remains inflated and
therefore limits the benefit of IABP. When deflation is Late deflation
very early, it may cause harm. Deflation sees the aortic When deflation begins too late, systole commences before
pressure drop markedly but there is now time for blood to complete emptying of the intra-aortic balloon.The typical
fill the space left by the balloon before systole commences. reduction of aortic end-diastolic pressure is not seen.When
Aortic end-diastolic pressure increases and may even significantly late, the end-diastolic pressure may even be

FIGURE 12.9 IABP during 1:2 assist. Early deflation. The balloon has been deflated well in advance of the
subsequent systole. The aortic pressure does drop off (not much from non-assisted diastole) but then begins to rise
again before the next systole gets underway, and may even exceed the normal end-diastolic pressure. Early deflation is
also obvious in 1:1 assist.

1:2 assist

1:1 assist
 CHAPTER 12 CARDIAC SURGERY AND TRANSPLANTATION 381

increased, prolonging the duration of the isovolumetric Alarm states

contraction phase and worsening afterload. As systole Alarm functions vary according to manufacturer and
occurs against an incompletely deflated balloon, the stroke model. The main alarm states common to most devices,
volume and cardiac output suffer and ventricular work and their causes and significance, are shown in Table
and oxygen demand increase (Figure 12.10). Deflation 12.4. Importantly, in most alarm states the pump consoles
should be set to earlier until the systolic upstroke emerges will revert to standby, suspending pumping. The balloon
out of the reduced end-diastolic pressure dip. is at risk of developing thrombi within the folds of

FIGURE 12.10 IABP during 1:2 assist. Late deflation. The late deflation is seen here as the sharp drop-off before
systole and a balloon assisted end-diastole that does not fall to below the normal patient end-diastolic pressure.

1:1 assist

1:2 assist

TABLE 12.4
Intra-aortic balloon pump alarm states

A L A R M S TAT E CAUSES / SIGNIFICANCE

Catheter alarm Obstruction (complete or subtotal) of the catheter, drive line or balloon
Device reverts to standby (non-assist); commonly due to catheter flexion at insertion site due to limb
position or excessive surface-to-vessel depth
Loss of trigger ECG trigger: signal disrupted or low in amplitude, or asystole
Pressure trigger: pulse pressure below threshold for detection
Pacer trigger: pacing spikes not detected or absent (including demand pacing)
Device reverts to standby until restoration of trigger; alternative trigger selection may be necessary
Gas loss alarms Leak in circuit/drive line or balloon; gas leak may be to the environment or into the patient as a helium embolus
Pump reverts to standby; refilling of circuit may be necessary
Low augmentation Augmented diastolic pressure is lower than operator-selected alarm level; pumping is not interrupted
Pneumatic drive Functional problem with the pump inflation/deflation pneumatic system
Device reverts to standby; alarm may sometimes be activated during tachycardia; 1:2 assist or assist at
reduced augmentation may be possible until a replacement device is accessed
Autofill failure Routine 2-hourly refilling of the system with helium may fail if gas tank is incompletely open or if circuit
leaks cause volume loss during the filling attempt
Device reverts to standby
System failure Console self-testing has identified component malfunction
Device reverts to standby; restarting may be possible but a replacement device should be accessed
Low helium supply Helium tank empty or incompletely opened
Low battery Reconnect to power and recharge
382 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

the balloon while deflated, and these can be liberated Patients with certain chronic heart, respiratory and
as arterial emboli on recommencement of pumping. lung diseases may be referred for organ transplantation
Therefore, it is important to treat alarm states promptly, assessment when their disease state is such that their life
to limit the duration of balloon stasis. If interruption to expectancy is less than 2 years and quality of life intoler-
pumping is prolonged, intermittent manual inflation of able. Patients who receive organ transplants are commonly
the balloon with a syringe is recommended (e.g. once debilitated and may have an acute on chronic presentation
every 5–10 minutes). at the time of surgery. The surgical procedure is lengthy,
up to 12 hours, and involves cardiopulmonary bypass.
Gas loss alarms The duration and nature of the surgery in patients with
Most devices will determine the severity of gas losses and severely compromised health status serve to compound
classify them as slow, rapid or disconnect. In all gas loss the often critical condition of such patients in the early
states it is imperative that assessments be made to exclude postoperative period.
balloon rupture and helium leak into the arterial circu- The immediate period following surgery is commonly
lation. Small gas losses of helium may or may not be of the first contact that critical care clinicians have with
clinical significance, but the delivery of sizeable helium transplant recipients and their families. The exception
volumes may behave as gas emboli and, if delivered into may be patients awaiting heart transplantation who are
the coronary circulation, may result in lethal arrhyth- supported by an intra-aortic balloon pump or mechanical
mias or neurological complications if delivered into circulatory support, also known as a ventricular assist device
the cerebral circulation.59 In all gas loss alarm states, the (VAD), as a ‘bridge to transplantation’ (see Figure 12.12).
helium drive line should be inspected for the presence Ideally, patients with mechanical circulatory support are
of blood to indicate loss of integrity of the balloon. If returned to a sound physical, mental and nutritional state
blood is present in the drive line (Figure 12.11), pumping prior to receiving a transplant and, as part of their recovery,
should be suspended and no attempts at recommencing await transplantation in the ward or home setting. For
balloon pumping should be made. Prompt removal and/ specific management of patients on mechanical circula-
or replacement, along with thorough patient assessment, tory support, readers are referred to specific resources (e.g.
is essential. websites and operating manuals for individual mechanical
circulatory support devices: HeartWare, Thoratec and
SynCardia).
FIGURE 12.11 Intra-aortic balloon rupture and Heart transplantation is a life-saving and cost-effective
presence of blood in the helium drive line. form of treatment that enhances the quality of life for many

people with chronic heart failure. Legislation that defined
brain death and enabled beating-heart retrieval was enacted
in Australia from 1982.This legislation heralded the estab-
,ĞůŝƵŵĚƌŝǀĞůŝŶĞ
ĨƵůůŽĨďůŽŽĚ
lishment of formal transplant programs. In Australia, the
first heart program commenced in 1983.72,73 The success
of transplantation in the current era as a viable option for
end-stage organ failure is primarily due to the discovery
of the immunosuppressive agent cyclosporin A.74 In this
section, heart transplantation as a component of critical
ZƵƉƚƵƌĞĚ care nursing is discussed, with reference to evidence-based
ďĂůůŽŽŶ practices.

History
Heart transplantation Heart transplant surgery for refractory heart failure
was first performed in Australia in 1968, only months
The ultimate goal of organ transplantation is to provide after the first heart transplant was performed in South
an improved quality of life and long-term survival for Africa in December 1967.75 However, high mortality
patients with end-stage heart disease. To optimise patient rates associated with severe acute rejection and infection
outcomes, the early postoperative management of these within months of surgery led to a reduction in the
patients requires critical care clinicians with specific number of heart transplants performed worldwide, and
expertise to collaborate with a multidisciplinary team in effect a moratorium occurred with the procedure.
of health professionals. In the following sections, the Heart transplantation was finally established in the
important management issues in the early postoperative modern era as a viable treatment option for end-stage
period for heart transplant recipients are discussed. The heart failure during the early 1980s when cyclosporin
major long-term complications of heart transplantation A, a then-novel immunosuppressive agent, dramatically
are also discussed briefly as survivors may be readmitted to improved patients’ survival rates by reducing episodes
critical care with life-threatening complications years after of acute rejection and lowering attendant infectious
their transplant. complications.76
 CHAPTER 12 CARDIAC SURGERY AND TRANSPLANTATION 383

FIGURE 12.12 Pump, monitor and controller. (A) HeartWareImplanted HVAD® Pump. (B) HeartWare® Monitor with
HeartWare® Controller and HeartWare® Batteries. (C) ThoratecHeartMate II (A) and (B) Published with permission from
HeartWare Inc. (C) Published with permission from Thoratec Corporation.

B C

Incidence at 81% to the first year and 70% at 2 years.80 The notion
of patients with VADs permanently due to advances in
Heart transplants in the modern era have been performed
device design and capability (e.g. fully implantable with
in Australia since 1986 and in New Zealand since 1987.
internal batteries) may not be as futuristic as once thought.
In 2013, 86 heart transplants were performed in Australia
and New Zealand.77 In Europe, 589 heart transplants were Outcomes from heart transplantation
performed, an annual figure that has been relatively static Currently, the centres around the world that submit data
for the past 5 years.78 As the annual number of transplants to an international registry achieve survival rates for heart
globally is likely to remain relatively stable because of transplant patients of 81% at 1 year, and 69% at 5 years,
limited organ availability, future management of end-stage with a median survival of 11 years.81 In Australia and New
heart failure may involve the insertion of a left ventricular Zealand, approximately 87% of heart transplant patients
assist device (LVAD) designed for long-term permanent survive to 1 year, and 82% survive to 5 years.82
mechanical circulatory support, so-called ‘destination
therapy’. In the early years, the VADs available were Indications
primarily used as ‘bridge to transplantation’ therapy (i.e. The vast majority of patients referred for heart trans-
support for a failing native heart until a suitable heart plantation have persistent NYHA functional class IV
became available), not ‘destination therapy’, although symptoms (see Chapter 10), secondary to ischaemic
both purposes were shown to be viable options in the heart disease or some form of dilated cardiomyopathy.81,83
REMATCH study.79 While this is still the case in Australia In ICUs and cardiac units, patients with cardiogenic
and New Zealand, recent global reports show about 40% of shock requiring either continuous intravenous inotropic
VADs are now used as ‘destination therapy’.80 This change support or cardiovascular support with an intra-aortic
has been facilitated by improvements in device technol- balloon pump or VAD are referred for transplant
ogies and the experiences of clinicians in managing this consideration.83 Commonly, patients listed for transplan-
unique cohort. Survival with continuous flowVADs is now tation have a life expectancy of less than 2 years without
384 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

transplantation. Accepted contraindications for heart sensitiser); antiarrhythmic drugs to suppress, or an internal
transplantation include active malignancy,84 complicated cardiac defibrillator to treat, potentially lethal arrhythmias;
diabetes,85 morbid obesity,86 uncontrolled infection, and insertion of a biventricular pacemaker (i.e. chronic
active substance abuse and an inability to comply with resynchronisation therapy) to re-establish atrioventricular
complex medical regimens.87,88 Currently, 50% of trans- synchrony (see Chapter 11).
planted patients globally are between 50 and 64 years of The average costs associated with heart transplantation
age.83Age has become a relative contraindication, with are high, at approximately A$35,000 for the first year and
16 days old being the youngest and 71 years of age being approximately A$15,000 for each ongoing year, depending
the oldest to have received a transplant to date.82 However, on the drug regimen and episodes of rejection or
the presence of multiple comorbidities in patients over infection.77 As some immunosuppressant drugs have come
70 years of age would be expected to exclude the majority off patent, these costs have been reduced. However, the high
of such patients from consideration.84,89 Other relative incidence of chronic heart failure and associated hospi-
contraindications include renal failure and an irreversible talisation costs are also considerable. During 2000, it was
high transpulmonary gradient (mean pulmonary artery estimated that over half a million Australians had chronic
pressure minus pulmonary artery wedge pressure) of heart failure (CHF), with 325,000 patients per annum
greater than 15 mmHg83,90 (see section on Early allograft experiencing symptoms.91 In Australia during 2007–2008,
dysfunction and failure later in this chapter). In the context 49,307 patients were hospitalised with a primary diagnosis
of a rigorous postoperative regimen of polypharmacy, of CHF (0.6% of all hospitalisations).3 Approximately 40%
frequent follow-up medical appointments and routine of patients admitted to hospital with heart failure will be
cardiac biopsies, a strong social support network, absence readmitted or die within one year.92 The cost of a single
of psychiatric illnesses and a willingness to participate hospital admission for CHF in Australia is currently approx-
actively in the recovery process are highly desirable char- imately A$6000.93 In New Zealand, hospital admissions for
acteristics of prospective recipients.90 heart failure consume approximately 1% of the healthcare
Patients referred for heart transplant assessment must budget.94 In the context of a 50% mortality rate within
have exhausted all other accepted pharmacological and 4 years of being diagnosed with chronic heart failure, a 50%
surgical treatment options for end-stage heart failure, such mortality rate within 1 year for patients with severe heart
as optimal therapeutic doses of common heart failure failure95 and the burden of care associated with heart failure
medications; revascularisation via coronary artery bypass exceeding that of all types of cancer,96 transplantation for
graft surgery or percutaneous transluminal coronary end-stage heart failure is actually a viable and economical
angioplasty; continuous IV infusions of dobutamine in the treatment option for individuals and society; it is, however, a
community/home setting; IV levosimendan (a calcium limited resource, available to only a few recipients.

FIGURE 12.13 Left: Completion of bicaval transplant technique, showing the inferior vena caval, superior vena caval,
aortic and pulmonary artery anastomoses. Right: Commencement of the left atrial anastomosis.

Adapted from Kirklin JK, Young JB, McGiffin DC. Heart transplantation. Philadelphia: Churchill Livingstone; 2002, with permission.
 CHAPTER 12 CARDIAC SURGERY AND TRANSPLANTATION 385

Forms of heart transplant surgery FIGURE 12.15 Heterotopic heart transplant

The most common heart transplant surgery is orthotopic (LVAD configuration).
transplantation, with two surgical techniques used: the
standard or bicaval approaches. The standard technique
69&
has been used since the 1960s and involves anastomoses
of the donor and native atria.97 Complications associated 69&
with the standard technique can include abnormal $2 $2
5$
atrial contribution to ventricular filling and tricuspid 3$
and mitral valve insufficiency.98,99 Since the mid-1990s, 3$
the bicaval technique as described by Dreyfus et al100 59
has gained favour. The main advantage of the bicaval /9 5$
approach is the maintenance of atrial conducting /9
pathways and the likelihood of promoting sinus rhythm
and its associated superior atrial haemodynamics100 (see 59
/$DSSHQGDJH
Figure 12.13). Reported potential disadvantages include
stenoses in the inferior and superior vena cava at the '2125 5(&,3,(17
anastomosis sites.100
Adapted from Newcomb AE, Esmore DS, Rosenfeldt FL,
The second form of heart transplant surgery is hetero- Richardson M, Marasco SF. Heterotopic heart transplantation:
topic transplantation, although these account for only a an expanding role in the twenty-first century? Ann Thorac Surg
handful of heart transplants globally.101 In this procedure, 2004;78(4):1345–50, with permission.
the donor heart is implanted in the right side of the chest
next to the native heart102 to augment native systolic
function. Figure 12.14 illustrates a chest X-ray of the Patient management
donor heart next to the native heart. Postoperative nursing and collaborative management
of orthotopic heart transplant recipients involve full
haemodynamic monitoring with a pulmonary artery
FIGURE 12.14 Chest X-ray showing heterotopic heart
transplant.
catheter (PAC), a triple- or quad-lumen central venous
catheter (CVC), arterial line, indwelling urinary catheter
and 5-lead cardiac monitoring to assist in arrhythmia
discrimination. A 12-lead ECG is also recorded. If the
orthotopic transplant is performed with the standard
technique, a remnant P wave from the native heart may
be visible on the ECG or cardiac monitor (see Figure
12.16). As the native sinus node cannot conduct across
the right atrial suture line, the recipient’s heart rate is
determined by the conduction system of the donor
heart, not the native heart. Of interest, it is possible for
the native heart to generate a P wave while the donor
heart is in atrial fibrillation or other arrhythmia. (More
detailed discussion of cardiac monitoring and haemo-
dynamic management of patients with a heterotopic
heart transplant is available.96,104) Monitoring data are
combined with physical assessment information from
all body systems to determine nursing and collabora-
Heterotopic heart transplantation is primarily tive interventions. Intensive continuous monitoring and
indicated in patients with pulmonary hypertension assessment of haemodynamic parameters according to
refractory to pulmonary vasodilator therapies. It may
also be considered in patients with a large body surface FIGURE 12.16 Rhythm strip post orthotopic transplant
area who are unlikely to receive a suitably large-sized (standard technique).
donor heart to enable an orthotopic procedure to take
place,97,103 or when the donated organ is unsuitable as an
orthotopic graft.103 Heterotopic transplantation is usually
performed to support the left ventricle (LVAD config-
uration), but can be configured to support biventricular
function (Biventricular ventricular assisted device config-
uration). The LVAD configuration for heterotopic heart
transplantation is illustrated in Figure 12.15.
386 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

evidence-based practices87–89 and overall clinical status rapid activation of the complement cascade, producing
allow nurses to detect and subsequently respond to severe damage to endothelial cells, platelet activation,
emergent postoperative complications. Comprehensive initiation of the clotting cascade and extensive micro-
guidelines for the care of heart transplant recipients, vascular thrombosis.109 There is no effective treatment for
supported by the level of evidence for relevant practices, hyperacute rejection apart from mechanical circulatory
are detailed in a paper published by the International support or interim retransplantation.
Society for Heart and Lung Transplantation (ISHLT).105
Full ventilatory support is required until the patient’s Acute rejection
haemodynamic status is stable. Respiratory status is Acute rejection can be classified as either cellular or
monitored via clinical, radiological and laboratory- humoral.110,111 Cellular rejection involves T-cell infiltra-
derived data (see Chapter 13). Enteral feeding is usually tion of the allograft. Cellular rejection occurs much more
commenced on the day of admission. Renal and neuro- commonly than humoral rejection, but both may occur
logical function are closely monitored, as cyclosporin simultaneously.112 Humoral or microvascular rejection is
has a deleterious effect on renal function and can lead to thought to be primarily mediated by antibodies. A recent
failure106 as well as neurotoxicity.107 For the small number review by key stakeholders has resulted in the publica-
of patients who develop allograft dysfunction requiring tion of standardised nomenclature for antibody-mediated
mechanical circulatory support (i.e. IABP, ECMO or rejection.110 Humoral rejection may occur due to the
Thoratec LVAD), or acute renal failure requiring haemo- presence of a positive donor-specific cross-match or
filtration, hospitalisation in the critical care unit tends to in a sensitised recipient with preformed anti-HLA
last weeks rather than days. antibodies.109
The immediate period after transplantation can be a Percutaneous transvenous endomyocardial biopsy
time of great hope and joy for recipients and their family is considered the gold standard for detecting cardiac
and friends; however, complications and setbacks can make rejection.113 Grading of cardiac rejection has a standardised
the path to recovery prolonged, unpredictable and difficult. nomenclature globally.114,115 In humoral rejection, endo-
The provision of psychosocial support by all members of myocardial biopsy reveals increased vascular permeability,
the transplant/critical care team to family members and microvascular thrombosis, interstitial oedema and haem-
friends is an important part of patients’ recovery from organ orrhage, and endothelial cell swelling and necrosis.110,113
transplantation. Meetings with family that convey honest An echocardiogram is also performed to evaluate systolic
and open information about patient progress need to be cardiac function.
conducted regularly. Supporting and managing patients Therapeutic interventions for rejection vary between
and families following transplant is consistent with support centres and are based on the grade of rejection, degree
provided to other critically ill patients (see Chapter 8). In of haemodynamic compromise, clinical findings and
addition, there is the issue of dealing with lost hope if the time elapsed since transplantation. Asymptomatic mild
transplant fails, a very distressing time for all involved. In the rejection (grade 1R) is rarely treated, the exception
immediate postoperative period, transplant recipients are at being if there is associated haemodynamic compromise;
risk of developing complications that include hyperacute and only 20–40% of mild cases progress to moderate
rejection, acute rejection, infection, haemorrhage and rejection (grade 2R), usually requiring treatment.109,116
renal failure. In the immediate postoperative period, heart Grade 3R rejection is always treated, as it represents
transplant recipients may experience morbidity specific myocyte necrosis. Cellular rejection is usually treated
to the heart transplant procedure, such as early allograft with higher doses of corticosteroids, such as ‘pulse’
dysfunction (i.e. organ failure due to preservation injury), doses of methylprednisolone (1–3 g IV over 3 days),
bleeding, right ventricular failure and acute rejection. and antilymphocyte antibody agents (ATG, ATGAM or
Long-term complications include chronic renal failure, OKT3). Humoral rejection is treated with plasmaphere-
hypertension, malignancy and cardiac allograft vasculopa- sis, high-dose corticosteroids, cyclophosphamide therapy
thy. The common immediate potential complications and and antilymphocyte antibody therapy.117,118 For both
associated clinical management for heart recipients are forms of rejection, other immunosuppressant agents such
discussed below. as the calcineurin inhibitor (cyclosporine, tacrolimus)
and an antiproliferative cytotoxic agent (azathio-
Hyperacute rejection prine, mycophenolate mofetil, sirolimus/rapamycin)
Hyperacute rejection is now a rare form of humoral are continued at the usual doses assuming levels were
rejection that occurs minutes to hours after transplantation therapeutic. It may be judicious to review the patient’s
and results from ABO blood group incompatibility or the medications during periods of rejection to ensure that
recipient having preformed, donor-specific antibodies.108 drugs capable of reducing cyclosporin or tacrolimus
ABO blood group and panel reactive screening of serum levels, such as certain anticonvulsants and antibi-
anti-human lymphocyte antigen (anti-HLA) antibodies otics, have not been taken. In addition to augmentation
preoperatively minimises the possibility of hyperacute of immunosuppression therapy, fluid, pharmacological
rejection, particularly in healthcare systems where blood and mechanical therapeutic interventions are instituted
that has been prospectively cross-matched is routinely used. to support cardiac function, depending on the degree of
If it occurs, hyperacute rejection leads to organ failure and ventricular dysfunction.
 CHAPTER 12 CARDIAC SURGERY AND TRANSPLANTATION 387

Nurses have an important role in detecting acute highlighted in the table, some immunosuppressive agents
rejection, as it is diagnosed by clinical signs and supported are cytotoxic (e.g. mycophenolate mofetil), requiring
by histological findings from an endomyocardial biopsy. safety measures during preparation, delivery and disposal.
Low-grade rejection can be suspected when non- Likewise, some immunosuppressive agents will be given
specific signs such as malaise, lethargy, low-grade fever and IV (e.g. azathioprine) until patients can eat and drink as
mood changes are present. Acute rejection causing cardiac they cannot be crushed for nasogastric administration.
irritation is revealed by a sinus tachycardia greater than In addition, as blood levels of some immunosuppression
120 beats/min; a pericardial friction rub; or new-onset agents (e.g. cyclosporine, sirolimus) are taken regularly to
atrial arrhythmias such as premature atrial contractions, assess efficacy, nurses need to be aware of timing blood
atrial flutter or fibrillation.116,119 More severe forms of sampling to dosage times in order to obtain accurate data
acute rejection are suspected when signs and symptoms to inform doses.
of varying degrees of heart failure emerge. If patients are
awake and alert, they may complain of severe fatigue, Infection
sudden onset of dyspnoea during minimal physical effort, Infection is a major risk factor for transplant recipients
syncope or orthopnoea. Physical assessment and haemo- due to their immunosuppressed state. The periods of
dynamic monitoring will reveal clinical signs of left and greatest risk for patients are the first 3 months after
right cardiac failure (see Chapter 9). transplantation, and after episodes of acute rejection
when immunosuppression agents are increased.128,129
Immunosuppression therapy In addition to the nosocomial bacterial infections that
In this section, a brief discussion of immunosuppression all surgical patients are exposed to in critical care (see
therapies and associated nursing implications is provided. Chapter 6), immunosuppressed transplant recipients are
To prevent rejection of the transplanted organ, recipients at risk of acquiring opportunistic bacterial, viral or fungal
receive a triple-therapy regimen of immunosuppression infections; latent infections acquired from the donor
agents for the remainder of their life.Triple-therapy usually organ such as cytomegalovirus (CMV); or reactivation
consists of corticosteroids (prednisolone or prednisone), of their own latent infections (e.g. CMV or Pneumocys-
a calcineurin antagonist (cyclosporine or tacrolimus tis carinii). To combat Pneumocystis carinii, patients receive
[FK506]) and an antiproliferative cytotoxic agent trimethoprim with sulfamethoxazole twice weekly.130
(mycophenolate mofetil, azathioprine or sirolimus/ Despite preoperative screening for CMV, the shortage
rapamycin).120,121 For some heart patients sirolimus, also of donor organs often necessitates CMV mismatching.
known as rapamycin, may be the cytotoxic drug of choice Effective prophylaxis for CMV infection is provided
because of a lower incidence of cardiac allograft vasculop- by administering CMV hyperimmune globulin to
athy at 6 and 24 months, and lower rejection rates with CMV-positive and CMV-negative recipients who receive
sirolimus compared with azathioprine.122 A later study a heart from a seropositive donor.131 This commences
also showed mycophenolate mofetil reduced mortality for within 24–48 hours of surgery.124 For CMV-negative
up to 36 months post-transplantation when compared to recipients of organs from seropositive donors, ganci-
azathioprine.123 clovir for 1–2 weeks followed by oral therapy for
Immunosuppression therapy is commenced pre- 3 months is required in addition to CMV hyperimmune
operatively or in the operating theatre. A maintenance globulin.105,131,132
immunosuppression regimen is usually instituted within To prevent infection, standard precautions and
hours of admission to ICU, with each patient’s immu- meticulous hand washing (see Chapter 6) are performed,
nosuppressive needs individually assessed. For instance, rather than isolation procedures.133 Mandatory measures
the administration time for introduction of the selected to prevent overwhelming sepsis are a high level of
immunosuppressive agent(s) may be delayed in patients vigilance by clinicians for signs of infection; obtaining
with preexisting renal dysfunction. When the adminis- empirical evidence from blood, sputum, urine, wound
tration of the usual regimen of immunosuppression is and catheter-tip cultures; and aggressive and prompt
delayed, induction therapy with anti-lymphocyte agents treatment for specific organisms. Although typical signs
(anti-thymocyte globulin (ATG), ATGAM or OKT3) and symptoms of infection are blunted in transplant
or interleukin-2 receptor antagonists (basiliximab, recipients, clinicians should suspect infections when
daclizumab) may be used in the immediate postopera- patients have a low-grade fever, hypotension, tachycar-
tive period.81,124,125 Induction therapy may also be used in dia, a high cardiac output/index, a decrease in systemic
circumstances of primary allograft failure perioperatively, vascular resistance (SVR), changes in mentation, a new
e.g. HLA mismatch (rare) or early humoral rejection, or cough or dyspnoea.121,134 Elevated white cell count, the
to allow for a delay in initiating cyclosporine in patients presence of dysuria, purulent discharge from wounds,
at risk of renal failure.119,126 A recent systematic review infiltrates on chest X-ray, sputum production or pain also
has found no support for the routine use of IL-2Ra indicate infection.
therapy as routine induction therapy to achieve a survival Prior to administering blood products, nurses must
benefit or reduction in cardiac allograft rejection.127 The ascertain the CMV status of the patient and donor.
common drugs used to suppress the immune system and Recipients who are seronegative for CMV and who
the nursing implications are illustrated in Table 12.5. As receive a heart from a seronegative donor must receive
388 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 12.5
Immunosuppression table124

DRUG NAMES TYPICAL DOSE IMPORTANT SIDE EFFECTS NURSING CONSIDERATIONS

Calcineurin antagonists Maintenance
cyclosporin 5–10 mg/kg/day Renal impairment Monitor renal and liver
(target blood levels) Hypertension function
tacrolimus 0.2–0.5 mg/kg/day Hypercholesterolaemia Mix oral liquid cyclosporin
(target blood levels) Abnormal liver function with orange juice or milk in
Headaches glass
Gingival hypertrophy Do not crush tablets
(cyclosporin only) Time sampling of serum drug
Hirsutism (cyclosporin only) levels with dosage times
Diabetes (tacrolimus only)
Corticosteroids Maintenance
prednisolone/prednisone 0.2–0.5 mg/kg/day Mood change Monitor blood glucose levels
Augmentation for rejection Weight gain
‘Pulse’ of 2 g over 3 days for Glucose intolerance
acute rejection Osteopenia
Muscle weakness
Antiproliferative cytotoxic agents Maintenance
azathioprine 1–2 mg/kg/day Bone marrow suppression Cytotoxic: take full
Gastrointestinal tract irritation precautions when preparing,
(especially mycophenolate administering and disposing
mycophenolate mofetil 2–3 g/day (adult) mofetil) of drugs
rapamycin Starting at 0.03 mg/kg/day Bone marrow suppression Minimise dietary cholesterol
(target blood levels) Hypercholesterolaemia Monitor platelets and serum
Hypokalaemia potassium
interleukin-2 receptor Induction of
antagonist immunosuppression
basiliximab 20 mg/kg preoperatively and Few and infrequent These drugs are often used in
day 4 patients with pre-existing renal
dysfunction
daclizumab 1 mg/kg preoperatively and
Other immunosuppression
days 14, 28, 42, 56
agents may be delayed with
the use of these agents
Little information about
compatibilities: avoid
concurrent administration
Antilymphocyte preparations Induction or augmentation for
rejection

ATGAM/OKT3 Various, may target T Anaphylaxis Premed of paracetamol,

lymphocyte levels Sterile meningitis promethazine and
Pulmonary oedema hydrocortisone 30 min prior to
Serum sickness slow infusion

Adapted from: Farmer DG, McDiarmid SV, Edelstein S, Renz JF, Hisatake G, Cortina G et al. Induction therapy with interleukin-2
receptor antagonist after intestinal transplantation is associated with reduced acute cellular rejection and improved renal function.
Transplant Proc 2004;36(2):331–2.

whole blood, packed/red cells or platelets that are fibrillation, impairment of hepatic function secondary
CMV-negative, leuco-depleted or both in order to avoid to right heart failure, redo surgery, surgical suture lines
development of a primary CMV infection.97,105,135 connecting major vessels and atria and a larger than usual
pericardium are all contributing factors. Good surgical
Haemorrhage/cardiac tamponade technique is mandatory in preventing postoperative
The risk of haemorrhage or cardiac tamponade is greater bleeding. As the promotion of haemostasis is a major
for heart transplant recipients than for patients undergoing therapeutic goal postoperatively, blood products, proco-
coronary artery bypass graft or valvular surgery. Preoper- agulants and antifibrinolytics are commonly administered
ative anticoagulation for end-stage heart failure or atrial according to laboratory and clinical data. Postoperative
 CHAPTER 12 CARDIAC SURGERY AND TRANSPLANTATION 389

mortality from bleeding has been reported to occur in up Heart transplants that encompass long distances
to 6.7% of cases.136 with ischaemic periods beyond 6 hours have been, and
Early detection of haemorrhage is achieved by close are likely to continue to be, performed in Australia
monitoring of the following: haematological status; chest and New Zealand and other countries, as excellent
tube patency, drainage volume and drainage consistency; short-term (30-day mortality) and long-term (ejection
and trends in haemodynamic data that suggest cardiac fraction at 1 year) outcomes have been reported.139
tamponade (see earlier in this chapter). Our clinical These outcomes were achieved by using innovative preser-
experience suggests that, if patients are hypotensive sporad- vation techniques and postoperative mechanical assistance
ically for no readily apparent reason, efforts should be made in the form of intra-aortic balloon counterpulsation
to eliminate the existence of cardiac tamponade. Suspicion and/or a right ventricular assist device.139,140 Adrenaline
of cardiac tamponade may be confirmed by chest X-ray is invariably commenced intraoperatively, irrespective of
or echocardiogram if the patient’s haemodynamic status ischaemic time, to provide inotropic support to the trans-
is stable. Sudden cardiac arrest or haemodynamic collapse planted heart.
secondary to cardiac tamponade warrants an immediate Early allograft dysfunction can present as left, right
return to theatre or a sternotomy in critical care. or biventricular dysfunction. Management of cardiac
dysfunction is dependent on clinical signs and underlying
Acute kidney injury aetiologies that include pulmonary hypertension, acute
Acute kidney injury or varying degrees of renal dysfunction rejection and ischaemic injury. Right ventricular dysfunc-
can occur in the initial postoperative period due to preexist- tion is usually secondary to pulmonary hypertension,
ing renal dysfunction, cyclosporin, nephrotoxic antibiotics whereas left ventricular or biventricular dysfunction
or sustained periods of hypotension secondary to cardio- results from acute rejection and ischaemic injury.
pulmonary bypass or allograft dysfunction. Diuretic therapy To prevent right ventricular dysfunction and failure
is invariably needed in the initial postoperative period due secondary to raised pulmonary pressures, prospective
to these factors, as well as the fluid retention effects of heart transplant recipients are screened preoperatively for
corticosteroids and raised filling pressures secondary to a the degree and reversibility of pulmonary hypertension.
transient loss of right and/or left ventricular compliance.137 Reversible pulmonary hypertension is a transpulmonary
High doses or continuous infusions of diuretics may be gradient less than 15 mmHg that responds to pulmonary
required in patients who were on diuretic therapy preop- vasodilator therapies, such as prostaglandin E1, prosta-
eratively. Close monitoring of serum electrolyte levels will cyclin or inhaled NO.141 Right ventricular dysfunction
indicate the need for any supplements. or failure can also occur in the postoperative context
In addition to all the usual nursing and collaborative due to ischaemic injury, an undersized heart (greater
measures that are taken to prevent, detect and support than 20% difference in body surface area between donor
renal dysfunction/failure in patients following cardiac and recipient) or hypoxic pulmonary vasoconstriction.97
surgery on cardiopulmonary bypass (see earlier in this Isoprenaline or milronine, dobutamine and adrenaline are
chapter and Chapter 18), the type and dose of immuno- administered in this situation.105
suppressive agents in the postoperative period are carefully Left ventricular dysfunction cannot be anticipated
selected and initiated according to individual risk factors preoperatively, so when signs first emerge peri- or post-
and clinical status. Experience suggests that early inter- operatively, fluid management strategies (filling or
vention with haemofiltration to support renal function diuresis as deemed appropriate) and inotropic agents are
is preferable to continued use of high-dose diuretics and commenced immediately.105 In patients with prolonged
deferred haemofiltration. This is because there is little ischaemic times, mechanical assistance in the form of an
scope to maintain low doses of renal toxic immunosup- IABP is invariably instituted perioperatively.
pressants for weeks given the imminent risk of rejection In the initial postoperative period, cardiac dysfunc-
and resultant allograft failure. tion can also occur as a result of a low SVR syndrome,
characterised by a calculated SVR of less than 750 dynes/
Early allograft dysfunction and failure sec/cm−5 in the presence of an unsustainable high cardiac
Primary allograft failure is the leading cause of death output.142,143 The cause of low SVR syndrome is not fully
in the first month and year after surgery.120,138 In the understood, although it has been linked with systemic
immediate postoperative period, myocardial performance inflammatory response syndrome (SIRS) associated with
is depressed due to the clinical sequelae of cardiopulmo- cardiopulmonary bypass (see Chapter 21), the chronic use
nary bypass and ischaemic injury associated with surgical of angiotensin-converting enzyme inhibitors for end-stage
retrieval, hypothermic storage, prolonged ischaemic times heart failure (see Chapter 10) and a deficiency of vasopres-
and reperfusion. Despite a preferred time period between sin.142,144 Noradrenaline is titrated to achieve a calculated
organ retrieval and reimplantation of 2–6 hours, the vast SVR within normal parameters and to lower the unsus-
distances between capital cities (up to 3000 km) over which tainably high cardiac index. In severe cases, vasopressin
donor hearts may be transported, and a decision to accept may be infused at doses of 0.04–0.1 units/min concur-
marginal, suboptimal organs, led Australian researchers and rently with noradrenaline.145 Experience suggests that the
transplant teams to pioneer prolonged ischaemic times of dose of adrenaline should be minimised in the presence of
up to 8 hours (New Zealand, 7 hours).139 metabolic acidosis, and the noradrenaline infusion increased
390 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

to achieve normotension, a calculated SVR higher than circulatory support with extracorporeal membrane
900 dynes/sec/cm-5 and a sustainable cardiac index. oxygenation (ECMO) is indicated when aggressive ther-
Patients with depressed left ventricular compliance apeutic regimens fail to produce a cardiac output that
and contractility due to cardiac dysfunction present provides adequate end-organ perfusion.105,149,150 As noted
clinically with reduced cardiac index, bradycardia, earlier, augmentation of the immunosuppression regimen
reduced tissue and end-organ perfusion (decreased may also be necessary to manage the acute rejection.
mental status, oliguria, poor peripheral perfusion, slow
capillary refill and raised serum lactate), low systemic Denervation
venous oxygenation and dyspnoea. Bradycardia may Donor heart implantation severs both afferent and
not be evident due to chronotropic support of the efferent nervous system connections to the heart. Hence,
denervated heart with atrial pacing and/or isoprena- the transplanted heart has no direct autonomic nervous
line. The following discussion focuses on management system innervation but is responsive to circulating cate-
of right heart dysfunction/failure and left heart cholamines. Denervation impairs circulatory system
dysfunction/failure (see also Chapter 10). homeostasis, as evidenced by: a volume-expanded state; a
Right heart dysfunction/failure is suspected in patients tendency to hypertension; no sensation of angina pectoris;
with preexisting pulmonary hypertension or a haemody- a high resting heart rate; a slow or absent baroreceptor
namic profile in the intra- or postoperative context that reflex (to increase heart rate/cardiac output in response
includes a rising CVP, low-to-normal pulmonary artery to hypotension); and no rises in heart rate and contractil-
diastolic/pulmonary artery wedge pressure (PAWP), ity due to hypovolaemia or vasodilation.97 As the cardiac
high calculated pulmonary vascular resistance, raised allograft is dependent on an adequate preload, the effects
pulmonary artery pressures, systemic hypotension and of postural changes in recipients are important. (A detailed
oliguria. The haemodynamic management of patients discussion of physiology of the transplanted heart is
with right ventricular dysfunction/failure involves provided elsewhere.97)
optimising right ventricular preload and afterload by There are four important clinical manifestations of
titrating fluid and pharmacological therapies to achieve denervation in the early postoperative period. First, drugs
adequate tissue and end-organ perfusion. Fluid resus- that act directly on the autonomic nervous system to modify
citation to a CVP between 14 and 20 mmHg and heart rate (e.g. atropine, digoxin) and vagal manoeuvres
inotropic therapy are necessary to ensure that the failing (carotid sinus massage) are ineffective. Amiodarone and
right ventricle continues to act as a conduit for the left adenosine are effective antiarrhythmic agents. Neither
ventricle. Nitric oxide by inhalation is the therapy of amiodarone nor sotalol interact with immunosuppressive
choice, as it provides selective pulmonary vasodilation at agents.105 However, as the denervated donor sinus node is
doses of 20–40 ppm, thereby reducing right ventricular more sensitive to exogenous adenosine than a sinus node
afterload without producing systemic hypotension.141,146 innervated in the normal way,151 it has been suggested
A secondary benefit of inhaled NO is improved oxygen- that adenosine be avoided.97 That is, a usual adenosine
ation due to reduced mismatching of ventilation/ dose may produce toxic-like effects in the context of a
perfusion.147 If inhaled NO is not available, IV prosta- denervated heart. Overdrive atrial pacing is a viable alter-
glandin E1 or prostacyclin may be used to reduce right native to drug therapy to treat a tachyarrhythmia such as
ventricular afterload when pulmonary pressures exceed atrial flutter.152
50 mmHg.148 Second, although a high resting heart rate is possible
Mild right ventricular dysfunction may be treated from efferent cardiac denervation, sinus or junctional
with milrinone at doses of 0.375–0.750 mcg/kg/min bradycardias may occur in the early postoperative period
or drug combinations that provide afterload reduction due to transient sinus node dysfunction or preoperative
and inotropic support (e.g. sodium nitroprusside and amiodarone. Studies suggest that sinus node dysfunc-
adrenaline). Appropriate respiratory management is tion occurs in about 20% of cases,153 although anecdotal
essential, as hypoxaemia and metabolic or respiratory experience suggests a higher percentage. To prevent
acidosis can exacerbate right ventricular failure. If pharma- low cardiac output secondary to bradycardias, atrial and
cological, fluid and inhaled NO therapies do not produce ventricular epicardial pacing wires are inserted and atrial
sustained improvement in right ventricular performance, a pacing of >90 beats/min,105 and often at 110 beats/min,
right VAD (e.g. Biomedicus centrifugal pump or Abiomed is commenced. Atrial pacing at 110 beats/min appears
BVS 5000) is indicated to provide temporary support for to ‘train’ the sinus node to conduct at rates of 70–100
the failing right ventricle. beats/min in the long term. A resting sinus or junctional
The immediate haemodynamic management of left heart rate below 70 beats/min prior to hospital discharge
ventricular dysfunction/failure secondary to acute rejection is predictive of long-term sinus node dysfunction.97
or ischaemic injury often involves fluid resuscitation to a Insertion of a permanent pacemaker for long-term heart
pulmonary artery diastolic of 16–20 mmHg, high-dose rate control is rarely required. Isoprenaline infusions at
inotropes, vasodilator agents and insertion of an IABP to doses of 0.5–2 mcg/min may be used for chronotropy
achieve a cardiac index greater than 2.2 L/min/m2 and in combination with atrial pacing. As noted earlier, atrial
adequate end-organ perfusion. The insertion of an LVAD arrhythmias such as atrial flutter may be an early indication
(e.g. Biomedicus centrifugal pump) or full mechanical of acute rejection. Ventricular arrhythmias are rare and
 CHAPTER 12 CARDIAC SURGERY AND TRANSPLANTATION 391

often lethal in spite of aggressive resuscitation attempts. The inability of patients to feel angina pectoris is important,
Persistent arrhythmias should always prompt investigation because all heart transplant recipients are at risk of developing
of the patient’s rejection level.105 accelerated allograft coronary artery disease.155 As part of
Third, as patients rely on circulating catecholamines, discharge education, patients are taught to identify clinical
orthostatic hypotension is common. Patients are educated signs of angina other than chest pain, such as shortness of
to sit up slowly from a lying position. Fourth, patients rarely breath and sweating. A summary of the main clinical mani-
feel anginal pain after surgery; however, there are some festations and nursing practice issues for patients following
reports of patients regaining feelings of angina pectoris.154 heart transplantation is included in Table 12.6.

TABLE 12.6
Nursing care of patients after heart transplantation

CLINICAL
M A N I F E S TAT I O N N U R S I N G P R A C T I C E C O N S I D E R AT I O N S

Acute rejection Detect acute rejection by clinical signs and endomyocardial biopsy
Suspect low-grade rejection when malaise, lethargy, low-grade fever and mood changes are present
Acute rejection is manifested by a sinus tachycardia >120 beats/min, a pericardial friction rub or new-
onset atrial arrhythmias
Suspect severe acute rejection with manifestations of left and right heart failure; awake patients may complain
of severe fatigue, sudden onset of dyspnoea during minimal physical effort, syncope or orthopnoea
Infection Standard infection control precautions and meticulous hand washing is required
Observe for signs of infection: low-grade fever, hypotension, tachycardia, a high cardiac output/index,
a decrease in systemic vascular resistance, changes in mentation, a new cough, dyspnoea, dysuria,
sputum production or pain
Monitor blood, sputum, urine, wound and catheter-tip cultures, infiltrates on chest X-ray and institute
aggressive and prompt treatment for specific infective organisms
Check CMV status before administering blood products
Haemorrhage/cardiac Monitor haematological status; chest tube patency, drainage volume and drainage consistency; and
tamponade trends in haemodynamic data that suggest cardiac tamponade
Patients who are hypotensive sporadically should be assessed to eliminate cardiac tamponade as a cause
Acute renal failure Support renal function, including titration of immunosuppressive agents to individual risk factors and
clinical status, and early haemofiltration
Early allograft dysfunction Augment the immunosuppression regimen to manage the acute rejection
Left heart failure Observe for depressed left ventricular compliance and contractility: reduced cardiac index, possible
bradycardia (may not be evident due to atrial pacing and/or isoprenaline), decreased mental status,
oliguria, poor peripheral perfusion, slow capillary refill and raised serum lactate, low systemic venous
oxygenation and dyspnoea
Fluid resuscitate to a PAWP of 14–18 mmHg, high-dose inotropes, vasodilator agents, IABP to achieve a
cardiac index >2.2 L/min/m2 with adequate end-organ perfusion
Insertion of full mechanical circulatory support (ECMO or LVAD) is indicated when other interventions do
not provide adequate end-organ perfusion
Right heart failure Observe for right heart dysfunction/failure: rising CVP, low-to-normal PAD/PAWP, high calculated
pulmonary vascular resistance, raised pulmonary artery pressures, systemic hypotension and oliguria
Optimise right ventricular preload and afterload: titrate fluid and medications to achieve adequate
end-organ perfusion; fluid resuscitate to a CVP of 14–20 mmHg; consider inhaled NO (selective
pulmonary vasodilation and improved oxygenation from reduced ventilation/perfusion mismatch),
prostaglandin E1 or prostacyclin, milrinone or drug combinations with afterload reduction and inotropic
support (e.g. sodium nitroprusside and adrenaline)
Institute appropriate respiratory management to minimise hypoxaemia and metabolic or respiratory acidosis
If no sustained improvement in right ventricular performance, a right VAD is indicated for temporary support
Denervation Drugs with direct autonomic nervous system actions on heart rate (e.g. atropine, digoxin) and vagal
manoeuvres (carotid sinus massage) are ineffective
Use overdrive atrial pacing to treat tachyarrhythmias
Sinus or junctional bradycardias may occur, and atrial/ventricular epicardial pacing is used to ‘train’ the
sinus node
Orthostatic hypotension is common: patients should sit up slowly from a lying position
Patients rarely feel anginal pain after surgery: they need to identify other clinical signs of angina, such as
shortness of breath and sweating
CMV = cytomegalovirus; CVP = central venous pressure; ECMO = extracorporeal membrane oxygenation; IABP = intra-aortic
balloon pump; LVAD = left ventricular assist device; PAD = pulmonary artery diastolic; PAWP = pulmonary artery wedge pressure.
392 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

and lymphoproliferative disorders,166,167 as a consequence

Practice tip of long-term immunosuppression therapy.81,168,169 Nurses
Heart transplant patients have a denervated heart, so play an important role in educating patients about how
carotid sinus massage will not slow a tachyarrhythmia to avoid and reduce the risks of sun exposure. Treatment
and atropine will not increase sinus node firing or options in transplant recipients are the same as for the
atrioventricular conduction. general population (e.g. chemotherapy, radiation therapy
and surgical excision), in addition to a reduction in immuno-
suppression therapy; however, outcomes remain poor.165
Medium- to long-term complications Long-term renal dysfunction occurs primarily
There are four long-term complications associated with post-transplantation due to cyclosporin nephrotoxicity.
heart transplantation: 1) cardiac allograft vasculopathy; 2) Careful monitoring of cyclosporin levels and avoidance of
malignancy; 3) renal dysfunction; and 4) hypertension.156 hypovolaemia and other nephrotoxic drugs are important
Cardiac allograft vasculopathy (CAV) is a diffuse, prolifera- measures in reducing progression to renal failure. Impor-
tive form of obliterative coronary arteriosclerosis that affects tantly, findings from recent research indicate that chronic
30–60% of heart transplant recipients in the first 5 years cyclosporin nephrotoxicity can be reversed by eliminat-
after surgery.157 Sudden death, ventricular arrhythmias and ing cyclosporin from immunosuppression regimens.108
symptoms of congestive heart failure may be the first signs End-stage renal failure requiring dialysis or renal trans-
of significant CAV.The aetiology of CAV is multifactorial, plantation has been reported in 3–10% of patients.170
including immunological factors (e.g. episodes of acute Systemic hypertension following transplantation has
rejection and anti-HLA antibodies), non-immunological been linked with cyclosporin-induced tubular nephro-
cardiovascular risk factors (e.g. hypertension, hyperlipid- toxicity, peripheral vasoconstriction and fluid retention.171
aemia, preexisting diabetes and new-onset diabetes), the Lifestyle modifications such as weight loss, low sodium
surgical procedure (e.g. donor age, ischaemic time and diet and exercise are recommended along with optimal
reperfusion injury) and side effects of immunosuppression therapeutic doses of cyclosporin, and combinations of
drugs such as cyclosporin and corticosteroids (e.g. CMV calcium channel blockers and angiotensin-converting
infection and nephrotoxicity).105,157–159 Statins at doses less enzyme inhibitors and blockers.105 Such approaches have
than that prescribed for hyperlipidaemia are commenced been reported to achieve blood pressure control in up to
within 2 weeks of surgery irrespective of cholesterol levels 65% of patients.172
to reduce episodes of rejection and CAV.105 Standard use
of cyclosporine may be augmented by mycophenolate Lifestyle issues
mofetil, everolimus or sirolimus as they have been shown Following such momentous surgery, patients require
to reduce the onset and progression of CAV.105 Diagnosis sound advice regarding returning to driving, work,
of CAV is difficult, due to allograft denervation, and exercise and sexual activity. Cardiac rehabilitation with
because coronary angiogram underestimates the extent of aerobic and resistance exercise is recommended to
the disease and is insensitive to early lesions.160 Currently, prevent short-term weight gain and glucose intolerance,
intravascular ultrasound provides the most reliable quan- as well as adverse effects of immunosuppressive therapy
titative information about the degree of CAV.160 As the on skeletal muscle.105 Return to work or education is
definitive treatment for CAV is retransplantation, ongoing expected and encouraged after surgery. Driving a vehicle
research into the prevention of CAV161 will be the can be considered once the patient’s gait, tremor and
most important factor in reducing the incidence and other neurological issues are normalised, and any brady-
associated mortality. cardia managed by pacemaker implantation.105 Pregnancy
All heart transplant recipients are at a greater is possible after 1 year following transplantation; but only
risk of developing malignancies than the general under the management of the multidisciplinary team who
population,162 particularly carcinoma of the skin162–165 will explain the considerable risks involved.105

Summary
Primary compromise of the cardiovascular system causes patients to require admission to a critical care area and the
need for specialised care including intra-aortic balloon pumping and post cardiac surgery management. Appropriate
assessment and management are essential to prevent secondary complications arising. Important principles of care are
summarised below.
Surgical procedures may be performed as treatment for structural abnormalities, ischaemic lesions within coronary
arteries and repair or replacement of cardiac valves. Haemodynamic stability constitutes the most common challenge in
the postoperative period and may be managed with fluids, cardiovascular medications, cardiac pacing and intra-aortic
balloon pumping. Bleeding in the postoperative period may be due to inadequate reversal or heparin, coagulopathy or
surgical bleeding; therefore, appropriate diagnosis must occur before relevant treatment is instigated.
 CHAPTER 12 CARDIAC SURGERY AND TRANSPLANTATION 393

Intra-aortic balloon pumping is one therapy that is used to provide support in the period after cardiac surgery. Major
benefits of IABP include increasing cardiac output, increasing myocardial oxygen supply and decreasing myocardial
oxygen demand. Appropriate timing is essential to obtain maximum benefits, so correction of timing errors forms
a central component of care. In addition, assessment of limb perfusion, with timely intervention when perfusion is
inadequate, is essential to prevent limb ischaemia.
Cardiac transplantation may also be used to provide support to the failing heart. Indications for heart transplanta-
tion include end-stage heart failure secondary to ischaemic heart disease and cardiomyopathy. Possible complications
in the early postoperative period include acute rejection, infection, haemorrhage, renal failure, right ventricular failure
and allograft dysfunction (left ventricular dysfunction/failure). A triple-therapy regimen consisting of corticosteroids,
a calcineurin antagonist and an antiproliferative cytotoxic agent is used to suppress the immune system after organ
transplantation. All cytotoxic agents necessitate specific administration and disposal procedures. Although early signs
of low-grade rejection can be non-specific, signs of moderate rejection usually present as organ dysfunction/failure.
Nursing practices for managing patients with heart transplantation focus on prevention and management of complica-
tions, maintenance of comfort and promotion of long-term recovery.

Case study
Mrs Murphy is a 78-year-old patient admitted for elective CABG surgery. Her past history includes ischaemic
heart diseases, hypertension, high cholesterol, type II diabetes and gout. She has had acute myocardial
infarction (AMI) 5 years ago, which was treated with percutaneous transluminal coronary angioplasty (PTCA)
and a drug-eluting stent to mid LAD lesion. She has had angina pain for the last 6 months and her coronary
angiography showed triple vessel diseases in circumflex artery, LAD above the old stent and posterior
descending artery (PDA) lesions. Her left ventriculogram revealed apical hypokenesis with moderate left
ventricle systolic dysfunction. Preoperative transthoracic echocardiography report revealed normal valves
and grade II left ventricle with moderate systolic dysfunction.
Surgery was reported as uncomplicated. Three bypass grafts were performed using left IMA to LAD,
left radial artery to mid circumflex artery and SVG to the PDA. Cardiopulmonary bypass was used for
79 minutes and aortic cross-clamp time was 58 minutes. Continuous infusion of glyceryl trinitrate (GTN) at
10 mcg/min and noradrenaline at 2 mcg/min were in progress.
On admission to the ICU the patient was intubated and ventilated. She had a right radial arterial line and
a right internal jugular PAC in situ. Two mediastinal and one pericardial drain tube had been placed and
had drained 50 mL of blood to the time of admission. There was a small air leak in under water seal
drainage system. A urinary catheter was also present. Early chest X-rays confirmed ETT, PAC and chest
tube placement. Left lower lobe collapse was noted.
The main dimensions of Mrs Murphy’s progress, care and management follow.

NEUROLOGICAL STATUS
She was kept sedated with propofol for 3 hours and then began to wake up, and was obeying commands,
able to move all limbs with equal strength. Pupils were normal size and reactive to light. Pain was managed
with regular intravenous tramadol, morphine (boluses) and paracetamol suppositories in the initial phase
and continued with tramadol for 48 hours and oral paracetamol for 4 days postoperatively.

VENTILATION
Initial parameters: ETT secured at lip level 22 cm, equal air entry bilaterally, but decreased in left lower base.
SIMV mode, tidal volume (VT) 500 mL (75 kg), rate 10/min, inspiratory flow 40 L/min, PEEP 5 cmH2O, FiO2
1.00, pressure support 10 cmH2O, producing acceptable peak inspiratory pressures of 22–24 cmH2O.
Admission ABG (after 20 minutes) revealed the following:
• PaO2 422 mmHg
• PaCO2 55 mmHg
• pH 7.30
• HCO3− 24 mmol/L
• SaO2 99.0%.
394 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

On the basis of the PaCO2 the SIMV rate was increased to 13 breaths per minute, which corrected the
PaCO2 and pH. FiO2 was progressively decreased to 0.40 over the next hour while pulse oximetry revealed
a SpO2 greater than 98%.
Sedation was reduced 3 hours after admission to ICU, and Mrs Murphy started to initiate spontaneous
breaths; therefore the ventilation mode switched to CPAP/PS. However, she required further sedation due
to events explained next.

CARDIOVASCULAR
Epicardial dual-chamber pacing wires were in place, but pacing was provided in the AAI mode at a rate
of 90 beats/min, with no evidence of AV block. Initially, Mrs Murphy’s blood pressure was maintained with
assistance of noradrenaline infusion at 2 mcg/min to keep MAP above 70 and systolic blood pressure of
110–120 mmHg. Filling pressure (CVP) was kept in the range 10–12 mmHg with colloid administration.
She was vasodilated, with an SVR of 676 dynes/sec/cm−5. Her core temperature on admission was
35.3°C, requiring active warming. Chest drainage remained high, with total blood loss of 150 mL in the
first hour, and continued to drain 120–150 mL/h for the next 3 hours. Multiple units of red blood cells,
fresh frozen plasma, platelets and cryoprecipitate were transfused. Mrs Murphy clinically deteriorated
with consistent low blood pressure that escalated the noradrenaline rate to 20 mcg/min and her filling
pressures were low, CVP of 5 mmHg and pulmonary artery diastolic pressure of 8 mmHg despite fluid
and blood products administration. Her initial cardiac index (CI) was 2.6 L/min/m2, which dropped to
1.7 L/min/m2 once she had deteriorated haemodynamically. Her heart rate remained the same at AAI
paced rate of 90 beats/min. The surgical team decided to take the patient back to theatre for exploration
and to achieve haemostasis.
On return to ICU, Mrs Murphy was sedated with propofol, on noradrenaline at 5 mcg/min and
milrinone at 0.250 mcg/kg/min infusions and IABP was inserted in theatre to assist with left ventricle
function and recovery (augmented diastolic pressure of 120, systolic pressure of 110, diastolic pressure
of 55 and mean arterial pressure of 80 mmHg). One litre of haemoserous collection from the left pleural
space and 350 mL from the pericardial sac were drained. The surgical team reported that a small
pericardial artery was bleeding, which was clipped. Haemostasis was achieved in theatre before closing
the sternum.
Despite returning to theatre, and escalation of care, Mrs Murphy was stable but remained intubated during
the night and sedation was turned off at 0600 in view of extubation. IABP was kept at a 1:1 ratio, noradrenaline
reduced to 2 mcg/min and milrinone to 0.125 mcg/kg/min, with a CI of 2.4 L/min/m2. Mrs Murphy was
extubated mid-morning and IABP was weaned (ratio wean) on postoperative day 2 over a period of 4 hours
without any compromise, and the IABP catheter was removed on day 2 post ICU admission.

FLUID BALANCE
Chest drainage for the first admission was around 750 mL over 3 hours but, after return to ICU for the
second time, the total drainage for 48 hours before the drains were removed was 440 mL. Mrs Murphy’s
urine output remained within the range 0.5–1 mL/kg/h with a small increase in serum urea and creatinine,
which returned to normal on day 7. Hourly fluid assessment was maintained for the duration of ICU stay
and a positive fluid balance was recorded, a total of 3.2 L positive before discharge from ICU on day 3.
Oral fluids were commenced 3 hours post extubation and within 24 hours a light diet was being tolerated.
Mrs Murphy remained in the ICU until the third postoperative morning and was then discharged to the
step-down unit after removal of all lines and tubes. Mrs Murphy was discharged from hospital to a cardiac
rehabilitation centre on day 9.

CASE STUDY QUESTIONS

1 Discuss the steps taken for the management of Mrs Murphy’s deterioration with increased drainage
from the drain tube post cardiac surgery.
2 Discuss the advantages and disadvantages of IABP counterpulsation use for Mrs Murphy.
 CHAPTER 12 CARDIAC SURGERY AND TRANSPLANTATION 395

RESEARCH VIGNETTE

Sethares KA, Chin E, Costa I. Pain intensity, interference and patient pain management strategies the
first 12 weeks after coronary artery bypass graft surgery. Appl Nurs Res 2013;26:174–9

Abstract
Pain is a distressing and often undertreated symptom of cardiac surgery. Little is known about pain levels,
interference and treatment strategies beyond the 9 week period. The purpose of this study was to describe
pain intensity, interference and strategies used to manage pain in post-operative CABG patients. Baseline data
were collected by interview in the hospital after CABG surgery using the Modified Brief Pain Inventory. One to
12 weeks after discharge, weekly telephone interviews were conducted to collect data. Pain levels and interference
with activities of daily living were greatest during hospitalization and decreased over 12 weeks. Pain interfered
the most with coughing and sleep. Once opioid medications ran out, activity modification was primarily used to
manage pain. Activity modification below recommended levels was reported as a pain management strategy.
Patients reported pain lasting longer than they expected and the need for more education about activity and pain
management strategies.

Critique
The management of postoperative pain is vital for a complete and timely recovery, and to prevent undesirable
complications. Few studies have tracked the intensity of pain and its interference with activities of daily living (ADLs)
due to cardiac surgical pain beyond the initial period. In this study, a convenience sample of 80 patients participated
weekly in telephone interviews for 12 weeks to report their pain intensity scores, sites of pain, how pain interfered
with ADLs and coping strategies used to minimise the impact of pain. The sample of patients in this study, 85% of
whom completed the study, was a stable, fairly uncomplicated cardiac surgical cohort; only two patients had a history
of chronic pain requiring opioid use.

The median pain scores reported from weeks 2 to 12 was below 3 (out of 10); however, the ranges were revealing
in that individual scores showed pain intensity up to 5.75 still at week 8. Pain scores for women were consistently
higher than men over the entire 12-week period, with statistical significance reached at weeks 4, 6, 10 and 11. The
introduction of arm exercises in week 7 during cardiac rehabilitation increased pain scores in the entire cohort. Less
than 15% of the cohort fulfilled their opioid prescriptions after the first month, instead choosing to minimise activities
as a strategy to minimise pain. At week 8, 10% of the cohort reported a coping strategy of ‘bearing it’ rather than
using analgesic. Based on these results, telephone follow-up is an ideal method of setting and clarifying patients’
expectations about pain and related activities, and managing individuals’ recoveries. Clearly, the reasons for higher
pain scores reported by women need to be considered and addressed. The study was conducted in a single centre
that had a number of ethic Portuguese patients who are known to be stoic; however, many patients in Australia
and New Zealand have ethnicities (e.g. Anglo-Celtic-Saxon) that have similar stoic attitudes that nurses need to be
mindful of while managing pain and recovery. Due to the single site nature of the study and convenience sample, the
results may not be generalisable to all cardiac surgical populations.

This article gives an insight into the recovery of patients beyond the early postoperative phase and the important role
nurses can play in managing patients’ recovery after discharge. Critical care nurses should always be mindful of the
education they provide to patients and give written information about expected complications due to incisional pain
and appropriate pain management and analgesic advice, including the use of alternatives such as complementary
therapies and activity restrictions that are reasonable and not reasonable. The issue of pain being different due to
gender is a consideration for all nurses managing post cardiac surgical patients.
396 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Lear ning a c t iv it ie s
1 Compare and contrast the automated and semi-automated modes of intra-aortic ballon counterpulsation.
2 Discuss with a senior colleague the reasons for reduction of IABP therapy complications rate.
3 Discuss how you would identify an intra-aortic balloon catheter rupture and immediate management.
4 Discuss the optimal ventilator setting before extubation of a cardiac surgical patient according to your unit
policy and procedures.
5 What haemodynamic values could assist you in deciding the choice of inotropes? Provide rationales.
6 Discuss the management of a patient with cardiac arrest due to pericardial tamponade when an operating
theatre is not available.

Online resources
Australian and New Zealand Intensive Care Society (ANZICS), www.anzics.com.au
Australian Institute of Health and Welfare, www.aihw.gov.au
Australian Organ Donor Register (AODR), www.medicareaustralia.gov.au/public/services/aodr/index.jsp
Cardiac Society of Australia and New Zealand, www.csanz.edu.au
Donate Life, www.donatelife.gov.au
National Heart Foundation of Australia, www.heartfoundation.org.au
National Heart Foundation of New Zealand, www.heartfoundation.org.nz
National Health Priorities and Quality, www.health.gov.au/internet/wcms/publishing.nsf/content/pq-cardio
The International Society for Heart and Lung Transplantation (ISHLT), www.ishlt.org
Transplant Nurses’ Association (TNA), www.tna.asn.au
Transplantation Society of Australia and New Zealand (TSANZ), www.tsanz.com.au

Further reading
Kurien S, Gallagher C. Ventricular assist device: saving the failing heart. Prog Transplant 2010;20:134–41.
Laing C. LVAD: left ventricular assist devices for end-stage heart failure. Nurse Pract 2014;39:42-7.
Pellegrino V, Hockings LE, Davies A. Veno-arterial extracorporeal membrane oxygenation for adult cardiovascular failure.
Curr Opin Crit Care 2014;20:484-92.
Ramakrishna H, Jaroszewski DE, Arabia FA. Adult cardiac transplantation: a review of perioperative management. Ann Card
Anaesth 2009;12:155-65.

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105 Costanzo MR, Dipchand A, Starling R, Anderson A, Chan M, Desai S et al. The International Society of Heart and Lung Transplantation
Guidelines for the care of heart transplant recipients. J Heart Lung Transplant 2010;29(8):914-56.
106 Busauschina A, Schnuelle P, van der Woude FJ. Cyclosporine nephrotoxicity. Transplant Proc 2004;36(2 Suppl):229S-233S.
107 Serkova NJ, Christians U, Benet LZ. Biochemical mechanisms of cyclosporine neurotoxicity. Mol Interv 2004;4(2):97-107.
108 Trento A, Hardesty RL, Griffith BP, Zerbe T, Kormos RL, Bahnson HT. Role of the antibody to vascular endothelial cells in hyperacute rejection
in patients undergoing cardiac transplantation. J Thorac Cardiovasc Surg 1988;95(1):37-41.
400 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

109 Laufer G, Laczkovics A, Wollenek G, Buxbaum P, Seitelberger R, Holzinge C et al. The progression of mild acute cardiac rejection evaluated by
risk factor analysis. The impact of maintenance steroids and serum creatinine. Transplantation 1991;51(1):184-9.
110 Berry GJ, Laczkovics A, Wollenek G, Buxbaum P, Seitelberger R, Holzinger C et al. The 2013 International Society for Heart and Lung
Transplantation Working Formulation for the standardization of nomenclature in the pathologic diagnosis of antibody-mediated rejection in
heart transplantation. J Heart Lung Transplant 2013;32(12):1147-62.
111 Stevenson LW,Miller LW. Cardiac transplantation as therapy for heart failure. Curr Probl Cardiol 1991;16(4):217-305.
112 Hammond EH. Pathology of cardiac allograft rejection. In: Cooper DKC, Miller LW, Patterson GA, eds. The transplantation and replacement of
thoracic organs. Boston: Kluwer; 1996, pp 239-52.
113 Caves PK, Stinson EB, Billingham ME, Rider AK, Shumway NE. Diagnosis of human cardiac allograft rejection by serial cardiac biopsy.
J Thorac Cardiovasc Surg 1973;66(3):461-6.
114 Billingham ME, Cary NR, Hammond ME, Kemnitz J, Marboe C, McCallister HA et al. A working formulation for the standardization of
nomenclature in the diagnosis of heart and lung rejection: Heart Rejection Study Group. The International Society for Heart Transplantation.
J Heart Transplant 1990;9(6):587-93.
115 Stewart S, Berry C, McMurray JJ. Revision of the 1990 working formulation for the standardization of nomenclature in the diagnosis of heart
rejection. J Heart Lung Transplant 2005;24(11):1710-20.
116 Lloveras JJ, Escourrou G, Delisle MB, Fournial G, Cerene A, Bassanetti I et al. Evolution of untreated mild rejection in heart transplant
recipients. J Heart Lung Transplant 1992;11(4 Pt 1):751-6.
117 Olsen SL, Wagoner LE, Hammond EH, Taylor DO, Yowell R, Ensley RD et al. Vascular rejection in heart transplantation: clinical correlation,
treatment options, and future considerations. J Heart Lung Transplant 1993;12(2):S135-42.
118 Partanen J, Nieminen MS, Krogerus L, Harjula AL, Mattila S. Heart transplant rejection treated with plasmapheresis. J Heart Lung Transplant
1992;11(2 Pt 1):301-5.
119 Williams TJ, Snell GI. Lung transplantation. In: Albert RK, Spiro SG, Jett JR, eds. Clinical respiratory medicine. Philadelphia: Mosby; 2004,
pp 831-45.
120 Taylor DO. Cardiac transplantation: drug regimens for the 21st century. Ann Thorac Surg 2003;75(6 Suppl):S72-8.
121 Wade CR, Reith KK, Sikora JH,Augustine SM. Postoperative nursing care of the cardiac transplant recipient. Crit Care Nurs Q, 2004;27(1):
17-28; quiz 29-30.
122 Keogh A. Calcineurin inhibitors in heart transplantation. J Heart Lung Transplant 2004;23(5 Suppl):S202-6.
123 Eisen HJ, Kobashigawa J, Keogh A, Bourge R, Renlund D, Mentzer R et al. Three-year results of a randomized, double-blind, controlled trial of
mycophenolate mofetil versus azathioprine in cardiac transplant recipients. J Heart Lung Transplant 2005;24(5):517-25.
124 Farmer DG, McDiarmid SV, Edelstein S, Renz JF, Hisatake G, Cortina G et al. Induction therapy with interleukin-2 receptor antagonist after
intestinal transplantation is associated with reduced acute cellular rejection and improved renal function. Transplant Proc 2004;36(2):331-2.
125 Morris PJ, Monaco AP. A meta-analysis from the Cochrane Library reviewing interleukin 2 receptor antagonists in renal transplantation.
Transplantation 2004;77(2):165.
126 Carey JA, Frist WH. Use of polyclonal antilymphocytic preparations for prophylaxis in heart transplantation. J Heart Transplant 1990;9(3 Pt 2):
297-300.
127 Moller CH, Gustafsson F, Gluud C, Steinbruchel DA. Interleukin-2 receptor antagonists as induction therapy after heart transplantation:
systematic review with meta-analysis of randomized trials. J Heart Lung Transplant 2008;27(8):835-42.
128 Mason VF, Konicki AJ. Left ventricular assist devices as destination therapy. AACN Clin Issues 2003;14(4):488-97.
129 Miller LW, Naftel DC, Bourge RC, Kirklin JK, Brozena SC, Jarcho J et al. Infection after heart transplantation: a multiinstitutional study. Cardiac
Transplant Research Database Group. J Heart Lung Transplant 1994;13(3):381-92; discussion 393.
130 Hughes WT, Rivera GK, Schell MJ, Thornton D, Lott L. Successful intermittent chemoprophylaxis for Pneumocystis carinii pneumonitis. N Engl
J Med 1987;316(26):1627-32.
131 Kocher AA, Bonaros N, Dunkler D, Ehrlich M, Schlechta B, Zweytick B et al. Long-term results of CMV hyperimmune globulin prophylaxis in
377 heart transplant recipients. J Heart Lung Transplant 2003;22(3):250-7.
132 Couchoud C. Cytomegalovirus prophylaxis with antiviral agents for solid organ transplantation. Cochrane Database Syst Rev 2000(2):CD001320.
133 Walsh TR, Guttendorf J, Dummer S, Hardesty RL, Armitage JM, Kormos RL et al. The value of protective isolation procedures in cardiac
allograft recipients. Ann Thorac Surg 1989;47(4):539-44; discussion 544-5.
134 Rourke TK, Droogan MT, Ohler L. Heart transplantation: state of the art. AACN Clin Issues 1999;10(2):185-201; quiz 307-9.
135 Bowden RA, Slichter SJ, Sayers M, Weisdorf D, Cays M, Schoch G et al. A comparison of filtered leukocyte-reduced and cytomegalovirus
(CMV) seronegative blood products for the prevention of transfusion-associated CMV infection after marrow transplant. Blood
1995;86(9):3598-603.
136 Luckraz H, Goddard M, Charman SC, Wallwork J, Parameshwar J, Large SR. Early mortality after cardiac transplantation: should we do
better? J Heart Lung Transplant 2005;24(4):401-5.
137 Cooper DKC, Lidsky NM. Immediate postoperative care and potential complications. In: Cooper DKC, Miller LW, Patterson GA, eds. The
transplantation and replacement of thoracic organs. Boston: Kluwer; 1996, pp 221-7.
138 McCrystal GD, Pepe S, Esmore DS, Rosenfeld FL. The challenge of improving donor heart preservation. Heart Lung Circ 2004;13:74-83.
139 Rosenfeldt FL, McCrystal G, Pepe S, Esmore D. Myocyte or heart preservation. In: Large S. Towards optimising donor heart quality.
Cambridge: publisher; 2002.
 CHAPTER 12 CARDIAC SURGERY AND TRANSPLANTATION 401

140 Esmore DS, Rosenfeldt FL, Mack JA, Waters KN, Bergin P. Long ischaemic time allografts (>6 hr) further expand the transplant donor pool.
Washington: International Society of Heart and Lung Transplantation Conference Abstracts; 2002.
141 Kieler-Jensen N, Lundin S, Ricksten SE. Vasodilator therapy after heart transplantation: effects of inhaled nitric oxide and intravenous
prostacyclin, prostaglandin E1, and sodium nitroprusside. J Heart Lung Transplant 1995;14(3):436-43.
142 Kristof AS, Magder S. Low systemic vascular resistance state in patients undergoing cardiopulmonary bypass. Crit Care Med 1999;27(6):1121-7.
143 Myles PS, Leong CK, Currey J. Endogenous nitric oxide and low systemic vascular resistance after cardiopulmonary bypass. J Cardiothorac
Vasc Anaesth 1997;11(5):571-4.
144 Landry DW, Levin HR, Gallant EM, Ashton RC Jr, Seo S, D’Alessandro D et al. Vasopressin deficiency contributes to the vasodilation of septic
shock. Circulation 1997;95(5):1122-5.
145 Argenziano M, Choudhri AF, Oz MC, Rose EA, Smith CR, Landry DW. A prospective randomized trial of arginine vasopressin in the treatment
of vasodilatory shock after left ventricular assist device placement. Circulation 1997;96(9 Suppl):II-286-90.
146 Ardehali A, Hughes K, Sadeghi A, Esmailian F, Marelli D, Moriguchi J et al. Inhaled nitric oxide for pulmonary hypertension after heart
transplantation. Transplantation 2001;72(4):638-41.
147 Rossaint R, Falke KJ, Lopez F, Slama K, Pison U, Zapol WM. Inhaled nitric oxide for the adult respiratory distress syndrome. N Engl J Med
1993;328(6):399-405.
148 Armitage JM, Hardesty RL, Griffith BP. Prostaglandin E1: an effective treatment of right heart failure after orthotopic heart transplantation.
J Heart Lung Transplant 1987;6:348-51.
149 Wang SS, Ko WJ, Chen YS, Hsu RB, Chou NK, Chu SH. Mechanical bridge with extracorporeal membrane oxygenation and ventricular assist
device to heart transplantation. Artif Organs 2001;25(8):599-602.
150 Karamlou T, Gelow J, Diggs BS, Tibayan FA, Mudd JM, Guyton SW et al. Mechanical circulatory support pathways that maximize post-heart
transplant survival. Ann Thorac Surg 2013;95(2):480-5; discussion 485.
151 Ellenbogen KA, Thames MD, DiMarco JP, Sheehan H, Lerman BB. Electrophysiological effects of adenosine in the transplanted human heart.
Evidence of supersensitivity. Circulation 1990;81(3):821-8.
152 Macdonald P, Hackworthy R Keogh A, Sivathasan C, Chang V, Spratt P. Atrial overdrive pacing for reversion of atrial flutter after heart
transplantation. J Heart Lung Transplant 1991;10(5 Pt 1):731-7.
153 Mackintosh AF, Carmichael DJ, Wren C, Cory-Pearce R, English TA. Sinus node function in first three weeks after cardiac transplantation.
Br Heart J 1982;48(6):584-8.
154 Stark RP, McGinn AL, Wilson RF. Chest pain in cardiac-transplant recipients. Evidence of sensory reinnervation after cardiac transplantation.
N Engl J Med 1991;324(25):1791-4.
155 Parry A, Roberts M, Parameshwar J, Wallwork J, Schofield P, Large S. The management of post-cardiac transplantation coronary artery
disease. Eur J Cardiothorac Surg 1996;10(7):528-32; discussion 53.
156 Shiba N, et al. Analysis of survivors more than 10 years after heart transplantation in the cyclosporine era: Stanford experience. J Heart Lung
Transplant 2004;23(2):155-64.
157 Valantine H. Cardiac allograft vasculopathy after heart transplantation: risk factors and management. J Heart Lung Transplant 2004;23
(5 Suppl):S187-93.
158 Kobashigawa J. What is the optimal prophylaxis for treatment of cardiac allograft vasculopathy? Curr Control Trials Cardiovasc Med 2000;1:166.
159 Rose EA, Pepino P, Barr ML, Smith CR, Ratner AJ, Ho E et al. Relation of HLA antibodies and graft atherosclerosis in human cardiac allograft
recipients. J Heart Lung Transplant 1992;11(3 Pt 2):S120-3.
160 Johnson DE, Alderman EL, Schroeder JS, Gao SZ, Hunt S, DeCampli WM et al. Transplant coronary artery disease: histopathologic
correlations with angiographic morphology. J Am Coll Cardiol 1991;17(2):449-57.
161 Keogh A, Richardson M, Ruygrok P, Spratt P, Galbraith A, O’Driscoll G et al. Sirolimus in de novo heart transplant recipients reduces acute
rejection and prevents coronary artery disease at 2 years: a randomized clinical trial. Circulation 2004;110(17):2694-700.
162 Na R, Grulich AE, Meagher NS, McCaughan GW, Keogh AM, Vajdic CM. De novo cancer-related death in Australian liver and cardiothoracic
transplant recipients. Am J Transplant 2013;13(5):1296-304.
163 Krikorian JG, Anderson JL, Bieber CP, Penn I, Stinson EB. Malignant neoplasms following cardiac transplantation. JAMA 1978;240(7):639-43.
164 Ong CS, Keogh AM, Kossard S, Macdonald PS, Spratt PM. Skin cancer in Australian heart transplant recipients. J Am Acad Dermatol
1999;40(1):27-34.
165 Veness MJ, Quinn DI, Ong CS, Keogh AM, Macdonald PS, Cooper SG et al. Aggressive cutaneous malignancies following cardiothoracic
transplantation: the Australian experience. Cancer 1999;85(8):1758-64.
166 Armitage JM, Kormos RL, Stuart RS, Fricker FJ, Griffith BP, Nalesnik M et al. Posttransplant lymphoproliferative disease in thoracic organ
transplant patients: ten years of cyclosporine-based immunosuppression. J Heart Lung Transplant 1991;10(6):877-86; discussion 886-7.
167 Cole WH. The increase in immunosuppression and its role in the development of malignant lesions. J Surg Oncol 1985;30(3):139-44.
168 Penn I. Cancers following cyclosporine therapy. Transplantation 1987;43(1): 32-5.
169 Penn I, First MR. Development and incidence of cancer following cyclosporine therapy. Transplant Proc 1986;18(2 Suppl 1):210-5.
170 Greenberg A, Thompson ME, Griffith BJ, Hardesty RL, Kormos RL, el-Shahawy MA et al. Cyclosporine nephrotoxicity in cardiac allograft
patients – a seven-year follow-up. Transplantation 1990;50(4):589-93.
171 Eisen HJ. Hypertension in heart transplant recipients: more than just cyclosporine. J Am Coll Cardiol 2003;41(3):433-4.
172 Ventura HO, et al. Mechanisms of hypertension in cardiac transplantation and the role of cyclosporine. Curr Opin Cardiol 1997;12(4):375-81.
Chapter 13

Respiratory assessment
and monitoring
Mona Ringdal, Janice Gullick

KEY WORDS
Learning objectives
After reading this chapter, you should be able to: arterial blood
gases
• understand respiratory anatomy and normal physiology
capnography
• understand mechanisms contributing to altered respiratory function
diagnostic imaging
• identify key principles underpinning assessment and monitoring of
respiratory function gas exchange
hypoxaemia
• describe nursing assessment and monitoring activities for critically
ill patients with respiratory dysfunction oxygen delivery
• discuss the importance of patient assessment skills, and the pulse oximetry
contribution of diagnostic and laboratory findings to ongoing clinical work of breathing
management
• outline the physiological basis for different types of monitoring
• describe common diagnostic procedures used in critical care.

Introduction
The respiratory system ensures adequate tissue and cellular oxygenation for
the body. It is responsible for gas exchange through the uptake of oxygen and
excretion of carbon dioxide (CO2); assists in optimal organ function; contributes
to acid–base balance; and therefore plays a large role in maintaining homeostasis.
As respiratory conditions account for 20–26% of admissions to intensive care
units (ICUs) in the USA and UK,1 and up to 33% in Australian hospitals,2 a
thorough understanding of the anatomy, physiology and pathophysiology of this
complex system is required to accurately assess critically ill patients and monitor
response to treatment or early signs of deterioration.
This chapter provides a comprehensive description of the principles and
practice of respiratory assessment, monitoring and diagnostics. These are foun-
dational concepts underpinning timely and effective interventions for critically
ill patients. Management of respiratory alterations, oxygenation and ventilation
are discussed in Chapters 14 and 15.
 CHAPTER 13 RESPIRATORY ASSESSMENT AND MONITORING 403

Related anatomy and nasal conchae create turbulent gas flow. Mucus is moved
by the cilia at the top of the epithelial cells lining the
physiology conducting airways. Mucus moves towards the pharynx
at a rate of 1–2 cm per minute, providing filtration and
The thoracic cavity contains the trachea and bronchial cleaning of the inhaled air. One litre of mucus is produced
tree, the two lungs, pleura and diaphragm. The media- every day with only a small part not reabsorbed by
stinum, located between the lungs, houses and protects the the body.6,7
heart, great vessels and the oesophagus.Twelve pairs of ribs The pharynx is a muscular tube that transports food
cover the lungs.Ten are connected to the spine posteriorly, to the oesophagus and air to the larynx. Inferior to the
and to the sternum or to the cartilage of the above rib pharynx, the larynx consists mostly of cartilage attached
anteriorly (ribs 8–10). The 11th and 12th ribs have no to other surrounding structures and houses the vestibular
anterior attachment (see Figure 13.1).3 (false) vocal folds, which do not produce any sounds but
The respiratory system is divided into upper and lower help to close the larynx during swallowing.The lower true
respiratory tracts: the upper airways consist of the nose, vocal cords create the vocal sounds (see Figure 13.2).8 The
nasal conchae, sinus and pharynx; the lower respiratory pyramid-shaped arytenoids, an important pair of cartilages
tract includes the larynx, trachea, bronchi and lungs.5 within the larynx, act as attachment points for the vocal
Larger airways are lined with stratified epithelial tissue, cords. This area is easily damaged by pressure from endo-
which has a relatively high cellular turnover rate; these cells tracheal tubes; the most significant independent risk factor
protect and clear these large airways. Additional specialised for injury to the arytenoids is the length of intubation
features of this tissue include an extensive distribution of time.9 The thyroid cartilage (‘Adam’s apple’) and the
mucus/goblet cells and cilia, which facilitate the airways’ cricoid cartilage protect the glottis and entrance to the
mucociliary clearance system. trachea.7 Another cartilage in the larynx is the triangular-
shaped elastic epiglottis, which protects the lower airways
Upper respiratory tract from aspiration of food and fluids into the lungs. The
The nasal cavities contain an extremely vascular and epiglottis usually occludes the inlet to the larynx during
mucoid environment for warming and humidifying swallowing.The primitive cough, swallow and gag reflexes
inhaled gases.To maximise exposure to this surface area, the further protect the airway.7

FIGURE 13.1 Ventilatory structures of the chest wall and lungs, showing the ribs and lobes of the lungs.4

Thyroid cartilage
Cricoid cartilage
Upper lobe
Trachea of left lung
Clavicle
Upper lobe
of right lung
Scapula 1 1

2 2

3 3

Sternum 4
4

5 5
6 6

dle lobe 7 7 Lower lobe

er lobe of left lung
8 8
9 9

Rib cartilages 10 10

Adapted from Urden L, Stacy K, Lough M. Critical care nursing: Diagnosis and management. 6th ed. St Louis: Mosby; 2010,
with permission.
404 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

FIGURE 13.2 Larynx. (A) Cartilages and ligaments. (B) Neck muscles.10

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Lower respiratory tract participate in gas exchange but form the anatomical dead
space (approximately 150 mL).11
The trachea is a hollow tube approximately 11 cm long
and 2.5 cm in diameter that marks the beginning of the Larger airways have a greater proportion of supporting
lower respiratory tract. The trachea is supported by 16–20 cartilage, ciliated epithelium, goblet and serous cells and,
C-shaped cartilages and is another area at risk of pressure hence, a mucous layer. As the airways become smaller,
damage from artificial airways. The trachea divides cartilage becomes irregularly dispersed. The number of
at the carina into the left and right main bronchi. The goblet cells and amount of mucus decrease until, at the
bronchial tree has two mainstem bronchi that are struc- alveolar level, there is only a single layer of squamous
turally different. The right bronchus is wider and angles epithelial cells. Alveolar macrophages present among
slightly where it divides further into the three lobes of the these epithelial cells phagocytose any small particles that
right lung. The most common site of aspiration of foreign enter the alveoli. Smooth muscle surrounds and supports
objects is the right bronchus because of its anatomical the bronchioles, enabling airway diameter change and
position. The acutely-angled left main bronchus divides subsequent changes in airway resistance to gas flow.12
further into the two lobes of the left lung.
The airways within each lung branch further into Thorax/lungs
secondary (or lobar) bronchi then tertiary (or segmental) The lungs and heart are protected within the thoracic
bronchi. Further divisions within these conducting cage. When inspiration is triggered, expansion of the
airways end with the terminal bronchioles, the smallest thorax creates a negative pressure causing air to flow into
airways without alveoli. These conducting airways do not the lungs. The thorax then passively compresses to expel
 CHAPTER 13 RESPIRATORY ASSESSMENT AND MONITORING 405

air from the lungs during expiration. The diaphragm Pleura

separates the thorax from the abdomen and is the most Each lung is contained within a continuous thin
important inspiratory muscle, performing approximately membrane called the pleura, creating the pleural sac that
80% of the work of breathing. Inspiration is initiated surrounds each lung. The two pleural sacs, one on each
from the medulla, sending impulses through the phrenic side of the midline, are completely separate from each
nerve to stimulate the diaphragm to contract and flatten. other. The parietal pleura lines the inner surface of the
The phrenic nerve originates in the cervical plexus and chest wall and is in close contact with the visceral pleura,
involves the third to fifth cervical nerves. It splits into two which covers the lungs. The pleural space, between these
parts, passing to the left and right side of the heart before two layers, contains a small amount of serous fluid, which
it reaches the diaphragm. For this reason, patients can have limits friction during lung expansion.
ventilation difficulties if phrenic nerve damage results The intrapleural pressure in the pleural space under
from C3–C5 trauma.12,13 normal circumstances is always negative with a range of
The conducting airways, ending in the terminal bron- −4 to −10 cmH2O; this negative pressure keeps the lungs
chioles, move inspired air towards the respiratory unit. inflated. During inhalation the pressure becomes more
The respiratory unit comprises the respiratory bronchi- negative as both the lungs and the chest wall are elastic
oles, alveolar ducts and alveolar sacs where the diffusion structures. These elastic fibres of the lung pull the visceral
of gas molecules, or gas exchange, occurs. The respiratory pleura inwards while the chest wall pulls the parietal
unit makes up most of the lung with a volume of 2.5–3 L pleura outward. The pressure difference between the
during rest11 (see Figure 13.3). alveolar pressure (0 cmH2O pressure in the lungs) and
the intrapleural pressure (−4 cmH2O) across the lung
Surfactant wall is termed the trans-pulmonary pressure (+4 cmH2O
Of particular importance to the structure and function [0 − (−4) = +4]), and is the force that holds the lungs
of the respiratory system are the type I and II alveolar open6,7 (see Figure 13.4).
epithelial cells. Type I cells provide support of the alveolar
unit walls. Type II cells produce an important lipoprotein, Pulmonary circulation
surfactant, that lines the inner alveolar surface lowering The circulatory system of the lung receives the entire
alveolar surface tension, stabilising the alveoli to optimise cardiac output but operates as a low pressure system; it
lung compliance and facilitating expansion during inspira- only directs blood back to the left side of the heart (unlike
tion.11 If surfactant synthesis is reduced due to pulmonary the systemic circulation, which pumps blood to different
disease, lung compliance decreases and the work of regions of the entire body). Within the pulmonary circu-
breathing increases.14 lation, the right ventricle pumps oxygen-depleted blood

FIGURE 13.3 Lower airway branches.10

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406 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

FIGURE 13.4 Changes in intrapleural and FIGURE 13.5 Terminal ventilation and perfusion units
intrapulmonary pressure during inspiration and of the lung.10
expiration.7
Terminal
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Adapted from Marieb E, Hoehn K. Human anatomy and

physiology. 4th ed. San Francisco: Pearson Benjamin
Cummings; 2010, with permission.

to the lungs via the pulmonary artery, with oxygen-rich

blood returning to the left atrium via the pulmonary veins.
Pulmonary blood vessels follow the path of the bronchi-
oles, with capillaries forming a dense network in the walls FIGURE 13.6 Comparison of pressure in the
of the alveoli. As illustrated in Figure 13.5,10 the entire pulmonary and systematic circulations (mmHg).15
surface area of the alveolar wall is covered by capillaries,
just large enough for a red blood cell to pass through, Mean = 15 Mean = 100
allowing gas exchange.
25/8 120/80
Pulmonary vessels are short and thin and have relatively Artery Artery
little smooth muscle. The pressure inside the vessels is 12 Pulmonary Systemic 30
remarkably low (normal pulmonary artery pressure is
25/0 120/0
only 25/8 mmHg; mean 15 mmHg).11 This low pressure
system ensures that right heart workload is minimised, Cap RV LV
Cap 20
while promoting efficient gas exchange in the lungs11 (see
RA LA
Figure 13.6).
8 2 5
Bronchial circulation 10
The bronchial circulation, part of the systemic circula- Vein Vein
tion, supplies oxygenated blood, nutrients and heat to the
conducting airways (to the level of the terminal bronchi-
oles) and to the pleura. Drainage of this deoxygenated blood Adapted from West J. Respiratory physiology: the essentials.
8th ed. Philadelphia: Lippincott, Williams & Wilkins; 2008,
is predominantly through the bronchial network, although with permission.
some capillaries drain into the pulmonary arterial circu-
lation, contributing to venous admixture or right-to-left
shunt11 (see Pathophysiology below for further discussion). chemoreceptors and mechanoreceptors. There are also
protective reflexes such as coughing and sneezing that
Control of ventilation respond to respiratory tract irritation.
Normal breathing occurs automatically and is a complex
function not fully understood. It is coordinated by Controller
the respiratory centre, regulated by controllers in the In the brainstem, the medulla oblongata and the pons regulate
brain, effectors in the muscles and sensors including automatic ventilation while the cerebral cortex regulates
 CHAPTER 13 RESPIRATORY ASSESSMENT AND MONITORING 407

voluntary ventilation (see Figure 13.7). The respiratory muscles, lifting the thorax up and out. This action lowers
rhythmic centre in the medulla can be divided into inspira- pressure within the alveoli (intra-alveolar pressure)
tory and expiratory centres, with the following functions:12 relative to atmospheric pressure. Air rushes into the lungs
• The inspiratory centre (or dorsal respiratory group) to equalise the pressure gradient. After contraction has
triggers inspiration. ceased, the ribs and diaphragm relax, the pressure gradient
• The expiratory centre (or ventral respiratory group) reverses, and air is passively expelled from the lungs, which
only functions during forced respiration and active return to their resting state due to elastic recoil.
expiration. Sensors
• The pneumotaxic and apneustic centre in the pons A chemoreceptor is a sensor that responds to a change
adjusts the rate and pattern of breathing.
in the chemical composition of the blood; there are two
• The cerebral cortex provides conscious voluntary types: central and peripheral. Central chemoreceptors
control over the respiratory muscles. This voluntary account for 70% of the feedback controlling ventilation,
control cannot be maintained when the partial pressure
and respond quickly to changes in the pH of cerebrospinal
of carbon dioxide in the arterial blood (PaCO2 )
fluid and increases in PaCO2.7,13 If the PaCO2 remains
and the hydrogen ion (H+) concentration become
markedly elevated; an example is the inability to hold high for a prolonged period, as in chronic obstructive
your breath for very long.12 Emotional and autonomic pulmonary disease (COPD), a compensatory change in
activities also affect the pace and depth of breathing. bicarbonate (HCO3−) occurs and the pH in cerebrospinal
fluid returns to its near normal value.11
Effectors Central chemoreceptors located in the medulla
The diaphragm is the major muscle of inspiration, respond to changes in H+ concentration in the surround-
although the external intercostal muscles also contribute. ing cerebrospinal fluid. A change in the PaCO2 causes
The accessory muscles of inspiration (scalenes, sterno- movement of CO2 across the blood–brain barrier into
cleidomastoid muscles and the pectoralis minor) are active the cerebrospinal fluid and alters the H+ concentration.
only during exercise or strenuous breathing. Expiration is This increase in H+ stimulates ventilation. Central chemo-
a passive act and only the internal intercostal muscles are receptors do not, however, respond to changes in the
involved at rest. During exercise, the abdominal muscles partial pressure of oxygen in arterial blood (PaO2). Opiates
also contribute to expiration. Inspiration is triggered by also have a negative influence on these chemoreceptors,
stimulus from the medulla, causing downward contraction reducing sensitivity to changing H+ concentration.11
of the diaphragm, and contraction of external intercostal Hyperventilation may reduce PaCO2 to a level that could

FIGURE 13.7 Respiratory centres and reflex.7

Higher brain centers

(cerebral cortex—voluntary
control over breathing)

Other receptors (e.g., pain) +

–
and emotional stimuli acting
through the hypothalamus
+
– Respiratory centers
(medulla and pons)

Peripheral
chemoreceptors +
O2 , CO2 , H+
+ – Stretch receptors
in lungs
Central
chemoreceptors
CO2 , H+ –
+ Irritant
receptors
Receptors in
muscles and joints

Adapted from Marieb E, Hoehn K. Human anatomy and physiology. 4th ed. San Francisco: Pearson Benjamin Cummings; 2010,
with permission.
408 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

cause accidental unconsciousness if the breath is held or in disease states, compliance is increased or decreased.
after hyperventilation. This phenomenon is well known Ranges of lung volumes and capacities are illustrated in
amongst divers and is due to increasing levels of CO2 as Figure 13.8. Tidal volume is the volume of air entering
the primary trigger of breathing. If the CO2 level is too the lungs during a single inspiration and is normally equal
low due to hyperventilation, the breathing reflex is not to the volume leaving the lungs on expiration (around
triggered until the level of oxygen has dropped below 500 mL). During inspiration, the tidal volume of inspired
what is necessary to maintain consciousness. air is added to the 2400 mL of air already in the lungs.
Peripheral chemoreceptors also play a role in controlling This remaining volume of air in the lungs after normal
ventilation, although to a lesser extent.16 Located in the expiration is the functional residual capacity,7 which:
common carotid arteries and in the arch of the aorta,
peripheral chemoreceptors detect changes in PaCO2
• has an important role in keeping small alveoli open
and avoiding atelectasis
and H+ concentration/pH in arterial blood.13 Peripheral
chemoreceptors are sensitive to changes in PaO2 and are • can be reduced during anaesthesia or neuromuscular
the primary responders to hypoxaemia, stimulating the blockade, most likely due to loss of muscle tone21
glossopharyngeal and vagus nerves and providing feedback • if reduced, results in the smallest alveoli closing at the
to the medulla. In response to low PaO2, such as below end of the expiration (the ‘closing volume’).
70 mmHg (8 kPa),11 they are stimulated and contribute The closing volume plus the residual volume is called
to maintaining ventilation. the ‘closing capacity’. The closure of the smallest airways
may occur because dependent areas of the lungs are
BOX 13.1 compressed, although this is not the only mechanism as
these airways also close in the weightlessness of space. The
Patients with chronic respiratory conditions, including
closing volume is dependent on patient age: in a young
COPD, often exhibit signs of hypoxia and hypercarbia,
healthy person it is 10% of vital capacity while, for an
particularly during an acute exacerbation of a chronic
individual aged 65 years, it increases to 40%, approximat-
condition. There is a strongly held belief that patients
ing total functional residual capacity (FRC).11
who chronically retain CO2 no longer have a central
chemoreceptor response to increased PaCO2 and their Alveolar ventilation
drive to breathe is in relation to peripheral chemoreceptor
Minute volume represents the volume of gas inhaled or
response, which detects hypoxia. However, the control of
exhaled in one minute and is calculated by multiplying
ventilation in such patients is highly complex and involves
the tidal volume by respiratory frequency (e.g. 500 mL
adaptations of the respiratory control system including
× 12 breaths per minute = 6000 mL). In this example
changes to respiratory muscles, chemoreceptor signaling
only the first 350 mL of inhaled air in each breath reaches
and central respiratory drive.17 While it is true that an
the alveolar exchange surface, with 150 mL remaining in
uncontrolled administration of oxygen to patients who
the conducting airways, referred to as the ‘anatomic dead
chronically retain CO2 results in hypercarbia, this is mainly
space’. Alveolar ventilation is the amount of inhaled air
because of reversal of hypoxic vasoconstriction and
that reaches the alveoli each minute (e.g. 350 mL × 12 =
changes to ventilation and perfusion matching. To a lesser
4200 mL of alveolar ventilation).12
extent, arterial CO2 increases because of a rightward shift
in the CO2 dissociation curve (the Haldane effect).18 Work of breathing
Those patients most likely to develop hypercarbia At rest, the energy required to breathe is minimal (less
associated with oxygen administration are also those than 5% of total O2 consumption).11 However, changes in
with significant hypoxaemia. For patients who chronically airway resistance and lung compliance affect the work of
retain CO2 and are hypoxic, the hypoxia must be treated breathing, resulting in increased oxygen consumption.22
and should be tailored to the patient’s clinical condition. As noted earlier, the lungs are very distensible, expanding
Evidence suggests that aiming for oxygen saturation during inspiration. This expansion is called the elastic
between 88% and 92% results in improved patient or compliance work and refers to the ease with which
outcome.19,20 For a more in-depth description of the lungs expand under pressure. Lung compliance is often
physiological changes associated with COPD please refer monitored when patients are mechanically ventilated, and
to Further reading at the end of this chapter. is calculated by dividing the change in lung volume by
the change in trans-pulmonary pressure.6 For the lung to
Other receptors include stretch receptors located in expand, it must overcome lung viscosity and chest wall
the lungs, which inhibit inspiration and protect the lungs tissue (called ‘tissue resistance work’). Finally, there is
from over-inflation (Hering-Breuer reflex), and in the airway resistance work – movement of air into the lungs
muscles and joints (see Figure 13.7). via the airways. The work associated with resistance and
compliance is easily overcome in healthy individuals but, in
Pulmonary volumes and capacities pulmonary disease, both resistance work and compliance
In healthy individuals, the lungs are readily distensible or work are increased.6,23 During exertion, when increased
compliant; when exposed to high expanding pressures muscle function heightens metabolic rate, oxygen
 CHAPTER 13 RESPIRATORY ASSESSMENT AND MONITORING 409

FIGURE 13.8 For lung volume measurements, all values are approximately 25% lower in women.3 ERV = expiratory
reserve volume; FRC = functional residual capacity; IC = inspiratory capacity; IRV = inspiratory reserve volume;
RV = residual volume; TLC = total lung capacity; VC = vital capacity; VT = tidal volume.

6000

5500

5000

4500
Total amount of air in lungs (ml)

4000

3500

3000

2500

2000

1500

1000

500

0
Measure TLC VT FRC IC IRV ERV RV VC

Value (ml) 5800 500 2300 3500 3000 1100 1200 4600
6000 2400 3600 3100 1200 1300 4800

demand rises to match consumption and avoid anaerobic Oxygen transport

metabolism, and work of breathing is increased. The term In oxygenated blood transported by the pulmonary capil-
‘work of breathing’ is often used in critical illness, when laries, there is 20 mL of oxygen in each 100 mL of blood.
basic respiratory processes are challenged and breathing Oxygen is transported in two ways: dissolved in plasma
consumes a far greater proportion of total energy. (about 0.3 mL; 1.5%) with the remainder bound to haemo-
Principles of gas transport and globin.12 Measured by arterial blood gases (ABGs), the 1.5%
of oxygen dissolved in blood constitutes the PaO2.7 One
exchange in alveoli and tissues gram of haemoglobin carries 1.34 mL of oxygen. The level
Oxygen and CO2 are transported in the bloodstream of saturation within the total circulating haemoglobin can
between alveoli and the tissue cells. Delivery of oxygen be measured clinically, by pulse oximetry. The amount of
to tissues and transfer of CO2 from the tissues to the oxygen actually bound to haemoglobin compared with the
capillaries occurs by diffusion and is therefore dependent amount of oxygen the haemoglobin can carry is commonly
on the pressure gradient between the capillary and the reported as arterial oxygen saturation or SaO2. Oxygen is
cell. Diffusion involves molecules moving from areas of attached to the haemoglobin molecule at four haem sites.
high concentration to low concentration. Other deter- As the majority of oxygen transport is via haemoglobin, if
minants of the rate of diffusion include the thickness of all four sites are occupied by oxygen molecules the blood is
the alveolar membrane, the surface area of the membrane determined to be ‘fully saturated’ (SaO2 = 100%).23
available for gas transfer and the inherent solubility of A large reserve of oxygen is available if required,
the gas. CO2 diffuses about 20 times more rapidly than without the need for any increase in respiratory or cardiac
oxygen, being much more soluble in blood.11 At the most workload. Oxygen extraction is the percentage of oxygen
distal ends of the conducting airways lay an extensive extracted and utilised by the tissues. At rest, just 25%
network of approximately 300 million alveoli. The surface of the total oxygen delivered to the tissue is extracted,
area of the lungs, if spread out flat, would be about 90 m2 although this amount does vary throughout the body,
– about 40 times greater than the surface area of the skin.7 with some tissue beds extracting more and others taking
Gas exchange occurs through the exceptionally thin less. Normally, the oxygen saturation of venous blood
alveolar membranes. Oxygen uptake takes place from the is 60–75%; values below this indicate that more oxygen
external environment via the lungs through to the blood than normal is being extracted by tissues. This can be due
in the adjacent alveolar capillary networks. Similarly, CO2 to a reduction in oxygen delivery to the tissues or to an
diffuses from capillaries to the alveoli and is then expired. increase in the tissue consumption of oxygen.12,13
410 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Oxygen delivery and oxygen consumption are

important considerations in the management of critically FIGURE 13.9 Shift of the oxygen–haemoglobin
dissociation curve: (A) to the right and (B) to the left.25
ill patients. Normal oxygen delivery in a healthy person
at rest is approximately 1000 mL/min. Normal oxygen

2VDWXUDWLRQ
consumption is 200–250 mL/min,13 but this can increase 
significantly during episodes of sepsis, fever, hypercatab-

olism and shivering.23 The difference between normal &XUYHEHIRUH
delivery and normal consumption highlights the large  VKLIW
degree of oxygen reserve available to the body. &XUYHVKLIWVWRULJKW
 DVS+&2
Oxygen–haemoglobin dissociation curve WHPSHUDWXUH
,QFUHDVHG 
As blood is transported to the tissues and end-organs, the R[\JHQ
tendency of haemoglobin and oxygen to combine decreases, UHOHDVH 
relative to the surrounding arterial oxygen tension. This WRWLVVXH      
relationship is illustrated by the oxygen–haemoglobin disso- 32 PP+J
ciation curve (see Figure 13.9).As oxygen is offloaded at the 32LQWLVVXH
tissue level, CO2 binds more readily with haemoglobin, to
be transported back to the lungs for removal.7 ,QWKHWLVVXHVWKHR[\JHQ²KDHPRJORELQGLVVRFLDWLRQ
The oxygen–haemoglobin dissociation curve relates FXUYHVKLIWVWRWKHULJKW$VS+GHFUHDVHV3&2
the partial pressure of oxygen to the haemoglobin LQFUHDVHVRUDVWHPSHUDWXUHULVHVWKHFXUYH EODFN 
saturation in blood.While the initial part of the curve rises VKLIWVWRWKHULJKW EOXH UHVXOWLQJLQDQLQFUHDVHG
steeply, the latter part of the curve flattens representing the UHOHDVHRIR[\JHQ
binding of oxygen to haemoglobin in the lungs. In the $
upper part of the curve (within the lungs), relatively large
changes in the PaO2 cause only small changes in haemo- ,QFUHDVHG
globin saturation. Therefore, if the PaO2 drops from 100 XSWDNHRI 
to 60 mmHg (14–8 kPa), the saturation of haemoglobin R[\JHQ
changes only 7% (from a normal 97% to 90%). As long as LQOXQJV 
&XUYHVKLIWVWROHIW
PaO2 remains above 60 mmHg (7.8 kPa) haemoglobin DVS+&2

will be more than 90% saturated. The minimal changes
2VDWXUDWLRQ

WHPSHUDWXUH
in O2 binding within this substantial PO2 range allow 
survival at high altitudes.7,12,24 &XUYHEHIRUH
The lower portion (steep component) of the oxygen–  VKLIW
haemoglobin dissociation curve, between 40 and 60

mmHg (5–8 kPa), represents the release of oxygen      
from haemoglobin in tissue capillaries. At this point, a 32 PP+J
small drop in PaO2 will cause a large increase in oxygen
32LQOXQJV
unloading. As haemoglobin is further de-saturated, larger
amounts of oxygen are released for tissue use, ensuring an
,QWKHOXQJVWKHR[\JHQ²KDHPRJORELQGLVVRFLDWLRQ
adequate oxygen supply to peripheral tissues, even when FXUYHVKLIWVWRWKHOHIW$VS+LQFUHDVHV3&2
oxygen delivery is reduced. Oxygen saturation remains at GHFUHDVHVRUDVWHPSHUDWXUHIDOOVWKHFXUYH EODFN 
70–75%, leaving a significant amount of oxygen in reserve. VKLIWVWRWKHOHIW EOXH UHVXOWLQJLQDQLQFUHDVHGDELOLW\
Normally only 25% of bound oxygen is unloaded during RIKDHPRJORELQWRSLFNXSR[\JHQ
one systemic circuit. However, during exercise when the %
muscles need more oxygen, the PaO2 drops and more
oxygen dissociates from haemoglobin for use by muscle Adapted from Seely R, Stephens T, Tate P. Anatomy and
cells without any complementary increase in respiratory physiology. 7th ed. Boston: McGraw Hill; 2006.
rate or cardiac output.7,12
The relationship between the two axes of this curve
assumes values for haemoglobin, pH, temperature, PaCO2 there is a reduced capacity for oxygen binding to haemo-
and 2,3-bisphosphoglycerate (BPG), a product of the globin in the lungs but oxygen is more readily released
breakdown of red blood cells that binds reversibly with to the tissues. At a local level, in active tissue such as
haemoglobin, are normal. Changes to any of these values working muscle that generates lactic acid, acid release
will shift the curve to the right or left and therefore reflect lowers the pH resulting in release of oxygen from haemo-
different values for PaO2 and SaO212 (see Figure 13.9). globin molecules to the surrounding tissue. The same
Both the binding and dissociation of oxygen to process occurs when active skeletal muscle generates heat.
haemoglobin are reversible reactions depending on the The increase in local temperature leads to oxygen release
surrounding tissue. When the curve shifts to the right for use by the surrounding muscle.7,12
 CHAPTER 13 RESPIRATORY ASSESSMENT AND MONITORING 411

As blood is transported to the tissues and end-organs, apices receive less perfusion compared with the bases.11 In
the binding affinity of haemoglobin and oxygen decreases the supine position, apical and basal perfusions are almost
relative to the surrounding arterial oxygen tension. As equal, but the posterior (dependent) portion of the lungs
oxygen is offloaded at the tissue level, CO2 binds more receives greater perfusion than the anterior lung area.
readily with haemoglobin, to be transported to the lungs Ventilation is also uneven throughout the lung, with the
for removal.7 bases receiving more ventilation per unit volume than
the apices.11
Carbon dioxide transport Pressure within the surrounding alveoli also influences
CO2 is transported by blood in three forms: combined blood flow through the pulmonary capillary network.The
with water as carbonic acid (80–90%), dissolved (5%) pressure gradients between the arterial and venous ends
or attached to plasma proteins (5–10%), including of a capillary network normally determine blood flow.
haemoglobin. The dissolved CO2 constitutes PaCO2 However, alveolar pressure (PA) can be greater than venous
and is measured by ABGs. The greater solubility of CO2 (Pv) and/or arterial (Pa) pressure, and therefore influences
compared with oxygen results in its rapid diffusion blood flow and gas exchange.
across the capillary membranes, and its easy removal.7 For a patient in an upright position, perfusion and
As a byproduct of cellular respiration, CO2 is produced ventilation vary as follows:
at a rate of 200 mL/min, with only minor differences • Zone 1 (upper area of the lungs): alveolar pressure
in normal concentrations in arterial (480 mL/L) and is generally greater than both arterial and venous
venous (520 mL/L) blood.13 capillary pressure [PA>Pa>Pv], and blood flow is
reduced, leading to alveolar dead space (alveoli
Relationship between ventilation ventilated but not adequately perfused).
and perfusion • Zone 2 (middle portion of the lungs): perfusion
Gas exchange is the key function of the lungs, and the and gas exchange are influenced more by pressure
unique anatomy of capillaries and alveoli facilitates this differences between arterial and alveolar pressures
process. However, because of a number of physiological than by the usual difference between arterial
factors, the ventilation to perfusion ratio (V/Q) is not and venous pressures [Pa>PA>Pv], with a normal
matched in a 1:1 relationship. As normal alveolar ventila- V/Q ratio.
tion is about 4 L/min and pulmonary capillary perfusion • Zone 3 (lung bases): alveolar pressure is lower than
is about 5 L/min, the normal V/Q is 0.8.11 In addition, both arterial and venous pressures [Pa>Pv>PA],
pressure in the pulmonary circulation is low relative to and ventilation is reduced, leading to intrapulmonary
systemic pressure, and is influenced much more by gravity shunting (alveoli perfused but not adequately
and hydrostatic pressure. In the upright position, lung ventilated)11 (see Figure 13.10).

FIGURE 13.10 The effects of gravity and alveolar pressure on pulmonary blood flow. Notice the three lung zones.26
(published with permission).

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Adapted from Seely R, Stephens T, Tate P. Anatomy and physiology. 7th ed. Boston: McGraw Hill; 2006, with permission.
412 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

These physiological relationships are more complex states including respiratory failure, pneumonia, acute respir-
in a critically ill patient when ventilation and/or lung atory distress syndrome, asthma and COPD are described
perfusion is further compromised by disease processes and in Chapter 14.
positive pressure ventilation, and the patient is in a supine
or semi-recumbent position.11 Hypoxaemia
Hypoxaemia describes a decrease in the PaO2 of less than
Acid–base control: respiratory 60 mmHg (7.8 kPa).7 This leads to less efficient anaerobic
mechanisms metabolism at the tissue and end-organ level, and compro-
mised cellular function. Hypoxia is abnormally low PO2
The respiratory system plays a vital role in acid–base
in the tissues, and can be due to:
balance. Changes in respiratory rate and depth can produce
changes in body pH by altering the amount of carbonic • ‘hypoxic’ hypoxia – low PaO2 in arterial blood due to
acid (H2CO3) in the blood. The body has substantial pulmonary disease
control over acid–base balance by altering alveolar venti- • ‘circulatory’ hypoxia – reduction of tissue blood flow
lation and the elimination of CO2 through the lungs. The due to shock or local obstruction
elimination of acid through the lungs is more than 100 • ‘anaemic’ hypoxia – reduced ability of the blood to
times more efficient than the elimination of acid through carry oxygen due to anaemia or carbon monoxide
the kidneys. If CO2 in body water increases due to low poisoning
alveolar ventilation, more H+ will be produced because
CO2 combines with H2O to form H2CO3. This breaks • ‘histotoxic’ hypoxia – a cellular environment that does
not support oxygen utilisation due to tissue poisoning
down to HCO3− and H+ resulting in a decrease in pH. (e.g. cyanide poisoning).11
CO2 + H2O ↔ H2CO3 ↔ HCO3− + H+ A hypoxic patient can show symptoms of fatigue and
shortness of breath if the hypoxia has developed gradually.
The strength of the dissociation is defined by the If the patient has severe hypoxia with rapid onset, they will
Henderson-Hasselbach equation, which describes the have ashen skin and blue discolouration (cyanosis) of the
relationship between HCO3−, CO2 and pH, and explains oral mucosa, lips and nail beds. Confusion, disorientation
why an increase in dissolved CO2 causes an increase in the and anxiety are other symptoms. In later stages, uncon-
acidity of the plasma, while an increase in HCO3− causes sciousness, coma and death occur.27
the pH to rise resulting in more alkaline plasma: Acute respiratory failure is a common patient presen-
tation in ICU that is characterised by decreased gas
(HCO3−) exchange with resultant hypoxaemia.28 Two different
pH = 6.1 + log
(CO2 ) mechanisms cause acute respiratory failure:Type I presents
with low PaO2 and normal PaCO2; Type II presents with
where 6.1 = the negative logarithm of the acid dissocia- low PaO2 and high PaCO23 (see Chapter 14 for further
tion constant in plasma for carbonic acid.11 discussion).
Respiratory acidosis is caused by CO2 retention and In general, impaired gas exchange results from alveolar
increases the denominator in the Henderson-Hasselbach hypoventilation, ventilation/perfusion mismatching and
equation resulting in a decreased pH level. In a spontan- intrapulmonary shunting, each resulting in hypoxaemia.
eously breathing patient, this condition occurs due to Hypercapnia may also be present depending on the
hypoventilation from either shallow breaths and/or a underlying pathophysiology.29
low respiratory rate. In the acute state the body cannot Alveolar hypoventilation occurs when the metabolic
compensate. If the patient develops chronic CO2 retention needs of the body are not met by the amount of oxygen
over a long period, there will be a renal response to the delivered and CO2 removed from the alveoli. Alveolar
increase in CO2.The renal system retains HCO3− to return hypoventilation causing hypoxaemia is usually extra-
the pH to normal (i.e. respiratory acidosis is compensated). pulmonary (e.g. altered metabolism, interruption to
Respiratory alkalosis occurs when a patient hyper- neuromuscular control of breathing/ventilation) and is
ventilates and alveolar ventilation is increased as a result associated with hypercapnia.3,29
of large, frequent breaths; CO2 decreases in arterial blood V/Q mismatch results when areas of lung that are
and the pH rises. If this condition is maintained (e.g. perfused are not ventilated (no participation in gas
walking at high altitude), the kidneys excrete HCO3− and exchange) because alveoli are collapsed or infiltrated with
the pH returns to normal (i.e. the respiratory alkalosis is fluid from inflammation or infection (e.g. pulmonary
compensated).11 oedema, pneumonia). This results in an overall reduction
in blood oxygen levels, which is usually countered by
Pathophysiology compensatory mechanisms.3
Intrapulmonary shunting is an extreme case of V/Q
Three common pathophysiological concepts that mismatch. Shunting occurs when blood passes alveoli
influence respiratory function in critically ill patients are that are not ventilated. If there is significant intrapul-
hypoxaemia, inflammation and oedema. Related disease monary shunting, there may be overwhelming reductions
 CHAPTER 13 RESPIRATORY ASSESSMENT AND MONITORING 413

Changes to the oxygen–haemoglobin dissociation

FIGURE 13.11 Ventilation perfusion mismatch.30 curve also occur in states related to hypoxia. The curve
shifts to the right when there is acidosis and/or raised
)URP levels of PaCO2 as commonly seen in respiratory failure.
SXOPRQDU\
DUWHU\
$LUZD\ ,PSDLUHG The shift in the oxygen–haemoglobin dissociation
YHQWLODWLRQ curve to the right means that, in the lung, fewer oxygen
$OYHROXV molecules attach to the haemoglobin molecule, resulting
in a decrease in arterial oxygen saturation. However, what
oxygen does attach to the haemoglobin molecule is more
$OYHRORFDSLOODU\ readily released at the tissue level.11
PHPEUDQH 7R +\SR[DHPLD
1RUPDO94 SXOPRQDU\YHLQ /RZ94
Compensatory mechanisms to
optimise oxygenation
,PSDLUHGSHUIXVLRQ
When PO2 in the alveoli is reduced, regional hypoxic
%ORFNHG
YHQWLDWLRQ pulmonary vasoconstriction occurs, with contraction of
&ROODSVHG
$OYHRODU smooth muscles in the small arterioles, directing blood
GHDGVSDFH flow away from the hypoxic area of the lung.11 Peripheral
DOYHRXV
chemoreceptors also detect hypoxaemia and initiate
compensatory mechanisms to optimise cellular oxygen
delivery. Initial responses are increased respiratory rate
and depth, resulting in increased minute ventilation, and
+\SR[DHPLD +\SR[DHPLD
raised heart rate with possible vasoconstriction as the
6KXQW YHU\ORZ 94 +LJK94
body attempts to maintain oxygen delivery and uptake.
This overall upregulation cannot be sustained indefinitely,
particularly in a person who is critically ill, and compensa-
in PaO2.30 CO2 levels may still be normal but, depending
tory mechanisms begin to fail with worsening hypoxaemia
on the onset and progression of respiratory pathophys-
and cellular and organ dysfunction. Unless the hypoxaemia
iology, compensatory mechanisms may not be able to
is reversed and/or respiratory and cardiovascular support is
maintain homeostasis3,13 (see Figure 13.11). provided, irreversible hypoxia and death will ensue.
Tissue hypoxia Inflammation
There are few physiological changes with mild hypoxaemia Inflammatory processes can occur at a local level (e.g. as
(when O2 saturation remains at 90% despite a PaO2 of a result of inhalation injuries, aspiration or respiratory
60 mmHg [8 kPa]), with only a slight impairment in mental infections) or are secondary to systemic events (e.g. sepsis,
state. If hypoxaemia deteriorates and the PaO2 drops to trauma). Damage to the pulmonary endothelium and
40–50 mmHg (5.3–6.7 kPa), severe tissue hypoxia ensues. type I alveolar cells appears to play a key role in the
Hypoxia at the central nervous system level manifests with inflammatory processes associated with acute respiratory
headaches and somnolence. Compensatory mechanisms distress syndrome (ARDS).32 Once triggered, inflamma-
include catecholamine release, and a decrease in renal tion results in platelet aggregation and complement release.
function results in sodium retention and proteinuria.31 Platelet aggregation attracts neutrophils, which release
Different tissues vary in their vulnerability to hypoxia, inflammatory mediators (e.g. proteolytic enzymes, oxygen
with the central nervous system and myocardium at most free radicals, leukotrienes, prostaglandins and platelet-
risk. Hypoxia in the cerebral cortex results in a loss of activating factor). Neutrophils also appear to play a key
function within 4–6 seconds, loss of consciousness in role in the perpetuation of ARDS.3 As well as altering
10–20 seconds and irreversible damage in 3–5 minutes. pulmonary capillary permeability, resulting in haemorrhage
In an environment that lacks oxygen, cells function by and leaking of fluid into the pulmonary interstitium and
anaerobic metabolism and produce much less energy. alveoli, mediators released by neutrophils and some macro-
For example, with aerobic metabolism 38 molecules of phages precipitate pulmonary vasoconstriction. Resulting
adenosine triphosphate are generated compared with pulmonary hypertension leads to diminished perfusion to
2 molecules of adenosine triphosphate generated in some lung areas, with dramatic alterations to both perfusion
anaerobic metabolism. During anaerobic metabolism, lactic and ventilation leading to significant V/Q mismatch, and
acid also increases.With less available energy, the efficiency the subsequent signs and symptoms typically seen in patients
of cellular functions such as the sodium–potassium pump, with pulmonary inflammation/oedema.
nerve conduction, enzyme activity and transmembrane
receptor function diminishes.31 The overall effect of inter- Oedema
ruption to these vital cellular activities is a reduction in Pulmonary oedema also alters gas exchange, and results
organ or tissue function, which in turn compromises from abnormal accumulation of extravascular fluid
system and body functions. in the lung. Two main reasons for this are an increase
414 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

in hydrostatic or osmotic forces, as seen in left ventricular in condition and the impact of treatment. Depending
dysfunction or volume overload, and increased membrane on a patient’s situation, assessment can be either brief
permeability of the lung epithelium or endothelium, or detailed.
allowing accumulation of fluid. This is referred to as
non-cardiogenic pulmonary oedema. ARDS may result Patient history
from increased permeability of the epithelium. A more History taking determines a patient’s baseline respir-
detailed discussion of ARDS is provided in Chapter 14. atory status on ICU admission. If the patient is distressed
only a few questions should be asked but, if the patient is
Changes to respiratory function able, a more comprehensive interview can be performed,
During the early exudative phase of ARDS, tachypnoea, focusing on four areas: the current problem, previous
signs of hypoxaemia (apprehension, restlessness) and an problems, symptoms and personal and family history.
increase in the use of accessory muscles are usually evident. Question a family member or close friend if a patient is
These symptoms result from infiltration of fluid into the unable to provide their own history.
alveoli.With impaired production of surfactant during the When introducing yourself, ask the patient’s name,
proliferative phase, respiratory function deteriorates, and seek eye contact and create a rapport with the patient
dyspnoea, agitation, fatigue and the emergence of fine and the family. Ensure that the patient is in a comfort-
crackles on auscultation are common.3,31 Airway resistance able position, ideally sitting up in bed. Provide privacy so
is increased when oedema affects larger airways. Lung that the interview is confidential. The physical examina-
compliance is reduced as interstitial oedema interferes tion should maintain the patient’s dignity and modesty. To
with the elastic properties of the lungs, and it may become minimise distress for a patient who is acutely breathless,
challenging to adequately ventilate patients. Infiltration the use of short closed questions is preferable.
of type II alveolar cells into the epithelium may lead to
interstitial fibrosis on healing,33 causing chronic lung Practice tip
dysfunction.
History taking by the nurse should be an interactive
Respiratory dysfunction: changes to experience, especially the initial interview where both
work of breathing the patient and nurse learn a lot about each other.
This knowledge has considerable influence on rapport
Without reversal of respiratory compromise, significant building between patient and nurse.
increases to the work of breathing will result. Clinical
manifestations include tachypnoea, tachycardia, dyspnoea,
low tidal volumes and diaphoresis. Hypercapnia ensues, Current respiratory problems
which further compromises respiratory muscle function Begin by asking why the patient is seeking care. If possible,
and precipitates diaphragmatic fatigue. Oxygen consump- let the patient describe the respiratory problem in his or
tion during breathing can be so great that reserve capacity her own words. Be focused and listen actively. Ask for
is reduced. If patients with pre-existing COPD (who may location, onset and duration of the respiratory symptoms.
breathe close to the fatigue work level) experience an
acute exacerbation, this can easily tip them into a fatigued Previous respiratory problems
state. Early identification and management of respir- Many respiratory disorders can be chronic and pulmonary
atory compromise before these stages improves patient diseases may recur (e.g. tuberculosis). New diseases can
outcomes.31 complicate existing ones.34 Problems with breathing and
chest problems, number of hospitalisations, treatments and
Assessment childhood respiratory diseases should be discussed with
the patient.
Respiratory insufficiency is a common reason for admission
to ICU, for either a potential or an actual problem, so Symptoms
comprehensive and frequent respiratory assessments are an Assess the onset and duration, pattern, severity and episodic
essential practice role. This section outlines history taking, or continuous nature of presenting symptoms. Also ask
physical examination, bedside monitoring and diagnostic about the patient’s perception of their respiratory problem,
testing focused on a critically ill patient with respiratory their opinion about its cause and, if the symptoms cause
dysfunction. fatigue, anxiety or stress. Ask specifically about dyspnoea,
Assessment is a systematic process comprising history cough, sputum production, haemoptysis, wheezing, chest
taking of a patient’s present and previous illnesses and pain or other pain, sleep disturbances and snoring.
physical examination of their thorax, lungs and related Dyspnoea (shortness of breath) is subjective and
systems. History taking and physical examination can therefore difficult to grade. The mechanism that underlies
occur simultaneously if the patient is very ill. Related the sensation of dyspnoea is poorly understood but it is
diagnostic findings inform an accurate and comprehensive extremely uncomfortable and frightening.34 Assess the
assessment. A thorough assessment, followed by accurate severity of dyspnoea by asking about breathing in relation
ongoing monitoring, enables early detection of changes to activities (e.g. breathlessness when dressing or walking
 CHAPTER 13 RESPIRATORY ASSESSMENT AND MONITORING 415

across a room).Ask the patient how many pillows they need children who are close to the patient, as innocuous viral
to sleep as this may indicate the severity of any orthopnoea infections in small children may account for severe disease
(shortness of breath when lying flat). Orthopnoea can be in adults.34 Also check for a family history of cancer and
a symptom of increased blood in the pulmonary circu- heart or respiratory diseases.
lation due to left ventricular failure, pulmonary oedema,
bronchitis, asthma or obstructive sleep apnoea. Physical examination
A cough can be dry or productive, episodic or The four activities of physical examination are
continuous and, if exacerbated when the patient is lying inspection, palpation, percussion and auscultation. Prior
flat, can imply heart failure. A cough can also be related to to commencing the examination, prepare the patient as
viral infections and allergies or may indicate intrathoracic well as possible by providing privacy, warmth, good light
disease. Ask the patient if they wake at night due to the and quiet surroundings. Explain that the examination is
cough, how long the cough has been present and if it is a standard procedure and you will use your eyes, hands
getting better or worse. and a stethoscope. Help the patient into a comfortable
Sputum production should be considered for amount, sitting position in the bed if possible and have all necessary
colour or the presence of blood. Yellow or green sputum equipment easily accessible.
is typical in bacterial infection. Haemoptysis or sputum
mixed with blood is a significant finding and can indicate Inspection
tuberculosis or lung cancer. Wheezing can indicate vocal Inspection involves carefully observing the patient from
cord disorder or asthma.34 head to toe for signs of respiratory problems. Focus on:
Chest pain can result from multiple causes; therefore patient position, chest wall inspection, respiratory rate and
appropriate assessment is essential. Chest pain that occurs rhythm, respiratory effort, central or peripheral cyanosis
during inspiration can be due to irritation or inflamma- and clubbing. Note what position appears preferable
tion of the pleural surface. Pleural pain is experienced for the patient; whether they look comfortable in bed,
mostly on one side of the chest, is knifelike in character have trouble breathing or appear anxious. Observe chest
and occurs in pneumonia, pleurisy and pneumothorax. wall symmetry during the respiratory cycle, anatomical
Chest pain also occurs with fractured ribs. structures and for the presence of scars.The most important
The most ominous chest pain occurs as a result of sign of respiratory distress is respiratory rate and rhythm.
myocardial ischaemia, due to poor oxygen delivery to the Count the rate for a 1-minute period. Normal respiratory
coronary vessels. This pain is termed angina pectoris and rate for adults is 12–15 per minute.7 Abnormal breathing
can arise from chronic stable angina or acute coronary patterns are noted in Table 13.1. Observe respiratory effort,
syndrome34 (see Chapter 10 for further discussion). in particular the use of accessory muscles, abdominal
Sleep disturbance and snoring may be related to obstructive muscles, nasal flaring, body position and mouth-breathing.
sleep apnoea. If the patient complains about drowsiness in Inspect the lips, tongue and sublingual area for central
the daytime, ask how many hours of continuous sleep they cyanosis (a late sign of hypoxia that is almost impossible to
have at night, and whether they take a nap during the day. detect in a patient with anaemia).3 Observe the extrem-
ities for oedema (can be a sign of heart failure), fingers
Personal and family history and toes for peripheral cyanosis and clubbing of the nail
Family history and environment can influence pulmonary beds. Peripheral cyanosis may indicate low blood flow to
presentations. The focus of this questioning is on: tobacco peripheral areas. Clubbing of finger or toe nail beds can
use, allergies, recent travel, occupational risk, home situation be idiopathic or more commonly due to respiratory or
and family history. Use of tobacco, current or past, is circulatory diseases (e.g. chronic hypoxia in congenital
important in evaluating pulmonary symptoms. Ask the heart disease).23,34
patient to quantify the amount of cigarette packs per week Note also if the patient requires oxygen and record
and how many years they have smoked. The majority of the dose. If the patient is intubated and mechanically
smokers have reduced lung function. Tobacco smoking is ventilated (monitoring is explained later in this chapter),
responsible for 80–90% of the risk of developing COPD but ensure the airway is adequately secured. If the patient is
only 10–15% of these patients will develop clinically signif- orally intubated, observe the mouth for the presence of
icant symptoms.35 Exposure to secondhand smoke may lesions or pressure on the oral mucosa and lips; and observe
also be of interest, with evidence that extended exposure the size of the tube, the length at the lips or teeth margin
is a major cause of chronic bronchitis.36 A history of recent and how it is secured. If the patient has a tracheostomy,
travel increases possible exposure to infectious respiratory observe the stoma for signs of infection or pressure areas,
diseases.37 Recent long flights increase the possibility of the type and size of tracheostomy tube, the length at the
deep venous thrombosis, which can lead to pulmonary hub if it is a tracheostomy with an adjustable flange and
embolism.38 An occupation with exposure to allergens and the manner of securement.
toxins is important to document as this can be associated
with declining lung function.39 Ask about the patient’s Palpation
home situation and whether they live with someone Palpate the patient’s chest with warm hands, focusing
with an illness such as influenza or tuberculosis. Ask about on: areas of tenderness, tracheal position, presence of
416 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 13.1
Description of different respiration patterns23

Normal Air trapping

Regular and comfortable at a rate of
12–20 per minute Increasing difficulty in getting breath out

Bradypnea Slower than 12 breaths per minute Cheyne-Stokes

Varying periods of increasing depth
interspersed with apnea

Tachypnea Kussmaul
Faster than 20 breaths per minute
Rapid, deep, labored

Hyperventilation
Biot Irregularly interspersed periods of apnea
(hyperpnea)
Faster than 20 breaths per minute, deep in a disorganised sequence of breaths
breathing

Sighing Ataxic
Significant disorganisation with irregular
Frequently interspersed deeper breath and varying depths of respiration

Adapted from: Morton P, Rempfer K. Patient assessment: respiratory system. In: Morton P, Fontaine D (eds). Critical care nursing:
A holistic approach. 9th ed. Philadelphia: Wolters, Kluwer/Lippincott Williams & Wilkins; 2009.

subcutaneous emphysema and tactile fremitus. Assess Palpation is also used to assess for tactile (vocal)
for symmetry (left compared to right) and follow a fremitus, a normal palpable vibration. Place your hands
systematic sequence of palpation over anterior and on the patient’s chest and ask them to vocalise repeatedly
posterior surfaces (see Figure 13.12). Check the thorax the term ‘ninety-nine’. Fremitus is decreased (that is,
for areas of tenderness or bony deformities and note impaired transmission of sounds) in pleural effusion and
symmetry of chest movement during breathing. Use pneumothorax. Fremitus is increased over regions of lung
the palm of your hand to assess skin temperature, where transmission is increased (e.g. pneumonia, consoli-
noting clammy, hot or cold skin. To test for chest wall dation).34 In mechanically ventilated patients, fremitus can
symmetry on inspiration, place both hands with thumbs be detected when there are secretions in the airways.
together on the patient’s posterior thorax and ask them
to take a deep breath. Your thumbs should separate Percussion
equally 3–5 cm during normal deep inspiration1 (see By tapping the chest with the bony structures of the hands,
Figure 13.13). Asymmetry can occur in pneumothorax, percussion can help to determine if the lung spaces are
pneumonia or other lung disorders where inspiration filled with air, fluid or sputum consolidation. Place your
is affected. non-dominant hand with your middle finger extended
Palpation of the tracheal position is useful to detect over the area of chest to be examined. Using the middle
a mediastinal shift; deviation of the trachea from midline finger of your dominant hand, tap on the distal knuckle of
may indicate a pulmonary problem such as large pneu- the finger resting on the chest wall. Starting from the upper
mothorax or previous pneumonectomy.41 The presence of chest wall and moving from side to side, following the same
subcutaneous emphysema indicates air in the subcutan- sequence as for auscultation (see Figure 13.12), compare
eous tissue and feels like crackling under your fingers due one side to the other for variation in sound. Normally, the
to air pockets in the tissue.42 It most commonly occurs in chest has a resonant percussion tone. A flat percussive note,
the face, neck and chest after blunt or penetrating trauma soft and high-pitched, may indicate a large pleural effusion.
to the chest (e.g. stabbing, gun shot, fractured ribs); facial A dull percussive note with medium intensity and pitch
fractures; tracheostomy; respiratory tract surgery; and in is heard in the presence of atelectasis, pulmonary oedema,
patients who are mechanically ventilated. pulmonary haemorrhage or pneumonia.23
 CHAPTER 13 RESPIRATORY ASSESSMENT AND MONITORING 417

FIGURE 13.12 Sequence of systematic movements for auscultation, percussion and palpation of the anterior and
posterior chest. Comparison of the right and left sides of the chest should be performed by moving from side to side,
beginning proximally and moving distally down the chest wall.40

Adapted from Weber J, Kelly J. Health assessment in nursing. Philadelphia: Lippincott, Williams & Wilkins; 2010, with permission.

FIGURE 13.13 Assessment of thoracic expansion. A Exhalation. B Inhalation.4 (Published with permission.)

$ %
418 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Identify and become familiar with normal breath

Practice tip sounds before beginning to listen and identify abnormal
When performing palpation or percussion of the chest breath sounds. Abnormal breath sounds are either
with your hand and auscultation of the chest with a continuous or discontinuous. Continuous sounds include
stethoscope, the patient will appreciate the hand and wheezes and rhonchi, while discontinuous sounds include
stethoscope being warmed prior to placing them on
crackles (see Table 13.3). Stridor is an abnormal, loud,
the skin
high-pitched breath sound caused by obstruction in the
upper airways as a result of a foreign body, tissue or vocal
cord swelling; this emergent condition requires immediate
Practice tip attention.43 Absent or diminished breath sounds also
require immediate treatment, indicating no airflow
When performing chest inspection, percussion and through that area of the lung.34,44
auscultation, always compare one side of the body with
the other. Practice tip

Respiratory rate is an early warning sign for respiratory

Auscultation
distress. If the patient has a high respiratory rate it
Careful interpretation of breath sounds and integration can be a sign of hypoxia as the patient attempts to
of this assessment data with other findings can provide compensate for low PaO2.
important information about lung disorders. Use the
diaphragm of the stethoscope and ensure full contact with
the skin for optimal listening. For a spontaneously breathing Documentation and charting
patient, ask them to breathe through their mouth (nose Document the findings of your respiratory assessment in
breathing may alter the pitch of the breath sounds). Auscul- the patient’s chart; if this is the first respiratory assessment,
tation is performed in a systematic way so as to compare describe the patient’s respiratory history carefully. Any
the symmetry of breath sounds (see Figure 13.12). Normal abnormal findings including abnormal sounds and their
breath sounds reflect air movement through the bronchi, characteristics should be described to enable subsequent
and sounds change as air moves from larger to smaller re-assessment.43
airways. Sounds also change when air passes though fluid or
narrowed airways. Breath sounds therefore differ depending Respiratory monitoring
on the area auscultated. The three types of normal breath
A thorough and comprehensive assessment, with accurate
sounds are bronchial, bronchovesicular and vesicular breath ongoing monitoring, enables early detection of changes
sounds (see Table 13.2), and these should be heard only in and assessment of responses to treatment for the critically
the areas specific to their region. ill. This section describes the main aspects of bedside
respiratory monitoring and the instruments used to assess
TABLE 13.2 the efficiency of a patient’s gas transfer mechanisms,
Characteristics of normal breath sounds including pulse oximetry, capnography, airway pressures
and ventilator waveforms and loops.
SOUND CHARACTERISTICS

Vesicular Heard over most of the lung field; low

Pulse oximetry
pitch; soft and short exhalation and Pulse oximetry is a non-invasive device that measures the
long inhalation oxygen saturation of haemoglobin in a patient’s arterial
Bronchovesicular Heard over main bronchus area and
blood. The technology is common in critical and acute
over upper right posterior lung field; care areas. It is important to note that the device does
medium pitch; exhalation equals not provide information on the patient’s ventilatory
inhalation state, but may determine oxygen saturation and detect
hypoxaemia.45 This prompt, non-invasive detection of
Bronchial Heard only over trachea; high pitch;
hypoxaemia enables detection of clinical deterioration and
loud and long exhalation
more rapid treatment to avoid associated complications.46
Adapted from: Urden L, Stacey K, Lough M. Critical care Pulse oximetry works by emitting two wavelengths of
nursing: Diagnosis and management. 6th ed. St Louis: light, red and infrared, that pass through a pulsatile flow
Mosby; 2010. Table 22.2. of blood from a diode (positioned on one side of the probe)
to a photodetector (positioned on the opposite side). The
signal emitted is measured over five pulses, causing a
Practice tip slight delay when monitoring. Oxygenated blood absorbs
Use an alcohol wipe to clean the earpieces on the
light differently from deoxygenated blood; the oximeter
stethoscope prior to use to protect yourself from
measures the amount of light absorbed by the vascular bed
infection.
and calculates the percentage of haemoglobin saturation
in the capillaries.
 CHAPTER 13 RESPIRATORY ASSESSMENT AND MONITORING 419

Table 13.3 FIGURE 13.14 Common pulse oximetry waveforms.

Description of abnormal breath sounds

ABNORMAL
SOUND DESCRIPTION CONDITION

Absent breath No airflow to Pneumothorax

sounds particular portion Pneumonectomy
of lung Emphysematous blebs NORMAL SIGNAL
Pleural effusion
Lung mass
Massive atelectasis
Complete airway
obstruction
Diminished Little airflow to Emphysema
breath sounds particular portion Pleural effusion MOTION ARTEFACT
of lung Pleurisy
Atelectasis
Pulmonary fibrosis
Displaced Bronchial Atelectasis with
bronchial sounds heard in secretions
sounds peripheral lung Lung mass with LOW PERFUSION
fields exudates
Pneumonia
Pleural effusion
Practice tip
Pulmonary oedema
Crackles (rales) Short, discrete Pulmonary oedema In cool environments, wrap the hand or foot that has the
popping or Pneumonia sensor attached. This may improve saturation readings.
crackling sounds Pulmonary fibrosis
Atelectasis It is important to understand that pulse oximetry
Bronchiectasis
measures the saturation of haemoglobin as an estimate of
Rhonchi Coarse, rumbling, Pneumonia peripheral arterial oxygen saturation (SpO2). SpO2 differs
low-pitched Asthma from PaO2. SaO2 and PaO2 are physiologically related
sounds Bronchitis and this relationship is illustrated by the two axes of the
Bronchospasm
oxygen–haemoglobin dissociation curve (see Figure 13.9,
Wheezes High-pitched, Asthma and the previous physiology section for more discussion). A
squeaking, Bronchospasm fit healthy adult with a normal haemoglobin level breathing
whistling sounds room air would usually have an SpO2 of 97–99%.47
Pleural friction Creaking, Pleural effusion
rub leathery, loud, Pleurisy Practice tip
dry, coarse
sounds Try to place the pulse oximeter on the finger of the
Adapted from: Urden L, Stacey K, Lough M. Critical care
opposite arm to where blood pressure is taken,
nursing: Diagnosis and management. 6th ed. St Louis: particularly if you have no arterial line and are doing
Mosby; 2010, Table 22.3. frequent non-invasive BPs.

Indirect measurement of arterial oxygen saturation

Limitations of pulse oximetry
via the peripheral circulation using pulse oximetry is • Pulse oximetry in isolation does not provide all
referred to as SpO2 (the symbol ‘p’ denotes peripheral) the necessary information to evaluate oxygenation,
and is displayed digitally on the monitor as a percentage, ventilation status or acid–base balance. ABG testing is
along with heart rate and a plethysmographic waveform. required to assess other parameters.48
Interpreting this waveform is essential in distinguishing a • Pulse oximetery readings are reasonably reliable
true oximetry signal from one displaying dampening or when the SaO2 is 90% or above; accuracy deteriorates
artefact (see Figure 13.14).The probe is commonly placed when the SaO2 falls to 80% or less.46 When low SpO2
on a finger, but can also be placed on the toe, earlobe readings occur and you are confident that the device
or forehead. Change the probe position frequently to is not influenced by artefact, formal ABG analysis
maintain adequate perfusion of the site and skin integrity.45 should be conducted.
420 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

• Satisfactory arterial perfusion of the monitored tissue • Injection of intravenous dyes may lead to a false
is required; low cardiac output states, vasoconstriction, underestimation of SpO2 for up to 20 minutes after
peripheral vascular disease and hypothermia can their administration (methylene blue, indocyanine
cause inaccurate pulse signals and falsely low oxygen green, indigo carmine).46
saturation readings. In such cases, confirm oxygen
saturation with intermittent ABG testing. Practice tip
• Cardiac arrhythmias can impair perfusion and flow,
Correlate the heart rate reading displayed in the pulse
and so signal quality may be compromised (see
Figure 13.14). In these cases, moving the probe to oximetry section of the monitor to the heart rate
another location, such as the earlobe or forehead, can calculated by the ECG. If they don’t correlate, this may
improve signal quality. indicate that not all pulsations are being detected and
the pulse oximetry reading may not be accurate.
• Motion artefact (see Figure 13.14), caused by patient
movement or shivering, is a significant cause of
erroneously low readings and false alarms.49 Keeping the Practice tip
patient warm (if not contraindicated) and encouraging
them to minimise movement may limit this problem. Patients with COPD who are hypoxic (SpO2 <88%)
Using an ear probe may also reduce motion artefact. should receive supplemental oxygen. The SpO2 targets
• There is conflicting evidence as to whether nail varnish for patients with COPD are lower with SpO2 generally
or acrylic nails interfere with SpO2 readings.49 Blue, maintained at >92% during an exacerbation if the patient
green and black nail varnishes are the most likely to is at risk of hypercapnia. It is important to frequently
affect SpO2 accuracy. Placing the sensor probe sideways assess these patients receiving oxygen so that any
on the finger may avoid this effect. To ensure accuracy, compromise in breathing is noted and acted upon.
it is recommended that nail varnish and acrylic nails be
removed if possible. Newer technology pulse oximeters Capnography
are less susceptible to these limitations.46
Capnography, using infrared spectrometry, monitors
• As skin pigmentation allows a constant level of expired CO2 during the respiratory cycle and is referred
absorption, and pulse oximetry relies on the change to as end-tidal CO2 (PetCO2). The percentage of exhaled
in absorbance throughout the cardiac cycle,50 CO2 at end-expiration is displayed on the monitor.
theoretically darker skin should not affect the A waveform, called a capnogram3 is also produced (see
performance of the device. However, dark skin has Figure 13.15). Continuous capnography detects subtle
been linked to falsely elevated SpO2 values, especially changes in patients’ lung dynamics (i.e. changes to phys-
saturation levels below 80%.46 iological shunting or alveolar recruitment) and can be
• External light, especially fluorescent light and heat measured in both intubated and non-intubated patients.
lamps, can lead to an over- or underestimation of
SpO2.48 Covering the probe with an opaque barrier,
such as a washcloth, can prevent this problem. FIGURE 13.15 Normal capnogram. (A) End inspiration;
(B) expiratory upstroke; (C) expiratory plateau; (D) end-
• Dyshaemoglobins, particularly carboxyhaemoglobin and
tidal carbon dioxide tension (PetCO2).
methaemoglobin, render SpO2 monitoring unreliable.46
The pulse oximetry sensor cannot differentiate
between oxyhaemoglobin, carboxyhaemoglobin
and methaemoglobin, and therefore provides a false
estimation of oxygen saturation.48 An example of '
high levels of non-functioning haemoglobin is that of 
&
carbon monoxide poisoning; high carboxyhaemoglobin
3&2 PP+J

levels give a falsely high SpO2 reading, leading to an

overestimation of oxygenation.51
• In the presence of anaemia it is possible to have good
 %
oxygen saturation of available haemoglobin but poor
tissue oxygenation due to a deficiency in the ability
of the blood to transport oxygen. In anaemia, the
pulse oximetry readings may be accurate, but it is
the clinician’s interpretation of these readings that $
is important. If we are looking at SpO2 as a marker 
of oxygenation, a reduced amount of functioning
haemoglobin may be well saturated with oxygen but is
a poor reflection of tissue oxygenation.51 Correction of 7LPH ([SLUDWLRQ,QVSLUDWLRQ
anaemia is required to improve tissue oxygenation.
 CHAPTER 13 RESPIRATORY ASSESSMENT AND MONITORING 421

It can be used to estimate PaCO2 levels in patients with a and their response to treatment: ABG analysis; blood
normal ventilation–perfusion ratio (usually 1–5 mmHg less testing; and sputum and tracheal aspirates.
than PaCO2). Levels are, however, affected by conditions
common in the critically ill (e.g. low cardiac output states, Arterial blood gases
elevated alveolar pressures, sepsis, hypo/hyperthermia, ABGs are one of the most commonly performed laboratory
pulmonary embolism), so use PetCO2 to estimate PaCO2 tests in critical care.Therefore, accurate ABG interpretation
levels in these patients with caution.50 Investigate any is an important clinical skill. ABG measurements enable
sudden changes in PetCO2 levels with ABG analysis. rapid assessment of oxygenation and ventilation, and all
Despite this limitation, PetCO2 monitoring has many ICUs are recommended to have a blood gas analyser as a
uses in the critical care unit: minimum standard.55
Blood for ABG analysis is sampled by arterial puncture
• indicating correct endotracheal tube (ETT) or, more commonly in critically ill patients, from an arterial
placement while awaiting CXR, assessing tube
patency and detecting leaks or disconnection of the catheter usually sited in the radial or femoral artery. Both
circuit techniques are invasive and only allow for intermittent
analysis.The advantage of the arterial catheter is that it facil-
• monitoring ventilation status during and after itates ABG sampling without repeated arterial punctures.
weaning from mechanical ventilation
Continuous blood gas monitoring is possible using an
• assessing the effectiveness of cardiopulmonary in-line fibre optic sensor as part of the arterial line, but this
resuscitation compressions and detecting return of practice is yet to have wide application in Australasia due
spontaneous circulation to cost and accuracy concerns.56 Questions also remain
• monitoring ventilation continuously during sedation regarding the possibility for arteriovenous shunting, blood
and anaesthesia loss and infection risk with continuous systems.57
• assessing ventilation/perfusion status.52,53 Sampling technique
A correct sampling technique is essential for accurate results.
Practice tip
Prior to arterial sampling from the radial artery, a modified
Allen’s test should be performed.The patient should clench
The capnography monitoring line can fill with con-
their fist tightly. Occlusive pressure is then applied to both
densation, particularly if the patient has a humidified
the ulnar and radial arteries, to obstruct blood flow to the
ventilator circuit. Regularly check for this and drain
hand. While maintaining this pressure, ask the patient to
or replace the line as necessary. Condensation can
relax their hand, and check whether the palm and fingers
interfere with the reading.
have blanched. Then release the occlusive pressure on the
Capnography is recommended as a standard ulnar artery only. The modified Allen’s test is positive if the
component of respiratory monitoring in mechani- hand flushes within 5–15 seconds, indicating that the ulnar
cally ventilated patients in the ICU, during transport of artery has good blood flow and radial sampling is safe.58
critically ill patients and during anaesthesia.54 Approximately 1 mL of arterial blood is collected
anaerobically and aseptically using a premixed syringe
Ventilation monitoring containing dry heparin. If drawing the sample from
an intra-arterial line, a portion of blood is discarded to
Mechanical ventilation is a common intervention for prevent dilution and contamination of the sample from
patients who require respiratory support in the ICU. the saline in the flush line. The discard amount is twice
Advances in ventilation technology have enhanced our the dead space volume to ensure clinically accurate ABG
ability to monitor many ventilator parameters. A detailed and electrolyte measurement, and to prevent unneces-
understanding of mechanical ventilation principles and sary blood loss.59 Dead space is defined as the priming
functions enables patient data to be interpreted accurately volume from the sampling port to the catheter tip; this
and managed appropriately. Chapter 15 provides a detailed differs depending on the arterial line set-up used. Arterial
discussion of mechanical ventilation, including ventila- blood exerts its own pressure, which is sufficient to fill the
tion monitoring; airway pressures (peak airway pressure, syringe to the required level; active negative pressure is to
plateau pressure and positive end-expiratory pressure); and be avoided, as this causes frothing. Any excess air will cause
waveforms and loop displays. inaccurate readings and is expelled before the syringe is
capped with a hub, preventing further air contamination.
Bedside and laboratory The sample is analysed within 10 minutes if not packed in
ice, or within 60 minutes if iced; delays cause degradation
investigations of the sample. Degradation also occurs if the sample is
Bedside and laboratory investigations add to available shaken; therefore gently roll the syringe/collection tube
information about a patient’s respiratory status and assist in between your fingers to mix the sample with the heparin
diagnosis and treatment. This section focuses on common and prevent clotting.60 The frequency of ABG sampling
investigations used to assess a patient’s respiratory status should be carefully considered and based on patient
422 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

need. ABG sampling may lead to losses of up to 70 mL

per day and the cumulative effect may worsen anaemia TABLE 13.5
and increase the need for transfusion. This is particularly Steps for arterial blood gas interpretation
important in the paediatric population.59
STEP I N T E R P R E TAT I O N

Arterial blood gas analysis 1 Assess oxygenation ... PaO2 <60 mmHg
ABG analysis includes measurement of the PaO2, the (<8 kPa) indicates hypoxaemia
PaCO2, the H+ concentration (pH) and the concen- 2 Assess the pH level ... <7.35 indicates
tration of chemical buffer, HCO3−. Normal values for acidosis, >7.45 indicates alkalosis
ABG parameters are listed in Table 13.4. Use a systematic 3 Assess PaCO2 level ... <35 mmHg (<4.7 kPa)
approach when interpreting the results of ABG analysis indicates respiratory acidosis; >45 mmHg
(see Table 13.5). (>6.0 kPa) indicates respiratory alkalosis
Assessing oxygenation: when assessing oxygenation, 4 Assess HCO3− level ... <22 indicates metabolic
hypoxaemia (PaO2 <60 mmHg or <7.8 kilopascals or kPa) acidosis; >32 indicates metabolic alkalosis
will be the most common abnormality and may indicate
5 Assess pH, CO2 and HCO3−. Is there an acid–
the need for supplemental oxygen to maintain adequate
base disturbance and is it fully compensated,
arterial oxygenation. Conversely, hyperoxia rarely occurs partially compensated or uncompensated?
unless a patient is receiving supplemental oxygen therapy.
Oxygen can be toxic to cells if delivered at high concen- 6 Assess other ABG results. Are they within
normal limits for the patient?
trations for a prolonged period.61
Assessing the pH: the body’s acid–base balance is
affected by both the respiratory and metabolic systems61
and is evaluated by measuring the pH of arterial blood. form carbonic acid (H2CO3), so can alter the pH of blood.
On the pH scale of 1 to 14 (where 1 = the strongest acid Retention of CO2 through hypoventilation or air trapping
and 14 = the strongest alkali), a pH of 7.4 is the middle leads to increased H+ ions resulting in a lower pH and
of the normal range. Acidaemia is present with a pH of development of respiratory acidosis. Alternatively, a loss
<7.35; alkalaemia is present with a pH of >7.45. The pH of CO2 through hyperventilation results in a higher pH
changes depending on the amount of H+ or HCO3− in and development of respiratory alkalosis.62 A PaCO2
the blood with H+ reflecting the acidic component and of >45 mmHg (6 kPa) indicates alveolar hypoventila-
HCO3− the base or buffer. tion, due to COPD, asthma, pulmonary oedema, airway
Assessing for respiratory mechanisms: PaCO2 obstruction, over-sedation, narcosis, drug overdose,
indicates the effectiveness of ventilation and rises when pain, neurological deficit or permissive hypercapnia in
ventilation is suboptimal. CO2 combines with water to mechanically ventilated patients.63 Conversely, a PaCO2 of

TABLE 13.4
Arterial blood gas normal values*

BLOOD GAS MEASUREMENT DESCRIPTION N O R M A L VA L U E

Temperature (T) Patient’s body temperature. Analyser defaults to 37°C if not 37°C
entered
Haemoglobin (Hb) Samples should be fully mixed so should be constantly agitated Females: 115–165 g/L
until analysed Males: 130–180 g/L
Acid–base status (pH) Overall acidity or alkalinity of blood 7.35–7.45
(36–44 nmol/L)
Carbon dioxide (CO2) Partial pressure of arterial CO2. A potential acid 35–45 mmHg
(4.7–6.0 kPa)
Oxygen (O2) Partial pressure of O2. Varies with age 80–100 mmHg
(10.7–13.3 kPa)
Bicarbonate (HCO3−) Standardised HCO3− (actual HCO3− minus the HCO3− produced 22–26 mmol/L
by respiratory dysfunction) estimates true metabolic function.
An alkali or base
Base excess (BE) Measures acid–base balance. The number of molecules of acid or −3 to +3 mmol/L
base required to return 1 L of blood to the normal pH (7.4)
Oxygen saturation (SaO2) Haemoglobin saturation by oxygen in arterial blood 94.5–98.2%

*Institutional norms may vary slightly.

 CHAPTER 13 RESPIRATORY ASSESSMENT AND MONITORING 423

<35 mmHg (4.7kPa) reflects alveolar hyperventilation, The degree of compensation depends on whether the pH
and can be due to hypoxia, pain, anxiety, pregnancy, returns to normal; full compensation results in a normal pH
permissive hypocapnia in mechanically ventilated patients whereas, in partial compensation, the pH remains outside
or as a compensatory mechanism for metabolic acidosis.63 normal limits. In an uncompensated acid–base imbalance,
Assessing for renal mechanisms: HCO3− is there has been no attempt by the body to correct the acid–
regulated by the renal system. A [HCO3−] of <22 mmol/L base imbalance and the pH, as well as either the CO2 or
can lead to metabolic acidosis, caused by renal failure, HCO3−, is abnormal.
ketoacidosis, lactic acidosis, diarrhoea or cardiac arrest. A To assess compensation, pH, CO2 and HCO3− are
HCO3− of >26 can lead to metabolic alkalosis, caused by examined in the context of a patient’s clinical presentation:
severe vomiting, continuous nasogastric suction, diuretics,
corticosteroids or excessive citrate administration from • In a fully compensated state, the pH is returned to
stored blood or renal replacement therapy.63 within normal limits, but the other two parameters will
Base excess is an additional value included in the ABG be outside normal limits as the body has successfully
report and it reflects the excess (or deficit) of base to acid in manipulated CO2 and HCO3− levels to restore the pH.
the blood. Normal base excess ranges from −2 to +2. If the • In a partially compensated state, the pH is not within
base excess (BE) is +2 mmol/L, removal of 2 mmol of base normal limits, and the other parameters will also be
per litre of blood is required to return the pH to 7.4. If the outside of normal limits but not enough to bring the
BE is −2 mmol/L (i.e. a base deficit), 2 mmol of base per pH back to normal.
litre of blood needs to be added to achieve a pH of 7.4.A BE
greater than +3 indicates that there is more base than acid
• In a non-compensated state, the pH will be outside
normal limits, and the primary disruption (either CO2
present and therefore alkalosis.A BE below −3 indicates that or HCO3−) will also be outside normal limits while
there is more acid than base. Understanding this concept is the remaining parameter has not compensated for this
useful as it can determine how much treatment is necessary derangement and has stayed within normal limits.
to restore a patient’s pH to normal.62,64,65
Assessing for compensation: the final step of inter- It can be difficult to differentiate the patient’s primary
pretation is to examine the pH, CO2 and HCO3− levels problem from their compensatory response. As a quick
collectively, to determine if the patient has either fully or guide, if the CO2 is moving in the opposite direction to pH,
partially compensated the primary dysfunction, or is in an then the primary disruption is respiratory; if the HCO3−
uncompensated state.With the respiratory system regulating is moving in the same direction as pH, the disruption is
CO2 and the metabolic system regulating HCO3−, resto- metabolic.65 Table 13.6 provides a guide to ABG findings
ration of normal acid–base balance and homeostasis is for each acid–base disorder. Other parameters measured
possible.62 The ability of the body to achieve homeostasis on the ABG sample, such as lactate, electrolytes, haemo-
and acid–base balance depends on the ability of the respira- globin and glucose, are also considered in determining
tory and renal systems to adjust to the underlying imbalance. patient status.

TABLE 13.6
Arterial blood gas findings for acid–base disturbances

PH P a C O 2 , M M H G ( K PA ) H C O 3− , M M O L / L
R E S P I R AT O RY A C I D O S I S
Uncompensated <7.35 >45 (6.0) Within normal limits
Partially compensated <7.35 >45 (6.0) >26
Fully compensated Within normal limits >45 (6.0) >26
R E S P I R AT O RY A L K A L O S I S
Uncompensated >7.45 <35 (4.7) Within normal limits
Partially compensated >7.45 <35 (4.7) <22
Fully compensated Within normal limits <35 (4.7) <22
M E TA B O L I C A C I D O S I S
Uncompensated <7.35 Within normal limits <22
Partially compensated <7.35 <35 (4.7) <22
Fully compensated Within normal limits <35 (4.7) <22
M E TA B O L I C A L K A L O S I S
Uncompensated >7.45 Within normal limits >26
Partially compensated >7.45 >45 (6.0) >26
Fully compensated Within normal limits >45 (6.0) >26
424 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

The Stewart approach (<13.3 kPa) indicates severe ARDS. For example, in
a patient receiving a FiO2 of 0.65 who has a PaO2 of
As an adjunct to traditional ABG interpretation, Peter
90 mmHg (12 kPa), their PaO2/FiO2 ratio would be
Stewart’s seminal concepts on acid–base assessment66
138.5 mmHg, indicating a moderate ARDS state. A
suggest that, in our body’s fluids, pH and HCO3− are merely
diagnosis of ARDS also requires the above reductions in
dependent variables that cannot be directly manipulated.
PaO2/FiO2 ratio to be present with the patient receiving
Stewart was particularly interested in considering the at least 5 cmH2O of positive end-expiratory pressure or
influence of resuscitation fluid management on acid–base continuous positive airway pressure. It requires this state
balance. He developed six equations to assist clinicians to to have developed within 1 week of a known clinical
analyse the physiological basis of acid–base shifts, consid- insult or worsening respiratory symptoms. A chest X-ray
ering the impacts of strong cations, the total concentration (CXR) should show bilateral opacities not fully explained
of weak acids and CO2.67 Stewart’s intention was not to by other causes and respiratory failure not fully explained
replace traditional methods of determining acid–base by cardiac failure or fluid overload.72
balance, but to extend their usefulness and to further
explain the physiological basis of complex disorders.67 An Transcutaneous blood gas monitoring
example of the utility of Stewart’s work is evident in a A transcutaneous monitor provides an estimate of the
recent study of 300 patients with abdominal sepsis. This PaO2 and PaCO2 by measuring these partial pressures
report demonstrated that a modification of the Stewart at the skin surface. This form of monitoring is useful
approach was able to identify mixed acid–base disorders where arterial access is not obtainable, or there is a need
which would otherwise remain undetected.68 to monitor continuous readings of oxygen and CO2 with
Stewart’s complex equations have been made more minimal drawing of blood. Transcutaneous monitoring is
user-friendly with the development of online calculators69 most appropriate to obtain continuous trend data; its use
where the clinician can enter patient chemistry data online for intermittent readings is not appropriate.73 Transcutan-
to receive an online decision support related to complex eous monitoring is a common approach with neonates
acid/base disorders (see Online resources). Once patient because neonatal skin is particularly thin;74 however, it
data are entered, the site offers clinicians a breakup of the may also prove useful for adult monitoring. Possible uses
relative contributions to the overall disturbance in pH by include evaluation of hypoventilation during management
its main controlling elements. When displayed graphically, and weaning of mechanical ventilation, during bronch-
this gives the user a sense of the severity of each contrib- oscopy or other procedures requiring sedation, during
uting factor, and allows input of these individual factors sleep studies or pulmonary function studies, apnoea testing
into virtual scenarios to predict the possible impact of or titration of long-term oxygen therapy and to monitor
specific interventions.67 tissue perfusion and revascularisation at the site of a wound.
It is also useful to monitor a patient’s response to therapy
Oxygen tension-derived indices in diabetic ketoacidosis as transcutaneous measurement of
The alveolar–arterial gradient is a marker of intrapul- CO2 closely correlates with serum HCO3− levels.73
monary shunting (i.e. blood flowing past collapsed areas Transcutaneous monitoring devices increase the local
of alveoli not involved in gas exchange). The index is skin temperature at the sensor site resulting in increased
calculated as PAO2 − PaO2 (where PAO2 is the partial local capillary perfusion. This increases the metabolic rate
pressure of oxygen in the alveoli). PAO2 is determined by of the skin and the solubility of CO2, which in turn leads
a complex equation, the alveolar gas equation. PAO2 and to local production of CO2. A temperature correction
PaO2 are equal when perfusion and ventilation are perfectly then addresses the heightened local CO2 production that
matched. The gradient increases with age but a value of results from heating the skin.75
5–15 mmHg is normal up until approximately middle The partial pressure of transcutaneous oxygen
age. Despite questions about its clinical usefulness, partic- (PtcO2) is measured using a Clark polarographic heated
ularly in the critically ill,70 it is used in clinical practice as electrode.74 The skin probe temperature needs to be
a trending tool to track intrapulmonary shunting. Simply 44°C to achieve an accurate PtcO2 and this may lead to
put, the larger the gradient between PAO2 and PaO2, the thermal injury, particularly if the skin is thin or damaged.
larger the degree of intrapulmonary shunting.71 Because of this risk, the site for transcutaneous electrodes
The ratio of PaO2 to fraction of inspired oxygen (FiO2), should be observed and alternated every 4–6 hours75 and
commonly referred to as the PaO2/ FiO2 (or P/F) ratio, as often as every 2 hours in small, premature neonates.
was introduced as a simple way of estimating pulmonary PtcO2 is an indirect measure of PaO2 that is not reflective
shunting, even though it does not formally measure of oxygen content or delivery and requires a knowledge
alveolar partial pressure. A recent consensus paper outlines and consideration of both haemoglobin saturation and
criteria known as the Berlin Definition72 to define stages of cardiac output.73
ARDS. According to this definition, a PaO2/FiO2 ratio The partial pressure of transcutaneous CO2 (PtcCO2) is
of 200–300 mmHg (≤39.9 kPa) indicates mild ARDS, a usually measured using a Severinghaus electrode. PtcCO2
ratio of 100–200 mmHg (≤26.6 kPa) indicates moderate is much less reliant on a higher skin temperature. Accuracy
ARDS while a ratio of less than or equal to 100 mmHg may be achieved with skin probe temperatures as low as
 CHAPTER 13 RESPIRATORY ASSESSMENT AND MONITORING 425

37°C making longer probe dwell times possible. Although

PtcCO2 is an indirect measure of PaCO2, it remains a Practice tip
useful assessment of ventilation.73 When comparing transcutaneous and arterial partial
Skin preparation is important for accurate readings and pressures of carbon dioxide, PtCO2 is typically higher
should include removal of soaps, oils and dead skin cells. than PaCO2. An acceptable range of agreement
To secure the electrode, a sensor fixation ring should be between arterial and transcutaneous measures is
placed in a highly vascularised location. In neonates and ± 7 mmHg.
small children the upper chest is an ideal location. Alterna-
tive sites include the ear lobe, cheeks, forehead or over the
zygomatic bone, the inner aspect of the thigh or forearm, Blood tests
the buttock or the lateral aspect of the abdomen.73 Once Haematology and biochemistry investigations should
the fixation device is secured, 1–2 drops of either normal inform treatment for patients with respiratory dysfunction.
saline or contact gel is placed inside the fixation ring to Full blood count, including a leukocyte differential count,
improve the diffusion of gases and, in turn, maximise the can monitor white cell activity for patients with a confirmed
accuracy of the sensor. The sensor then snaps into place. or suspected infective process. When infections are severe,
A good seal should be sought between the sensor and the full blood count will show a dramatic rise in the number
fixation device as leaks or the formation of air bubbles can of immature neutrophils. Blood cultures can also assist in
affect the accuracy of transcutaneous readings.73 diagnosis of bacterial or yeast infections and isolation of the
A number of conditions should be documented in causative organism.Viral studies may aid diagnosis for respi-
relation to transcutaneous monitoring results including ratory infections of unknown origin. Where pulmonary
the respiratory rate, the patient’s position and level of embolism is suspected, a D-dimer test can assist diagnosis of
activity; the fraction of inspired oxygen and the oxygen a thrombus. Routine measurement of urea and electrolytes
delivery device including ventilator mode and settings; the can track renal function and acid–base status.76
site, temperature and time of electrode placement; and the
clinical appearance of the patient and the results of simul- Practice tip
taneous ABGs, specifically PaO2, PaCO2 and pH.73
Monitoring lactate levels is important as the levels can
Limitations of transcutaneous be used to assess the effectiveness and efficiency of
monitoring resuscitative therapies. A persistently elevated lactate
Following electrode placement 5–10 minutes should level is associated with higher morbidity and poorer
be allowed before taking transcutaneous readings. Poor patient outcomes.
calibration, trapped air or leaks in the fixation device
or damage to the membranes can result in inaccurate Sputum, tracheal aspirates and
readings. Generally speaking, PtcO2 underestimates PaO2 nasopharyngeal aspirates
while PtCO2 overestimates PaCO2. In addition, falsely
elevated or diminished readings may occur due to: Colour, consistency and volume of sputum provide useful
information in determining changes in a patient’s respir-
• high arterial oxygen levels (PaO2 >100 mmHg, atory status and progress. Regular cultures of tracheal
13.3 kPa) (overestimates PtcO2) sputum reveal colonisation by opportunistic organisms,
• hypoperfusion (as in shock or acidosis) or vasoactive and can identify the cause of an acute chest infection
drug use (underestimates PtcO2 and PtcCO2); the use or sepsis. Many ICUs have routine (weekly or twice-
of more contemporary transcutaneous devices and weekly) surveillance monitoring of tracheal aspirates in
placement of the sensor close to the carotid artery long-term mechanically ventilated patients. In spontan-
may limit this effect eously breathing patients, sputum specimens can be
• thickened or oedematous skin or subcutaneous tissue collected in a sterile specimen receptacle. Specimens are
(underestimates PtcO2 and PtcCO2) best collected early in the morning and teeth cleaning
prior to sample collection may reduce secondary contam-
• poor skin preparation or poor electrode fixation ination. In intubated patients, using a sputum trap between
(underestimates PtcO2 and PtcCO2)
the suction catheter and suction tubing assists sputum
• distal placement of the electrode in the presence of collection. A sterile technique should be maintained to
vasoconstriction (underestimates PtcO2 and PtcCO2)
reduce sample contamination.77
• active or passive patient movement causing increased If obtaining an adequate sputum specimen in
capillary blood flow (overestimates PtcO2 and non-intubated patients is difficult, there is evidence that
PtcCO2). administration of nebulised saline (isotonic or hypertonic)
Transcutaneous oxygen and CO2 readings should may assist sputum collection.78 There is no evidence to
be validated by comparing them with simultaneous support this among mechanically ventilated patients but,
ABG results at baseline measurement and periodically anecdotally, nebulised normal saline may assist sputum
thereafter.73 production by moistening the airways and thinning
426 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

secretions. Physiotherapy79 in the form of manual hyper- tests and bronchoscopy to determine the cause and
inflation and head-down tilt during therapy has been shown severity of the illness episode, relevant comorbidities and
to increase sputum production for sample collection.80,81 the patient’s response to treatment.
Instilling normal saline in an ETT to facilitate clearance
and/or collection of tenacious sputum remains a contro- Medical imaging
versial issue.There is no evidence that instillation facilitates A range of imaging techniques may be available for
secretion clearance, while there is some evidence that it supporting care of a critically ill patient with a respiratory
increases both patient discomfort and the risk of bacterial dysfunction, depending on the level of broader health
contamination of the lower airway.Therefore, this practice service resources available. This sub-section describes
is not recommended.82 X-ray, ultrasound, computerised tomography, magnetic
Nasopharyngeal aspirate or swabs may be necessary resonance imaging and ventilation/perfusion scan
to diagnose viral respiratory infections. The nasopharyn- techniques.
geal aspirate is collected by inserting a fine, sterile suction
catheter (8 or 10 F) attached to a sputum trap through Chest X-ray
the nare and back to the nasopharynx. Suction is applied Chest radiography is a common diagnostic tool used for
while withdrawing and slowly rotating the catheter. The respiratory examination of critically ill patients. CXR
catheter is flushed through to the sputum trap with sterile allows basic information regarding abnormalities in the
normal saline or transport medium if available. A nasopha- chest to be obtained relatively quickly.The image provides
ryngeal swab is collected by inserting a specially designed information about lung fields and other thoracic structures
swab to the back of the nasopharynx and rotating for 5–10 as well as the placement of invasive lines and tubes.84,85 In
seconds. The swab is then withdrawn slowly and placed the ventilated patient, serial CXRs also enable sequential
in the plastic vial containing transport medium. As close assessment of lung status in relation to therapy.85
contact with the patient is necessary, and the procedure In-unit X-rays of patients using portable equipment
can generate aerosols and droplets, personal protective are inferior to those taken using a fixed camera in the
equipment should be worn.83 radiology department. Patient preparation is therefore
important to optimise the quality of the film. Patients
should ideally be positioned sitting or semi-erect; CXRs
Diagnostic procedures using a supine position are less effective at revealing
Assessment and monitoring of the respiratory status of a gravity-related abnormalities such as haemothorax.
critically ill patient may rely on various medical imaging Lateral view CXRs may assist identification of lesions in

FIGURE 13.16 Chest X-ray, PA view.

Trachea

Scapula Clavicle

Vertebrae

Aortic arch

Right main
bronchus Carina

Right hilum Left main

bronchus

Lung Left hilum

Rib Heart
Diaphragm
Gastric air
Costophrenic bubble
angle

Liver Stomach

Published with permission, University of Auckland Faculty of Medical and Health Sciences.
 CHAPTER 13 RESPIRATORY ASSESSMENT AND MONITORING 427

TABLE 13.7
Guide to normal chest X-ray interpretation84

Technical issues • Check X-ray belongs to correct patient; note date and time of film
• Ensure you are viewing X-ray correctly (i.e. right and left markings correspond to thoracic structures)
• Determine whether X-ray was taken supine or erect, and whether PA or AP
• Check X-ray was taken at full inspiration (posterior aspects of 9th/10th ribs and anterior aspects of
5th/6th ribs should be visible above diaphragm)
• Note the penetration of the film: dark films are overpenetrated and may require a strong light to view; white
films are underpenetrated; good penetration will allow visualisation of the vertebrae behind the heart
Bones • Check along each rib from vertebral origin, looking for fractures
• Ensure clavicles and scapulas are intact
Mediastinum • Check for presence of trachea and identify carina (approximately level of 5th–6th vertebrae)
• Check width of mediastinum: should not be more than 8 cm
Apex • Ensure blood vessels are visible in both apices, particularly looking to rule out pneumothoraces that present
as clear black shading on the X-ray. Erect X-rays are essential to facilitate visibility of pneumothoraces
Hilum • Check for prominence of vessels in this region: it generally indicates vascular abnormalities such as
pulmonary oedema or pulmonary hypertension, or congestive heart failure
Heart • Cardiac silhouette should be not more than 50% of the diameter of the thorax, with {1/3} of heart
shadow to the right of the vertebrae and {2/3} of shadow to the left of the vertebrae; this positioning
helps to rule out a tension pneumothorax. It should be noted that, post-cardiac surgery, if the
mediastinum is left open the heart may appear wider than this; also in AP films this may be the case due
to the plate being further away from the heart
Lung • Identify the lobes of the lungs and determine if infiltrate or collapse is present in one or more of them.
Lobes are approximately located as follows:
—left upper lobe occupies upper half of lung
—left lower lobe occupies lower half of lung
—right lower lobe occupies costophrenic portion of lung
—right middle lobe occupies cardiophrenic portion of lung
—right upper lobe occupies upper portion of lung
Diaphragm • Check levels of diaphragm: right diaphragm will normally be 1–2 cm above the left diaphragm to
accommodate the liver
Gastric Check for pneumoperitoneum and dilated loops of bowel
Catheters and lines • Identify distal end of endotracheal tube and ensure above the carina (i.e. not in the right main bronchus)
• Trace nasogastric tube along length and ensure tip is in stomach, or below stomach if nasoenteric tube
• Check position of intra-aortic balloon pump and ensure it is in the descending thoracic aorta
• Trace all central catheters and ensure distal tip is in correct location
• Identify other lines (e.g. intercostal catheters, pacing wires) and note location

PA = posteroanterior; AP = anteroposterior.
Adapted from: Lareau C, Wootton J. The “frequently” normal chest x-ray. Can J Rural Med 2004;9(3):183–6.

the thorax. Film plate location against the patient’s thorax CXR interpretation follows a systematic process
determines the view: for posteroanterior (PA) the plate is designed to identify common pathophysiological processes
positioned against the anterior thorax (see Figure 13.16) and the locations of lines and other items. Table 13.7
while the anteroposterior (AP) view has the plate against provides a comprehensive guideline for viewing and inter-
the patient’s back. For mobile CXRs, the AP view is used. preting a CXR.
The AP view can magnify thoracic structures and can be Common abnormalities that can be detected by CXR
less distinct or even distorted, so interpret findings with include:
caution, particularly if comparing them with previous PA
images.86 • Lobar collapse or atelectasis: loss of lung volume,
displacement of fissures and vascular markings
and/or diaphragmatic elevation on the affected
Practice tip side.
When preparing your patient for a CXR, minimise • Pneumothorax: lack of pulmonary vascular markings
the number of monitoring leads and unnecessary on the affected side so the lung field appears black.
equipment in the CXR field to optimise the image. There will be mediastinal and possible tracheal shift
away from the affected side in tension pneumothorax.
428 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

• Pleural effusion: in the dependent areas of the pleural requirements and maintenance of infusions during
spaces, costophrenic angles are blunted by fluid and scanning. Portable CT scanners are available in some
there may be a mediastinal shift away from a large centres, and may reduce the risks associated with trans-
effusion. Effusions are best visualised with the patient portation of critically ill patients to fixed CT scanners.94
upright, and will only be evident on an AP image See Chapter 6 for discussion of in-hospital transfers, and
with 200–400 mL of fluid in the pleural space. Chapter 23 for inter-hospital transport.
• Pulmonary oedema: lung fields, particularly central
Magnetic resonance imaging
and perihilar areas, appear white. Kerley B lines (small
horizontal lines <2 cm long) may be present in the Magnetic resonance imaging (MRI) uses radiofrequency
lung periphery near the costophrenic angles. waves and a strong magnetic field rather than X-rays to
provide high contrast, detailed pictures of internal organs
• Pulmonary embolism: although not the optimal
and soft tissues that are clearer than those generated by
diagnostic tool, areas of infarction may be visualised
X-ray or CT scans. The strong magnetic field around
on CXR and may be mistaken for collapse or
the scanner means that ferromagnetic objects containing
consolidation.
material that can be attracted by magnets, such as iron
• Pneumoperitonium: free air under the diaphragm or steel, can become potentially fatal projectiles. MRI
elevates the diaphragm.86,87 scans may therefore be unsuitable for some patients.
American95 and European guidelines96 discourage the
Ultrasound use of MRI where permanent pacemakers and implant-
Ultrasound imaging (sonography) is a useful bedside able defibrillators are in situ; however, recent research
diagnostic tool for a select group of critically ill patients88 suggests MRIs may be safe for many of these patients.97,98
and can add to the diagnostic information provided by Some types of neurostimulation devices99 and intra-
CXR and computerised tomography (CT) scanning. cranial aneurysm clips100 have been designed for safe
Ultrasound uses high-frequency sound waves which, use in MRI but careful screening should precede MRI
when probed on the body, reflect and scatter. The to determine patient and device-specific risks. Dental
advantages are that the procedure can take place within fillings, braces and retainers are usually safe but may
the ICU, and it is radiation-free. Ultrasound is most useful distort images of the face or brain.101 MRI in people
for patients with fluid in the pleural space (i.e. pleural with such devices should be used where the potential
effusion, haemothorax or empyema), and provides more benefit clearly outweighs the risks. The strong magnetic
detailed diagnostic information than CXR alone.89 fields also have the potential to interfere with ventilators,
Ultrasound allows an estimate of the volume and exact infusion pumps and monitoring equipment.102
location of the fluid present and reduces the potential for
serious complications during aspiration of fluid or chest Ventilation/perfusion scan
tube insertion.90 A V/Q scan is indicated when a mismatch of lung venti-
lation and perfusion is suspected, most commonly for
Computed tomography pulmonary embolism. The ventilation scan is performed
CT is a diagnostic investigation that provides greater with the patient inhaling a radioisotopic gas, while the
specificity in chest anatomy and pathophysiology than a perfusion scan is performed using an intravenous radio-
plain CXR, using multiple beams in a circle around the isotope that reveals the distribution of blood flow in the
body. These beams are directed to a specific body area pulmonary vessels.103 These two scans are then compared,
and provide detailed, consecutive cross-sectional slices seeking mismatches between perfusion and ventilation.
of the scanned regions. CT scans can be performed with In larger centres, the V/Q scan has been superseded
or without intravenous contrast.91 Contrast improves by the CT pulmonary angiogram for detection of
diagnostic precision but is used with caution in patients pulmonary embolism.
with renal impairment; renal failure may preclude a
patient from receiving contrast. CT scanning is useful Bronchoscopy
in the detection and diagnosis of pulmonary, pleural and Bronchoscopy is a bedside technique used for both
mediastinal disorders (e.g. pleural effusion, empyema, diagnostic and therapeutic purposes. The bronchoscope
haemothorax, atelectasis, pneumonia, ARDS).92 CT can be either rigid or flexible, with the flexible fibre
pulmonary angiography produces a detailed view of blood optic bronchoscope most widely used in critical care. A
vessels and is therefore the most definitive method for flexible fibre optic bronchoscope allows direct visualisa-
diagnosing pulmonary embolism.93 tion of respiratory mucosa and thorough examination of
A significant limitation of CT scanning is that the patient the upper airways and tracheobronchial tree. The scope
is transported away from the ICU. Transport increases the is passed into the trachea via the oropharynx or nares. In
risks for critically ill patients and usually requires at least mechanically ventilated patients, the scope can be passed
two appropriately trained staff to accompany the patient. quickly and easily down the ETT or tracheostomy tube
Detailed planning by the healthcare team (including using a specially adapted valve that allows passage of the
imaging staff) includes ventilator support, monitoring scope without disconnection of mechanical ventilation.104
 CHAPTER 13 RESPIRATORY ASSESSMENT AND MONITORING 429

During bronchoscopy, supplemental oxygen can be arrhythmia, pneumothorax and pneumonia occur
administered in non-intubated patients and FiO2 can rarely.106 Patient preparation may include CXR; haemo-
be increased in intubated patients. Accurate continuous globin and coagulation profile, particularly if a biopsy is to
monitoring during the procedure includes continuous be performed; baseline ABGs; and fasting or cessation of
pulse oximetry, electrocardiography, respiratory rate, feeds for 4–6 hours prior.
heart rate and blood pressure. Equipment for advanced Diagnostic indications for bronchoscopy include
airway management, suctioning, cardiac defibrillation further investigation of poor gas exchange; evaluation
and advanced life support medications is immediately of haemoptysis; collection of specimens (e.g. broncho-
available.105 In intubated patients, one person is responsible alveolar lavage, bronchial washings, bronchial brushings,
for security of the airway to reduce the risk of displace- lung biopsy); diagnosis of infection, interstitial lung
ment during the procedure. disease, rejection post lung transplantation, malignancy;
When performed by an experienced operator, fibre and diagnosis of airway injury due to burns, aspiration
optic bronchoscopy is a relatively safe procedure in critically or chest trauma. Therapeutic indications include removal
ill patients. In mechanically ventilated patients, the correct of mucous plugs; removal of foreign bodies; treatment
diameter of bronchoscope relative to the endotracheal of atelectasis; assistance during tracheostomy; airway
tube diameter is important to avoid decreases in tidal and dilation and stenting for tracheobronchomalacia and
minute volumes,104 decreased PaO2 and increased PaCO2. tracheobronchial stenosis; and lung volume reduction for
Serious complications such as bleeding, bronchospasm, emphysema.107,108

Summary
In this chapter a comprehensive overview of assessment and monitoring of a patient with respiratory dysfunction to
aid clinical decision making is provided. Acute respiratory dysfunction is a major cause for admission to a critical care
unit. Whether due to a primary or secondary condition, compromise of the respiratory system can be a life-threatening
situation. This chapter outlines related respiratory physiology, pathophysiology, assessment and respiratory monitoring,
bedside laboratory investigations and medical imaging:
• Critical care nurses are in a prime position to provide systematic and dynamic bedside assessments of a patient’s
respiratory status including past and presenting respiratory history, and physical examination of the thorax and lungs
using inspection, palpation and auscultation techniques.
• Monitoring a patient’s respiratory function includes pulse oximetry and capnography. Bedside and laboratory
investigations including ABG analysis, blood tests and sputum and tracheal aspirates add to available information
and assists in both diagnosis and treatment. ABG testing is common and ABG interpretation is an important
clinical skill for critical care nurses.
• CXR is the most common diagnostic imaging tool in the ICU. CXR interpretation follows a systematic process to
identify common pathologies and to locate lines and other items. Bronchoscopy is a useful bedside diagnostic and
therapeutic device. CT provides greater specificity than CXR. Ultrasound imaging is useful to diagnose fluid in the
pleural space. MRI and V/Q scans are more sophisticated diagnostic tools.
Careful patient assessment is essential, as respiratory dysfunction can be immediately life-threatening. Contempo-
rary critical care practice involves comprehensive clinical assessment skills and use of a range of monitoring devices
and diagnostic procedures. This challenges critical care nurses to be adaptable and willing to embrace new skills
and knowledge.

Case study
Presenting history: Max is a 63-year-old man who presented to the emergency department with a
3–4 week history of shortness of breath and a dry cough, worsening over the past week. Max weighs
122 kg and has a body mass index of 42.
Past medical history: Max had atrial fibrillation, obstructive sleep apnoea and hypertension and was an
ex-smoker of 25 packet-years.
Medications: warfarin, digoxin, diltiazem and atenolol.
Social history: Max works as a taxi driver, lives at home with his wife and walks independently.
430 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

ON ADMISSION
Inspection: on arrival to the emergency department Max was speaking in short sentences. Respiratory
rate was 32 breaths per minute, temperature 38°C and SpO2 74% on room air. Max appeared to have an
increased respiratory effort. It was difficult to assess his use of accessory muscles of respiration due to
excess adipose tissue. He reported no chest pain.
Palpation: Max’s apex beat was 92 beats per minute and irregular and BP was 107/79 mmHg. The nurse
noted grade II bilateral pedal oedema with chronic skin changes. His peripheries were warm and pink and
capillary refill time less than 2 seconds. Vocal fremitus was difficult to determine and chest wall expansion
slightly diminished on the right side.
Percussion: there appeared to be dullness over the bases; however percussion was difficult to assess due
to excessive adipose tissue.
Auscultation: bilateral bronchial breath sounds over the bases and a mild expiratory wheeze.
Initial management: non-invasive ventilation, serial electrocardiograms (ECGs) and cardiac enzymes were
ordered. Bilevel positive airway pressure was commenced. Medical staff documented a target SpO2 range
of 88–92%.
Other assessment findings: ECG showed atrial fibrillation, rate 94 beats per minute. With no prior ECG
for comparison, the poor R wave progression in the precordial leads and non-specific T wave changes
in the context of raised cardiac enzymes suggested the possibility of a non-ST-elevation acute coronary
syndrome. High sensitivity troponin-T was elevated at 22 ng/mL. An echocardiogram showed mild left
ventricular hypertrophy with normal left ventricular ejection fraction. Right ventricular pressure was slightly
elevated. The white cell count was 4.00 (× 109 L).
Arterial blood gases: PaO2 = 67 mmHg (8.9 kPa), pH = 7.44, PaCO2 = 44 mmHg (5.9 kPa), BE= 5, SaO2 =
93%. The pH and PaCO2 are in the upper range of normal and the BE is abnormally high indicating a mixed
disorder that needs monitoring and consideration within the patient’s broader clinical picture.
Chest X-ray: bilateral fluffy interstitial opacities were noted, though they were more evident on the right
side. Costophrenic angles were visible indicating there was no effusion.
Assessment plan: sputum culture, urine specimen for pneumococcal antigens, a nasopharyngeal swab for
respiratory viruses, serial ECG and troponins, hourly urine measure and daily weight.
Management plan: Max had multifactorial Type 1 respiratory failure, including community-acquired
pneumonia and a likely component of congestive cardiac failure. IV antibiotics azithromycin and cefotaxime,
IV magnesium sulfate, IV hydrocortisone and nebulised salbutamol were prescribed and a respiratory
and ICU consult were organised. Max was transferred to the high dependency unit. IV Lasix 40 mg
daily, a 1500-mL fluid restriction and regular salbutamol via metered-dose inhaler with spacer were
prescribed.

DAY 1
Inspection: Max became drowsy. He was able to follow simple commands but was irritable when roused.
His respiratory rate was 28–38 breaths per minute and an increased work of breathing was noted despite
increasing non-invasive ventilation support.
Vital signs: temperature 39.2°C, atrial fibrillation rate 128 bpm and BP 134/69 mmHg.
Palpation: grade II pitting oedema to mid calves. Calf compressors applied.
Auscultation: loud bi-basal crackles, widespread wheeze and reduced air entry.
Management plan: Max was considered at high risk for further deterioration and was predicted to have a
difficult airway to manage under those circumstances. He was transferred to ICU.
On admission to ICU: ABG results were PaO2 58 mmHg (7.7 kPa), pH 7.33, PaCO2 68 mmHg (9 kPa) and
BE 7.8, indicating hypoxia and a partially compensated respiratory acidosis. Max’s doctor explained the
situation and received Max’s verbal consent for endotracheal intubation.

ONGOING PROGRESS
Max managed well on pressure support ventilation. He was repositioned regularly, including in a high sitting
position. He received frequent physiotherapy. His peripheral oedema reduced. Over time, nurses were
 CHAPTER 13 RESPIRATORY ASSESSMENT AND MONITORING 431

able to reduce Max’s FiO2. His PaO2 and PaCO2 began to normalise. After 4 days, Max was extubated and, after a further
week on the ward, he returned home. Follow-up was arranged with respiratory and cardiology doctors and a dietician and
arrangements were made for home continuous positive airway pressure therapy at night.

DISCUSSION POINTS
• Obesity increases the prevalence of respiratory failure and augments the risk of conditions such as obstructive sleep
apnoea, pulmonary embolism and pulmonary hypertension. Impaired lung mechanics in obese patients can facilitate the
development of pneumonia and, when mechanically ventilated, they have reduced respiratory compliance.109,110
• The reverse Trendelenburg position can improve oxygenation and functional residual capacity.109
• Vocal fremitus is easier to feel over a thin chest wall. The vibrations produced in vocal fremitus are dampened in patients
who are obese or heavily muscled.111 Breath sounds are diminished in obese patients, losing strength as they travel
through adipose tissue.112

CASE STUDY QUESTIONS

1 If a nurse anticipated Max might have areas of pulmonary consolidation, what changes would he/she expect to feel with
vocal fremitus and hear using percussion compared to normal areas of lung?
2 What indicates partially compensated respiratory acidosis in Max’s final ICU ABG prior to intubation? (PaO2 58 mmHg
[7.7 kPa], pH 7.33, PaCO2 68.3 mmHg [9.1 kPa], BE 7.8)
3 Consider the challenges that Max’s high BMI creates for respiratory assessment and the mechanics of breathing while
nursed in bed.

RESEARCH VIGNETTE

Lavelle C, Dowling M. The factors which influence nurses when weaning patients from mechanical ventilation:
findings from a qualitative study. Intensive Crit Care Nurs 2011;27:244–52

Abstract
The aim of the study was to describe the factors that influence critical care nurses when deciding to wean patients
from mechanical ventilation. The study adopted a qualitative methodology, using semi-structured interviews and a
vignette. An invited sample of critical care nurses (n = 24) from one Irish intensive care unit was employed. Each nurse
was interviewed once and a vignette was used to structure the interview questioning. The findings were analysed using
thematic content analysis. Six major themes influencing nurses’ decision to wean emerged: physiological influences;
clinical reassessment and decision making; the nurse’s experience, confidence and education; the patient’s medical
history and current ventilation; the intensive care working environment; and use of protocols. The findings highlight
the complex nature of weaning patients from mechanical ventilation and the major role of the nurse in this process.

Critique
This study is relevant to the area of respiratory assessment and monitoring because it explores the way critical care
nurses apply their assessment and monitoring skills to inform their decisions on weaning patients from mechanical
ventilation.

The authors situate the relevance of this work in the acknowledged role of critical care nurses in the weaning
process and the complexity of the process, despite the use of protocols. The role of nurses in weaning decisions
is described as evolving from the domain of the intensivist, extending through the addition of what were previously
seen as medical tasks and expanding through the growth of nursing knowledge. The critical nature of readiness
for weaning and its commencement as soon as appropriate is justified through discussion of the complications
associated with mechanical ventilation. These include increased mortality from ventilator-associated lung injury and
ventilator-associated pneumonia, along with an increased need for sedation and neuromuscular blockade. Weaning
that is undertaken too soon is discussed in terms of fatigue of respiratory muscles and cardiovascular instability.
The authors cite previous studies that demonstrate nurse involvement in weaning can improve patient care and
432 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

reduce weaning times. They note that, while in many countries nurses have a high level of autonomy and decision
making and may also work collaboratively with medical colleagues on the decision to extubate, there are variations
internationally in the nature and processes of nurse involvement. They draw attention, in particular, to the USA where
ventilation management is the role of respiratory therapists.
The authors used the Critical Appraisal Skills Programme (CASP) criteria for qualitative research appraisal, a useful tool
for considering methodological rigour, particularly in non-traditional qualitative methodologies. The aim and significance
of this study were clearly stated: to explore and describe the involvement of nurses in decisions relating to weaning from
mechanical ventilation in Ireland. The rationale was the lack of previous research on this topic in the Irish context and
it was inferred that previous work in the UK using a similar approach was limited by its small sample of seven nurses.
The chosen method was a qualitative design that employed use of a patient case vignette. This approach was
selected because it can provide insight into how participants might behave in a situation that could be difficult to
observe in real life and so reduced the need for lengthy interviews or questionnaires. A three-step model to enhance
the internal validity was utilised. This included grounding the vignette on the literature from case histories and weaning
from mechanical ventilation, review and modification of the vignette by an expert panel made up of senior medical
and nurse clinicians and pilot testing of the vignette with intensive care nurses.
The research setting, including the number of beds, typical APACHE 11 score and typical duration of ventilation, was
explained. The study was undertaken in a single setting. This reduces the transferability of the findings as it is difficult
to determine which findings might be attributed to the essential experiences of nurses working in critical care units
in Ireland and which are determined by the local workplace culture. Qualitative research frequently uses purposive
sampling that seeks the participants who can best illuminate the study question, rather than using probability
methods more often seen in positivist studies. These researchers have employed a more objective approach to
sampling; 57 possible participants were stratified into three levels of years of experience, and participants were
randomly chosen by a person who was not involved in the research drawing names from a hat. This method may
have been appropriately chosen to reduce the potential selection bias as at least one of the researchers knew and
worked with the participants. The relationship with participants was not discussed in detail other than to say one of
the researchers was a colleague of the participants and not working in a managerial role. It was not clear how this
relationship was managed to reduce coercion or reduce the influence on the answers given by participants. The
stratification of participants according to level of experience strengthened the research design and responses were
examined for relationship to the years of experience.
Twenty-five nurses were subsequently invited to participate in the research and all agreed. The authors note that one
participant had to withdraw for health reasons. They report the number of participants that were female, their level
of experience in other intensive care units and experience with weaning but do not comment on how these sample
characteristics compare with critical care nurses generally. Addressing this could help to inform the transferability of
the results.
The authors did not examine their own role in the research setting and the potential for bias or influence. There was
no reflexive statement about their personal motivations or opinions on the phenomenon under study. There was no
statement as to how previous working relationships might influence or be subsequently altered by the study.
The 24 semi-structured interviews were audiotaped and transcribed verbatim. The analytical method of Burnard’s
content analysis was described in detail and seemed appropriate to the study question and aims. To increase
the external validity, an independent expert nurse was brought in to independently recode the data to check for
similarities in theme choice. Member checking is sometimes used by qualitative researchers to allow participants
the opportunity to challenge the researcher’s perceptions or to confirm the accuracy of their preliminary results.
Although member checking is often viewed critically by interpretative qualitative researchers because of the nature
of interpretative analysis that co-creates meaning between researcher and participant, in descriptive methods such
as content analysis it is viewed as an important component of rigour. Member checking was used in this study, with
three of the participants asked to identify main points from their own transcribed interviews with the intention of
comparing these to the eventual themes and categories from the research analysis. Beyond noting that, due to the
complexity of vignette and the weaning process, there were no right or wrong answers in this member checking, it
was not made clear how the process influenced the researchers’ final analysis or decision making.
 CHAPTER 13 RESPIRATORY ASSESSMENT AND MONITORING 433

While a solid number of participants had been recruited and the sample appeared reasonably homogeneous, the
issue of data saturation was not discussed. It was therefore unclear how well developed these reported themes
were within the participant interviews. This can sometimes be addressed by noting how many of the participants
experienced this theme under discussion or how many participants were required to experience the main themes
before interviewing would be stopped.

The results are important as they highlight the way nurses synthesise their respiratory assessment findings into a
general clinical picture. They note the importance of an assessment of oxygenation and oxygen requirements to
the nurses’ understanding of readiness for weaning. Key aspects of continuous reassessment were ABGs, markers
of respiratory distress, changes in cardiovascular status and ‘the patient’. These were incorporated into decision
making and were mediated by the nurses’ experience and confidence. Findings are discussed and confirmed in
relation to contemporary literature. The value of the research is that it suggests weaning protocols are useful for junior
nurses, whereas senior nurses are more likely to use a more complex synthesis of respiratory assessment and clinical
judgement to inform their weaning decisions. In conclusion, this is a well-conducted qualitative study that used the
novel approach of a patient vignette to describe the factors that influence critical care nurses when deciding to wean
patients from mechanical ventilation. International readers should consider their local ICU culture and the level of
training and autonomy of their ICU nurses in relation to ventilation decisions when considering the transferability
of these findings.

Lear ning a c t iv it ie s
1 Describe what coarse crackles and wheezes sound like and the pathophysiological mechanisms that may lead
to reduced air entry when these abnormal sounds are heard.
2 Outline the correct sampling technique for drawing an ABG from an arterial line.
3 Define Type 1 and Type 2 respiratory failure.

Online resources
Acidbase.org, www.acidbase.org
American Association for Respiratory Care, www.aarc.org
ARDS Network, www.ardsnet.org
Asian Pacific Society of Respirology, www.apsresp.org
Australian & New Zealand Society of Respiratory Science, www.anzsrs.org.au
Australian Lung Foundation, www.lungnet.org.au
Basic Lung Sounds Tutorial, http://solutions.3m.com/wps/portal/3M/en_EU/3M-Littmann-EMEA/stethoscope/littmann-
learning-institute/heart-lung-sounds/lung-sounds/#rhonchi-low-pitched
Become an expert in spirometry, www.spirxpert.com
Capnography: a comprehensive educational website, www.capnography.com
Chest X-rays, www.learningradiology.com
Critical Care Medicine Tutorials, www.ccmtutorials.com
European Respiratory Journal, erj.ersjournals.com
Lung Health Promotion Centre, The Alfred Hospital, Victoria, www.lunghealth.org
Respiratory Care online, www.rcjournal.com
Respiratory Research, http://respiratory-research.com
Thoracic Society of Australia and New Zealand, www.thoracic.org.au
Thorax: An International Journal of Respiratory Medicine, http://thorax.bmj.com
World Health Organization, www.who.int/en
434 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Further reading
Abdo WF, Heunks LMA. Oxygen-induced hypercapnia in COPD: myths and facts. Crit Care 2012:16:323.
Dempsey JA, Smith CA. Pathophysiology of human ventilator control. Eur Respir J 2014;44:495–512.
Higginson R, Jones B. Respiratory assessment in critically ill patients: airway and breathing. Br J of Nurs 2009;18(8):458–61.
Jacono FJ. Control of ventilation in COPD and lung injury. Respir Physiol Neurobiol 2013;189:371–6.
Robinson TD, Freiberg DB, Regnis JA, Young IH. The role of hypoventilation and ventilation–perfusion redistribution in
oxygen-induced hypercapnia during acute exacerbations of chronic obstructive pulmonary disease. Am J Resp Crit Care
Med 2000;161:1524–9.
Siela D. Chest radiograph evaluation and interpretation. AACN Adv Crit Care 2008;19(4):444–73.
Spiegel J. End-tidal carbon dioxide: the most vital of vital signs. Anesthesiology News, October 2013, <http://www.
anesthesiologynews.com/download/Capnography_ANSE13_WM.pdf>; [accessed 30.07.14].
UK Resuscitation Council. Arterial blood gas analysis workshop, <http://www.resus.org. uk/pages/alsabgGd.pdf2012>;
[accessed 30.07.14].
Valdez-Lowe C, Ghareeb SA, Artinian NT. Pulse oximetry in adults. Am J Nurs 2009;109(6):52–9.
Van Gestel AJR, Steier J. Autonomic dysfunction in patients with chronic obstructive pulmonary disease (COPD). J Thorac
Dis 2010;2:215–22.

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87 Tarrac SE. A systematic approach to chest x-ray interpretation in the perianesthesia unit. J Perianesth Nurs 2009;24(1):41-7; quiz 7-9.
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89 Chen HJ, Yu YH, Tu CY, Chen CH, Hsia TC, Tsai KD et al. Ultrasound in peripheral pulmonary air-fluid lesions. Color Doppler imaging as an aid
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92 Hill JR, Horner PE, Primack SL. ICU imaging. Clin Chest Med 2008;29(1):59-76, vi.
93 Davies AR, Pilcher DV. Pulmonary embolism. In: Bersten AD, Soni N, eds. Oh’s intensive care manual. 6th ed. Philadelphia: Butterworth
Heinemann; 2009, pp 387-98.
94 Rumbolt Z, Huda W, All J. Review of portable CT with assessment of a dedicated head CT scanner. Am J Neuroradiol 2009;30:1630-6.
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 CHAPTER 13 RESPIRATORY ASSESSMENT AND MONITORING 437

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Lippincott Williams & Wilkins; 2014, pp 174.
Chapter 14

Respiratory alterations
and management
Sharon Wetzig, Bronagh Blackwood, Judy Currey

KEY WORDS
Learning objectives
After reading this chapter, you should be able to: acute respiratory
• describe the pathophysiological mechanisms of acute respiratory failure distress
and key principles of patient management syndrome
• differentiate between failure to oxygenate (hypoxaemic/type I) and failure acute respiratory
to ventilate (hypercapnoeic/type II) respiratory failure failure
• outline the incidence of respiratory alterations in the critical care context hypercapnoeic
• discuss the aetiology, pathophysiology, clinical manifestations and respiratory failure
management of common respiratory disorders managed in intensive care, hypoxaemic
specifically pneumonia, pandemic respiratory infections, asthma, chronic respiratory failure
obstructive pulmonary disease, acute lung injury, pneumothorax and
pulmonary embolism influenza
• describe the evidence base for key components of nursing and oxygenation
collaborative practice involved in the management of patients with acute pneumonia
respiratory failure in the intensive care unit
ventilator-
• outline the principles and immediate postoperative management for lung associated
transplant recipients. pneumonia

Introduction
The most common reason why patients require admission to an intensive care
unit (ICU) is for support of the respiratory system. Use of mechanical ventila-
tion is high with almost half of all patients admitted to ICU requiring this level
of support.1 Failure or inadequate function of the respiratory system occurs
as a result of direct or indirect pathophysiological conditions. The process of
mechanical ventilation may also injure a patient’s lungs, further impacting func-
tioning of the respiratory system. Preventing or minimising ventilator-associated
lung injury is therefore also a primary goal of patient care.
In chapter 13 the relevant assessment and monitoring practices for a patient
with life-threatening respiratory dysfunction were described. In this chapter
the incidence, pathophysiology, clinical manifestations and management of
common respiratory disorders that result in acute respiratory failure are described.
Specific conditions such as pneumonia, pandemic respiratory infections, asthma,
chronic obstructive pulmonary disease (COPD), acute lung injury (ALI), pneumo-
thorax and lung transplantation are discussed. Respiratory support strategies
including oxygenation and ventilation to support respiratory function during a
critical illness are presented in Chapter 15.
 CHAPTER 14 RESPIRATORY ALTERATIONS AND MANAGEMENT 439

Incidence of respiratory Importantly, respiratory failure can be an acute or

chronic condition. Whereas acute respiratory failure is
alterations characterised by life-threatening alterations in function,
the manifestations of chronic respiratory failure are more
Respiratory diseases are common and affect significant subtle and potentially more difficult to diagnose. Patients
numbers of people. They are among the leading causes of with chronic respiratory failure often experience acute
death worldwide. Lung infections (primarily pneumonia exacerbations of their disease, also resulting in the need
and tuberculosis), lung cancer and COPD together for intensive respiratory support.3
accounted for 17% of global deaths in 2008.These diseases
also accounted for one-tenth of the disability-adjusted Pathophysiology
life years lost worldwide in the same year.2 Respiratory Respiratory failure occurs when the respiratory system
diseases are also the most common illnesses responsible fails to achieve one or both of its essential gas exchange
for emergency admissions to hospital and visits to general functions – oxygenation or elimination of carbon dioxide
practitioners and represent the most frequently reported – and can be described as either type I, which is primarily
long-term illnesses in children.3 a failure of oxygenation, or type II, which is primarily a
Infective processes, such as influenza and pneumonia, failure of ventilation.3
COPD and asthma represent the three largest groups of
presentations requiring hospital admission. Conditions Type I respiratory failure – failure to
such as ALI, pneumothorax, pulmonary embolus and oxygenate
pulmonary oedema are relatively small groups. It should A patient with type I or ‘hypoxaemic’ respiratory failure
be noted, however, that these conditions often evolve presents with a low partial pressure of oxygen (PaO2)
throughout the course of an illness and may not, therefore, and a normal or low partial pressure of carbon dioxide
be included as the reason for admission.3 Common (PaCO2). Hypoxaemic respiratory failure may be caused
respiratory alterations managed in ICU are discussed in by a reduction in inspired oxygen pressure as might occur
the following sections. at extreme altitude, hypoventilation, impaired diffusion
or ventilation–perfusion mismatch. Most major respir-
Respiratory failure atory alterations cause type I respiratory failure, usually
Respiratory failure occurs when there is a reduction as a result of hypoventilation due to alveolar collapse or
in the body’s ability to maintain either oxygenation or consolidation, or a perfusion abnormality.
ventilation, or both. It may occur acutely, as observed in When there is mismatch between ventilation and
pneumonia and ALI, or it may persist in chronic form, as perfusion in the lungs, exchange of gases is impaired and
observed in asthma and COPD. hypoxaemia ensues (see Figure 14.1).3
In some cases, there may be reduced ventilation to
Aetiology of respiratory failure a certain area of lung tissue (e.g. pulmonary oedema,
For the respiratory system to function effectively, the rate pneumonia, atelectasis, ALI). A severe form of mismatch
and depth of breathing has to be controlled appropriately known as intrapulmonary shunting occurs when adequate
by the brain, the chest wall must expand adequately, air perfusion exists but there are sections of lung tissue that
needs to flow easily through the airways and effective are not ventilated. In these alveoli, the oxygen content is
exchange of gases needs to occur at the alveolar level. similar to that of the mixed venous blood and the carbon
Conditions that impact on one or more aspects of normal dioxide is elevated. In other instances, ventilation may
physiological functioning of the respiratory system can be adequate but perfusion is impaired (e.g. pulmonary
cause respiratory failure, for example: embolus). In its severe form, this is known as dead space
ventilation as the lungs continue to be ventilated but there
• decreased respiratory drive may be caused by brain is limited or no perfusion, and therefore no gas exchange.
trauma, drug overdose or anaesthesia/sedation
In this situation, the alveolar oxygen content is similar to
• decreased respiratory muscle strength may be caused that of the inspired gas mixture and the carbon dioxide is
by Guillain-Barré syndrome, poliomyelitis, myasthenia minimal (see Chapter 13 for further discussion).
gravis or spinal cord injury
• decreased chest wall expansion may be caused by Type II respiratory failure – failure to
postoperative pain, rib fractures or a pneumothorax ventilate
• increased airway resistance may be caused by asthma A patient with type II respiratory or ‘hypercapnoeic/
or COPD hypoxaemic’ failure presents with a high PaCO2 as well as
• increased metabolic oxygen requirements may be a low PaO2. This failure is caused by alveolar hypoventi-
caused by severe sepsis lation, where the respiratory effort or minute ventilation
• decreased capacity for gas exchange may be caused is insufficient to allow adequate exchange of oxygen and
by impairment in either ventilation (e.g. pulmonary carbon dioxide. This may be caused by conditions that
oedema, pneumonia, ALI, COPD) or pulmonary affect respiratory drive such as neuromuscular diseases,
perfusion (e.g. pulmonary embolism), or a chest wall abnormalities or severe airways disease (e.g.
combination of the two. asthma or COPD).
440 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

FIGURE 14.1 Ventilation–perfusion mismatches.3 Ventilation-perfusion (V/Q) ratio displays the normal balance (star)
between alveolar ventilation and vascular perfusion allowing for proper oxygenation. When ventilation is reduced, the
V/Q ratio decreases, in the most extreme case resulting in pure shunt, where V/Q = 0. When perfusion is reduced,
the V/Q ratio increases, in the most extreme case resulting in pure dead space, where V/Q = infinite (∞).

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textbook of respiratory medicine. 5th ed. Philadelphia: Saunders; 2010.

Clinical manifestations comfort and compliance with the ventilation mode, ABG
analysis and pulse oximetry guide any titration of respir-
Patient presentations in acute respiratory failure can be
atory support. The key goals of management are to treat
quite diverse and are dependent on the underlying patho-
the primary cause of respiratory failure, maintain adequate
physiological mechanism, the specific aetiology and any
comorbidities that may exist.3 Specific clinical manifesta- gas exchange and prevent or minimise the potential
tions for the disorders discussed in this chapter are provided complications of positive pressure mechanical ventilation.3
in each section. Dyspnoea is the most common symptom Comorbidities add to the complexity of managing
associated with acute respiratory failure; this is often accom- a patient’s primary condition and increase the risk of
panied by an increased rate and reduced depth of breathing additional organ dysfunction or failure. Chronic respiratory
and the use of accessory muscles. Patients may also present conditions can have a significant impact on the severity
with cyanosis, anxiety, confusion and/or sleepiness.4 of respiratory infections, while cardiovascular and renal
A systematic approach to clinical assessment and diseases impact on disease severity and the management of
management of patients with acute respiratory failure is many respiratory alterations. Other factors such as smoking
crucial, given the large number of possible causes. Clinical and alcohol use, living conditions and lifestyle impact on
investigations to assess the cause of respiratory failure vary the predisposition and clinical course of an illness.2
depending on the suspected underlying aetiology and the Maintaining oxygenation
progression of disease. Continuous monitoring of oxygen
saturation using pulse oximetry, arterial blood gas (ABG) The therapeutic aim is to titrate the fraction of inspired
analysis and analysis of chest X-rays (CXR) are used in oxygen (FiO2) to achieve a PaO2 of 65–70 mmHg and
almost all cases of respiratory failure. Other more specialised to maintain minute ventilation to achieve PaCO2 within
tests such as computed tomography (CT) of the chest and normal limits where possible.3 Nursing staff in ICU are
microbiological cultures may be used in specific circum- commonly responsible for titration of oxygen therapy to
stances.5 With ABG analysis, the measurement of PaO2, maintain a specific PaO2 or SpO2 and the alteration of
PaCO2, alveolar–arterial PO2 difference and patient response respiratory rate and/or tidal volume to maintain a specified
to supplemental oxygen are key elements in determining PaCO2. One concern that often arises, particularly with
the cause of acute respiratory failure5 (see Chapter 13). patients who require high concentrations of oxygen, is
the risk of oxygen toxicity. The link between prolonged
Patient management periods of oxygen concentrations approaching 100%
The primary survey (airway, breathing and circulation) and oxidant injuries in airways and lung parenchyma has
and immediate management form initial routine practice.6 been established, although mostly from animal research.3
Frequent assessment and monitoring of respiratory Although it remains unclear how these data apply to
function, including a patient’s response to supplemental human populations, most consensus groups have argued
oxygen and/or ventilatory support, is the focus. Patient that FiO2 values less than 0.4 are safe for prolonged periods
 CHAPTER 14 RESPIRATORY ALTERATIONS AND MANAGEMENT 441

of time and that FiO2 values of greater than 0.8 should be Development of ventilator-associated respiratory
avoided if possible3 (see Chapter 15 for further detail on muscle weakness has been reported as a significant issue
assessment and management of oxygenation). when the respiratory muscles are rendered inactive
through adjustment of ventilator settings and adminis-
Supporting ventilation tration of pharmacotherapy. While it is not yet possible
Ventilator-associated lung injury is also a concern when to provide precise recommendations for interventions to
managing patients with acute respiratory failure. A lung avoid this, clinicians are advised to select ventilator settings
can be injured when it is stretched excessively as a result that provide for some respiratory muscle use.7
of tidal volume settings that generate high pressures, Prevention or minimisation of complications associ-
often referred to as barotrauma or volutrauma. The most ated with positive pressure mechanical ventilation remains
common injury is that of alveolar rupture and/or air in the a major focus of nursing practice. These complications
pleural space resulting in a pneumothorax. An approach may relate to the patient–ventilator interface (artificial
known as ‘lung protective ventilation’ aims to minimise airway and ventilator circuitry), infectious complica-
over-distension of the alveoli through careful monitoring tions or complications associated with sedation and/
of tidal volumes and airway pressures. This method should or immobility. Some common complications and the
be considered for all ventilated patients. The approach appropriate management strategies are briefly outlined in
may result in tolerance of higher PaCO2 than normal in Table 14.13,8,9,10 and are discussed further in Chapter 15.
patients presenting with acute lung injury 3 (see Chapter 15 A patient with acute respiratory failure requires
for further discussion). extensive multidisciplinary collaboration between nurses,

TABLE 14.1
Complications of mechanical ventilation and associated management strategies3,8,9,10

PAT I E N T – V E N T I L AT O R
I N T E R FA C E C O M P L I C AT I O N M A N A G E M E N T S T R AT E G I E S
Airway dislodgement/disconnection Endotracheal tube or tracheostomy tube is secured to optimise ventilation and prevent
airway dislodgement or accidental extubation
Circuit leaks Cuff pressure assessment
Circuit checks
Exhaled tidal volume measurement
Airway injury from inadequate heat/ Maintain humidification of the airway using either a heat–moisture exchanger or a water-
humidity bath humidifier
Obstructions from secretions Assess the need for suctioning regularly and suction as required
Tracheal injury from the artificial airway Assessment of airway placement and cuff pressure (minimal occlusion method)
I N F E C T I O U S C O M P L I C AT I O N M A N A G E M E N T S T R AT E G I E S
Ventilator-associated pneumonia Alcohol-based hand hygiene
(VAP) Appropriate antibiotic therapy
Oral decontamination
Selective digestive decontamination
Semi-recumbent positioning, 30–45°
Daily sedation holds
Peptic ulcer disease prophylaxis
Minimising interruptions to ventilator circuit (e.g. closed suctioning technique)
Use of oropharyngeal vs nasopharyngeal feeding tubes
Drainage of sub-glottic secretions
Small bowel feeding rather than gastric feeding
Aerosolised antibiotics for patients who are colonised
Weaning and discontinuation of ventilatory support as soon as possible, including using
nurse-led weaning protocols
Early tracheostomy
Prophylactic probiotics
C O M P L I C AT I O N A S S O C I AT E D
W I T H I M M O B I L I T Y / S E D AT I O N M A N A G E M E N T S T R AT E G I E S
Gastrointestinal dysfunction Prokinetic medication
Constipation – bowel therapy regimen
Muscle atrophy Passive limb movements, foot splints (see Chapter 6) and early activity/mobility (see Chapter 4)
Pressure injuries Pressure-relieving mattresses, regular repositioning
Assessment of risks and management of pressure injuries by wound care specialists,
nutrition advice
442 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

physiotherapists, specialist medical staff, speech and (see Chapters 11 and 21). As the use of medications will
occupational therapists, dieticians, social workers, radiolo- vary depending on the underlying cause of respiratory
gists and radiographers, pharmacists and microbiologists. failure, these are discussed separately in the sections below.
Patients may require intervention to improve capacity for
oxygen delivery through an adequate haemoglobin level Practice tip
and a cardiac output sufficient to supply oxygenated blood
to the tissues.3 At times this may require blood transfusion Respiratory failure in pregnancy
and/or the use of vasoactive medications (see Chapters 11 Respiratory physiology and the respiratory tract itself are
and 21). altered during pregnancy; this may result in exacerbation
Chest physiotherapy is a routine activity for managing of pre-existing respiratory disease or increased sus-
patients with acute respiratory failure. This involves ceptibility to disease (see Chapter 28). Upper airway
positioning, manual hyperinflation, percussion and mucosal oedema may increase the likelihood of upper
vibration and suctioning. The evidence base for these respiratory tract infection. Lung function and lung
techniques is limited, however, with a systematic review volume are also altered, compensated by an increase
reporting no improvement in mortality for patients with in respiratory drive and minute ventilation. The impact
pneumonia.8 Guidelines for physiotherapy assessment on the fetus of infection, hypoxia and drug therapy is an
have enabled identification of patient characteristics important consideration.3
for treatments to be prescribed and modified on an
individual basis. Table 14.23,8,11 provides an outline of
management interventions for patients with respiratory Practice tip
failure, particularly those who may require prolonged
mechanical ventilation. Respiratory failure in the elderly

Medications The elderly have ageing organs and systems and

other comorbidities that may exacerbate their respir-
Medications commonly prescribed in respiratory failure atory dysfunction. Drug metabolism and excretion is
include inhalation/intravenous steroids and broncho- slowed, complicating drug dosing and response.150
dilators, antibiotic therapy, analgesia and sedation to Metabolism of anaesthetic agents is slower due to
maintain patient–ventilator synchrony, but may also the diminished physiology of ageing organs. Common
involve nitric oxide, glucocorticoid or surfactant admin- comorbidities may also be present, including obesity,
istration. A patient’s condition, comorbidities and the heart disease, diabetes and renal impairment or
above-mentioned pharmacological therapy may also be muscle wasting.3
supported with inotropic and other resuscitation therapies

TABLE 14.2
Long-term patient management in respiratory failure3,8,11

MANAGEMENT BEST PRACTICE

Timing of tracheostomy Where mechanical ventilation is expected to be 10 days or more, tracheostomy should be performed
insertion as soon as identified. Early tracheostomy is associated with less nosocomial pneumonia, reduced
ventilation time and shorter ICU stay
Weaning protocols Specific plan is patient dependent; better outcomes are achieved when there is an agreed and well
communicated weaning plan (see Chapter 15)
Nutrition Consider adequate nutrition for physiological needs – important to not overfeed as this increases CO2
production – and the need to have a balance of vitamins and minerals
Swallow assessment Assess for dysphagia
Mobilisation Sitting out of bed, mobilising (see Chapter 4)
Communication Communication aids, speaking valves
Activities Activity plan/routine, entertainment (TV/films), visitors, outings
Sleep Clustering cares, reducing stimuli to promote sleep (see Chapter 7)
Family support Importance of providing physical, emotional and/or spiritual support to family members (see Chapter 8)
Tracheostomy follow-up Outreach team: follow-up care by nurses experienced in tracheostomy care can prevent complications
and improve outcomes
End-of-life decisions in See Chapter 5
acute respiratory failure
 CHAPTER 14 RESPIRATORY ALTERATIONS AND MANAGEMENT 443

Pneumonia Aetiology
Pneumonia is infection of the lung. Depending on the Pneumonia is caused by a variety of microorganisms,
type and severity of the infection and the overall health including bacteria, viruses, fungi and parasites. In many
of the person, it may result in acute respiratory failure. cases, the causative organism may not be known and
Pneumonia can be caused by most types of microorgan- current practice in many cases is to initiate antimicrob-
isms, but is most commonly a result of bacterial or viral ial treatment as soon as possible, based on symptoms
infection. In critical care the key distinctions in assessing and patient history, rather than waiting for microorgan-
and managing a patient with pneumonia relate to the ism culture results.14 The true incidence of pneumonia is
specific aetiology or causative organism. This section not well known as many patients do not require hospi-
reviews the pathophysiology, aetiology, clinical presenta- talisation. Different ages and characteristics of patients
tion and management of two types of pneumonia: are often associated with different causative organisms.
Viral pneumonias, especially influenza, are most common
1 community-acquired pneumonia (CAP)
in young children, while adults are more likely to have
2 ventilator-associated pneumonia (VAP) and pneumonia caused by bacteria such as Streptococcus
ventilator-associated events (VAE). pneumoniae and Haemophilus influenzae.3
As a result of the complexity and ambiguity associated
with previous definitions of VAP, there has been a signifi- Practice tip
cant shift towards measuring VAE as a way of monitoring
Pneumonia in the elderly
ventilator-associated complications more broadly.12 A
VAE is said to have occurred when a decline in respir- Pneumonia is a particular concern among elderly
atory function occurs (defined by a significant increase adults as they experience an increase in the frequency
in FiO2 or positive end-expiratory pressure [PEEP]) in a and severity of pneumonia. This is largely due to the
ventilated patient after a period of initial stability. Patients decline in immune system response that is associated
who are identified as having had a VAE are then reviewed with age and with the presence of comorbid disease,
to determine if clinical signs and symptoms meet the such as cardiac and respiratory disease. CAP is a
criteria for an infective ventilator-associated complication. major cause of morbidity and mortality in elderly
Further investigation of microbiological culture results patients. Streptococcus pneumoniae is the most
then determines if the definition of VAP applies.13 common causative organism, with an increase in drug-
resistance being reported more widely in the over-65
Pathophysiology age group. Immunisation with pneumococcal and
The normal human lung is sterile, unlike the gastro- influenza vaccines is beneficial in the prevention of
intestinal tract and upper respiratory tract, which have pneumonia in elderly patients.3
resident bacteria. A number of defence mechanisms exist
to prevent microorganisms entering the lungs, such as
particle filtration in the nostrils, sneezing and coughing
Community-acquired pneumonia
to expel irritants and mucus production to trap dust The International CAP Collaboration Cohort study15
and infectious organisms and move particles out of the provides information from a pooled multicentre data set
respiratory system. Infection occurs when one or more of of patients with CAP. This study reports that around 30%
these defences are not functioning adequately or when an of patients with CAP require hospital admission and up
individual encounters a large amount of microorganisms to 20% require ICU admission. The causative organism is
at once and the defences are overwhelmed.3 An invading frequently unidentified.
pathogen provokes an immune response in the lungs, Clinical assessment, especially patient history, is
resulting in the following pathophysiological processes: important in distinguishing the aetiology and likely
causative organism in patients with CAP. Specific informa-
• alteration in alveolar capillary permeability that leads tion regarding exposure to animals, travel history, nursing
to an increase in protein-rich fluid in the alveoli; this
home residency and any occupational or unusual exposure
impacts on gas exchange and causes the patient to
may provide the key to diagnosis.14 Personal habits such
breathe faster in an effort to increase oxygen uptake
as smoking and alcohol consumption increase the risk of
and remove carbon dioxide
developing pneumonia and should be explored. Many
• mucus production increases and mucous plugs may patients admitted to hospital with CAP have comorbidi-
develop that block off areas of the lung, further ties, suggesting that those who are chronically ill have an
reducing capacity for gas exchange increased risk of developing acute respiratory failure. The
• consolidation occurs in the alveoli, which fill with most common chronic illnesses involved are respiratory
fluid and debris; this occurs particularly with bacterial disease, including smoking history, COPD and asthma,
pneumonia where debris accumulates from the large congestive cardiac failure and diabetes mellitus. Table 14.3
number of white blood cells involved in the immune outlines aspects of the clinical history associated with
response.3 particular causative organisms in CAP.3,16,17
444 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 14.3
Clinical history/comorbidities associated with particular causative organisms in community-acquired pneumonia3,16,17

CONDITION C A U S AT I V E O R G A N I S M S
I N D I V I D U A L FA C T O R S
Alcoholism S. pneumoniae (including penicillin-resistant), anaerobes, gram-negative bacilli (possibly K. pneumoniae),
tuberculosis
Poor dental hygiene Anaerobes
Elderly Group B streptococci, M. catarrhalis, H. influenzae, L. pneumophila, gram-negative bacilli,
C. pneumoniae and polymicrobial infections
Smoking (past or present) S. pneumoniae, H. influenzae, M. catarrhalis, Aspergillus spp.
IV drug use S. aureus, anerobes, M. tuberculosis, S. pneumoniae
COMORBIDITIES
COPD S. pneumoniae, H. influenzae, M. catarrhalis, Aspergillus spp.
Post influenza pneumonia S. pneumoniae, S. aureus, H. influenzae
Structural disease of lung P. aeruginosa, P. cepacia or S. aureus
(e.g., bronchiectasis, cystic
fibrosis)
Sickle cell disease, Pneumococccus, H. influenzae
asplenia
Previous antibiotic P. aeruginosa
treatment and severe
pulmonary comorbidity,
(e.g. bronchiectasis, cystic
fibrosis, and severe COPD)
Malnutrition-related Gram-negative bacilli
diseases
E N V I R O N M E N TA L E X P O S U R E
Air conditioning L. pneumophila
Residence in nursing home S. pneumoniae, gram-negative bacilli, H. influenzae, S. aureus, C. pneumoniae; consider
M. tuberculosis; consider anaerobes, but less common
Homeless population S. pneumoniae, S. aureus, H. influenzae, C. gattii: caused by inhalation of spores while sleeping,
associated with red gum trees (Australia, Southeast Asia, South America)
Suspected bioterrorism Anthrax, tularaemia, plague
ANIMAL EXPOSURE
Bat exposure H. capsulatum
Bird exposure C. psittaci, C. neoformans, H. capsulatum
Rabbit exposure F. tularensis
Exposure to farm animals C. burnetii (Q fever)
or parturient cats
T R AV E L H I S T O RY
Travel to southwestern USA Coccidioidomycosis; hantavirus in selected areas
Travel to southeast Asia Severe acute respiratory syndrome (coronavirus), M. tuberculosis, melioidosis
Residence or travel to rural Melioidosis (B. pseudomallei)
tropics
Travel to area of known Avian influenza (H5N1), swine influenza (H1N1) and severe acute respiratory syndrome (coronavirus)
epidemic

COPD = chronic obstructive pulmonary disease; IV = intravenous. B. pseudomallei = Burkholderia pseudomallei; C. burnetii =
Coxiella burnetii; C. gattii = Cryptococcus gattii; C. neoformans = Cryptococcus neoformans; C. pneumoniae = Chlamydophila
pneumoniae; C. psittaci = Chlamydia psittaci; F. tularensis = Francisella tularensis; H. capsulatum = Histoplasma capsulatum;
H. influenzae = Haemophilus influenzae; K. pneumoniae = Klebsiella pneumoniae; L. pneumophila = Legionella pneumophila;
M. catarrhalis = Moraxella catarrhalis; M. tuberculosis = Mycobacterium tuberculosis; P. aeruginosa = Pseudomonas aeruginosa;
P. cepacia = Pseudomonas cepacia; S. aureus = Staphylococcus aureus; S. pneumoniae = Streptococcus pneumoniae.
 CHAPTER 14 RESPIRATORY ALTERATIONS AND MANAGEMENT 445

Diagnosis BOX 14.1

Routine screening of patients with suspected pneumonia
continues to rely on microscopy and culture of lower Severity scoring in CAP
respiratory tract specimens, blood cultures, detection of CURB65/CUR6519
antigens in urine and serology. Methods for detection The score is an acronym for each of the risk factors
of antigens are now widely available for several pneumonia measured. One point is allocated for each risk factor
pathogens, particularly S. pneumoniae, Legionella and some present, with maximum scores of 5 and 4, respectively:
respiratory viruses. Culture of respiratory secretions may • C – confusion: a new onset of confusion, defined as
be limited due to difficulty in obtaining sputum samples. an abbreviated mental test score of 8 or less
For this reason, nasopharyngeal aspirates or swabs may be
taken as part of the routine screening for CAP.18 • U – urea: blood urea nitrogen level >19 mg/dL
• R – respiratory rate: ≥30 breaths per minute
Severity assessment scoring • B – blood pressure: ≤90 mmHg systolic or
International guidelines recommend a severity-based ≤60 mmHg diastolic (not measured as part of
approach to management of CAP, in relation to the CUR65 scoring system)
initial site of treatment (e.g. home, hospital ward, ICU), • 65 – age: ≥65 years
and appropriate level of intervention, including antibiotic
therapy.15 Several severity scores have been developed and Pneumonia Severity Index20
validated; however, to date there is no agreement on the The PSI considers a range of patient characteristics,
optimal tool or an agreed definition of the term ‘severe comorbid diseases, signs and symptoms and laboratory
pneumonia’.19 CUR65/CURB65 and the Pneumonia findings with the intent of classifying the severity of a
Severity Index are the most widely recommended systems patient’s pneumonia at a risk level ranging from I to V,
that produce scores and assess severity based on patient with V being the most severe. An online PSI calculator
demographics, risk factors, comorbidities, clinical pres- (see Online resources for link) is available to assist
entation and laboratory results. Recent evaluation of these clinicians in applying the scoring system.
tools found no significant differences in their ability to • PSI risk class I – patient can be sent home on oral
predict mortality in hospitalised patients.20 antibiotics
The Australian CAP Collaboration team devised and
• PSI risk class II–III – patient should be treated with
validated the SMART-COP scoring system for predicting
IV antibiotics and may need to be monitored in
the need for intensive respiratory or vasopressor support
hospital for 24 hours
in patients with CAP. The acronym relates to the factors:
low Systolic blood pressure, Multilobar involvement, • PSI risk class IV–V – patient should be hospitalised
low Albumin level, high Respiratory rate, Tachycardia, for treatment
Confusion, poor Oxygenation and low arterial pH.21
Adapted from Singanayagam A, Chalmers JD, Hill AT. Severity
Hospital-acquired and ventilator- assessment in community-acquired pneumonia: a review.
QJM 2009;6:379–88, with permission.
associated pneumonia (VAP)
Hospital-acquired pneumonia is defined as pneumonia
occurring more than 48 hours after hospital admission.16 It VAP are associated with multiple organisms.As in CAP, the
is the second most common nosocomial infection and the presence of comorbidities and other risk factors influences
leading cause of death from infection acquired in-hospital. the causative organism.3
VAP is a form of hospital-acquired pneumonia that occurs
in patients who are mechanically ventilated. The incidence Diagnosis
of VAP is reported at 10–30% among patients who require VAP can be difficult to diagnose, as clinical features can be
mechanical ventilation for greater than 48 hours.22 non-specific and other conditions may cause infiltrates on
Critically ill ventilated patients commonly experience CXR. In addition to this, ambiguity in the definition of
chest colonisation as a result of translocation of bacteria VAP has led to inconsistencies in interpretation and appli-
from the mouth to the lungs via the endotracheal tube cation of the definition, which has meant that comparison
(ETT) or via contamination of the ventilator circuit. of incidence and/or treatment effects has been difficult.
This may lead to clinical signs of infection, or the patient The current definition used by the Centres for Disease
may remain colonised without an infective process. The Control in the USA focuses on more objective data.13
patient’s severity of disease, physiological reserve and VAP is suspected when additional support is required
comorbidity influence the development of infection.3 to maintain oxygenation, such as increased FiO2 or
Most cases of VAP are associated with infection involving higher PEEP, clinical signs of infection begin to develop,
gram-negative bacilli such as Pseudomonas aeruginosa and including new onset of pyrexia or raised white blood cell
Acinetobacter spp. A high number of cases are associated counts, or when indicated by microbiological culture.13
with gram-positive Staphylococcus aureus. Many cases of Specific risk factors associated with increased mortality
446 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

in VAP have been identified over the past decade. The outcome measures, have made interpretation of these data
most widely-recognised risk-minimisation factor is the complex. In addition, the high mortality reported to be
provision of appropriate antibiotic treatment, which associated with VAP has also been questioned,27 leading
has reduced mortality and the rate of complications. clinicians to debate the benefit of implementing inter-
Timeliness of antibiotic administration is an independent ventions that reduce the incidence of VAP but may not
risk factor for mortality – mortality was increased where impact on patient outcome measures.
administration of antibiotics was delayed for more than Effective oral hygiene care has been recommended in
24 hours after diagnosis.22 ventilated patients, especially when performed with chlor-
When VAP is suspected there are two treatment hexidine as this is associated with a 40% reduction in the
strategies that are commonly used, and a systematic review odds of developing VAP. Despite this reduction, there is no
of these strategies was not able to demonstrate any differ- evidence of it influencing other outcome measures such as
ences in patient outcome measures including mortality, mortality, duration of mechanical ventilation or duration
length of ICU stay or length of ventilation period:23 of ICU stay.28
1 Clinical strategy: involves treatment of patients with The Surviving Sepsis Campaign Guidelines29
new antibiotics, based on patient risk factors and the recommend that selective oral decontamination and
local microbiological and resistance patterns. Therapy selective digestive decontamination be introduced and
is adjusted based on culture results and the patient’s investigated as a method to reduce the incidence of VAP.
response to treatment. The aim of selective digestive decontamination is to prevent
or eradicate the abnormal colonisation of potentially
2 Invasive strategy: involves collection and quantitative
pathogenic microorganisms, such as gram-negative aerobic
analysis of respiratory secretions from samples microorganisms and methicillin-sensitive Staphylococcus
obtained by bronchoalveolar lavage to confirm the aureus and yeasts, from the oropharyngeal and intestinal
diagnosis and causative organism. Antibiotic therapy is tracts. Although this strategy has been shown to be effective
then guided by specific protocols. in reducing morbidity and mortality30, with antibiotic
Clinical manifestations resistance being controlled, it is yet to be widely adopted in
clinical practice.31 Recent review of nursing considerations
Symptoms for pneumonia are both respiratory and
for administration of selective digestive decontamination
systemic. Common characteristics include fever, sweats,
highlights the importance of a comprehensive education
rigours, cough, sputum production, pleuritic chest pain,
program and an implementation plan that considers patient
dyspnoea, tachypnoea, pleural rub, inspiratory crackles on
safety issues as well as the impact on nursing practice.32
auscultation, plus radiological evidence of infiltrates or
Several other new strategies have been suggested and
consolidation.3 Cough is the most common finding in
evaluated for their effectiveness in reducing VAP rates.
CAP and is present in up to 80% of all patients.16
These include: specialised ETTs that allow for aspiration of
Patient management subglottic secretions; continuous maintenance of appropri-
ate ETT cuff inflation pressures; modified shape of ETT cuff;
VAP prevention strategies ETTs that have an external silver/antimicrobial coating; and
Prevention of VAP is a key emphasis in the care of all administration of probiotics. These have been shown to be
mechanically ventilated patients and involves a number of effective, but need evaluation in large randomised clinical
interventions. One approach in encouraging the imple- trials before practice recommendations can be made.33
mentation of VAP prevention was the combination of key
aspects of patient management into an evidence-based Management
guideline, the Ventilator Care Bundle, which advocates Early recognition of pneumonia, timely administration of
semi-recumbent positioning, sedation holds, peptic ulcer appropriate antibiotic therapy and supportive care are key
disease prophylaxis and deep vein thrombosis prophylaxis.24 aspects in pneumonia management. Supportive ventilation
A number of different VAP bundles, clinical guidelines or is a key focus for managing patients with pneumonia. In
checklists have been reported. A VAP prevention bundle some instances this may include increased oxygen delivery
used in Scotland, which included head elevation, oral care and PEEP to maintain oxygenation and prevent alveolar
with chlorhexidine, sedation interruptions and a ventilator collapse. Chest physiotherapy remains a key component
weaning protocol, demonstrated a reduced VAP rate in a of management of all ventilated patients. However, its
before-and-after study.25 A CanadianVAP prevention bundle contribution towards improving mortality in patients with
demonstrating a reduction in VAP rate included preferential pneumonia is unclear.8 Upright positioning and early
use of oral versus nasal tubes for access to the trachea or mobilisation are important elements of both prevention
stomach and subglottic secretion drainage, in addition to and management of pneumonia. The evidence supporting
semi-recumbent positioning and sedation holds.26 use of additional strategies, such as beds with a continuous
Further evaluation of the effectiveness of these strategies lateral rotation or a vibration function, is limited and has
and the issues associated with implementation has been been associated with complications, so recommendations
performed. However, differences in the definitions used for their use cannot be made.33 See Chapter 15 for further
for VAP/VAE, combined with a limited impact on patient discussion.
 CHAPTER 14 RESPIRATORY ALTERATIONS AND MANAGEMENT 447

Medications Respiratory pandemics

Antibiotic administration is fundamental to a patient’s
clinical progress. As noted earlier, the importance of Serious outbreaks of respiratory infections that spread
accurate and timely administration of antibiotics directly rapidly on a global scale are termed pandemics. Their
impacts on patient outcome. In particular, the first dose spread is rapid because the infection is usually associated
of antibiotics is required as soon as possible after the with the emergence of a new virus where the majority of
diagnosis of pneumonia has been made.29 Antibiotic cover the population has no immunity.These infections are char-
for pneumonia depends on the causative organism and acterised by extremely rapid ‘transmission with concurrent
sensitivity to drugs (see Table 14.43). outbreaks throughout the globe; the occurrence of disease
outside the usual seasonality, including during the summer
Practice tip months; high attack rates in all age groups, with high levels
of mortality particularly in healthy young adults; and
Pneumonia during pregnancy multiple waves of disease immediately before and after the
Pneumonia is a leading cause of maternal and fetal
main outbreak’.14
morbidity and mortality. It also increases the likelihood of
Several severe respiratory infections have progressed
the complications of pneumonia, including requirement
to become pandemics in recent years; these have been
for mechanical ventilation. Bacterial pneumonia is the
associated with the coronavirus and influenza viruses.
most common type experienced in pregnancy although
Prediction of the interval between pandemics is difficult,
diagnosis is often delayed as a result of the reluctance to
but occurrence is likely to continue and therefore
obtain a CXR. Management is similar to a non-pregnant
requires that the healthcare community be well prepared.
patient with antibiotic therapy adjusted to consider the
The InFACT H1N1 Research Collaborative is a global
impact on the fetus.3
initiative aimed at reducing the mortality associated with
H1N1 through clinical research groups and professional

TABLE 14.4
Preferred antimicrobial agents in pneumonia3

TYPE OF INFECTION PREFERRED AGENT(S)

C O M M U N I T Y- A C Q U I R E D P N E U M O N I A

Streptococcus pneumoniae Penicillin-susceptible organisms: penicillin G, amoxicillin, clindamycin, doxycycline, telithromycin

Penicillin-resistant organisms: cefotaxime, ceftriaxone, vancomycin, fluoroquinolone
Mycoplasma Doxycycline, macrolide
Chlamydophila pneumoniae Doxycycline, macrolide
Legionella Azithromycin, fluoroquinolone (including ciprofloxacin), erythromycin (rifampicin)
Haemophilus influenzae Second- or third-generation cephalosporin, clarithromycin, doxycycline, beta-lactam/
beta-lactamase inhibitor, trimethoprim/sulfamethoxazole, azithromycin, telithromycin
Moraxella catarrhalis Second- or third-generation cephalosporin, trimethoprim–sulfamethoxazole, macrolide
doxycycline, beta-lactam–beta-lactamase inhibitor
Neisseria meningitidis Penicillin
Streptococci (other than Penicillin, first-generation cephalosporin
S. pneumoniae)
Anaerobes Clindamycin, beta-lactam–beta-lactamase inhibitor, beta-lactam + metronidazole
Staphylococcus aureus
Methicillin-susceptible Oxacillin, nafcillin, cefazolin; all + rifampin or gentamicin
Methicillin-resistant Vancomycin, rifampicin or gentamicin
Klebsiella pneumoniae and Third-generation cephalosporin or cefepime (all + aminoglycoside), carbapenem
other Enterobacteriaceae
(excluding Enterobacter spp.)
H O S P I TA L - A C Q U I R E D I N F E C T I O N S

Enterobacter spp. Carbapenem, beta-lactam–beta-lactamase inhibitor, cefepime, fluoroquinolone; all +

aminoglycoside in seriously ill patients
Pseudomonas aeruginosa Anti-pseudomonal beta-lactam + aminoglycoside, carbapenem + aminoglycoside
Acinetobacter Aminoglycoside + piperacillin or a carbapenem
448 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

organisations working together to gain a rapid under- USA. This virus contained genes from avian, human and
standing of the epidemiology and clinical presentation of swine influenza viruses and affected millions of people
the disease, and the identification of effective management worldwide. Patients typically presented with nonspecific
strategies.34 flu-like symptoms; however, in a quarter of patients this
was accompanied by diarrhoea and vomiting. The disease
Aetiologies of severe acute spread globally with millions of cases reported and resulted
respiratory syndrome and influenza in over 16,000 deaths by March 2010.36
In 2002–03 an outbreak of a novel coronavirus occurred Australian and New Zealand communities had a high
in China and rapidly spread throughout the world. proportion of cases of H1N1 influenza A infection, with
The infection was highly virulent with over 8000 cases 856 patients being admitted to ICU, 15 times the incidence
reported and a mortality rate of 11%. The infection was of influenza A in other recent years. Infants (aged 0–1
called severe acute respiratory syndrome (SARS) due to years) and adults aged 25–64 years were at particular risk;
the severity of the disease, characterised by diffuse alveolar others at increased risk were pregnant women, adults with
infiltrates, resulting in about 20% of patients requiring a body mass index over 35 and indigenous Australian and
respiratory support. The outbreak provoked a rapid and New Zealand populations. Australian and New Zealand
intense public health response coordinated by the World Intensive Care Society investigators prepared a report
Health Organization, resulting in a cessation of disease based on the Australian and New Zealand experience to
transmission within 10 months.14 assist those in the northern hemisphere to better prepare
Epidemics of influenza occur regularly and are for their winter influenza season.37
associated with high morbidity and mortality. Incidence The emergence of a novel swine-origin influenza A
is usually highest in the young, while mortality is highest virus was not anticipated and it is unlikely, given the lim-
in the elderly population. Those with pre-existing respir- itations of current knowledge, that future pandemics can
atory conditions such as asthma or COPD experience be predicted. The threat of pandemic disease from avian
particularly high morbidity and mortality. In contrast, influenza remains high with the rapid evolution of H5N1
when influenza occurs on a pandemic scale it has been viruses; however, the direction this will take is unpredict-
shown to affect greater numbers of younger and otherwise able. Priorities for prevention and management of future
healthy people. influenza pandemics therefore involve development of an
A feature of the influenza virus that explains why it international surveillance and response network for early
continues to be associated with epidemic and pandemic detection and containment of the disease, local prepara-
disease is its high frequency of antigenic variation. This tion for controlling the spread of the infection and further
occurs in two of the external glycoproteins and is referred development of vaccines and antiviral agents.36
to as antigenic drift or antigenic shift, depending on the Patient management
extent of the variation.The result of this is that new viruses
are introduced into the population and, due to the absence Vaccination
of immunity to the virus, a pandemic of influenza results.3 Influenza vaccines are formulated annually based on
Pandemics of influenza were observed a number of current and recent viral strains. Success in protecting an
times in the twentieth century, and were believed to have individual against influenza requires that the virus strains
involved viruses circulating in humans that originated included in the vaccine are the same as those currently
from influenza A viruses in birds. The ‘Spanish influenza’ circulating in the community. Vaccines are commonly
pandemic of 1918–19 resulted in the deaths of over 50 effective in preventing influenza in 70–90% of healthy
million people worldwide and remains unprecedented in adults younger than 65 years of age. Efficacy appears lower
its severity.14 in elderly persons. Healthcare workers are a key target
The first reported infection of humans with avian group for the influenza vaccine, at the very least to reduce
influenza viruses occurred in Hong Kong in 1997, with six absenteeism over what is often the busiest period for most
recorded fatalities. The increased virulence of this disease hospitals and health services and to reduce the risk of
was observed in the acuity of those affected by the outbreak nosocomial influenza in hospitals.14
of the highly pathogenic avian influenza virus (H5N1)
in 2004–05.14 Most patients presented with non-specific Isolation precautions and personal
symptoms of fever, cough and shortness of breath. In many protective equipment
patients this progressed rapidly to acute respiratory failure Key aspects of infection control in an epidemic or pandemic
requiring ventilation and other supportive measures. The situation focus on limiting opportunities for nosocomial
majority of people affected (90%) were less than 40 years spread and the protection of healthcare workers. Guide-
of age with case fatality rates highest in the 10–19-year- lines for institutional management of these infections
old age group.35 involve designing and implementing appropriate isolation
The most recent influenza pandemic was declared by procedures and recommending appropriate personal pro-
the World Health Organization in 2009 when a novel tective equipment. The importance of adequate personal
H1N1 influenza A virus emerged in Mexico and the protective equipment was highlighted particularly during
 CHAPTER 14 RESPIRATORY ALTERATIONS AND MANAGEMENT 449

the SARS epidemic where there was overrepresentation patients with pneumonia. The risk of developing ARDS
of healthcare workers who became patients infected with increases significantly when more than one predisposing
the virus.14 factor is present.38
Specific infection control guidelines are usually
developed for individual institutions, based on government Pathophysiology
recommendations for management of staff, appropriate Inflammatory damage to alveoli from locally or system-
personal protective equipment and isolation procedures. ically released inflammatory mediators causes a change
This topic is covered in detail in Chapter 6. in pulmonary capillary permeability, with resulting fluid
and protein leakage into the alveolar space and pulmonary
Acute lung injury/acute infiltrates. Dilution and loss of surfactant causes diffuse
alveolar collapse and a reduction in pulmonary compliance
respiratory distress syndrome and may also impair the defence mechanisms of the lungs.
Intrapulmonary shunt is confirmed when hypoxaemia
ALI is a generic term that encompasses conditions causing does not improve despite supplemental oxygen adminis-
physical injury to the lungs. Acute respiratory distress tration. The characteristic course of ARDS is described as
syndrome (ARDS) is a severe form of ALI resulting from having three phases:39
bilateral and diffuse alveolar damage due to an acute insult,
and is the predominant form of ALI observed in ICU.3 1 Oedematous phase: involves an early period
of alveolar damage and pulmonary infiltrates
Aetiology resulting in hypoxaemia. This phase is characterised
ARDS is a characteristic inflammatory response of by migration of neutrophils into the alveolar
the lung to a wide variety of insults. Epidemiological compartment, releasing a variety of substances
studies show a variable incidence of ARDS. For example, including proteases, gelatinases A and B and reactive
estimates of incidence from studies conducted in the nitrogen and oxygen species that damage the alveoli.
USA range from 64 to 79 cases per 100,000 person-years, Further damage is caused by resident alveolar
whereas estimates from other areas are substantially lower macrophages and release of proinflammatory
with Northern Europe reporting 17 cases per 100,000, cytokines that amplify the inflammatory response
Spain reporting 7.2 cases per 100,000 and Australia/New in the lung. Significant ventilation–perfusion
Zealand reporting 34 cases per 100,000. Reasons for (intrapulmonary shunt) mismatch evolves, causing
this variation may include differences in demographics, hypoxaemia.
healthcare delivery systems and clinical coding practices.38 2 Proliferative phase: begins after 1–2 weeks as
Regardless of the variations in incidence, ARDS remains pulmonary infiltrates resolve and fibrosis and
a syndrome of significant impact with an in-hospital remodelling occur. This phase is characterised
mortality rate of approximately 40%.39 by reduced alveolar ventilation and pulmonary
Clinical disorders that are commonly associated compliance and ventilation–perfusion mismatch.
with ARDS can be separated into those that directly or Reduced compliance causes further atelectasis in
indirectly injure the lung16 (see Table 14.5). the mechanically ventilated patient as alveoli are
The most common cause of indirect injury resulting damaged by increased volume and/or pressure on
in ALI/ARDS is sepsis, followed by severe trauma and inspiration.
haemodynamic shock states. Transfusion-related ALI 3 Fibrotic phase: the final phase where alveoli become
is not common but is observed in ICU. ARDS arising fibrotic and the lung is left with emphysema-like
from direct injury to the lung is most commonly seen in alterations.
Diagnosis
TABLE 14.5 A standardised definition of ARDS was first described in
Direct and indirect causes of acute lung injury16 1988, with three clinical findings; 1) hypoxia, 2) decreased
pulmonary compliance and 3) diffuse infiltrates observed
D I R E C T L U N G I N J U RY I N D I R E C T L U N G I N J U RY
on CXR. The Murray Lung Injury Score was developed
Pneumonia Sepsis as a method for clarifying and quantifying the existence
Aspiration of gastric contents Multiple trauma and severity of the disease.40 The American-European
Pulmonary contusion Cardiopulmonary bypass Consensus Conference on ARDS provided the following
Fat, amniotic fluid or air Drug overdose definition: acute onset of arterial hypoxaemia (PaO2/
embolus Acute pancreatitis FiO2 ratio <200) and bilateral infiltrates on CXR without
Near drowning Transfusion of blood evidence of left atrial hypertension or congestive cardiac
Inhalational injury (chemical products
or smoke)
failure. The spectrum of disease was also acknowledged
Reperfusion pulmonary
and the term ALI was introduced to describe patients
oedema with a less severe but clinically similar form of respiratory
failure (PaO2/FiO2 ratio <300).41
450 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Recent review of the American-European Consensus development. The use of small tidal volumes and
Conference definition and drafting of the Berlin definition adequate levels of PEEP, along with careful attention
of ARDS42 have resulted in a definition that is feasible, to fluid status and patient–ventilator synchrony, may be
reliable and prognostic. Major changes include: sufficient to maintain oxygenation at an appropriate level
while minimising further damage from barotrauma and
• replacing the term ALI with three levels of ARDS nosocomial pneumonia.44
severity, based on PaO2/FiO2 measured with at least
5 cmH2O of applied PEEP The use of rescue therapies, when refractory
hypoxaemia does occur, is controversial. Ideally, such
• defining ‘acute’ as less than 7 days from the therapies should improve oxygenation but also improve
predisposing clinical insult survival, and need to be considered safe and effective
• eliminating pulmonary wedge pressure cut-off values regardless of the particular patient issues.
that discriminate ARDS from cardiogenic pulmonary Some therapies have demonstrated improved oxygen-
oedema. ation, which may be an important goal in many patients
who experience severe hypoxaemia. The key focus of
Clinical manifestations rescue ventilatory strategies is alveolar recruitment.
Although no specific test exists to determine whether a An evidence-based approach is likely to involve lung-
patient has ARDS, it should be considered in any patient protective ventilation (volume and pressure limitation
with a predisposing risk factor who develops severe with modest PEEP) requiring permissive hypercapnia
hypoxaemia, reduced compliance and diffuse pulmonary and permissive hypoxaemia.44,45 Strategies to support gas
infiltrates on CXR.38 ARDS usually occurs 1–2 days exchange, such as the use of extracorporeal membrane
following onset of a presenting condition and is character- oxygenation, may also be used for patients with ARDS.
ised by rapid clinical deterioration. Common symptoms This strategy is described in more detail in Chapter 15.
include severe dyspnoea, dry cough, cyanosis, hypoxaemia The recently reported findings that high-frequency
requiring rapidly escalating amounts of supplemental oscillatory ventilation in patients with ARDS resulted in
oxygen and persistent coarse crackles on auscultation.3 an increased mortality (most likely due to the elevated
mean airway pressures affecting venous return and venous
Assessment resistance) has meant that this therapy is no longer used as
A patient with ARDS requires ongoing monitoring of a rescue strategy.46
oxygenation and ventilation through pulse oximetry and
ABG analysis, especially PaCO2 to monitor permissive Prone positioning
hypercapnia. Monitoring of ventilatory pressures and Use of prone positioning in patients with ARDS was
volumes ensures that additional lung injury is prevented. described almost 30 years ago as a means of improving
As many patients with ARDS require cardiovascular oxygenation. This improvement is largely due to the
support, assessment of haemodynamics and peripheral effect that the prone position has on chest wall and lung
perfusion is important to ensure oxygen delivery to cells compliance. The result is a more homogeneous ventila-
is achieved.3 tion of the lungs and improved ventilation–perfusion
matching.16 For many years, investigation into the effective-
Patient management ness of this as a therapy in ARDS has noted improvement
The key principles of management are treatment of the in oxygenation, but no corresponding improvement in
precipitating cause and providing supportive care during mortality. However, a recent clinical trial found that use
the period of respiratory failure. The most significant of prone positioning can improve survival in patients with
advances in the supportive care of ARDS patients have ARDS and severe hypoxaemia when applied early and
been associated with improved ventilator management. for relatively long periods.47 See Chapter 15 for further
Several clinical trials have shown that a large number discussion.
of pharmacological strategies have not been effective in
reducing mortality.43 Medications
Other strategies include cautious fluid management, A number of non-ventilatory strategies may form part
adequate nutrition, prevention of ventilator-associated of the treatment of patients with ARDS. Neuromuscu-
pneumonia, prophylaxis for deep vein thrombosis and lar blocking agents are used to promote patient–ventilator
gastric ulcers, weaning of sedation and mechanical synchrony, especially when non-conventional modes of
ventilation as early as possible and physiotherapy and ventilation are used. Improvements in oxygenation are
rehabilitation. Management involves a coordinated collab- usually observed and may be attributed to reduction in
orative approach including supportive ventilation, patient oxygen consumption and improved chest wall compliance.
positioning and medication administration. However, as the use of neuromuscular blocking agents
is also associated with an increased risk of myopathy,
Ventilation strategies demonstration of a clinically significant improvement in
The key focus of ventilation in ARDS is the prevention oxygenation with one dose prior to continuous adminis-
of refractory hypoxaemia rather than its reversal after tration is recommended.48
 CHAPTER 14 RESPIRATORY ALTERATIONS AND MANAGEMENT 451

Inhaled nitric oxide therapy may be used to improve of cases, asthma is well controlled; however, there are
oxygenation through selective vasodilation of the pulmon- approximately 180,000 deaths worldwide each year. Most
ary blood vessels, promoting improvement in ventilation– deaths occur in the pre-hospital setting although, in the
perfusion matching. Improvement in oxygenation should USA, 2–20% of admissions to ICU are attributed to
be observed within the first hour of treatment to support severe asthma60 with a 10–20% mortality rate in intubated
its ongoing use.48 Some groups have reported the use patients.61
of inhaled nitric oxide to be harmful, especially to renal
function, and recommend that it not be used,49 given the Pathophysiology
lack of evidence demonstrating reduction in mortality.50 A Asthma is a complex syndrome of unknown aetiology.
similar effect, in terms of pulmonary vasodilation, has been However, it is known to be influenced by genetic,
achieved using inhaled prostacyclins, which remains under immunological and environmental factors, and epidemi-
investigation as an alternative therapy.51 ological studies show strong associations with respiratory
A number of drug therapies continue to be inves- pathogens.62 The factors that contribute to asthma lead
tigated to treat ARDS in acute and subacute exudative to infection and allergic responses, inflammation and
phases. These include agents that target the disrupted smooth airway muscle contraction resulting in wheezing,
surfactant system (exogenous surfactant therapy), oxidative breathlessness and coughing. The pathophysiology of
stress and antioxidant activity (antioxidants), neutrophil life-threatening asthma involves constriction of the bron-
recruitment and activation, activation of the coagulation chioles and subsequent air trapping in the alveoli beyond
cascade (immune-modulating agents, heparin, aspirin the constriction, leading to hyperinflation and generation
and statins), microvascular injury and leak (beta-2- of intrinsic positive end-expiratory pressure. This is exac-
agonists, ACE inhibitors), and tissue regeneration (growth erbated by increased resistance in expiratory gas flow due
factors, stem cell therapy).To date, however, the advantages to a loss of elastic recoil and rapid respiratory rates. The
that have been observed in initial investigations have not patient increases the work of breathing, becomes rapidly
been shown in human trials.52,53,54 Although an improve- fatigued and anxious and there is diminished gas exchange.
ment in oxygenation has been reported, improvements in These factors reduce carbon dioxide elimination while
other outcomes such as duration of mechanical ventila- increasing its production and eventually will progress to
tion, length of ICU stay or improved survival have not respiratory failure and hypoxaemia.63
been shown.54 The use of low-dose corticosteroids has In 2014, the International European Respiratory
been associated with improved outcomes for patients with Society/American Thoracic Society published new
ARDS, although its use remains controversial and further guidelines on the definition, evaluation and treatment of
investigation is ongoing. severe asthma targeted mainly to respiratory specialists. In
common with previous guidelines, they do not address
issues of management in intensive care. In this respect,
Asthma and chronic the Australian Asthma Handbook and the British Thoracic
obstructive pulmonary disease Society are more specific in their recommendations,
recommending admission to ICU or a high dependency
Asthma is a chronic respiratory condition where airflow unit for deteriorating respiratory function, oxygenation
limitation may be fully or partially reversible either spon- and reduced level of consciousness.64
taneously or with treatment.55,56 COPD is a chronic In contrast to asthma, COPD is a preventable and
respiratory condition where airflow limitation is progres- treatable disease associated with an inflammatory response
sive and not fully reversible, although there may be some to harmful gases or particles. Inflammation causes signif-
reversibility of airflow limitation with bronchodilators. icant airflow narrowing that results in a permanent and
The partial airflow responsiveness to therapy in COPD progressive condition. Smoking (both active and passive)
results in a clinical overlap between COPD and asthma, is the cardinal risk factor and continuation is the most
as well as chronic bronchitis and emphysema. A non- significant determinant for disease progression.65,66
proportional Venn diagram (see Figure 14.2), originally However, only 25% of smokers actually develop clinically
used by the American Thoracic Society57 and now in the significant COPD,67,68 suggesting that other factors are
Australian and New Zealand expert guidelines,58 depicts also involved including environmental and occupa-
this overlap between conditions. It is not uncommon for tional pollutants, genetic predisposition, hyper-responsive
people with an obstructive lung disease to share clinical airways and respiratory infections.69,70 Disease progression
characteristics for more than one respiratory condition, in susceptible individuals is most likely to be dependent
although the dominant clinical symptom is usually on the synergistic effects of these factors. It is estimated
indicative of the underlying condition.59 It is, however, that approximately 210 million people worldwide have
important to differentiate between COPD and asthma as COPD71 and, despite public health effects, the World
they have different management and illness trajectories. Health Organization has predicted that by 2030 it will be
Asthma affects approximately 150 million adults and the third most common cause of death.72
children worldwide, with Australia, New Zealand and The airflow limitation characterised in COPD may
the UK having the highest incidences.59 In the majority be a result of three different pathological mechanisms.
452 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

First, chronic inflammation leads to fibrosis of the small (32% versus 16%) and that COPD was associated with
airways. Second, loss of elastic support and recoil leads prolonged mechanical ventilation and prolonged weaning.
to airway collapse because the small airways close on The authors also reported that the use of non-invasive
expiration. Third, the mucous and plasma exudate from ventilation within the COPD cohort more than doubled
the inflammation obstructs the airway lumen. These during the study period, and that this was associated with
mechanisms lead to air trapping and lung hyperinflation, a reduction in mortality.80
which consequently produces dyspnoea and exercise
limitation for the patient.73 Assessment and diagnostics
Perfusion abnormalities arise from hypoxaemia- Communication with patients that builds trust, through
induced vasoconstriction of the capillary beds. Pulmonary honesty and effective intervention, contributes consid-
ventilation/perfusion abnormalities and hyperinflation erably to the de-escalation of panic and fear in patients
contribute to increased pulmonary vascular resistance, and presenting with hypoxaemia. Creating a calm and trusting
respiratory muscle fatigue.74 Increased pulmonary vascular environment is paramount for those struggling for breath.
resistance and hypoxaemia require the right side of the Forward-planning for potential deterioration and constant
heart to work harder and may lead to right ventricular assessment of respiratory, cardiovascular and neurological
hypertrophy, dysfunction and failure (cor pulmonale).75 systems are fundamental in determining optimal clinical
The incidence of right ventricular hypertrophy is progress for these patients. Diagnostic tests and procedures
approximately 40% for patients with moderate levels of involve peak flow monitoring, spirometry, radiology
COPD (i.e. FEV1 <1000 mL).55 The left ventricle may and ABGs.56
also be compromised by hyperinflation, which generates The ‘gold standard’ for diagnosing COPD is
increased afterload. Pulmonary hypertension, coronary spirometry.69,81,82,83 Although there is no gold standard in
artery disease and arrhythmias are therefore a frequent the diagnosis of asthma, spirometry is the lung function
concomitant condition with COPD76 (see Chapter 11 test of choice.81 Respiratory function tests are usually
for further discussion). Impaired ventilation and perfusion performed according to standard principles.84 Values
leads to hypoxaemia and mechanical dysfunctions, with obtained are expressed at body temperature, ambient
the primary cause of adverse lung mechanics being pressure, saturated with water vapour, in absolute units
hyperinflation. (L or L/s) and as a percentage of predicted normal values.
COPD is not just a disease of the lungs. COPD and The carbon monoxide pulmonary diffusing capacity may
systemic inflammation have been widely studied and be measured using the single breath technique modified by
inflammation has been considered an important key Krogh.84 Diffusing capacity indicates the available surface
linking the disease and systemic manifestations. It has been area for gas exchange, and is reduced with emphysema
established that systemic inflammation is present during but can be normal with asthma.85 The carbon monoxide
both stable phases and acute exacerbations of COPD. pulmonary diffusing capacity can be a directly measured
Increased numbers of leucocytes, acute phase response value or expressed as a percentage of predicted normal
proteins, cytokines and tumour necrosis factor are found for age, sex, height and weight. A number of reference
in the blood of COPD patients.77 COPD is associated with tables of predicted normal values enable comparison
quite significant systemic abnormalities including kidney with population norms.85 A continuing lack of consensus
and hormonal imbalances, malnutrition, muscle-wasting, remains for differentiating asthma and COPD. The most
osteoporosis and anaemia. What is not clear, however, is commonly used criterion in Australia and New Zealand is
if the systemic abnormalities are a consequence of the airway reversibility in response to bronchodilator therapy:
pulmonary disorder or if COPD is a systemic disease.78 <15% reflects COPD; >15% reflects asthma.70
Clinical manifestations Patient management
With asthma and COPD, a patient may present with Contemporary management of asthma follows an asthma
wheeze, cough and/or dyspnoea. History and physical management plan, to minimise acute exacerbation and
assessment are fundamental to determining the severity any subsequent respiratory arrest. Many presentations will
of presentation. Presence of diminished or silent breath be managed in the emergency department (see Chapter
sounds, central cyanosis, an inability to speak, an altered 23 for further discussion). For patients requiring ventila-
level of consciousness, an upright posture and diaphoresis tory support, they are better managed with non-invasive
indicate a life-threatening case.56 Chest pain or tightness ventilation, as mechanical ventilation is associated with
may be present. Underestimation of severity is associated significant mortality and morbidity80 from hyperinfla-
with higher mortality.56 Large longitudinal datasets for tion and aggravation of bronchospasm.60 Contemporary
Australia and New Zealand, the UK and Saudi Arabia79 management of COPD has advocated a care plan for patients
show hospital survival rates ranging from 90% to 100%, in the community setting.This has an effect on prompting
largely due to the reversibility of the condition. Conversely, patients to recognise a change in their symptoms and seek
the largest epidemiological study of COPD in Europe appropriate care. However, improving symptom recogni-
showed that hospital mortality of patients admitted to ICU tion does not reduce healthcare utilisation.86 Patients with
due to COPD was double that of patients without COPD acute exacerbations of COPD managed with non-invasive
 CHAPTER 14 RESPIRATORY ALTERATIONS AND MANAGEMENT 453

ventilation in a timely manner have a reduced need for can present with symptoms similar to asthma, including
endotracheal intubation and reduced mortality rate.87,88 respiratory distress, wheeze, tachycardia, tachypnoea,
In patients with COPD who are mechanically ventilated, desaturation, hyper-expansion, agitation and decreased
a weaning strategy that includes non-invasive ventilation air entry.90 Fortunately, tension pneumothorax is a far
has been shown to reduce mortality and VAP without less common condition, and the patient is more likely
increasing the risk of re-intubation or weaning failure. to report additional chest pain. The actual incidence of
There are published guidelines on the prevention, identi- tension pneumothorax is relatively unexamined, but
fication and management of asthma60 and COPD.65 it is more likely to occur in a ventilated patient where
a pneumothorax has been missed on assessment.91
Medications
Administration of oxygen and beta-agonists (salbutamol) Pathophysiology
are first-line therapies. Nebulised salbutamol is the preferred Tension pneumothorax occurs when a one-way valve
route, with intravenous administration considered for forms, allowing air to flow into the pleural space but
patients not responding to nebulised medication. See stopping air from flowing out. The volume of intrapleural
Table 14.660 for key medications used in the treatment air increases with each inspiration. Consequently, pressure
of asthma. rises within the thoracic cavity, the lung collapses and
hypoxaemia ensues. Further pressure causes a media-
Pneumothorax stinal shift that subsequently compresses the lung (causing
further hypoxaemia) and the superior and inferior vena
Pneumothorax describes air that has escaped from a defect cava entering the right atrium of the heart (causing
in the pulmonary tree and is trapped in the potential compromised venous return). Untreated, the hypoxaemia,
space between the two pleura. A pneumothorax can be metabolic acidosis and decreased cardiac output lead to
classified as spontaneous, traumatic or iatrogenic and can cardiac arrest and death.91
be life-threatening. A spontaneous pneumothorax can be
primary (in persons without lung disease) or secondary (in Clinical manifestations
persons with lung disease). A pneumothorax is traumatic Severe presentations are identified by history and clinical
if caused by a blunt or penetrating injury or iatrogenic if examination (respiratory distress, cyanosis, tachycardia,
caused by complications from diagnostic or therapeutic tracheal shift and unilateral movement of the chest). They
interventions.89 are also detected on CXR with a translucent appearance
In some cases, the amount of air trapped increases of the air and absence of lung markings92 (see Chapter 13
markedly if the defect in the pulmonary tree functions as for information on CXR interpretation).
a one-way valve. In this case, air enters the pleural cavity
on inspiration but is unable to exit on expiration, leading Patient management
to increasing intrapleural pressure.This is termed a tension It is essential to check airway, breathing and circulation in
pneumothorax. A patient with tension pneumothorax all patients with chest trauma. Upright positioning may

TABLE 14.6
Key medications in an acute episode of asthma60

TYPE OF GENERIC
DRUG M E D I C AT I O N ACTION N U R S I N G C O N S I D E R AT I O N S

Beta-agonist salbutamol Produces relaxation of bronchial Metered-dose inhaler – one to two puffs (100–200 mcg)
smooth muscle by action at beta- 4-hourly and as required. Also continuous nebulisation
2-receptors via ultrasonic nebuliser and intravenous administration
Steroids hydrocortisone Starts effect 6–12 hours after Glucocorticoid dramatically reduces inflammation by
administration its profound effects on concentration, distribution and
Increases beta-responsiveness of function of peripheral leucocytes and a suppressive
airway smooth muscle effect on inflammatory cytokines and chemokines
methyl-prednisolone Decreases inflammatory response A synthetic adrenal steroid with similar glucocorticoid
Decreases mucus secretion activity, but considerably less severe sodium and water
retention effects than those of hydrocortisone
Xanthine aminophylline Bronchodilator Administration can be in oral or intravenous form. The
Inhibits the inflammatory phase half-life is variable dependent on age, liver and thyroid
in asthma function. This is a drug now used with decreasing
Stimulates the medullary frequency
respiratory centre
454 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

be beneficial if there is no contraindication. Penetrating Pulmonary embolism

wounds should be covered immediately with an occlusive
or pressure bandage. If a tension pneumothorax is Deep vein thrombosis and pulmonary embolism (PE)
suspected, a thin needle can be used to relieve the pressure are two aspects of the disease process known as venous
and allow the lung to re-inflate. If this is unsuccessful, thromboembolism. Certain factors lead to higher
insertion of a thoracic underwater seal drain will allow the incidence, immobilisation (due to long bone, pelvic and
collapsed lung to re-expand. If a haemothorax is present, spinal fractures) and closed head injury in particular (see
suction on the underwater seal drain (20–60 mmHg) will Table 14.8 for a list of risk factors).96
expedite drainage and re-expansion of the lung.93 There In addition, critically ill patients have many additional
are no reported differences in short- and long-term health risk factors, such as the need for surgery, catheters,
outcomes between insertion of an underwater seal drainage immobility and use of sedatives and paralytic agents.97
system and simple aspiration of the air for patients with a Most PEs originate in the lower limbs, pelvic veins or
spontaneous primary pneumothorax.92 Pain management inferior vena cava.
and facilitation of respiratory care with oxygen therapy, Three predisposing risk factors for thrombosis are
non-invasive or invasive ventilation, positioning and deep venous stasis, vein wall injury and hypercoagulability of
breathing and coughing, and the monitoring of the chest blood. Clinical risk factors are immobility, surgery, trauma,
tube and drainage for the presence of air leak and serous malignancy, pregnancy or thrombophilia. PE may have no
drainage, are key to recovery without development of clinical consequence or it may be catastrophic, causing
further complications.94 Chapter 12 discusses chest tube sudden death. Terms such as ‘massive’, ‘sub-massive’ and
management in more detail. ‘non-massive’ are often found in the literature, although
they are ambiguous.98 Outcomes from PE vary substan-
Medications tially depending on patient characteristics; for example, a
Management of pain associated with chest trauma is guided non-massive PE may be associated with a high risk for
by the presence of comorbidities. Epidural or intravenous complications in a patient with COPD or congestive
opioids are the most effective pain management strategies heart failure.99 International registries maintained over
(see Table 14.7).95 two decades affirm that hypotension and cardiac arrest

TABLE 14.7
Common medications prescribed with chest injury: pneumothorax95

TYPE OF GENERIC
DRUG M E D I C AT I O N ROUTE / ACTIONS N U R S I N G C O N S I D E R AT I O N S

Opioids morphine Intravenous Sedative effect with respiratory depression,

Activates opioid receptors in the brain and decreased cough reflex, bradycardia
spinal cord Histamine release may lead to flushing of face
Depresses respiratory centre and cough reflex or hypotension, nausea and vomiting
Alters pain perception and CNS modulation of Reduces gastrointestinal motility
painful stimuli Reversed by naloxone
fentanyl Epidural and intravenous Sedative effect with respiratory depression
A synthetic phenylpiperidine derivative Can obscure the clinical course of patients
Pharmacological actions are similar to those of with head injury
morphine, but action is more prompt and less Slow intravenous injection reduces the risk of
prolonged, and fentanyl appears to have less respiratory muscle rigidity
emetic activity Use with caution in patients with renal
and hepatic impairment, as action will be
prolonged
Respiratory depression can be reversed by
naloxone Bradycardia can be reversed by
atropine
Antibiotic cephalosporin Intravenous Active against a wide range of gram-positive
(1st generation) Bactericidal as a result of inhibition of bacterial and gram-negative bacilli. Highly active
for 24 hours cell wall synthesis against Staphylococcus aureus, including
strains resistant to penicillin

Adapted from Adrales G, Huynh T, Broering B, Sing RF, Miles W, Thomason MH et al. A thoracostomy tube guideline improves
management efficiency in trauma patients. J Trauma 2002;52(2):210–16, with permission.
 CHAPTER 14 RESPIRATORY ALTERATIONS AND MANAGEMENT 455

thrombosis, 40–50% may progress to develop a PE. PE

TABLE 14.8 occurs 3–7 days after the onset of deep vein thrombosis
Risk factors for venous thromboembolism96 and in 10% of cases may be fatal within 1 hour after
symptoms develop.102
Individual Age
The consequences of acute PE are primarily haemo-
Pregnancy and the puerperium
Active or occult malignancy
dynamic. Pulmonary artery obstruction causes release
Previous venous thromboembolism
of vasoactive agents from accumulating platelets, with
Varicose veins subsequent raised pulmonary vascular resistance and
Marked obesity acute pulmonary hypertension. The arterial obstruction
Prolonged severe immobility (bed rest, long causes severe shunting and life-threatening hypoxaemia.
haul flights) Early recognition is of utmost importance, but may be
Oestrogen-containing hormone replacement difficult in the ICU setting. In the mechanically ventilated
therapy or oral contraceptives patient, difficulty to wean or sudden incidences of hypo-
Inherited or acquired thrombophilia tension, tachycardia and hypoxia may be a consequence
Medical Acute or acute on chronic chest infection of an undetected PE.104 In 90% of cases, PE is suspected if
Heart failure patients develop dyspnoea (most common), pleuritic chest
Myocardial infarction pain and haemoptysis. Physical signs of tachypnoea, fever,
Stroke with immobility tachycardia and right ventricular dysfunction may also be
Some forms of cancer chemotherapy present. If a massive PE has occurred, the patient exhibits
Acute inflammatory bowel disease hypotension with pale, mottled skin and peripheral and/
Surgical All surgical procedures, especially abdominal, or central cyanosis.105
pelvic, thoracic, orthopaedic
Leg injury that requires surgery or prolonged
Assessment and diagnostics
immobilisation Several clinical prediction scoring tools to estimate the
ICU Presence of central venous catheters
probability of PE have been developed. The two most
Mechanical ventilation
validated are the Modified Wells Scoring System106 and the
Pharmacological paralysis Revised Geneva Scoring System.107 These tools are based
Acquired coagulation disorders on a list of criteria of known risk factors and clinical signs:
points are assigned to each criterion to produce a score
Adapted from National Health and Medical Research indicating clinical probability of a PE. Evidence-based
Council (NHMRC). Clinical practice guideline for the literature supports the practice of using these tools before
prevention of venous thromboembolism in patients admitted
proceeding to diagnostic testing. Diagnostic investiga-
to Australian hospitals. Melbourne: NHMRC, <https://www.
nhmrc.gov.au/_files_nhmrc/publications/attachments/ tions include compression ultrasonography for a suspected
guideline_prevention_venous_thromboembolism.pdf>; deep vein thrombosis, pathology test for elevated levels
2009 [accessed 09.07.14]. of D-dimer in plasma and a ventilation–perfusion isotope
scan, CT and pulmonary angiography (helical CT) scan
for PE.96
are associated with increased mortality in acute PE. The
International Cooperative Pulmonary Embolism Registry Patient management
reported the 90-day mortality rate of patients with acute Due to the high risk of venous thromboembolism in
PE and a systolic blood pressure <90 mmHg as 52% the critically ill, ICUs should have a policy for thrombo-
in comparison with 15% for normotensive patients.100 embolic prophylaxis.108 It is recommended that patients
The Management Strategy and Prognosis of Pulmonary undergo a risk assessment prior to initiating preventa-
Embolism Registry reported in-hospital mortality rates of tive therapies. Recommended prophylactic interventions
8.1% for haemodynamically stable patients versus 25% for include anticoagulant-based prophylaxis or, for patients
those with cardiogenic shock and 65% for those requiring with a high risk of bleeding, mechanical prophylaxis with
cardiopulmonary resuscitation.101 A number of interna- either graduated anti-embolic compression stockings
tional clinical practice guidelines have been published alone or stockings combined with intermittent pneumatic
to address this significant health issue.102,103 They address compression devices. Combined pharmaceutical and
risks and benefits of treatment for medical, surgical and mechanical prophylaxis has been shown to significantly
oncology patients. reduce the incidence of deep vein thrombosis, but it has
not been studied in the ICU setting.109
Clinical manifestations The management of PE in the ICU can be complex,
In most cases, PE is a consequence of deep vein thrombosis, hence the need for an ongoing risk assessment. For
therefore clinical manifestations should be considered example, multisystem organ failure (particularly of the
together. The risk of venous thromboembolism is highest liver and kidney) and the need for invasive procedures
during the first 2 weeks after surgery and remains high or surgery may complicate decisions on anticoagulant
for 2–3 months. In patients with a symptomatic deep vein therapy. Providing there are no contraindications, the first
456 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

line of treatment is subcutaneous or intravenous heparin anticoagulant similar to low-molecular weight heparin.110
or non-heparin based anticoagulant therapy. If anti- In high-risk PE with cardiogenic shock, thrombolytic
coagulation therapy is absolutely contraindicated or has therapy, for example recombinant tissue plasminogen
failed, surgical pulmonary embolectomy or percutaneous activator or streptokinase, is the first line of treatment.111
catheter embolectomy can be used in high-risk patients. Table 14.9112 outlines some of the key medications recom-
A further technique that can be used if thrombolysis is mended and prescribed for patients with PE.
contraindicated is the deployment of a filter in the inferior
vena cava.105 Lung transplantation
Medications Transplantation is a life-saving and cost-effective form of
Medications commonly prescribed in PE include inotropes, treatment that enhances the quality of life for people with
analgesics, thrombolytic and anticoagulant therapy. chronic respiratory disease. Lung transplantation is facili-
Supportive treatment of acute right ventricular failure and tated by organ donation from patients with brain death or
hypotension is vital. Inotropic drugs such as adrenaline, donation after cardiac death. Donation after cardiac death
noradrenaline and dobutamine need to be carefully significantly increased the number of organs available
administered because of associated peripheral vasodilation, for lung transplantation.113,114 Encouragingly, results of a
which may exacerbate the problem.96 In general, antico- large multicentre study demonstrate early and intermedi-
agulation treatment plays the major role in patient therapy. ate patient outcomes for patients with transplants arising
Rapid anticoagulation is achieved with intravenous from organ donation after cardiac death are equivalent
unfractionated heparin, subcutaneous low-molecular to outcomes for donation after brain death.115 In 1985,
weight heparin or subcutaneous fondaparinux, a synthetic 13 lung transplant procedures were reported worldwide.

TABLE 14.9
Medications for pulmonary embolism112

TYPE OF DRUG G E N E R I C M E D I C AT I O N ACTION N U R S I N G C O N S I D E R AT I O N S

Opioid morphine Pain relief See Table 14.7

Anticoagulant unfractionated heparin A strongly acidic mucopolysaccharide Prophylaxis and treatment of
with rapid anticoagulant effects venous thromboembolism, PE
Inhibits thrombin and potentiates and disseminated intravascular
naturally occurring inhibitors of coagulopathy
coagulation, antifactor X (Xa) and To prevent clotting in extracorporeal
antithrombin III blood circuits (e.g. renal dialysis or
No effect on existing thrombi intravascular catheters)
Standard heparin has a molecular weight Prophylaxis of arterial thrombosis
of 5000–30,000 daltons (e.g. after vascular surgery,
interventional radiology or
after thrombolysis for an acute
myocardial infarction)
Low-molecular-weight LMW heparin ranges from 1000–10,000 Administered subcutaneously
(LMW) heparin daltons, resulting in distinct properties
LMW-heparin binds less strongly to
protein, has enhanced bioavailability,
interacts less with platelets and yields
a very predictable dose response,
eliminating the need to monitor aPPT
Acetyl salicylic acid aspirin Preventive: inhibits thromboxane A2 The aspirin antiplatelet effect lasts
(platelet agonist), prevents formation of 8–10 days (the life of a platelet in
thrombi and arterial vasoconstriction general); aspirin should be stopped
1 week before surgery
Thrombolysis recombinant tissue-type Massive pulmonary embolism, where The risks of therapy include
plasminogen activator restoration of pulmonary arterial flow is haemorrhage. Safety and
(rt-PA) alteplase, urokinase urgently required due to right ventricular monitoring of the patient’s clinical
and streptokinase failure state are paramount

Adapted from Pastores SM. Management of venous thromboembolism in the intensive care unit. J Crit Care 2009;24(2):185–9,
with permission.
 CHAPTER 14 RESPIRATORY ALTERATIONS AND MANAGEMENT 457

In the 2013 report, the number of recipients worldwide most common indications.118 In terms of quality of life,
has steadily increased to be in excess of 3640 annually.116 prospective lung transplant recipients usually struggle
Patients have received lung transplants in Australasia to perform activities of daily living, may be oxygen-
since the early 1990s. Lung transplantation can be either dependent and have New York Heart Association
single or double, depending on a patient’s underlying functional class III or IV symptoms. As a result, most
disease state. In the postoperative period, clinicians patients presenting for surgery are at risk of being debil-
need to carefully balance fluid management to optimise itated and may be malnourished or over-nourished,
respiratory function without causing haemodynamic and therefore require specific interventions by health
compromise or renal dysfunction. As severe pain, particu- team members. A recent study found that, although no
larly for transverse thoracotomy incisions, can compromise specific nutritional deficit was predictive of long-term
recovery significantly, effective analgesic regimens to adverse outcomes, preoperative hypoalbuminaemia as a
facilitate physiotherapy are critical. marker of malnutrition (and critical illness) was associated
with poorer survival and postoperative infections; thus
Indications optimising nutritional state is critical.119
The two generally accepted criteria for lung transplanta-
tion in patients with end-stage pulmonary or pulmonary Description
vascular disease are a poor prognosis (less than 50% The four possible forms of lung transplantation, indi-
chance of surviving 2 years) and poor quality of life.117 cations for each form of surgery and salient nursing
About a third of recipients suffer from COPD, with implications are outlined in Table 14.10.120 Currently, lung
idiopathic pulmonary fibrosis and cystic fibrosis the next transplantation takes two main forms: bilateral sequential

TABLE 14.10
Comparison of the four standard lung replacement techniques, including their common indicators120

B I L AT E R A L
HEART–LUNG SEQUENTIAL LUNG SINGLE LUNG LIVE DONOR LOBAR
Incision Midline sternotomy Transverse sternotomy, i.e. Lateral thoracotomy Transverse sternotomy,
horizontal ‘clam shell’ i.e. horizontal ‘clam shell’
Anastomoses Tracheal Left and right bronchial Bronchial Lobar bronchus to
Right atrial ’Double’ left atrial Left atrial bronchus
Aortic Right and left pulmonary Pulmonary artery Lobar vein to superior
artery pulmonary vein
Lobar artery to main
pulmonary artery
Advantages Airway vascularity Access to pleural space Easiest procedure Increases donors
All indications No cardiac allograft Increases recipients Can be performed
Less cardiopulmonary ‘electively’
bypass
Disadvantages Cardiac allograft Airway complications Airway complications Complex undertaking
Organ ‘consumption’ Postoperative pain severe Poor reserve Donor morbidity
Common Congenital heart disease with Cystic fibrosis Emphysema Cystic fibrosis
indications pulmonary hypertension Bullous emphysema COPD Pulmonary fibrosis
Heart and lung disease Primary pulmonary Pulmonary fibrosis Primary pulmonary
Primary pulmonary hypertension hypertension bronchiectasis Primary pulmonary hypertension
hypertension
Nursing Recipients may be malnourished Pain must be optimally Risk of pulmonary Complex ethical issues
considerations and debilitated managed to facilitate dynamic hyperinflation in
Rarely performed due to use physiotherapy and timely obstructive disorders
of three organs. If native heart recovery Complex ventilatory issues
from heart–lung recipient is Postoperative management Postoperative
transplanted into another patient requires careful optimisation management requires
(’domino’), it is judicious to have of haemodynamic, careful optimisation
relatives in separate waiting respiratory and renal function of haemodynamic,
rooms during surgery (i.e. respiratory and renal
complex issues may arise) function

COPD = chronic obstructive pulmonary disease.

Adapted from Williams TJ, Snell GI. Lung transplantation. In: Albert RK, Spiro SG, Jett JR, eds. Clinical respiratory medicine.
St. Louis: Mosby; 2004, pp 831–45, with permission.
458 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

lung transplantation (BSLTx) and single-lung transplan- 72 hours is likely to be due to infection or hemidiaphragm
tation (SLTx). BSLTx is the most common form of lung paralysis secondary to phrenic nerve damage. Although
transplantation and has a survival advantage over and BSLTx is usually performed without cardiopulmonary
above SLTx. However, the advantage of SLTx over BSLTx bypass, for those patients who require cardiopulmonary
is that twice as many people receive life-saving surgery. bypass for surgery, it is recognised that there is a higher
For SLTx recipients with COPD, there is an increase in incidence of PGD.
the complexity of postoperative respiratory management
and, for this reason, some centres may perform BSLTx for Patient management
patients with COPD. SLTx is also utilised for patients with Severity of allograft dysfunction is assessed by ABG
idiopathic pulmonary fibrosis and other forms of intersti- analysis, respiratory function and patient comfort, CXR,
tial lung disease who have a high waiting list mortality.120 bronchoscopy and haemodynamic parameters. A careful
balance in the management of haemodynamic, respiratory
Clinical manifestations and renal status is vital in the first 12 hours, and their
Postoperative management of all lung transplant recipients optimisation should be achieved with inotropes (e.g.
involves intensive clinical monitoring similar to that adrenaline, noradrenaline) and judicious use of colloids
required for heart transplant recipients, with a focus on to ensure adequate end-organ perfusion without causing
the stabilisation and optimisation of haemodynamic, pulmonary overload. Fluid management should aim to
respiratory and renal status. Great skill by clinicians is keep filling pressures low to normal in light of a recent
required to manage this complex interplay. Respiratory retrospective review that found a high CVP (>7 mmHg)
dysfunction can develop due to severe dysfunction of was associated with prolonged mechanical ventilation and
the transplanted lung resulting from ischaemia–reperfu- high mortality. Importantly, there was no evidence of renal
sion injury, pulmonary oedema, hyperacute rejection and complications associated with these low filling pressures.
pulmonary venous or arterial anastomotic obstruction. Fluid resuscitation should include products to correct
Other major complications in the early postoperative anaemia and preoperative low plasma protein levels.125
period that affect respiratory management include severe For patients who have required intraoperative cardio-
pain, diaphragmatic dysfunction, acute rejection and pulmonary bypass, high doses of inotropes are often needed
infection. Patients who receive an SLTx for COPD are to overcome a transient relative hypovolaemia. Addition-
at risk of developing pulmonary dynamic hyperinflation, ally, gentle rewarming measures are needed to re-establish
requiring independent lung ventilation. Haemodynamic normothermia in order to prevent haematological and
function can be compromised in the early postoperative peripheral perfusion impairments associated with hypo-
phase due to cardiac and respiratory problems; renal and thermia. Gentle rewarming, and close monitoring of
gastrointestinal dysfunction is also prevalent. Long-term cardiac output/index and pulmonary haemodynamics
respiratory complications include airway anastomotic should minimise the development of pulmonary oedema
problems (stricture and dehiscence), suboptimal exercise at this time. For patients with allograft dysfunction accom-
performance and chronic rejection manifesting as bron- panied by high pulmonary pressures, inhaled nitric oxide
chiolitis obliterans syndrome.116 is useful in decreasing high pulmonary pressures and
reducing intrapulmonary shunting.126,127 Continuous
Respiratory dysfunction monitoring of cardiac output, haemodynamic parameters
Respiratory dysfunction within the first 24–48 hours post- and urine output assists in guiding haemodynamic thera-
operatively is usually caused by primary graft dysfunction peutic interventions (see Chapter 9).
(PGD), a syndrome characterised by non-specific alveolar To assess the causes and progress of allograft dysfunc-
damage, lung oedema and hypoxaemia.121 PGD may be tion, CXR provides vital information about line placement,
aggravated by factors associated with the donor (e.g. ETT position, lung expansion, lung size, position of the
trauma, mechanical ventilation, aspiration, pneumonia and diaphragm and mediastinum and the presence of pneumo-
hypotension), cold ischaemic storage120 or inadequate pres- thorax, oedema and atelectasis.128 Allograft dysfunction
ervation and disruption of pulmonary lymphatics. Clinical due to ischaemia–reperfusion injury appears on CXR as
signs of PGD range from mild hypoxaemia with infiltrates a rapidly developing diffuse alveolar pattern of infiltration
on CXR to severe ARDS requiring high-level ventila- that is greater in the lower regions,129 most commonly
tory support, pharmacological support and extracorporeal seen on the first postoperative day but may occur up to
membrane oxygenation.122 Australian researchers have 72 hours following surgery. The presence of rapidly
shown a decrease in the severity and incidence of PGD worsening pulmonary infiltrates (especially if associated
following the implementation of an evidence-based with low cardiac indices) should, however, prompt urgent
guideline for managing patients’ respiratory and haemo- echocardiography to assess cardiac function and pulmonary
dynamic status postoperatively.123 The guideline directs venous anastomosis patency.129 Beyond 72 hours, alveolar
clinicians to minimise crystalloid fluids, use vasopressors and interstitial infiltration may indicate either acute
as the first-line treatment to maintain blood pressure if rejection or an infective process. This information is
cardiac output is adequate and use lung-protective venti- combined with other respiratory and haemodynamic data
lation strategies.122,124 Respiratory dysfunction beyond to inform appropriate collaborative interventions.
 CHAPTER 14 RESPIRATORY ALTERATIONS AND MANAGEMENT 459

Commonly, ventilatory settings and respiratory Immediate management of the condition requires
weaning are guided by pH rather than PaCO2 levels. A attempts to minimise hyperinflation with altered venti-
modest degree of hypercarbia is anticipated postopera- latory settings and bronchodilators. If this fails, insertion
tively and resolves over time. Given that lung-protective of a dual-lumen ETT is required. Precise positioning
ventilation has been shown to have a positive impact and secure placement of the tube is vital, to avoid slight
on recovery and long-term outcomes in patients with movement of the position and consequent displacement
ARDS,130 it is now recommended that SLTx and BSLTx of correct cuff placement (see Figure 14.4 for correct
recipients receive similar ventilator settings.131 In SLTx positioning of a dual-lumen ETT).
recipients, ventilation/perfusion mismatches can also
be improved by inhaled nitric oxide and by positioning FIGURE 14.3 Chest X-ray of a patient with left single
patients regularly with the allograft uppermost. lung transplant for COPD who has developed PDH.
Allograft dysfunction can develop in SLTx recipients
with a remaining native COPD lung who are ventilated
via a single-lumen ETT, due to gas trapping in the
over-distensible native lung, a condition known as
pulmonary dynamic hyperinflation (PDH) (see Figure
14.2). Any condition that lowers the compliance of
the allograft can lead to PDH in these patients. Nurses
need to be aware of the patients who can potentially
develop PDH and to remain hypervigilant, as early
signs and opportunities to stabilise patients’ haemody-
namic and respiratory status quickly can be easily missed.
Initial presentation of PDH is usually an ABG showing
inadequate ventilation (hypercapnoea) and oxygena-
tion (hypoxaemia). For many critically ill patients the
response to this clinical presentation might be to increase
respiratory rate, tidal volume or PEEP. However, in the
patient who has received a lung transplant and exhibits
PDH, these actions will exacerbate the degree of native
lung hyperinflation. A more appropriate strategy would
be to reduce minute ventilation.131
Other common presenting cues of PDH include a
haemodynamic profile of cardiac tamponade, tracheal
deviation, obvious hyperinflation of the native lung with
or without mediastinal shift on CXR, decreased air entry
to the allograft on auscultation and pneumothorax. The
early stages of PDH in a patient with a left SLTx for
COPD can be seen on the CXR in Figure 14.3.
FIGURE 14.4 Correct positioning of a double-lumen
FIGURE 14.2 Mechanism of pulmonary dynamic endotracheal tube for pulmonary dynamic hyperinflation.
hyperinflation: distribution of inspiratory gas.
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460 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Independent lung ventilation is then established however, the insertion of an epidural catheter at the time
to ensure that the native lung receives no PEEP and a of surgery may be contraindicated due to preoperative
minimal tidal volume and rate.132 The allograft may require anticoagulation therapy. In these circumstances, epidural
high levels of PEEP to provide adequate oxygenation. analgesia should be instituted as soon as appropriate after
Ongoing assessment of respiratory function determines surgery. Higher failure rates of transition from epidural
the timing of weaning independent lung ventilation (i.e. to oral analgesia have been reported in lung transplant
replacement of the dual-lumen ETT with a single-lumen recipients than in other thoracotomy patients,134 and it is
ETT) and return to standard ventilatory practice. If PDH not uncommon for BSLTx recipients to require opiate
is not recognised until the patient has a cardiac arrest, the analgesia for a month after surgery in order to perform
single-lumen ETT should be pushed into the bronchus activities of daily living and physiotherapy.
of the transplanted lung in order to selectively ventilate
the allograft until the patient’s condition is stable and a Patient management
dual-lumen ETT can be safely inserted. Consultation with pain services to ensure that patients
Patients with allograft dysfunction are always assessed receive optimal analgesic regimens should be an integral
for the emergence of rejection and pulmonary infection component of patients’ postoperative management (see
using transbronchial biopsy and bronchoalveolar lavage in Chapters 7 and 26). Paracetamol is beneficial in relieving
critical care. Evidence of rejection will be treated with mild-to-moderate pain, and may be used as an adjunct to
changes in the immunosuppression regimen and appropri- centrally-acting analgesics for moderate-to-severe pain.134
ate ventilatory and haemodynamic support. Many patients The use of non-steroidal anti-inflammatory drugs should
with rejection in the immediate postoperative period may be avoided, due to their detrimental effects on renal and
not exhibit classic signs of rejection such as abrupt onset gastrointestinal function.135
of dyspnoea, cough and chest tightness while mechani- The nursing management of intercostal chest tubes is
cally ventilated. Subtle changes in respiratory effort, gas similar to that for cardiac surgical patients (see Chapter
exchange and minute ventilation may be the only signs 12), with a few additional considerations. Recipients of
to alert the nurse to respiratory dysfunction secondary to SLTx have one apical and one basal chest tube, whereas
rejection or infection during mechanical ventilation. BSLTx recipients have four chest tubes: two apical and
Classic clinical signs of pulmonary infection include two basal. Both BSLTx and SLTx recipients have one
a low-grade fever, increasing dyspnoea and sputum pleural space, so the amount and consistency of drainage
production, cough and infiltrates on a CXR. Hypo- from basal tubes will vary depending on patient position-
tension, a reduced cardiac index and subtle changes in ing. Apical chest tubes are removed prior to basal tubes.
respiratory parameters during mechanical ventilation Once lung expansion is optimal and any pneumothoraces
noted above may also be present. Pulmonary infections have resolved, the apical tubes are removed. Basal chest
may be acquired through nosocomial, community or tubes are removed once drainage is considered minimal
donor means, with recipient-colonised and opportunistic in volume (approximately 250 mL/day) and serous in
infections prevalent. Regardless of the means of acqui- nature.136
sition, all infections are treated promptly with specific
antibiotic, antifungal or antiviral therapies. The risk of Haemodynamic instability
developing cytomegalovirus and Pneumocystis carinii in As noted earlier, all lung transplant patients can experience
lung transplant recipients is somewhat higher than in heart haemodynamic compromise and renal impairment post-
transplant recipients, so prophylactic therapies for both operatively as a result of managing respiratory function.
infections are provided. Clinicians play an important role in Potential causes of a low cardiac output are outlined in
preventing the transmission of infection between patients Table 14.11. Patients with pulmonary hypertension must
and cross-contamination within patients. Meticulous hand be carefully managed in the early postoperative period
washing between patients and between procedures as well because of impaired cardiac output and changes in right
as minimising traffic into and out of patient care areas are ventricular dynamics. Prior to surgery, prolonged periods
important measures in reducing infection rates.133 of a high right ventricular afterload lead to right ventricu-
lar thickening and stiffness, accompanied by limited wall
Pain motion of the left ventricle.137
All recipients of lung transplantation can experience
severe pain afterwards due to the incisions and chest drains. Patient management
However, recipients of BSLTx in particular experience During arousal from anaesthesia and patient activity,
extremely severe postoperative pain secondary to the fluctuations in oxygenation and systemic and pulmonary
transverse sternotomy (clam-shell incision) and presence pressures exacerbate haemodynamic instability.138,139
of four chest tubes. The recent use of a minimally invasive When weaning from mechanical ventilation, as venti-
thoracotomy rather than transverse sternotomy for patients lation pressures fall, increases in preload may precipitate
with obstructive respiratory illnesses may also reduce the acute pulmonary oedema, even days after surgery.138
postoperative pain experienced by recipients. Ideally, all Conversely, if the patient is hypovolaemic at the time
lung transplant recipients should receive epidural analgesia; of weaning, right ventricular outflow obstruction may
 CHAPTER 14 RESPIRATORY ALTERATIONS AND MANAGEMENT 461

for ‘dry’ lungs postoperatively. Fortunately, the use of inter-

TABLE 14.11 leukin-2 receptor antibody drugs can assist in lowering
Possible causes of low cardiac output in the first week the doses of calcineurin inhibitor agents to offer some
after lung transplantation137 early protection to the kidneys without inducing acute
C A R D I O VA S C U L A R
rejection.140
Hypovolaemia Patient management
Haemorrhage Routine management of gut function is an important
Hypothermia
aspect of nursing practice, including the prevention of
Acute myocardial infarction
constipation (see Chapter 6). For patients receiving surgery
Pulmonary venous or arterial anastomosis obstruction
for cystic fibrosis, pancreatic enzyme supplements are
(embolism, clot, stitch, torsion)
Pulmonary embolism (thrombus or air)
required postoperatively. As these patients are invariably
Non-specific left ventricular dysfunction
debilitated preoperatively, enteral feeds that do not require
Arrhythmias pancreatic enzyme supplements should be commenced as
Coronary artery air embolism soon as possible after surgery, as these supplements cannot
P U L M O N A RY
be administered via enteral feeding tubes. Further specific
information on managing patients with cystic fibrosis is
Pulmonary dynamic inflation of native lung in single-lung
available.141
transplantation
Pneumothorax Psychosocial care
Oversized pulmonary allograft
In the early postoperative period, corticosteroids,
OTHER
sedatives, sleep deprivation and persistent pain contribute
Sepsis/infection (especially line or occult gut) to acute organic brain syndrome117 (see Chapter 7).
Sedatives Rejection episodes can be emotionally demanding, and
Analgesics (especially epidural) the requirement for higher doses of corticosteroids can
Transfusion reaction lead to irritability, insomnia, profound depression, mania
Anaphylaxis or psychosis.117
Hyperacute rejection (rare) Although lung transplantation offers recipients relief
Adapted from Birsan T, Kranz A, Mares P, Artemiou O, from shortness of breath and increased exercise tolerance,
Taghavi S, Zuckermann A et al. Transient left ventricular many patients have to continue managing other aspects
failure following bilateral lung transplantation for pulmonary of their underlying disease (e.g. cystic fibrosis). Thus, the
hypertension. J Heart Lung Transpl 1999;18(1):4–9, with burden of living with a chronic illness remains. Conversely,
permission.
some recipients experience wellness for the first time
in their life, and this can alter family and relationship
dynamics. In circumstances where lung function deterio-
occur.125 These potential events confirm that careful rates after initial success, patients and families experience
titration of fluid and inotropic therapies, guided by feelings of devastation and hopelessness. Counselling
frequent, accurate monitoring of invasive haemodynamic services are essential in both the preoperative and the
parameters, is required in patients with preoperative postoperative phase.142,143
pulmonary hypertension.
Long-term sequelae
Renal and gut dysfunction Long-term sequelae for lung transplant recipients include
Reasons for renal dysfunction in lung transplant recipients renal impairment, hypertension and increased risk of
in the early postoperative period are similar to those for malignancies, similar to those with heart transplantations.
heart recipients. The situation is, however, compounded Further information about long-term complications
in lung recipients due to aminoglycoside and non- specific to lung transplantation, such as bronchiolitis
steroidal anti-inflammatory drug use preoperatively, the obliterans syndrome and other non-pulmonary complica-
high number of patients with diabetes and a requirement tions, is available.144,145

Summary
Respiratory alterations, whether a primary condition or a secondary complication of comorbidity, are a common reason
for ICU admission.Vigilant assessment, monitoring and provision of a rapid response to a deteriorating state are central to
critical care nursing practice. Contemporary approaches to respiratory support focus on preserving a patient’s respiratory
function, including use of non-invasive ventilation, using less controlled ventilation when appropriate and consideration
of weaning from mechanical ventilation at the earliest opportunity. The current evidence base supports strategies to
prevent VAP, using daily checklists or care bundles.
462 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Case study
A 69-year-old man is admitted to the hospital because of a productive cough. The patient has a history
of alcohol abuse and is a 20 pack-year smoker. He has been in good health until 5 days ago when he
developed a cough, productive of yellow sputum. The cough is associated with fever and chills. He also has
dyspnoea with minimal exertion. He denies weight loss, night sweats and previous exposure to tuberculosis.
He periodically sees a general practitioner and is being treated for hypertension, increased cholesterol and
ischaemic heart disease. His current medications include captopril 6.25 mg twice daily, metoprolol 50 mg
twice daily and anginine as required.
On presentation he had mild respiratory distress and could only talk in short sentences. His clinical
observations were: GCS 15/15, temperature 38.5°C, respiratory rate 34 breaths/min, heart rate 110 beats/
min, blood pressure 150/80 mmHg, SpO2 (room air) 92%.
On physical examination crackles were audible on auscultation and percussion of the chest revealed
dullness over the right lower chest. Blood was taken and testing revealed normal serum electrolyte values,
haematocrit and platelet count, but his white blood cell count was elevated. A chest radiograph was taken
and showed a right pleural effusion and alveolar infiltrate involving the right middle and lower lobes.
Blood and expectorated sputum were obtained for gram-stain and culture. The patient was started on
erythromycin and vancomycin. Results of the blood cultures were negative but the sputum grew Streptococcus
pneumoniae, which is sensitive to penicillin, and appropriate changes to antibiotic therapy were made.
The patient continued to have difficulty breathing and arterial blood gas analysis provided the following
results: pH 7.29, PaCO2 55 mmHg, HCO3− 23 mmol/L, PaO2 47 mmHg, SaO2 86%. As a result of the
hypoxaemia demonstrated in this result, the patient was commenced on supplemental oxygen via a venturi
mask with FiO2 of 0.50.
Further clinical assessment revealed: pale, cool, dry skin; dry, cracked lips; decreased urine output (voided
once in 8 hours – volume 150 mL); history of poor food/fluid intake over the past 5 days; BGL 9.0 mmol/L.

DISCUSSION
The patient presents with signs of a lower respiratory tract infection including an increased respiratory rate
and difficulty breathing, low oxygen saturation, temperature and increased white cell count. Chest X-ray
and physical examination reveal involvement of the right middle and lower lobes of the lung. His history
includes increased alcohol intake and smoking, which are risk factors for developing respiratory infections.
Alveolar infiltrate will decrease ventilation relative to perfusion and this will contribute to decreased amounts
of oxygen in the arterial blood as evidenced through the SpO2 of 92%. The alveolar infiltrate and presence of
pleural effusion will increase the patient’s work of breathing. Supplemental oxygen is required as the PaO2
and SaO2 have both decreased. The patient also has increased carbon dioxide in the arterial blood despite
a significant increase in his respiratory rate, suggesting that ventilation perfusion mismatch is significant
and preventing adequate carbon dioxide removal.
The decreased oxygen present in the arterial blood is of particular concern given the patient has a history
of ischaemic heart disease and angina. His increased heart rate will be increasing the myocardial work and
myocardial oxygen demand and may predispose him to cardiac ischaemia.
Treating the underlying infection will be important in improving oxygenation and minimising the physiological
stress. As the patient already shows signs of sepsis, preventing transmission from the respiratory system
to the blood is paramount. Management of his apparent sepsis will involve fluid administration and other
evidence-based therapies, so the nurse must be vigilant to ongoing assessment of the patient’s response
and averting progression to full septic shock.

CASE STUDY QUESTIONS

1 There are several severity scoring systems that can be used in CAP (see Box 14.1) to determine the
severity of the patient’s condition and predict his need for further intervention and support. Using the
information provided in the case study, describe the severity of this patient’s presentation according to
one or more of the scoring systems outlined.
2 Interpret the results from the patient’s arterial blood gas analysis and outline the likely management
strategies that would be considered priorities in this situation.
3 Explain whether the ventilation–perfusion mismatch in this patient is due to alveolar hypoventilation,
intrapulmonary shunting, dead-space ventilation or a combination of these factors.
 CHAPTER 14 RESPIRATORY ALTERATIONS AND MANAGEMENT 463

RESEARCH VIGNETTE

Burns KEA, Meade MO, Premji A, Adhikari NKJ. Non-invasive positive-pressure ventilation as a weaning strategy
for intubated adults with respiratory failure. Cochrane Database Syst Rev 2013;12:CD004127

Abstract
Background: Non-invasive positive-pressure ventilation (NPPV) provides ventilatory support without the need for
an invasive airway. Interest has emerged in using NPPV to facilitate earlier removal of an endotracheal tube and to
decrease complications associated with prolonged intubation.
Objectives: We evaluated studies in which invasively ventilated (IPPV) adults with respiratory failure of any cause
(chronic obstructive pulmonary disease [COPD], non-COPD, postoperative, non-operative) were weaned by means
of early extubation followed by immediate application of NPPV or continued IPPV weaning. The primary objective
was to determine whether the non-invasive positive-pressure ventilation (NPPV) strategy reduced all-cause mortality
compared with invasive positive-pressure ventilation (IPPV) weaning. Secondary objectives were to ascertain
differences between strategies in proportions of weaning failure and ventilator-associated pneumonia (VAP), intensive
care unit (ICU) and hospital length of stay (LOS), total duration of mechanical ventilation, duration of mechanical
support related to weaning, duration of endotracheal mechanical ventilation (ETMV), frequency of adverse events
(related to weaning) and overall quality of life. We planned sensitivity and subgroup analyses to assess (1) the influence
on mortality and VAP of excluding quasi-randomized trials, and (2) effects on mortality and weaning failure associated
with different causes of respiratory failure (COPD vs mixed populations).
Search methods: We searched the Cochrane Central Register of Controlled Trials (The Cochrane Library, Issue 5,
2013), MEDLINE (January 1966 to May 2013), EMBASE (January 1980 to May 2013), proceedings from four
conferences, trial registration websites and personal files; we contacted authors to identify trials comparing NPPV
versus conventional IPPV weaning.
Selection criteria: Randomized and quasi-randomized trials comparing early extubation with immediate application
of NPPV versus IPPV weaning in intubated adults with respiratory failure.
Data collection and analysis: Two review authors independently assessed trial quality and abstracted data according
to pre-specified criteria. Sensitivity and subgroup analyses assessed (1) the impact of excluding quasi-randomized
trials, and (2) the effects on selected outcomes noted with different causes of respiratory failure.
Main results: We identified 16 trials, predominantly of moderate-to-good quality, involving 994 participants, most with
COPD. Compared with IPPV weaning, NPPV weaning significantly decreased mortality. The benefits for mortality were
significantly greater in trials enrolling exclusively participants with COPD (risk ratio [RR] 0.36, 95% confidence interval
[CI[ 0.24 to 0.56) versus mixed populations (RR 0.81, 95% CI 0.47 to 1.40). NPPV significantly reduced weaning failure
(RR 0.63, 95% CI 0.42 to 0.96) and ventilator-associated pneumonia (RR 0.25, 95% CI 0.15 to 0.43); shortened length
of stay in an intensive care unit (mean difference [MD] −5.59 days, 95% CI −7.90 to −3.28) and in hospital (MD −6.04
days, 95%CI −9.22 to −2.87); and decreased the total duration of ventilation (MD −5.64 days, 95% CI −9.50 to −1.77)
and the duration of endotracheal mechanical ventilation (MD −7.44 days, 95% CI −10.34 to −4.55) amidst significant
heterogeneity. NPPV weaning also significantly reduced tracheostomy (RR 0.19, 95% CI 0.08 to 0.47) and reintubation
(RR 0.65, 95% CI 0.44 to 0.97) rates. NPPV weaning had no effect on the duration of ventilation related to weaning.
Exclusion of a single quasi-randomized trial did not alter these results. Subgroup analyses suggest that the benefits
for mortality were significantly greater in trials enrolling exclusively participants with COPD versus mixed populations.
Authors’ conclusions: Summary estimates from 16 trials of moderate-to-good quality that included predominantly
participants with COPD suggest that a weaning strategy that includes NPPV may reduce rates of mortality and
ventilator-associated pneumonia without increasing the risk of weaning failure or reintubation.

Critique
Focus: Minimising the duration of mechanical ventilation is an important goal because of the risk of VAP resulting in
increased morbidity and mortality. This systematic review is clearly focused on evaluating the impact of weaning for
critically ill adults (population) using NPPV (intervention) versus IPPV (comparator) on mortality and VAP (outcomes).
464 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Methodological quality: The review has good methodological quality. The authors reported transparent processes
demonstrating robustness in meeting the PRISMA checklist standards.146 The search strategy was fairly comprehensive,
but somewhat geographically constrained because the authors searched the conference proceedings of the top
four USA and European meetings for unpublished research. It is possible that unpublished conference abstracts of
studies presented at top Australian, Asian or South American meetings may have been missed, resulting in potential
publication bias. Selection, data extraction and quality assessment of included studies were undertaken by two
authors independently; furthermore, all analyses were determined a priori and there was no deviation from the review
protocol. These practices demonstrate a reliable process and reflect high standards in conducting the review.
Characteristics and methodological quality of included studies: Characteristics related to study settings (i.e.
country; nurse- and doctor-to-patient ratios; presence of sedation or ventilator weaning protocols) were poorly
described in the review. This is an important omission as it minimises the ability to generalise to one’s own clinical
setting. The quality of the majority of studies was judged as moderate, yet more than 50% failed to report their
methods of generating and concealing randomisation. This means we cannot reliably determine the level of selection
bias in these trials. If clinicians had prior knowledge of group allocation, recruitment to the NPPV group may be
compromised because of clinician-perceived clinical assessment of risk.
Interpretation of results: Nine of the 16 studies exclusively studied patients with COPD, and the impact of NPPV
in this patient population was significantly more beneficial than IPPV weaning for all outcomes (except duration of
ventilator weaning and arrhythmias). While this is very encouraging, the strength of this conclusion is somewhat
limited because of the reported variability in weaning methods employed in both NPPV and IPPV groups; the low
event rate for deaths and VAP; and variability in selecting and reporting continuous outcomes. Variability is not a
new phenomenon and the extent of the problem has been reported elsewhere.147 Furthermore, we are unsure of the
contexts in which these trials were conducted. Knowledge of the presence or absence of particular ICU contextual
factors (i.e. staffing, workload, usual weaning processes, expertise with NPPV) is essential when considering if this
intervention could be implemented and sustained in clinical practice.148 The authors proposed further research
before recommending the routine use of NPPV as an adjunct for weaning and a multicentre trial is currently underway
in the UK.149

Lear ning a c t iv it ie s
1 A patient has severe ARDS following aspiration pneumonia. His FiO2 is 1.0 and PaO2 is 60 mmHg. Core
temperature is 40°C and the only medications are antibiotics. Any activity including suctioning causes profound
desaturation. What additional measures could be implemented to minimise this effect?
2 Assess the next five patients that you look after against current criteria for ARDS and see how many patients are
categorised as having mild, moderate or severe ARDS.
3 List the interventions required for a nurse to safely care for a patient with a provisional diagnosis of H1N1 influenza.
4 Describe and compare the differences between a simple, persistent and reoccurring pneumothorax.
5 Outline the clinical manifestations that may be present in a mechanically ventilated patient with a pulmonary
embolism.

Online resources
American Association for Respiratory Care, www.aarc.org
ARDS Network, www.ardsnet.org
Asthma Foundation, www.asthmaaustralia.org.au
Australian and New Zealand Society of Respiratory Science, www.anzsrs.org.au
Australian Lung Foundation, www.lungnet.org.au
Become an expert in spirometry, www.spirxpert.com
British Thoracic Society, www.brit-thoracic.org.uk
 CHAPTER 14 RESPIRATORY ALTERATIONS AND MANAGEMENT 465

Centers for Disease Control and Prevention, www.cdc.gov

Critical Care Medicine Tutorials, www.ccmtutorials.com
InFACT, www.infactglobal.org
Lung Health Promotion Centre, The Alfred Hospital, Victoria – resources, www.lunghealth.org
Organ and Tissue Authority: Donate Life Australia, www.donatelife.gov.au/discover/facts-and-statistics
Pneumonia Severity Index Calculator, http://pda.ahrq.gov/clinic/psi/psicalc.asp
Respiratory Care online, www.rcjournal.com
Respiratory Research, http://respiratory-research.com
Thoracic Society of Australia and New Zealand, www.thoracic.org.au
World Health Organization, www.who.int/en

Further reading
Fuller J, Fisher A. An update on lung transplantation. Breathe 2013;9(3):189–200.
George E, Guttendorf J. Lung transplant. Crit Care Nurs Clin N Am 2011;23(3):481–503.
Lawrence P, Fulbrook P. The ventilator care bundle and its impact on ventilator-associated pneumonia: a review of the
evidence. Nurs Crit Care 2011;16(5):222–34.
Rose L, Nelson S. Issues in weaning from mechanical ventilation: literature review. J Adv Nurs 2006;54(1):73–85.
Shi Z, Xie H, Wang P, Zhang Q, Wu Y, Chen E et al. Oral hygiene care for critically ill patients to prevent ventilator associated
pneumonia. Cochrane Database Syst Rev 2013;CD008367.

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Chapter 15

Ventilation and oxygenation

management
Louise Rose, Rand Butcher

KEY WORDS
Learning objectives
After reading this chapter, you should be able to: artificial airway
• describe complications associated with oxygen therapy and management mechanical
priorities ventilation
• state nursing priorities for airway management strategies including non-invasive
laryngeal masks, endotracheal tubes and tracheostomy tubes ventilation
• summarise current knowledge on the physiological benefits, indications oxygen therapy
for use, associated monitoring priorities, complications, modes, settings weaning
and interfaces for non-invasive ventilation
• state the indications for use, associated monitoring priorities,
complications, classification framework, modes and settings for invasive
mechanical ventilation
• outline the weaning continuum and current evidence for optimising safe
and efficient weaning from mechanical ventilation
• discuss ventilation management strategies for refractory hypoxaemia
• discuss ventilation management strategies for severe airflow limitation.

Introduction
Support of oxygenation and ventilation are two of the most common inter-
ventions in intensive care; in 2012–13, approximately 41% of patients in
Australian and New Zealand intensive care units (ICUs) received invasive
mechanical ventilation and 8% received non-invasive ventilation (NIV).1 Similar
numbers of critically ill patients receive ventilation in the UK,2 whereas in
the USA reported numbers range from 21% to 39%.3 The technology available
for supporting oxygenation and ventilation is complex, ranging from simple
interventions such as nasal cannulae through to invasive mechanical ventilation
and extracorporeal support. Additionally, the meaning of ventilator terminology
is often unclear and terms may be used interchangeably. Critical care nurses
must have a strong knowledge of the underlying principles of oxygenation and
ventilation that will facilitate an understanding of respiratory support devices,
associated monitoring priorities and risks.
 CHAPTER 15 VENTILATION AND OXYGENATION MANAGEMENT 471

Oxygen therapy symptoms may be mistakenly attributed to the underlying

illness, especially in a sedated and ventilated patient. Many
Oxygen is required for aerobic cellular metabolism and of the symptoms abate once the fraction of inspired
ultimately for human survival, with some cells, such as oxygen (FiO2) is reduced, although irreversible pulmonary
those in the brain, being more sensitive to hypoxia than fibrosis may occur (see Box 15.1). The concentration and
others. Refer to Chapter 13 for a discussion of oxygen duration of oxygen exposure that induces oxygen toxicity
delivery and consumption, the oxygen–haemoglobin varies between patients;7 the lowest possible FiO2 should
dissociation curve, hypoxaemia and tissue hypoxia; therefore be used to achieve the target partial pressure
this material provides rationales for clinical decisions of oxygen in arterial blood (PaO2) or peripheral oxygen
regarding the administration of oxygen therapy or venti- saturation (SpO2).
lation strategies. Oxygen therapy should be considered
for patients with a significant reduction in arterial oxygen BOX 15.1
levels, irrespective of diagnosis and especially if the patient
is drowsy or unconscious. Signs and symptoms of oxygen toxicity
Central nervous system:
Indications
• Nausea and vomiting
Indications for oxygen therapy include:
• Anxiety
• cardiac and respiratory arrest • Visual changes
• type I respiratory failure • Hallucinations
• type II respiratory failure • Tinnitus
• chest pain or acute coronary syndrome4 with hypoxia • Vertigo
(i.e. SpO2 <93%) or evidence of shock
• Hiccups
• low blood pressure, cardiac output
• Seizures
• increased metabolic demands
Pulmonary:
• carbon monoxide poisoning.
• Dry cough
Complications • Substernal chest pain
Administration of oxygen, regardless of the delivery
• Shortness of breath
device, has potential adverse effects. High concentrations
of oxygen cause nitrogen washout, resulting in absorption • Pulmonary oedema
atelectasis. • Pulmonary fibrosis

Hypoventilation and CO2 narcosis

High-dose oxygen therapy may lead to hypoventilation, Oxygen administration devices
hypercapnia and CO2 narcosis in a small proportion of
patients with chronic obstructive pulmonary disease Initial management of hypoxia in a spontaneously-
(COPD). The processes underpinning these physiologi- breathing patient with an intact airway is low-flow oxygen
cal changes are described in Chapter 13. These patients via nasal cannulae (up to 6 L/min) or face mask (up to
require close monitoring of PaCO2 levels when oxygen 15 L/min). Although oxygen devices have traditionally
therapy is instituted or increased. Although COPD had FiO2 ascribed to specific flow rates, the FiO2 delivered
patients frequently may have a lower baseline SpO2 to the alveoli is influenced by:
(88–94% compared to 96–100% in patients with no • patient factors – inspiratory flow rate, respiratory rate,
lung pathology), treatment of hypoxia is still essential, tidal volume (VT), respiratory pause
and oxygen should not be withheld or withdrawn while • oxygen device factors – oxygen flow rate, volume of
hypoxia remains, even if hypercapnia worsens.5,6 mask/reservoir, air vent size, tightness of fit.
Normal inspiratory flow in a healthy adult ranges
Practice tip between 25 and 35 L/min. Patients with respiratory failure
Oxygen should not be withheld or withdrawn while tend to increase their flow demand from 50 up to 300 L/
hypoxia remains, even if hypercapnia worsens. min. Patients in respiratory distress are characterised by
high respiratory rates and low VT7,8 that can significantly
decrease the FiO2 available via an oxygen delivery device,
Oxygen toxicity depending on the type in use.
Administration of high oxygen concentrations may lead All oxygen delivery devices use some type of reservoir
to oxygen toxicity; symptoms include non-productive to support oxygen delivery and prevent CO2 rebreath-
cough, substernal pain, reduced lung compliance, intersti- ing. For face masks, the reservoir is the mask; for nasal
tial oedema, and pulmonary capillary haemorrhage. These cannulae, it is the patient’s pharynx. Patients with high
472 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

inspiratory flow demand will deplete the reservoir faster Venturi systems
than it can be replenished, resulting in air entrainment and Venturi systems use the Venturi effect to entrain gas via
dilution of the oxygen concentration. a narrow aperture via a side port increasing gas speed
Variable flow devices and augmenting kinetic energy. FiO2 concentration can
be altered by widening or narrowing the Venturi device
Various low- or variable-flow oxygen delivery devices
aperture to a maximum FiO2 of 0.6. The FiO2 concen-
are available. These devices range from nasal cannulae and
tration using a Venturi system is less affected by changes
oxygen masks with different features, through to bag–
in respiratory pattern and demand compared to other
mask ventilation.
low-flow oxygen devices.8
Low-flow nasal cannulae
Bag–mask ventilation
Traditional low-flow nasal cannulae sit at the external
nares and deliver 3–4 L/min of oxygen. Higher flows may Bag–mask ventilation with a self-inflating bag (and
cause discomfort and damage from the drying effect on reservoir), non-return valve and mask delivers assisted
respiratory mucosa. Increased flow demand with respir- ventilation at an FiO2 of 1.0. Addition of a positive end-
atory distress dilutes the oxygen, reducing the FiO2 to the expiratory pressure (PEEP) valve will improve oxygen-
alveoli. ation. Manual ventilation requires a good seal between
the patient’s face and the mask; this may be difficult to
High-flow nasal cannulae achieve as a single operator. One person should hold the
High-flow nasal cannulae have slightly larger prongs that mask and lift the patient’s chin, while another squeezes
facilitate oxygen flow of up to 60 L/min, leading to less air the bag. Effective bag–mask ventilation is confirmed
entrainment than with other oxygen delivery systems.8,9 when the chest visibly rises as the bag is squeezed and
High-flow nasal cannulae generate low levels of end- oxygen saturations improve.20 Bag–mask ventilation may
expiratory pressure, though this is dependent on the flow cause gastric insufflation, increasing the risk of vomiting
rate, trachea size and mouth closing,10 and can therefore and subsequent aspiration.
reduce tachypnoea and work of breathing.11,12 The high
gas flow may flush CO2 from the anatomical dead space Practice tip
preventing CO2 rebreathing and thereby decreasing
Transparent face masks are recommended for bag–
PaCO2, although this is not well supported by the
mask ventilation as they allow immediate recognition if
literature.13,14 These systems are generally well-tolerated,
a patient vomits.
but must be used with heated humidification to avoid
drying the respiratory mucosa.12 High-flow nasal cannulae
are now used frequently in clinical practice to avoid, or
as an alternative to,15 more invasive therapies but there is
Airway support
limited high-quality evidence on their use in adults and The most common cause of partial airway obstruction in an
children other than neonates.16 unconscious patient is loss of oropharyngeal muscle tone,
particularly of the tongue.This may be alleviated by tilting
Oxygen masks the head slightly back and lifting the chin, or thrusting
Loose-fitting oxygen masks include simple (Hudson) face the jaw forward. The head-tilt/chin-lift manoeuvre is not
masks, aerosol masks used in combination with heated used if cervical spine injury is suspected.21 The jaw-thrust
humidification and nebuliser treatments, tracheostomy manoeuvre may require two hands to maintain.22 If more
masks and face tents. All are considered low-flow or prolonged support is required, an oro- or nasopharyngeal
variable-flow devices, with the delivered FiO2 varying airway can be used, which may also facilitate bag–mask
with patient demand. Flow rates ≥5 L/min minimise CO2 ventilation.
rebreathing.The addition of ‘tusks’ to a Hudson mask may
increase the oxygen reservoir17 but does not guarantee Oro- and nasopharyngeal airways
a consistent FiO2 and has probably been superseded by The Guedel oropharyngeal airway is available in various
high-flow systems.18 sizes (a medium-sized adult requires a size 4). The airway
Partial rebreather and non-rebreather masks have an is inserted into the patient’s mouth past the teeth, with
attached reservoir bag that enables delivery of higher levels the end facing up into the hard palate, then rotated 180°,
of FiO2. Both mask types have a one-way valve precluding taking care to bring the tongue forward and not push
expired gas entering the reservoir bag. A non-rebreather it back. Oropharyngeal airways are poorly tolerated in
mask has two one-way valves preventing air entrainment.19 conscious patients and may cause gagging and vomiting.20
The maximum FiO2 delivery with non-rebreather masks A nasopharyngeal airway (see Figure 15.1) is inserted
is 0.85 with low flow demand, with a steep decline in through the nares into the oropharynx; it can be difficult
alveolar oxygen concentration as minute volume increases. to insert and requires generous lubrication to minimise
Non-rebreather masks may perform worse than a Hudson trauma.This type of airway should not be used for patients
mask without a reservoir bag.8 with a suspected head injury. As well as opening the airway,
 CHAPTER 15 VENTILATION AND OXYGENATION MANAGEMENT 473

is most commonly used when a difficult intubation is

FIGURE 15.1 Nasopharyngeal airways. anticipated or encountered. This device has a handle and
is more rigid, wider and curved than the cLMA, enabling
passage of a purpose-made endotracheal tube.23
Combitube
The combitube is more widely used in North America for
emergency situations than in Australia and the UK.21 It is
a dual-lumen, dual-cuff oesophageal–tracheal airway that
enables ventilation if inserted into either the oesophagus or
trachea. Inexperienced operators may find a combitube more
difficult to insert correctly than a cLMA.25 Complications
may occur in up to 40% of patients and include aspiration
pneumonitis, pneumothorax, airway injuries and bleeding,
oesophageal laceration and perforation and mediastinitis.26
Endotracheal tubes
Endotracheal intubation is the ‘gold standard’ for airway
support, providing airway protection in the presence
of airway oedema, absent gag, cough or swallow reflex.
suction catheters can be passed to facilitate secretion Intubation facilitates mechanical ventilation and pulmon-
ary secretion clearance.22
clearance. Once inserted, these airways are better tolerated
Endotracheal tubes (ETT) have common design char-
than an oropharyngeal airway.
acteristics, are generally made from polyvinyl chloride, are
Laryngeal mask airway and insertion available with internal diameters ranging from 2–10 mm
(common adult sizes are 7–9 mm) and are up to 30 cm
The classic laryngeal mask airway (cLMA) (see Figure 15.2)
long. A longitudinal radio-opaque line allows visualisation
is positioned blindly into the pharynx to form a low-
of tube placement on a chest X-ray. Markings at 1-cm
pressure seal against the laryngeal inlet. It is easier and intervals indicate the length from the distal end, a design
quicker to insert than an endotracheal tube, and is feature that facilitates the ability to gauge insertion depth
particularly useful for operators with limited airway and monitor tube movement.27 Tubes are available with
skills; the cLMA does not carry the same potentially fatal and without a distal cuff, an inflatable balloon that seals
complications such as oesophageal intubation although the trachea, facilitates positive pressure ventilation and
the risk of aspiration remains.23 prevents aspiration of oropharyngeal contents. Cuffs come
Mechanical ventilation can be delivered with in a range of profiles and volumes, but are commonly
low-airway pressures (<20 cmH2O) via a cLMA. This high-volume, low-pressure enabling application of a safe
device is widely used in elective general anaesthesia,21 pressure over a larger surface area (see Figure 15.3). A
and can be used in critical care as an alternative to bag– smaller inflatable balloon, attached to the cuff via a pilot
mask ventilation23 or endotracheal intubation when initial line, provides a tactile gauge of cuff pressure and a small
attempts at intubation have failed.24 The ‘intubating’ LMA air reservoir to prevent minor changes in cuff pressure.28

FIGURE 15.2 Laryngeal mask airways. FIGURE 15.3 Endotracheal tubes.

474 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Endotracheal tubes reinforced with a wire coil

embedded within the plastic along the entire tube length Practice tip
prevent kinking and occlusion. These tubes are more During intubation, know who to call for help, and do not
commonly used in the operating room.29 The wire coils hesitate to do so.
can be irreversibly compressed by a strong bite occluding
the airway. Reinforced tubes also increase the risk of
tracheal damage and should be replaced with a standard Procedure
ETT on ICU arrival. Most ETTs have a ‘Murphy eye’, The patient is preoxygenated to minimise desaturation
an oval-shaped hole in the side of the tube between the during apnoea and laryngoscopy, commonly via bag and
cuff and the tube end that provides a patent aperture if the mask, although other methods such as non-invasive venti-
distal opening is occluded.30 lation have been suggested.32 The practice of apnoeic
oxygenation during endotracheal intubation through the
Preparation for intubation administration of 15 litres per minute via nasal cannula
Adequate preparation of the patient, equipment and envi- has become very popular in emergency departments.
ronment, as well as knowledge of emergency procedures, To date, there is insufficient evidence to recommend
is important to ensure safe and efficient intubation. Up its routine use during endotracheal intubation in the
to 50% of patients undergoing endotracheal intubation critically ill. Intubation in ICU is usually performed via
in the ICU experience complications; 28% will have a laryngoscopy with insertion of an oral ETT. Intubation
serious complication, including hypoxaemia, circulatory may be performed using a fibre optic bronchoscope when
collapse, cardiac arrhythmia, cardiac arrest, oesophageal difficulty is encountered, or for nasal intubation.
intubation, aspiration and death.31
Oral vs nasal intubation
Patient preparation Oral intubation is preferred unless there are specific indi-
If appropriate, and time permits, explain the procedure to cations for nasal intubation. Oral intubation is easier to
the patient and family. Prepare the patient with: perform and allows use of a larger diameter ETT. While
nasal intubation provides better splinting for the ETT
• reliable intravenous access established to allow rapid and facilitates oral hygiene, it can damage nasal structures,
fluid and drug administration
is contraindicated in skull fractures and increases the risk
• accurate blood pressure monitoring (preferably of maxillary sinusitis and ventilator-associated pneumonia
intra-arterial) (VAP).33
• continuous oxygen saturation and ECG monitoring Cricoid pressure
• nasogastric tube (if in situ) aspirated and placed on The cricoid cartilage, situated below the thyroid
free drainage
prominence, is a closed tracheal ring which, when
• positioning supine in the ‘sniff ’ position. compressed, closes the oesophagus while the trachea
Equipment and drugs remains open. Cricoid pressure is performed by placing
All equipment should be available and checked immedi- the thumb on one side of the patient’s trachea, middle
ately prior to intubation, including: finger on the other side and index finger directly on
the cricoid.34 Although widely used, its efficacy is ques-
• oxygen supply tionable as technique is frequently poor,35 and there is
• suction supply, with a range of Yankauer and wide anatomical variation in the exact orientation of the
y-suction catheters/closed suction device oesophagus in relation to the trachea.36
• laryngoscope blades and compatible holder, with a Backwards, upwards, rightward
functioning light
pressure manoeuvre
• appropriately-sized face mask The backwards, upwards, rightward pressure (BURP)
• manual ventilation (Ambu bag™) attached to oxygen manoeuvre on the thyroid cartilage was introduced in the
supply
mid-1990s to improve visualisation during difficult laryng-
• ETT cuff inflated in sterile water to ensure no leaks oscopy. The patient’s jaw is thrust forward, so the head is
and even inflation in the ‘sniffing’ position. The thumb and third finger are
• water-based lubricant applied to tube and cuff (while placed on either side of the thyroid cartilage and the index
maintaining sterility) finger on top. Pressure is applied in the sequence backwards
• capnography (chemical CO2 detectors are often used (towards the spine), upwards (towards the head), rightward
in emergency situations) (towards the patient’s right side). This is easier to perform
• ventilator and circuit following administration of muscle relaxants.
• emergency/resuscitation trolley at bedside Cuff management
• gloves, eye protection Endotracheal and tracheostomy tube cuffs prevent airway
• drugs (sedative and muscle relaxant). contamination by pharyngeal secretions and gastric
 CHAPTER 15 VENTILATION AND OXYGENATION MANAGEMENT 475

contents and loss of VT during mechanical ventilation. A variety of tracheostomy tubes are available that
The cuff does not secure the tube in the trachea. facilitate secretion clearance, communication and differing
patient anatomy. Inner cannulae (re-usable or disposable)
Confirmation of tube position prevent secretion build up on the tracheostomy tube,
The correct position of the ETT distal end is 3–5 cm while fenestrated and talking tracheostomies facilitate
above the carina. A lip level of 20 cm for women and communication, as do one-way speaking valves, such as
22 cm for men should prevent endobronchial intubation, the Passy-Muir® valve, used with the cuff deflated.
with the proximal end fixed at either the centre or side
of the mouth.37 Confirmation of the ETT position is Tracheostomy care
required immediately following intubation and at regular The aim of tracheostomy care is to keep the stoma free of
intervals thereafter as tube movement can occur. infection, and prevent tube blockage or dislodgement.The
Chest auscultation and observation of chest expansion stoma is cleaned with normal saline and fixation devices
to confirm ETT position is unreliable, as the chest may are changed at least 12-hourly with two nurses required to
appear to rise with oesophageal intubation. Conversely, safely perform changes.43 Velcro tapes are easier to change
the chest may not rise with a correctly positioned tube if and more comfortable than cotton tape.44 Lint-free
the patient is obese or has a rigid chest wall. Patients with or superabsorbent foam dressings are used under the
left main bronchus intubation may exhibit bilateral breath flange to absorb secretions. Adequate humidification and
sounds.38 End-tidal CO2 monitoring is the ‘gold standard’ suctioning will usually prevent tube obstruction (see later
method for confirming ETT placement (see Chapter 13 in this chapter). The use of inner cannulae has obviated
for further information on end-tidal CO2 monitoring). the need for frequent tracheostomy tube changes. Single
Disposable devices that change colour in the presence of lumen (no inner cannula) tracheostomy tubes should be
CO2 are inexpensive and easy to use, but may be inaccurate changed every 7–10 days.43
during cardiopulmonary resuscitation, or if contaminated. Complications of endotracheal
Capnography is the most reliable technique to identify
ETT placement in both arrest and non-arrest situations.24 intubation and tracheostomy
Continuous end-tidal CO2 monitoring during intubation Tube blockage, tube dislodgement and aspiration are
is recommended as a minimum standard by the College major complications. Partial ETT or tracheostomy tube
of Intensive Care Medicine of Australia and New Zealand dislodgement can cause greater harm than complete
(CICM).39 removal because of delays in diagnosis and resultant
aspiration and worsening gas exchange. Tube dislodge-
Practice tip ment is most likely to occur when turning the patient,
in agitated patients or when nursing staff are distracted or
Always ensure there is someone who is skilled at intuba- on breaks.45 While physical restraint may be considered to
tion immediately available when extubating a patient. prevent tube dislodgement, multiple studies noted patients
were restrained when self-extubation or device removal
Tracheostomy occurred.46–51 Appropriate levels of analgesia and sedation
are therefore required for minimising self-extubation risk.
Tracheostomy may be required for upper airway obstruction, Complications during, and immediately after,
although it is most commonly performed for ICU patients endotracheal intubation and tracheostomy include
requiring prolonged mechanical ventilation.The advantages cardiovascular compromise, bleeding, tracheal wall injury,
of tracheostomy over endotracheal intubation include: vocal cord damage, pneumothorax, pneumomediasti-
decreased risk of laryngeal damage and subglottic stenosis; num and subcutaneous emphysema. Late complications
reduced airway resistance and dead space, which decreases of tracheostomy include tracheal stenosis, tracheomalacia
the work of breathing and therefore supports weaning;40 and tracheo-oesophageal fistula and infection. As noted
and improved patient tolerance enabling sedation reduction. earlier, damage to the trachea is exacerbated by high cuff
The optimum time to perform tracheostomy remains pressures.52 Percutaneous tracheostomy results in fewer
contentious, and is often influenced by patient diagnosis.41 wound infections, decreased incidence of bleeding and
Procedure reduced mortality compared to surgical tracheostomy.53
Tracheostomy can be performed using a surgical or percu-
taneous dilatational technique. Percutaneous dilatation is Managing endotracheal and
contraindicated in patients with anatomical anomalies of tracheostomy tubes
the neck and serious bleeding disorders, and should be
undertaken with caution in patients who are obese, have Tracheal suction
a cervical spine injury, coagulopathy, difficult airway or Patients with an ETT or tracheostomy tube require
require high levels of ventilatory support.42 Percutaneous tracheal suction to remove pulmonary secretions that can
dilatation is more commonly performed than the surgical lead to atelectasis or airway obstruction and impair gas
technique in Australian and New Zealand ICUs.42 exchange.54 Suction should be performed as clinically
476 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

indicated, with assessment of visible or audible secretions, hypertension and increased intracranial pressure. Tracheal
rising inspiratory pressure, decreasing VT or increased work suctioning causes discomfort, and should therefore be
of breathing.55 A sawtooth pattern on the flow–volume performed only when clinically indicated, such as audible
waveform may also indicate the need for suction.56 presence of secretions, desaturation and when a sawtooth
Preoxygenation using a FiO2 of 1.0 for approximately pattern is observed on the flow–time scalar and flow/
60 seconds prior to suctioning is commonly performed volume loop.57,58
though not supported by strong evidence unless the
patient is experiencing hypoxia or has compromised Securing endotracheal and
cerebral circulation.57 Preoxygenation of patients without tracheostomy tubes
hypoxia should be avoided as it may cause harm associated The purpose of ETT and tracheostomy tube fixation
with oxygen toxicity. If a patient’s oxygen saturation is to maintain the tube in the correct position, prevent
declines to an unacceptable level during suctioning, the unintended extubation or dislodgement and facilitate
FiO2 should be increased to 1.0. Manual hyperinflation mechanical ventilation while maintaining skin integrity
should be discouraged due to the risk of haemodynamic and oral hygiene.61 ETT fixation methods include:
compromise, derecruitment and barotrauma and lack of
evidence of benefit.58 Similarly, installation of saline is not • tying cotton tape around the tube, then around the
supported due to increased risk of flushing pathogens into neck
distal lung regions.59 • taping the tube to the face using medical adhesive
tape
Methods • commercial tube holders of varying designs.
The three methods of suctioning are: There is no evidence supporting a preferred method62
1 Open suction: a suction catheter is passed with each having specific strengths and weaknesses.
under aseptic technique directly into the ETT/ A manikin study comparing cotton tapes with the
tracheostomy after disconnection from the ventilator Thomas™ Endotracheal Tube Holder demonstrated less
circuit. Disadvantages include loss of PEEP resulting ETT movement with the commercial tube holder.63
in alveolar derecruitment and increased risk of Two nurses are required to prevent ETT dislodgement
transmission of infective organisms. A surgical mask during fixation. Although there is also no evidence
and protective eyewear should be worn.60 recommending a preferred frequency, ETT fixation is
2 Semi-closed suction: a suction catheter is passed generally changed at least daily, to allow assessment of the
through a swivel connector with a self-sealing underlying skin with particular attention to the ears and
rubber flange. corners of the mouth and to facilitate oral hygiene.61 The
3 Closed suction: an in-line system is attached between
ETT position in the mouth is alternated at this time.
the ETT/tracheostomy tube and the ventilator
circuit where the suction catheter is contained in Practice tip
an integrated plastic sleeve. Alveolar derecruitment Adhesive devices may become dislodged as facial hair
occurs to a lesser degree than with open suction. grows under them.
There is no difference between techniques in relation
to development of VAP and quantity of secretions Cuff pressure management
removed.
The suction catheter diameter should not be greater Cuff inflation pressures should be maintained at 20–30
than half the airway diameter, using the formula: suction cmH2O (15–22 mmHg). Tracheal wall damage may occur
catheter size [French] = (ETT size [mm] − 1) × 2. The if cuff pressure exceeds tracheal capillary perfusion pressure
suction catheter should be inserted to the carina, then (27–40 cmH2O/20–30 mmHg). Cuff inflation pressures
withdrawn 2 cm before suction is applied to prevent ≤20 cmH2O (≤15 mmHg) are associated with an increased
damage. Suction should only last 15 seconds, using risk of aspiration and a 2.5-fold increase in VAP.64
continuous, rather than intermittent, suction. Suction There are four methods for assessing cuff inflation:
pressure should be set as low as possible with <150 mmHg 1 minimal occluding volume
recommended for adults and <100 mmHg for neonates.59 2 minimal leak test
Use of ETTs or tracheostomy tubes with integrated 3 cuff pressure measurement
subglottic suction ports may assist in preventing VAP,
especially when performed with other prevention 4 palpation.
strategies such as semirecumbant positioning and good In Australia and New Zealand, cuff pressure measure-
cuff seal management. ment is most commonly used,65 in contrast to the UK66
and North America67 where it is used less frequently. Cuff
Adverse effects pressure measurement requires a manometer attached
Adverse effects of suctioning include hypoxaemia, intro- to the pilot balloon. Cuff pressure varies with head and
duction of infective organisms, tracheal trauma, bradycardia, body position, tube position and airway pressures.68,69
 CHAPTER 15 VENTILATION AND OXYGENATION MANAGEMENT 477

The optimum frequency of cuff pressure monitoring is Extubation

unclear; at a minimum it should be done post-intubation,
Following successful weaning from mechanical ventilation
on arrival in ICU and once per nursing shift. Recently,
(see later in this chapter), assessment of the patient prior to
continuous cuff pressure measurement has been shown to
extubation should indicate adequate gas exchange, respir-
reduce VAP.70 Even with appropriate cuff inflation, micro-
atory rate and work of breathing on minimal support;
aspiration occurs via the longitudinal folds in the cuff.71
respiratory muscle strength; the ability to cough and clear
If performing minimal occluding volume and minimal
secretions spontaneously; and a stable haemodynamic
leak tests, aspiration should be prevented by semirecum-
status and mental status.75 Serious post-extubation compli-
bent positioning, suctioning the back of the mouth (as far
cations of laryngospasm and stridor cannot be reliably
back as tolerated), aspiration of the nasogastric tube and
predicted,76 so the ease/grade of intubation should be
discontinuation of feeds before cuff deflation.
considered prior to extubation and provision made for
Subglottic secretion management immediate reintubation.77
For the intubated patient, oropharyngeal secretions drain
into the subglottic space, pool above the cuff and gradually Mechanical ventilation
leak via the longitudinal cuff folds to the lungs increasing the
The most recent international study of mechanical venti-
risk of pneumonia. Subglottic secretion drainage, a dedicated
lation practices, reporting data from 4968 patients in
lumen within the ETT dorsal wall that exits above the cuff,
349 ICUs and 23 countries, found the median duration
enables removal of subglottic secretions either continuously
of ventilation was 4 days (interquartile range 2–8 days).78
via low pressure suction or intermittently via suction or
In this patient cohort the three most common reasons
a syringe.27 A recent systematic review and meta-analysis
for mechanical ventilation were postoperative respiratory
found subglottic secretion drainage reduced the risk of
failure, coma and pneumonia. This international report
VAP by 48% though there was no evidence of effect on
did not include data from Australia and New Zealand. As
ICU or hospital mortality or duration of ventilation.72
stated in the introduction, 41% of patients in Australian
Managing emergencies associated with and New Zealand ICUs received invasive mechanical
ventilation and 8% received NIV in 2012–13.1 The
endotracheal and tracheostomy tubes median duration of invasive mechanical ventilation for
Pilot tube these patients was 2.5 days. A study describing ventila-
If the pilot tube for the ETT or tracheostomy tube is acci- tion and weaning practices of 55 ICUs in Australia and
dentally cut or a hole is suspected in the tubing or balloon, New Zealand in 2005 reported a similar profile as inter-
cannulate the tubing with a 23- or 24-gauge needle to national studies for the most common indications for
reinflate the cuff and clamp the tubing. If using a clamp mechanical ventilation.79
with serrations, place gauze between the tube and the Principles of mechanical ventilation
clamps to avoid further damage to the pilot tube.
Mechanical ventilation describes the application of positive
Cuff herniation or negative pressure breaths using non-invasive or invasive
ETT cuff herniation occurs infrequently with low techniques. Indications for initiation of mechanical venti-
pressure high volume cuffs, may be difficult to diagnose, lation are discussed below. Table 15.1 lists the patient
but can cause life-threatening bronchial obstruction.73 If parameters typically observed in acute and chronic respir-
cuff herniation is suspected (profound desaturation, loss atory failure that may influence the decision to ventilate.
of breath sounds), deflate and reinflate the cuff, checking During positive pressure ventilation, the type of ventila-
the cuff pressure is within normal range. If the problem tion used most commonly in critical care, the ventilator
persists the tube will need changing. delivers a flow of gas into the lungs during inspiration
using a pneumatic system. Expiration is passive.
Persistent cuff leaks
The equation of motion
Cuff leaks may be categorised as leaks around an intact cuff
or those due to structural damage to the cuff.74 Structural The equation of motion for the respiratory system is a
damage generally requires replacement of the tube, partic- mathematical model that relates pressure, volume and flow
ularly if leaks are large and ventilation is ineffective. during breath delivery, with the pressure required to deliver
a volume of gas determined by the elastic and resistive
properties of the respiratory system80 (see Table 15.2).
Practice tip

A persistent cuff leak as indicated by bubbling or other

Compliance and elastance
noises suggestive of gas leak and loss of VT or cuff Compliance refers to the ease with which lung units
pressures of ≥30 cmH2O (≥22 mmHg) indicating failure distend. Elastance is the tendency of the lung units to
to generate a seal should be reviewed. Check ETT return to their original form once stretched. Compliance
position for migration and refer to medical staff. is defined as the change in volume that occurs due to a
change in pressure and is expressed as C = ΔV/ΔP.
478 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 15.1
Physiological indications suggesting the need for mechanical ventilation

PA R A M E T E R N O R M A L VA L U E S ARF CRF ASSOCIATED SIGNS AND SYMPTOMS

Respiratory rate 12–20 ≥28 ≥30 Dyspnoea, increased activation of accessory

muscles and active expiration
pH 7.35–7.45 <7.30 7.35–7.40 Failure to adequately ventilate: elevated
No compensatory May be normal PaCO2, acidic pH, headache, confusion or
changes due to metabolic other mental status change, tachypnoea
compensation (RR >30), flushed skin
PaCO2 35–45 mmHg >50 mmHg and >50 mmHg and
rising rising
PaO2 80–100 mmHg <65 mmHg and <50 mmHg and Failure to adequately oxygenate: decreased
falling falling PaO2 and SpO2, tachycardia, hyper- or
Hb/HCT elevated hypotension, dyspnoea, gasping, nasal
as compensatory flaring, use of accessory muscles, anxiety,
mechanism agitation and altered mental status, cyanosis
HCO3− 22–26 mmol/L Within normal limits If chronic hypercapnia, then HCO3− >26 mmol/L is a compensatory
mechanism
If CRF is primarily failure to oxygenate, then HCO3− will be within
normal limits

ARF = acute respiratory failure; CRF = chronic respiratory failure; HCT = haematocrit; RR = respiratory rate.

length (including the artificial airway), the gas flow rate

TABLE 15.2 and the density and viscosity of the inspired gas. During
Equation of motion mechanical ventilation, bronchospasm, airway oedema,
EQUATION:
endotracheal tube lumen size, increased secretions and
P T (PAIRWAY + P MUSCLE ) = V T /C + V T /T I × R + PEEP T inappropriate setting of flow rates can influence airway
resistance. Normal resistance for intubated patients is
Abbreviations PT = total pressure – the sum of the
pressure in the proximal airway and the
6 cmH2O/(L/s).81
pressure generated by the respiratory
muscles Ventilator graphics
VT = tidal volume Analysis of ventilator graphics provides clinicians with the
C = compliance ability to assess patient–ventilator interaction, appropriate-
TI = inspiratory time ness of ventilator settings and lung function.
R = resistance
PEEPT = total positive end-expiratory
Scalars: Pressure/time, flow/time,
pressure – alveolar pressure at the
end of expiration and is the sum of volume/time
PEEP applied by the ventilator and any Many ventilators now offer integrated graphic displays
intrinsic (auto) PEEP as waveforms that plot one of three parameters,
Notes VT/C: describes the elastic properties of pressure, flow or volume, on the vertical (y) axis against
the respiratory system time, measured in seconds, on the horizontal (x) axis
VT/TI: reflects flow in the system referred to as scalars. Examination of scalars can assist
VT/TI × R: resistance of the respiratory with assessment of patient–ventilator synchrony, patient
system triggering, appropriateness of inspiratory/expiratory
times, presence of gas trapping, appropriateness and
Lung tissue and the surrounding thoracic structures adequacy of flow, lung compliance and airway resistance
contribute to respiratory compliance. Normal compliance and circuit leaks.82, 83
for a mechanically ventilated patient ranges from 35 to
50 mL/cmH2O.81 Pressure vs time scalar
The morphology of this waveform depends on the control
Resistance variable (volume or pressure), breath type (mandatory or
Resistance refers to the forces that oppose airflow. Resist- spontaneous) and whether the breath is initiated by the
ance in the airways is affected by their diameter and ventilator or the patient’s inspiratory effort.84 Pressure–time
 CHAPTER 15 VENTILATION AND OXYGENATION MANAGEMENT 479

waveforms reflect airway pressure (Paw) during inspira- appearance depending on the control variable (volume vs
tion and expiration and can be used to evaluate peak and pressure). In volume-control breaths (see Figure 15.4) the
plateau inspiratory pressures and end-expiratory pressures, inspiratory waveform continues to rise until peak inspi-
inspiratory and expiratory times and appropriateness of ratory pressure is achieved according to VT set. If an
flow (see Figure 15.4). The peak pressure represents the inspiratory hold is applied a plateau pressure will be
maximum pressure achieved during inspiration. The generated. As the patient expires airway pressure will drop
plateau pressure is measured during an inspiratory hold back to the set PEEP level. In pressure control breaths, the
and represents the pressure applied to the small airways and inspiratory waveform reaches its peak at the beginning of
alveoli. The expiratory pressure is the pressure measured inspiration and remains at this elevation until cycling to
once the patient has expired. Pressure–time scalars vary in expiration.

FIGURE 15.4 Pressure, flow, volume and time waveforms.

Inspiratory
hold

3 Peak Inspiratory pressure Circuit pressure

U
H Alveolar pressure
V Plateau
V pressure
X
U
H End expiratory pressure

0 cmH2O

Inspiratory
flow
Period Period
) of no of no
O flow flow
R
Z 0 lpm

Expiratory
flow

9
R Inspiratory Inspiratory Expiratory
O volume hold volume
X
P
H

0 mls
480 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

When interpreting the pressure waveform it is ventilator can also be identified as negative deflections in
important to recognise that the graphic waveforms the pressure waveform without corresponding responses
display circuit pressure, which does not always represent from the ventilator.85 Appropriateness of flow can be
alveolar pressure. Periods of no flow (inspiratory and detected from the pressure–time scalar. If the flow is set
expiratory holds/pauses) are required to estimate alveolar too high or the rise time is too short this can be seen as a
pressure. The plateau pressure is a more reliable estimate sharp peak in the waveform (see Figure 15.5). Conversely,
of inspiratory alveolar pressure than the peak inspiratory if flow is inadequate or the rise time is too long, the incline
pressure. An expiratory hold is required to determine end- of the inspiratory portion of the pressure waveform may
expiratory alveolar pressure. Estimating alveolar pressure be dampened or even negative.82
may be useful to assess the patient’s respiratory resistance Flow vs time scalar
and compliance. Comparing the difference between
The flow–time scalar presents the inspiratory phase above
the peak inspiratory pressure and plateau pressure can
the horizontal axis and the expiratory phase below (see
give an indication of the patient’s inspiratory resistance.
Figure 15.6). The shape of the inspiratory flow waveform
Comparing the difference between the plateau pressure
is influenced by the selection of flow pattern (constant,
and the end-expiratory pressure can provide information decelerating, sinusoidal) in volume-control breaths or the
about the patient’s compliance. A large difference between variable and decelerating flow waveform associated with
peak and plateau pressures indicates high airway resistance. pressure-control breaths. The inspiratory flow waveform
An elevated plateau pressure indicates reduced compliance. of spontaneous breaths, those triggered and cycled by
Spontaneous triggering of ventilation can be the patient, is influenced by the presence or absence of
identified by examination of the pressure–time scalar at pressure support and the expiratory sensitivity.82
the beginning of inspiration. A small negative deflection Evaluation of the expiratory limb of the flow–time
indicates patient effort. When pressure-triggering is used, scalar assists with detection of gas trapping and the
a breath is triggered when the pressure drops below patient’s response to bronchodilators. In the absence of
baseline. The depth of the deflection is proportional to gas trapping, the expiratory limb drops sharply below
patient effort required to trigger inspiration (see Figure baseline then gradually returns to zero before the next
15.5). A flow-triggered breath occurs when the flow breath. Failure to return to baseline indicates gas trapping
rises above baseline, although this is frequently accompa- whereby the inspired gas is not totally expired. Gas
nied by a small negative deflection in the pressure–time trapping results in development of intrinsic or ‘auto-
scalar. Patient inspiratory attempts that fail to trigger the PEEP’.This can adversely affect a patient’s haemodynamic

FIGURE 15.5 Triggering and rise time.

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 CHAPTER 15 VENTILATION AND OXYGENATION MANAGEMENT 481

FIGURE 15.6 Flow vs time waveform.

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status and cause patient–ventilator asynchrony.86 Gas Loops: Pressure/volume, flow/volume

trapping may occur in patients with airflow limitation Most contemporary critical care ventilators allow for
such as those with COPD and asthma. Consequences monitoring of pressure, flow and volume parameters
of gas trapping include dynamic hyperinflation, reduced
integrated into graphic loops enabling measurement of
respiratory compliance and respiratory muscle fatigue.87
airway resistance, chest wall and lung compliance.
Evaluation of the expiratory flow waveform also enables
evaluation of the effects of bronchodilator therapy as, if Pressure–volume loops
efficacious, the expiratory flow waveform will return to The two parameters, Paw and VT are plotted against each
baseline (see Figure 15.7).86 Patient–ventilator asynchrony
other, with Paw on the x axis. For mandatory breaths,
can be detected in the flow waveform as abrupt decreases
the loop is drawn counterclockwise (see Figure 15.9).
in expiratory flow in the expiratory limb and abrupt
increases in flow in the inspiratory limb.85 Spontaneous (triggered and cycled) breaths are drawn
in a clockwise fashion. When low gas flow is delivered
Volume vs time scalar and the patient is unable to initiate ventilation, pressure–
The volume–time waveform originates from the volume loops may be used to identify the lower and
functional residual capacity (baseline), rises as inspiratory upper inflection points.The lower inflection point begins
flow is delivered to reach the maximum inspiratory VT, near the beginning of inspiration as the Paw starts to rise
then returns to baseline during expiration. The volume with little change in VT. As Paw continues to rise, the VT
waveform is useful in troubleshooting circuit leaks (see increases exponentially as alveoli are recruited, resulting
Figure 15.8) as it will fail to return to baseline if a leak in in a marked increase in the inspiratory limb slope. This
the circuit–patient interface is present. point represents alveolar recruitment and is referred to
482 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

FIGURE 15.7 AutoPEEP and gas trapping.

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as the lower inflection point, and may be used to guide

FIGURE 15.8 Tidal volume vs time, with and
PEEP selection.88,89 The inspiratory limb continues
without leak.
until peak inspiratory pressure and maximal VT are
achieved. The bend in the inspiratory limb towards the
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 CHAPTER 15 VENTILATION AND OXYGENATION MANAGEMENT 483

FIGURE 15.9 Pressure–volume loop. Ventilator circuits

Delivery of mechanical ventilation requires a ventilator
9ROXPH circuit to transport gas flow to the patient. To prevent
condensation from cooling of warm humidified gas,
([SLUDWLRQ % inspired gas is heated via a wire inside the circuit wall
in either the inspiratory limb alone or both the inspir-
atory and expiratory limbs.94 Historically, ventilator
circuits were changed frequently (48–72 hours) to decrease
the risk of VAP.95 Current guidelines for VAP prevention
found evidence that the frequency of ventilator circuit
changes had no relationship to the VAP incidence and,
,QVSLUDWLRQ therefore, recommended routine circuit changes were
$ 3UHVVXUH not necessary and circuits should only be changed when
soiled or damaged.96
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www.draeger.com/sites/assets/Publixhingimages/Products/ Humidification
savina-300/UK/9097421-Fibel-Curves_Loops-en.pdf, p 26,
Humidification warms and moistens gas to facilitate
with permission.
cilia action and mucus removal as well as to prevent
drying and irritation of respiratory mucosa and solidi-
in a clockwise fashion, reflecting patient effort. The fication of secretions. During endotracheal intubation
loop then shifts to the right of the y axis and moves and mechanical ventilation, the normal humidification
in a counterclockwise fashion as the ventilator assumes processes of the nasopharynx are bypassed.This, in combi-
the work of breathing.81 Pressure–volume loops reflect nation with the use of dry medical gas at high flow rates,
dynamic compliance between the lungs and the ventilator means alternative methods of humidification are required.
circuit. Decreased compliance requires greater pressure The best conditions for mucosal health and function over
to achieve VT and is reflected in a flattened pressure– prolonged periods are when inspired gas is warmed to
volume loop.92 The area between the loops represents core body temperature and is fully saturated with water.97
the resistance to inspiration and expiration, known as
hysteresis. As resistance increases, less VT is delivered Absolute and relative humidity
resulting in a shorter and wider loop; conversely, as Absolute humidity refers to the amount of water vapour
resistance decreases, a longer, wider loop is generated in a given volume of gas at a given temperature. Absolute
(see Figure 15.10).93 humidity rises with increasing temperature; during
mechanical ventilation gas is heated to increase the
Flow–volume loops amount of water vapour it will hold. Relative humidity
Flow–volume loops recorded during positive pressure is expressed as a percentage, and is the actual amount of
ventilation depict inspiration above the baseline and water vapour in a gas compared to the maximum amount
expiration below it. These loops are useful in determin- this gas can hold (ratio of absolute to maximal humidity).
ing response to bronchodilators and examining changes in Ideal humidification is achieved when the:
airway resistance. 1 inspired gas delivered into the trachea is at 37°C with
a water content of 30–43 g/m3 (relative humidity is
FIGURE 15.10 Pressure–volume loop representing 100% at 37°C in the bronchi)
resistance changes. 2 set temperature remains constant without fluctuation
3 humidification and temperature are unaffected by
large or differing types of gas flow

4 device is simple to use
9ROXPH P/

 5 humidifier can be used with spontaneously breathing

+LJK5DZ and ventilated patients
 6ROLGOLQH 6 safety alarms prevent overheating, overhydration and
electrocution

7 resistance, compliance and dead space characteristics
do not adversely affect spontaneous breathing modes
     8 sterility of the inspired gas is not compromised.98
3UHVVXUH FP+2 Humidification is applied using either a heat–moisture
'DVKHGOLQHGHSLFWVQRUPDO5DZ exchanger (HME) or a heated water bath reservoir device
in combination with a heated ventilator circuit.
484 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Heat–moisture exchanger
Practice tip
HMEs conserve heat and moisture during expiration
enabling inspired gas to be heated and humidified. Two When other members of the ICU team use the term
types of HMEs exist: hygroscopic and hydrophobic. BiPAP/BIPAP, clarify if they are referring to non-invasive
Hygroscopic HMEs absorb moisture onto a chemically or invasive ventilation.
impregnated foam or paper material and have been shown
to be more effective than hydrophobic HMEs.99 HMEs
muscle fatigue through the addition of inspiratory positive
are placed distally to the circuit Y-piece in line with the
pressure, thus reducing inspiratory muscle work.104 Appli-
ETT and increase dead space by an amount equal to
cation of positive pressure during inspiration increases
their internal volume.100 HMEs should be changed every
transpulmonary pressure, inflates the lungs, augments
24 hours or when soiled with secretions and are usually
alveolar ventilation and unloads the inspiratory muscles.105
reserved for short-term humidification.
Augmentation of alveolar ventilation, demonstrated by
Heated humidification an increase in VT, increases CO2 elimination and reverses
Generally, heated humidification is used for patients acidaemia. High levels of inspiratory pressure may also
requiring more than 24 hours of mechanical ventilation. relieve dyspnoea.106
Various models of heater bases and circuits are on the The main physiological benefit in patients with
market and we recommend their use in accordance with congestive heart failure (CHF) is attributed to the increase
manufacturer instructions. A recent systematic review in functional residual capacity associated with the use
and meta-analysis reported no overall effect on artificial of PEEP that reopens collapsed alveoli and improves
airway occlusion, mortality, pneumonia or respiratory oxygenation.107 Increased intrathoracic pressure associated
complications when HMEs were compared to heated with the application of positive pressure also may improve
humidification, although it noted that the PaCO2 and cardiac performance by reducing myocardial work and
minute ventilation were increased and body temperature oxygen consumption through reductions to ventricu-
was lower with the use of HMEs.101 lar preload and left ventricular afterload.107–109 NIV also
preserves the ability to speak, swallow, cough and clear
secretions, and decreases risks associated with endotracheal
Non-invasive ventilation intubation.110
NIV is an umbrella term describing the delivery of Indications for NIV
mechanical ventilation without the use of an invasive
airway, via an interface such as an oronasal, nasal or full-face The success of NIV treatment is dependent on appropri-
mask or helmet. NIV techniques include both negative ate patient selection.111 Table 15.3 outlines indications and
and positive pressure ventilation, although in critical care contraindications to NIV.
positive pressure ventilation is primarily used. Acute respiratory failure
Terminology Evidence supporting the role of NIV in patients with
Positive pressure NIV can be further categorised as hypoxaemic respiratory failure is limited and conflict-
non-invasive positive pressure ventilation (NIPPV) or ing.107 For patients with community-acquired pneumonia,
continuous positive airway pressure (CPAP). NIPPV is NIV has been shown to reduce intubation rates, ICU
the provision of inspiratory pressure support, also referred length of stay and 2-month mortality but only in the
to as inspiratory positive airway pressure (IPAP), usually subgroup of patients with COPD.112 Pneumonia also has
in combination with positive end-expiratory pressure been identified as a risk factor for NIV failure.113
(PEEP). PEEP is also referred to as expiratory positive
airway pressure (EPAP). CPAP does not actively assist Acute exacerbation of COPD and CHF
inspiration but provides a constant positive airway pressure Strong evidence exists to support the use of NIV for
throughout inspiration and expiration.102 patients with acute exacerbation of COPD and CHF.
The terms biphasic (or bilevel) positive airway pressure Three meta-analyses have shown a reduction in intubation
(BiPAP®) and non-invasive pressure support ventilation rates, hospital length of stay and mortality for COPD
(NIPSV) are also used to refer to NIPPV.103 The acronym patients managed with NIPPV compared to standard
BiPAP® is registered to Respironics (Murrayville, PA), a medical treatment.114–116 COPD patients most likely
company that produces non-invasive ventilators including to respond favourably to NIPPV include those with an
the BiPAP® Vision, which is commonly used in the ICU. unimpaired level of consciousness, moderate acidaemia, a
The acronym NIPSV is primarily used in European respiratory rate of <30 breaths/minute and who demon-
descriptions of NIPPV. strate an improvement in respiratory parameters within
2 hours of commencing NIPPV. 104,117
Physiological benefits Early use of NIV in combination with standard
The efficacy of NIV in patients with acute respiratory therapy for patients with CHF has also been shown to
failure is, at least in part, related to avoidance of inspiratory reduce intubation rates and mortality when compared
 CHAPTER 15 VENTILATION AND OXYGENATION MANAGEMENT 485

to standard therapy alone.118–120 The most recent meta- caution once respiratory failure has developed and should
analysis including 32 trials found NIV reduced hospital not delay the decision to reintubate.106
mortality and reintubation rates by nearly 50% compared
to standard medical care and no increased risk of acute Other indications
myocardial infarction.121 The authors recommended Other indications for NIV include:
CPAP may be considered as the first option for NIV due • asthma126,127
to more robust evidence for its effectiveness, safety and
lower cost compared with NIPPV.121 Practice surveys • pulmonary infiltrates in immunocompromised
patients
indicate CPAP may be the preferred method of NIV for
patients with CHF in Australia and internationally. • neuromuscular disorders (e.g. muscular dystrophy,
amyotrophic lateral sclerosis)
NIV in weaning • fractured ribs
NIV may be used as an adjunct to weaning to reduce the • obesity and central hypoventilation syndromes
duration of invasive ventilation and associated compli-
cations.122 Patients are extubated directly to NIV and
• palliation.128
then weaned to standard oxygen therapy. This use of Patient selection
NIV differs from its role in preventing reintubation in Selection of patients to receive NIV depends on the
patients that develop, or who are at high risk of, post- presence of an indication listed above as well as bedside
extubation respiratory failure.123 A recent systematic observations and gas exchange parameters found in
review and meta-analysis of 16 trials with 994 participants Table 15.3.
(mostly COPD) using NIV immediately after extubation
reported reductions in mortality, weaning failure, VAP, Interfaces and settings
tracheostomy, reintubation, ICU and hospital lengths of NIV requires an interface that connects the patient to a
stay and total duration of ventilation.124 Conversely, the ventilator, portable compressor or flow generator with a
effectiveness of NIV for postextubation respiratory failure CPAP valve. The selection of an appropriate interface can
is not so clear. The largest study of NIV use in postextu- influence NIV success or failure. Oronasal masks cover
bation respiratory failure reported worsened survival rates both the mouth and nose and are the preferred mask type
hypothesised to be as a result of delayed reintubation.125 for the management of acute respiratory failure.129 Nasal
A subsequent meta-analysis suggested NIV may have a masks enable speech, eating and drinking, and therefore
role in preventing the development of respiratory failure are employed more frequently for long-term NIV use.
postextubation for those at risk, but should be used with An oronasal mask enables delivery of higher ventilation

TABLE 15.3
Indications and contraindications for non-invasive ventilation

I N D I C AT I O N S

Bedside observations Increased dyspnoea; moderate-to-severe tachypnoea:

>24 breaths per min [obstructive]
>30 breaths per min [restrictive]
Signs of increased work of breathing, accessory muscle use and abdominal paradox
Gas exchange Acute or acute-on-chronic ventilatory failure (best indication), PaCO2 >45 mmHg, pH <7.35
Hypoxaemia (use with caution), PaO2/FiO2 ratio <200
C O N T R A I N D I C AT I O N S

Absolute Respiratory arrest

Unable to fit mask
Relative Medically unstable: hypotensive shock, uncontrolled cardiac ischaemia or arrhythmia, uncontrolled
upper gastrointestinal bleeding
Agitated, uncooperative
Unable to protect airway
Swallowing impairment
Excessive secretions not managed by secretion clearance techniques
Multiple (i.e. two or more) organ failure
Recent upper airway or upper gastrointestinal surgery

PaCO2 = partial pressure of carbon dioxide in arterial blood; PaO2 = partial pressure of oxygen in arterial blood; PaO2/FiO2 = ratio of
partial pressure of oxygen in arterial blood to fraction of inspired oxygen.
486 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

pressures with less leak and greater comfort for the the initiation and stabilisation period, patients should be
patient.130 Other interfaces include full-face masks130 that monitored using a nurse-to-patient ratio of 1:1 with
seal around the perimeter of the face and cover the eyes ongoing coaching to promote NIV tolerance throughout
as well as the nose and mouth, nasal pillows, mouthpieces the early stabilisation period.
that are placed between the patient’s lips and helmets
that cover the whole head and consist of a transparent Practice tip
plastic hood attached to a soft neck collar. These alterna-
tive interfaces may increase patient tolerance by reducing NIV tolerance may be promoted with a simple
pressure ulceration, air leaks and patient discomfort.131 explanation of the therapy, reassurance and constant
monitoring for your patient. During initiation, allow
Initiation and monitoring priorities them to take short breaks from the mask if they are in
Successful initiation of NIV is dependent on patient discomfort or experiencing claustrophobia.
acceptance and tolerance. Patient acceptance may be aided
by a brief explanation of the procedure and its benefits. Potential complications
Strategies to enhance patient tolerance include: use of an
interface that fits the patient’s facial features, commencing Masks need to be tight-fitting to reduce air leaks;
with low pressure levels, holding the mask gently in however, this contributes to pressure ulceration on the
position prior to securing with the straps/headgear and bridge of the nose or above the ears (due to mask straps/
ensuring straps prevent major leaks but are not so tight headgear). Air leaks may cause conjunctival irritation
they increase discomfort. Once NIV is commenced, the and the high flow of dry medical gas results in nasal
patient should be monitored for respiratory and haemo- congestion, oral or nasal dryness and insufflation of air
dynamic stability, response to NIV treatment, ongoing into the stomach. Claustrophobia associated with the
tolerance and presence of air leaks (Table 15.4). Arterial NIV interface may also lead to agitation, reducing the
blood gas analysis should be performed at baseline and efficacy of NIV treatment due to poor coordination of
within the first 1 to 2 hours of commencement.132 During respiratory cycling between the patient and NIV unit.104
More serious, yet infrequent, complications include
aspiration pneumonia, haemodynamic compromise
TABLE 15.4 associated with increased intrathoracic pressures and
Monitoring priorities for non-invasive ventilation pneumothorax.105
PRIORITY ASSESSMENT
Detecting NIV failure
Patient comfort Restlessness
Failure to respond to NIV within 1–2 hours of commence-
Mask tolerance
ment is demonstrated by unchanged or worsening
Anxiety level
gas exchange, as well as ongoing or new onset of rapid
Dyspnoea score
Pain score
shallow breathing and increased haemodynamic instabil-
ity.130 Decreased level of consciousness may be indicative
Conscious level Glasgow Coma Score
of imminent respiratory arrest.
Work of Chest wall motion
breathing Accessory muscle activation Weaning from NIV
Respiratory rate
Existing guidelines provide little guidance on weaning
Gas exchange Continuous SpO2 of NIV.133 In many cases, NIV may be simply withdrawn
parameters Arterial blood gas analysis (baseline and as opposed to weaned.132 Those commencing on high
1–2 hourly subsequently) levels of IPAP and/or EPAP may need weaning based
Patient colour on ongoing assessment of dyspnoea and chest wall
Haemodynamic Continuous heart rate movement, as well as ventilation and oxygenation
status Intermittent blood pressure parameters. Another weaning method may be progressive
Ventilator Air leak around mask extension of time off NIV, while monitoring tolerance.
parameters Adequacy of pressure support (VT, pH,
PaCO2)
Adequacy of peak end-expiratory
Invasive mechanical ventilation
pressure (SpO2, PaO2) Critically ill patients with persistent respiratory insuffi-
ciency (hypoxaemia and/or hypercapnia), due to drugs,
PaCO2 = partial pressure of carbon dioxide in arterial blood;
PaO2 = partial pressure of oxygen in arterial blood; SpO2 =
disease or other conditions, may require intubation and
saturation of peripheral oxygen; VT = tidal volume. mechanical ventilation to support oxygenation and
Adapted from Rose L, Gerdtz M. Use of non-invasive
ventilatory demands. Clinical criteria for intubation
ventilation in Australian emergency departments. Int J Nurs and ventilation should be based on individual patient
Stud 2009;46(5):617–23, with permission. assessment and patient response to measures aimed at
reversing hypoxaemia.
 CHAPTER 15 VENTILATION AND OXYGENATION MANAGEMENT 487

Indications BOX 15.2

Indications for intubation and mechanical ventilation include:
Mechanical ventilation of the elderly patient
• apnoea • Elderly survivors of mechanical ventilation may have
• inability to protect airway; e.g. loss of gag/cough a greater increase in disability than those hospitalised
reflex; decreased Glasgow Coma Scale score and not requiring ventilation;136 this is information that
• clinical signs134indicating respiratory distress; e.g. should be shared with patients and family members
tachypnoea, activation of accessory and expiratory when considering treatment options.
muscles, abnormal chest wall movements,135 • Frail elderly are at increased risk of delirium
tachycardia and hypertension resulting in prolonged mechanical ventilation.137
• inability to sustain adequate oxygenation for
metabolic demands; e.g. cyanosis, SpO2 <88%, with
supplemental FiO2 ≥0.5 both inspiratory and expiratory breath phases. Parameters
commonly manipulated during mechanical ventilation
• respiratory acidosis (e.g. acute decrease in pH <7.25) are detailed in Table 15.5. Parameters often observed and
• postoperative respiratory failure documented are discussed below.
• shock. Phases of breath delivery
The goals of mechanical ventilation are to achieve and
maintain adequate pulmonary gas exchange, minimise the The respiratory cycle comprises both inspiratory and
risk of lung injury, reduce patient work of breathing and expiratory phases (see Figure 15.11). Pressure, flow,
optimise comfort. volume and time are parameters used to describe or
classify mechanical ventilator breaths during the phases
Mechanical ventilators of inspiration. Ventilator breaths are classified by: 1) the
Contemporary ventilators use sophisticated microproces- mechanism (ventilator or patient) that ‘triggers’ the start of
sor controls with sensitive detection, response and control inspiration; 2) the parameter that is ‘targeted’ (also referred
of pressure and gas flow characteristics. These ventila- to as ‘controlled’ or ‘limited’) during inspiration; and 3)
tors are more sensitive to patient ventilatory demands, the parameter that ‘cycles’ the breath from inspiration to
enabling improved patient–ventilator synchrony during expiration.138

TABLE 15.5
Set ventilator parameters

PA R A M E T E R DESCRIPTION

Fraction of inspired oxygen (FiO2) The fraction of inspired oxygen delivered on inspiration to the patient
Tidal volume (VT) Volume (mL) of each breath
Set breath rate (f) The clinician-determined set rate of breaths delivered by the ventilator (bpm)
Inspiratory trigger or sensitivity Mechanism by which the ventilator senses the patient’s inspiratory effort. May be
measured in terms of a change in pressure or flow
Inspiratory pressure (Pinsp, Phigh) Clinician-determined pressure that is targeted during inspiration
Inspiratory time (Tinsp) The duration of inspiration (s)
Inspiratory : expiratory ratio (I:E) The ratio of the inspiratory time to expiratory time
·
Flow ( V) The speed gas travels during inspiration (L/min)
Pressure support (PS) The flow of gas that augments a patient’s spontaneously initiated breath to a
clinician-determined pressure (cmH2O)
Positive end-expiratory pressure (PEEP) Application of airway pressure above atmospheric pressure at the end of expiration
(cmH2O)
Rise time Time to achieve maximal flow at the onset of inspiration for pressure-targeted breaths
Expiratory sensitivity During a spontaneous breath, the ventilator cycles from inspiration to expiration once
flow has decelerated to a percentage of initial peak flow
Minute volume (VE) Generally not set directly but is determined by VT and f settings. Tidal volume multiplied
by the respiratory rate over one minute (L/min)
Airway pressure (Paw) The pressure measured in cmH2O by the ventilator in the proximal airway
Plateau pressure (Pplat) The pressure, measured in cmH2O, applied to the small airways and alveoli. Pplat is not
set but can be measured by performing an inspiratory hold manoeuvre
488 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

FIGURE 15.11 Phases of breath delivery.

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Pressure vs volume delivery inspiratory flow requirements can lead to dyssynchrony.

Traditionally, clinicians have favoured volume control Another disadvantage of VCV is the lack of control over
peak airway pressure that changes in response to altered
ventilation (VCV) due to the ability to regulate minute
compliance and resistance. Elevated plateau pressure may
ventilation (VE) and CO2 elimination with straightforward cause alveolar overdistension, barotrauma and haemo-
manipulation of respiratory rate and VT.139 VCV provides dynamic effects such as reduced venous return and cardiac
consistent VT delivery, independent of lung mechanics. output resulting in hypotension and thus decreased organ
The set VT and flow rates used in VCV mean that the perfusion.140 Clinicians need to carefully monitor ventila-
ventilator is unable to increase volume or flow rates in tion to avoid injurious pressures. In VCV the peak airway
response to the patient’s inspiratory demands during pressure is achieved towards the end of inspiration, and only
mandatory breaths.This inability to respond to the patient’s for a short duration; therefore, distribution of gas may not
 CHAPTER 15 VENTILATION AND OXYGENATION MANAGEMENT 489

be optimised and shearing stress can occur.141 This can be time. This promotes recruitment of alveoli with high
overcome with the use of a decelerating waveform and an opening pressures and long time-constants.
inspiratory time that produces an inspiratory hold.
Pressure controlled ventilation (PCV) allows control over Ventilator parameters
the peak inspiratory pressure and inspiratory time. Clinicians Fraction of inspired oxygen
must monitor minute ventilation and gas exchange due to
The FiO2 is expressed as a decimal, between 0.21 and 1.0,
the lack of a guaranteed VT and possible changes in respi-
ratory compliance and resistance. The variable flow and when supplemental oxygen is applied. Room air has an
VT mean that there is the potential for greater interaction oxygen content of 0.21 (21%). Ventilation is commonly
between patient efforts and ventilator breaths than is present commenced on a high FiO2 setting but, as noted earlier,
in volume controlled ventilation. The variable and decelerat- clinicians should consider the risks of oxygen toxicity,
ing inspiratory gas flow pattern of PCV enables rapid alveolar which include disruption to the alveolar-capillary
filling and more even gas distribution compared to the membrane and alveolar wall fibrosis.146
constant flow pattern that may be used with volume control.
This decelerating flow pattern also results in improved gas Tidal volume
exchange, decreased work of breathing and prevention of VT is the volume, measured in mL, of each breath. Set
overdistension in healthy alveoli.142–145 During PCV, the or targeted VT is calculated using the patient’s ideal body
set inspiratory pressure is achieved at the beginning of weight using height and gender-specific tables147 to achieve
the inspiratory cycle and maintained for the set inspiratory 6–8 mL/kg (see Table 15.6). Strong evidence indicates

TABLE 15.6
ARDSnet tables for predicted body weight for females and males
PBW AND TIDAL VOLUME FOR FEMALES HEIGHT, CENTIMETRES PBW AND TIDAL VOLUME FOR MALES
PBW 4 ML 5 ML 6 ML 7 ML 8 ML (INCHES) PBW 4 ML 5 ML 6 ML 7 ML 8 ML
31.7 127 159 190 222 254 137 (54) 36.2 145 181 217 253 290
34 136 170 204 238 272 140 (55) 38.5 154 193 231 270 308
36.3 145 182 218 254 290 142 (56) 40.8 163 204 245 286 326
38.6 154 193 232 270 309 145 (57) 43.1 172 216 259 302 345
40.9 164 205 245 286 327 147.5 (58) 45.4 182 227 272 318 363
43.2 173 216 259 302 346 150 (59) 47.7 191 239 286 334 382
45.5 182 228 273 319 364 152.5 (60) 50 200 250 300 350 400
47.8 191 239 287 335 382 155 (61) 52.3 209 262 314 366 418
50.1 200 251 301 351 401 157.5 (62) 54.6 218 273 328 382 437
52.4 210 262 314 367 419 160 (63) 56.9 228 285 341 398 455
54.7 219 274 328 383 438 162.5 (64) 59.2 237 296 355 414 474
57 228 285 342 399 456 165 (65) 61.5 246 308 369 431 492
59.3 237 297 356 415 474 167.5 (66) 63.8 255 319 383 447 510
61.6 246 308 370 431 493 170 (67) 66.1 264 331 397 463 529
63.9 256 320 383 447 511 172.5 (68) 68.4 274 342 410 479 547
66.2 265 331 397 463 530 175 (69) 70.7 283 354 424 495 566
68.5 274 343 411 480 548 178 (70) 73 292 365 438 511 584
70.8 283 354 425 496 566 180 (71) 75.3 301 377 452 527 602
73.1 292 366 439 512 585 183 (72) 77.6 310 388 466 543 621
75.4 302 377 452 528 603 185.5 (73) 79.9 320 400 479 559 639
77.7 311 389 466 544 622 188 (74) 82.2 329 411 493 575 658
80 320 400 480 560 640 190.5 (75) 84.5 338 423 507 592 676
82.3 329 412 494 576 658 193 (76) 86.8 347 434 521 608 694
84.6 338 423 508 592 677 195.5 (77) 89.1 356 446 535 624 713
86.9 348 435 521 608 695 198 (78) 91.4 366 457 548 640 731

PBW = predicted body weight.

The formulae, when using height in centimetres, are:
• Females = 45.5 + 0.91 × (height in cm − 152.4)
• Males = 50 + 0.91 × (height in cm − 152.3).
Adapted from information courtesy of ARDSnet. Further information available at http://www.ardsnet.org/node/77460.
490 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

a mortality benefit for using 6 mL/kg in patients with mandatory breaths and pressure support for spontan-
acute respiratory distress syndrome (ARDS).148,121 Increas- eous breaths. Reducing the rise time to its lowest value
ingly, evidence indicates protective lung ventilation using will enable the ventilator to reach target pressure in the
6 mL/kg as a target for patients without ARDS is associated shortest time frame resulting in a more rapid delivering of
with improved clinical outcomes.149–151 While further flow in the early phase of inspiration.This reduces work of
studies are required, clinicians should consider aiming for breathing and improves synchrony. In patients with a high
6–8 mL/kg in all ventilated patients. airway resistance (e.g., severe asthma), a short inspiratory
time may cause oscillation and overshoot of the pressure
Respiratory rate waveform. The clinical relevance of this is questionable
Mandatory frequency (f) or respiratory rate (RR) is set but it produces an abnormal pressure waveform and results
with consideration of the patient’s own respiratory effort, in alarm violations. Increasing the rise time may alleviate
anticipated ventilatory requirements and the effect on the this problem. In other patients, an increased rise time may
I:E ratio. Use of high doses of sedation with or without unnecessarily increase their work of breathing.156
neuromuscular blockade requires setting a mandatory rate
that facilitates adequate gas exchange and meets oxygen- Inspiratory time and inspiratory-to-
ation requirements. A lower frequency can be set for a expiratory ratio
patient able to breathe spontaneously in modes such as The total time available for each mandatory breath
synchronised intermittent mandatory ventilation (SIMV) is determined by the set inspiratory time and breath
and assist control (A/C) (see below) to enable spontaneous frequency. Normal inspiratory time is 0.8 to 1.2 seconds.
triggering. Physiologically normal respiratory rates are Total breath time comprises the inspiratory and expiratory
12–20 breaths per minute. Patients with hypoxaemic respir- time, which is expressed as the I:E ratio. In normal spon-
atory failure generally breathe 20–30 breaths per minute.152 taneous breathing, expiratory time is approximately twice
the inspiratory time (1:2 ratio). Gas flow also influences
Triggering of inspiration inspiratory time, with higher gas flows resulting in
Depending on the ventilation mode, breaths are triggered decreased time to achieve the target VT. The I:E ratio
by the ventilator or patient in various sequences. A breath can be manipulated to create an inverse relationship (1:1,
may be triggered by the ventilator in response to time 2:1, 4:1) with the goal of increased mean airway pressure
elapsed in modes with clinician-determined set frequency, resulting in alveolar recruitment and improved oxygen-
such as controlled mandatory ventilation (CMV), and ation. Prolonging the inspiratory time beyond normal
in A/C and SIMV in the absence of spontaneous effort. or using inverse ratio ventilation in any mode can result
Patient triggering requires the ventilator to sense the in patient ventilator dyssynchrony and increased risk of
patient’s inspiratory effort. Most modern ventilators barotrauma.157
now use flow triggering, as evidence indicates that flow
triggering may be more responsive to patient effort than Inspiratory flow and flow pattern
pressure triggering.153 Pressure triggering requires the The flow rate refers to the speed of gas, is measured in
patient to create a negative pressure within the ventilator litres per minute (L/min) and generally delivered at speeds
circuit of sufficient size to enable the ventilator to sense of 30–60 L/min. Higher flow rates cause turbulent gas
the effort and commence flow of gas. Flow triggering flow, resulting in increased peak airway pressures. Lower
is sometimes used in conjunction with a predetermined flow rates result in laminar flow, increased inspiratory
flow of gas, usually 5–10 L/min, referred to as the bias (or time, improved gas distribution and lower peak airway
base) flow, that travels continuously through the ventilator pressures.158 The flow of inspiratory gas can be delivered
circuit. When the patient makes an inspiratory effort, in three styles: constant or square wave, decelerating ramp
they divert flow, which is sensed by the ventilator. If the and sinusoidal pattern (see Figure 15.6). In a constant flow
flow diversion reaches a clinician-determined set value, pattern, the peak flow is achieved at the beginning of
a breath is initiated.154 The flow trigger is usually set at inspiration and is held constant throughout the inspiratory
1–3 L/min (1 L/min represents less patient effort and phase. This may result in higher peak airway pressures.
3 L/min represents greater patient effort). Despite advances Using a decelerating ramp, the gas flow is highest at the
in ventilator technology, various studies continue to beginning of inspiration and tapers throughout the inspir-
identify missed patient triggers that contribute to patient– atory phase. Sinusoidal gas flow resembles spontaneous
ventilator asynchrony.155 Conversely, ‘auto-triggering’ is ventilation.
ventilator triggering in the absence of spontaneous inspir-
atory effort. Auto triggering is sometimes observed in Peak airway pressure
patients with an increased cardiac output, such as those Airway pressures vary across the respiratory cycle with
fulfilling brain death criteria. a number of pressures identifiable (e.g. peak inspiratory,
end-expiratory). The airway pressure (Paw) is an important
Rise time parameter in assessing respiratory compliance and patient–
The rise time controls how quickly the ventilator reaches ventilator synchrony, and will vary depending on VT, RR,
the clinician-determined inspiratory pressure (Pinsp) for ventilator flow pattern, dynamic compliance and airway
 CHAPTER 15 VENTILATION AND OXYGENATION MANAGEMENT 491

resistance. In pressure-targeted modes the peak inspiratory Ventilator modes

pressure is equivalent to the Pinsp. In volume-targeted
The mode of ventilation describes inspiratory phase
modes the peak inspiratory pressure is determined by the
variables; how the ventilator controls pressure, volume and
set VT and patient compliance and resistance.
flow during a breath; as well as describing how breaths
Positive end-expiratory pressure are sequenced. All breaths have trigger, limit and cycle
PEEP is the pressure applied at the end of the expiratory inspiratory phase variables.174 Each breath is triggered
cycle to prevent alveolar collapse. PEEP increases (started) either by the patient or by the ventilator. During
residual lung volume thereby recruiting collapsed alveoli, inspiration, the breath is limited to a set target of pressure,
improving ventilation/perfusion match and enhancing volume or flow. This target cannot be exceeded during
movement of fluid out of the alveoli.159,160 PEEP was each breath. The cycling variable determines the end of
originally introduced by Ashbaugh and colleagues161 in the the inspiratory phase. Again this variable may be pressure,
1960s as a technique for treating refractory hypoxaemia flow, volume or time. Gas delivery during each breath is
in patients with ARDS. Animal studies suggest ventilator- described by the control variable. There are five control
associated lung injury may be prevented using PEEP by variables: pressure, volume, flow, time and dual control
recruiting atelectic alveoli and bronchioles and preventing (such as used in the mode pressure-regulated volume
cyclic opening and closing of alveoli.162–165 PEEP may be control). Breath sequencing refers to the sequence of
beneficial, however, only if the lung is recruitable such as mandatory and spontaneous breath. A spontaneous breath
in collapsed, as opposed to consolidated, lung.159 Selection is one during which inspiration is both started (triggered)
of optimal PEEP remains controversial. Low PEEP levels and stopped (cycled) by the patient. Spontaneous breaths
have been shown to be associated with higher mortality may be assisted, as with pressure support, or unassisted.
for ARDS patients in several studies.166–169 Two randomised, Mandatory breaths are either triggered or cycled by the
controlled trials comparing low tidal volume ventilation ventilator.175 A complete mode description should include:
and conventional PEEP to low tidal volume ventilation 1) the control variable; 2) the breath sequence; and 3) the
and high PEEP, with and without additional recruitment targeting scheme (limit variable).
manoeuvres (40 cmH2O applied for 40 s),170, 171 did not Commonly employed ventilation
demonstrate a reduction in hospital170 or 28-day171 mortality.
modes
Pressure support Contemporary ventilators now provide a range of modes
When triggered by the patient, the ventilator delivers flow to facilitate mechanical ventilation. See Table 15.7.
to achieve the clinician-determined set pressure support.
The flow is variable, depending on the patient demand. Controlled mandatory ventilation
The VT achieved with pressure support is dependent CMV is a mandatory mode, and is the original and
on chest and lung compliance as well as airway and most basic mode of ventilation.176 CMV delivers all
ventilator resistance. Pressure support is generally set at breaths at a clinician-determined set frequency (rate);
5–20 cmH2O. Increasing the level of pressure support will the patient’s spontaneous effort is not acknowledged
result in increased VT and improvements in gas exchange by the ventilator.81 VCV requires clinician selection of
if compliance and resistance remain constant. the frequency, PEEP, FiO2, tidal volume, flow waveform,
peak inspiratory flow and either the inspiratory time
Expiratory sensitivity or I:E ratio. PCV requires clinician selection of rate,
Expiratory sensitivity describes the percentage of decay in PEEP, FiO2, inspiratory pressure, as opposed to tidal
peak flow reached during the inspiratory phase that signals volume, and inspiratory time or I:E ratio depending on
the ventilator to cycle to expiration for spontaneous the ventilator type. Peak inspiratory flow and the flow
breaths. In some ventilator models this is predetermined waveform are manipulated by the ventilator, to achieve
at 25%, while others allow clinician selection. Premature the clinician-selected inspiratory pressure within the set
termination of a breath will increase inspiratory muscle inspiratory time. The inability to breathe spontaneously
workload whereas delayed breath termination increases during CMV contributes to diaphragm muscle dysfunc-
expiratory muscle load.172 Reducing the expiratory sensi- tion and atrophy, which may result in difficulty weaning
tivity in patients with COPD may prolong the inspiratory from the ventilator.177
time, thereby increasing the VT and reducing the respir-
atory rate and gas trapping.173 Assist control
In A/C the patient can trigger the ventilator; however,
Practice tip unlike SIMV, every patient-initiated breath is assisted to
The Pinsp setting reflects a different value on different
the same clinician-determined VT (volume targeted) or
ventilators. Pinsp equals total pressure including PEEP
inspiratory pressure (pressure targeted). All breaths are
on some ventilators and Pinsp above PEEP on others.
cycled by the ventilator irrespective of being patient-
Use the pressure–time scalar to confirm.
or ventilator-triggered. In the absence of spontaneous
breathing, A/C resembles CMV.
492 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 15.7
Ventilator modes

MODE DESCRIPTION C L I N I C A L I M P L I C AT I O N S
Controlled All breaths are mandatory, no patient triggering is enabled. Patients with respiratory effort require sedation
mandatory Also called volume controlled ventilation (volume targeted) and neuromuscular blockade
ventilation (CMV) (VCV) and pressure controlled ventilation (pressure Potential for respiratory muscle atrophy due to
targeted) (PCV) disuse
Assist-control (A/C) Breaths may be either machine or patient triggered but Activation of the diaphragm with patient triggering
all are cycled by the ventilator. Assist control may be Potential for respiratory alkalosis if tachypnoea
delivered as volume (AC-VC) or pressure (AC-PC) targeted develops
Synchronised Mandatory breaths are delivered using a set rate and Reduced need for sedation
intermittent volume (SIMV-VC) or pressure (SIMV-PC). Mandatory Activation of the diaphragm with patient triggering
mandatory breaths are synchronised with patient triggers within a
ventilation (SIMV) timing window. Between mandatory breaths the patient
can breathe spontaneously
Pressure support All breaths are patient triggered and cycled. Pressure Reduced need for sedation
ventilation (PSV) applied by the ventilator during inspiration (pressure Facilitates ventilator weaning
support) augments patient effort Level of PS can be adjusted to achieve desired VT
Sustains respiratory muscle tone and decreases
work of breathing
Continuous All breaths are patient triggered and cycled. Positive Requires intact respiratory drive and patient
positive airway pressure is applied throughout inspiratory and expiratory ability to maintain adequate tidal volumes
pressure (CPAP) phases of the respiratory cycle
Volume support Spontaneous mode with clinician preset target tidal volume Requires intact respiratory drive
(VS) delivery achieved with the lowest inspiratory pressure
Pressure-regulated Mandatory rate and target tidal volume are set, and the Dual control of volume and pressure enables
volume control ventilator then delivers the breaths using the lowest guarantee of volume and pressure
(PRVC) achievable pressure
Airway pressure Ventilator cycles between 2 preset pressure levels for Reduced need for sedation
release ventilation defined time periods. I:E ratio is inverse, often with a Activation of the diaphragm with patient triggering
(APRV) prolonged inspiratory time (4 s) and shortened expiratory Promotes alveolar recruitment
time (0.8 s). Patient can breathe spontaneously at both Considered a rescue mode in ARDS when used
pressure levels with extreme inverse ratio
Biphasic positive As with APRV, the ventilator cycles between 2 preset Reduced need for sedation
airway pressure pressure levels for defined time periods and the patient Activation of the diaphragm with patient triggering
(BiPAP/ BILEVEL/ can breathe spontaneously at both pressure levels. The Promotes alveolar recruitment
Bivent) inspiratory time is generally shorter than, or the same
length, as the expiratory time
Mandatory minute The patient’s spontaneous minute ventilation is monitored Guarantees minute ventilation for patients
ventilation (MMV) by the ventilator. When the minute ventilation falls below with fluctuating respiratory drive and muscle
the clinician-determined target, the ventilator increases innervation such as patients awakening from
the mandatory rate or size of tidal volumes to regain the anaesthesia and those with Guillain–Barré
desired minute ventilation
Proportional assist Delivers positive pressure throughout inspiration in Requires intact respiratory drive
ventilation (PAV)269 proportion to patient generated effort, and dependent on Patients with high respiratory drive as the ventilator
the set levels of flow assist (offsets resistance) and volume may over-assist and continue to apply support
assist (offsets elastance)268 when the patient has stopped inspiration269
Proportional assist Clinician only sets a percentage of work for the ventilator. Requires intact respiratory drive
ventilation (PAV+™) The ventilator assesses total work of breathing by Decreases work of breathing and improves
randomly measuring compliance and resistance every patient ventilator synchrony
4–10 breaths Potential for use as a weaning mode
Adaptive support Automatic adaptation of respiratory rate and pressure Automatically sets all ventilator settings except
ventilation (ASV) levels based on a clinician-set desired percentage of PEEP and FiO2
minute ventilation270 Potential for use as a weaning mode
Volume assured The ventilator switches from pressure control to volume Enables maintenance of a preset minimum VT
pressure support control, or pressure support to volume control during and reduces work of breathing
(VAPS) inspiration
 CHAPTER 15 VENTILATION AND OXYGENATION MANAGEMENT 493

Synchronised intermittent mandatory breathing independent of ventilator cycling, using an

ventilation active expiratory valve that allows patients to exhale
even in the inspiratory phase.140,141,179,180 Both modes are
SIMV delivers breaths at a set frequency (rate), and can pressure-limited and time-cycled. In the absence of spon-
be either pressure- or volume-targeted. Setting of the taneous breathing, these modes resemble conventional
ventilator is similar to setting VCV or PCV. The availabil- pressure-limited, time-cycled ventilation.181 In North
ity of patient triggering with SIMV facilitates provision America the acronym BiPAP® is registered to Respiron-
of gas flow in recognition of a patient’s spontaneous ics non-invasive ventilators (Murrayville, PA). Therefore
effort. SIMV uses a timing window to deliver mandatory ventilator companies have developed brand names such as
breaths in synchrony with patient inspiratory effort.178 BiLevel (Puritan Bennett, Pleasanton, CA, GE Healthcare,
Additional spontaneous breaths occurring outside of the Madison, WI) Bivent (Maquet, Solna, Sweden), DuoPaP
timing window may be assisted with pressure support (Hamilton Medical, Rhäzüns, Switzerland), PCV+
to augment the patient’s spontaneous effort to a pre-set (Dräger Medical, Lübeck, Germany) or BiPhasic (Viasys,
pressure level. Conshocken, PA) to describe essentially equivalent
Pressure support ventilation modes. Ambiguity exists in the criteria that distinguish
APRV and BIPAP. When applied with the same I:E ratio,
Pressure support ventilation (PSV) is a spontaneous mode no difference exists between the two modes. APRV, as
in which the patient initiates and cycles all breaths, with opposed to BIPAP, however, is more frequently described
support of the patient’s inspiratory effort by the ventilator with an extreme inverse ratio and advocated as a method
using rapid acceleration of flow to achieve a preset level to improve oxygenation in refractory hypoxemia.182
of inspiratory pressure. Unlike CMV, SIMV or A/C, PSV
does not require setting of ventilator (mandatory) breaths. Automatic tube compensation
PSV is usually employed with PEEP, which maintains Automatic tube compensation is active during sponta-
partial inflation of alveoli during the expiratory phase to neous breaths and compensates for the work of breathing
promote alveolar recruitment and oxygenation. associated with ETT resistance via closed-loop control
Continuous positive airway pressure of continuously calculated tracheal pressure.183,184 During
spontaneous inspiration, a pressure gradient exists
CPAP applies a set baseline positive pressure throughout between the proximal and distal ends of the ETT due
the inspiratory and expiratory phases. In this sponta- to resistance created by the tube. A reduced pressure
neous breathing mode, unlike PSV, no additional positive at the proximal end of the tube means a patient needs
pressure is provided to the patient during inspiration. Due to produce a greater inspiratory force (greater negative
to nomenclature used on some ventilator models, PSV is pressure) to generate an adequate VT.185 Higher flow rates
frequently misrepresented as CPAP. generate larger pressure gradients and greater resistance.
Volume-targeted pressure control Automatic tube compensation requires the airway
type and size to be selected as well as a percentage of
breaths automatic tube compensation to be applied. It appears
A number of hybrid ventilator modes are commer- to have most use in reducing the work of breathing for
cially available that use an algorithm to target a set patients with high respiratory drive who require high
VT by regulating the inspiratory pressure during pres- inspiratory flow.186
sure-controlled breaths based on the patient’s resistance,
compliance and inspiratory effort. Examples include pres- Neurally adjusted ventilatory assist
sure-regulated volume control, available on the Servo 300 Neurally adjusted ventilatory assist is available on the
and Servo I (Maquet, Solna, Sweden) and SIMV with Servo-I ventilator (Maquet, Solna, Sweden) and uses the
autoflow (Dräger, Lübeck, Germany). On initiation of electrical activity of the diaphragm to control patient–
these modes the ventilator delivers a number of breaths ventilator interaction.187 Electrical activity of the diaphragm,
during a ‘learning period’ to establish an estimate of the measured using an oesophageal catheter, should result in
pressure required to achieve the targeted VT. The patient’s optimal patient–ventilator synchrony as it represents the
resistance, compliance and inspiratory effort continue to end point of neural output from the respiratory centres,
influence the pressure and flow delivered to attain the and thus is the earliest signal of patient inspiratory trigger
targeted VT. The ventilator constantly regulates inspiratory and expiratory cycling. Pressure delivered to the airways
pressure based on the pressure/volume calculation of the is proportional to inspiratory diaphragmatic electrical
previous breaths and the clinician-determined target tidal activity using a clinician-determined proportionality factor
volume. set on the ventilator.188 Neurally adjusted ventilatory assist
provides breath-by-breath assist in synchrony with, and
Airway pressure release ventilation and in proportion to, respiratory demand.189 Although clinical
biphasic positive airway pressure data on neurally adjusted ventilatory assist are currently
Airway pressure release ventilation (APRV) and BIPAP limited,188,190–192 this mode shows promise for improving
are ventilator modes that allow unrestricted spontaneous patient–ventilator synchrony.
494 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Managing the mechanically HFOV is generally considered a rescue mode for adult
patients with ARDS experiencing refractory hypoxaemia
ventilated patient and failing conventional ventilation.207, 208 A recent large,
multicentre, randomised controlled trial of HFOV was
Management of refractory stopped early for harm with increased mortality in the
hypoxaemia HFOV arm.209 A contemporaneous trial conducted in the
Refractory hypoxaemia may require strategies in addition UK found no effect for HFOV compared to usual venti-
to conventional lung-protective mechanical ventilation.148 latory care on 30-day mortality in patients undergoing
These include recruitment manoeuvres (RMs), high mechanical ventilation for ARDS.210
frequency oscillatory ventilation (HFOV), extracorporeal
membrane oxygenation (ECMO) and nitric oxide (NO).
Extracorporeal membrane oxygenation
ECMO improves total body oxygenation using an
Recruitment manoeuvres external (extracorporeal) oxygenator, while allowing
RMs refer to brief application of high levels of PEEP intrinsic recovery of lung pathophysiology by resting
to raise the transpulmonary pressure to levels higher the lung. Indications for ECMO include acute severe
than achieved during tidal ventilation with the goals of cardiac or respiratory failure such as severe ARDS and
opening collapsed alveoli, recruiting slow opening alveoli, refractory shock or as a bridge to transplantation.211 Due
preventing alveolar derecruitment and reducing shearing to the need for rescue treatment with ECMO during
stress.193–195 The most common RM is elevation of PEEP to the 2009 H1N1212 outbreak and a randomised clinical
achieve a peak pressure of 40 cmH2O for a sustained period trial indicating a survival benefit with venous–venous
of 40 s, although studies report peak pressure elevations ECMO compared to conventional ventilation,213 ECMO
ranging from 25–50 cmH2O for durations ranging from is being used more frequently for refractory respiratory
20–40 s.196 The best method in terms of pressure, duration failure. Bleeding as a complication of anticoagulation is
and frequency has yet to be determined.197 RMs in a major risk of ECMO, with cerebral bleeds being the
humans have not produced consistent results in clinical most catastrophic.214 Another serious complication is limb
studies,198,199 with a recent systematic review demon- ischaemia when the femoral artery is used.
strating no mortality benefit despite transient increases ECMO consists of three key components:
in oxygenation.196 Effective recruitment may be difficult 1 a blood pump (either a simple roller or centrifugal
to assess with the potential for either alveolar overdisten- force pump)
sion or failure to recruit.169 Once the RM is terminated, 2 a membrane oxygenator (bubble, membrane or
derecruitment may occur rapidly. Serious adverse effects hollow fibre)
have been noted during RMs due to increased intratho-
3 a countercurrent heat exchanger, where the blood is
racic and intrapulmonary pressures resulting in reductions
in venous return and cardiac output, cardiac arrest and exposed to warmed water circulating within metal
increased risk of barotrauma.195,200 tubes.
In addition, essential safety features include: bubble
High frequency oscillatory ventilation detectors that detect gas in the arterial line and shut
HFOV requires a specialised ventilator and manipula- the pump off; arterial line filters between the heat
tion of four variables: mean airway pressure (cmH2O), exchanger and arterial cannula, to trap air thrombi
frequency (Hz), inspiratory time and amplitude (or and emboli; pressure monitors placed before and after
power [ΔP]).201 Alveolar overdistension is limited the oxygenator that measure the pressure within the
through the use of sub-dead space tidal volumes whereas circuit and detect rising circuit pressures commonly
alveolar cyclic collapse is prevented by maintenance of caused by thrombus or circuit or cannulae occlusion;
high end-expiratory lung pressures.202,203 High frequency and continuous venous oxygen saturation and tempera-
(between 3 and 15 Hz) oscillations at extremely fast rates ture monitoring. On commencement of ECMO the
(300–420 breaths/min) create pressure waves enabling circuit is primed with fresh blood. The acid–base balance
CO2 elimination.162,204 Oxygenation is facilitated through and blood gas of the primer is adjusted to ensure that
application of a constant mean airway pressure via the the pH is within the normal range (7.35–7.45) and
bias flow (rate of fresh gas).204,205 In adults, recommen- PaO2 is adequate. ECMO can be delivered via veno-
dations for the initiation of HFOV state mean airway arterial access, which requires cannulation of an artery.
pressure should be set 5 cmH2O above the peak airway This method bypasses the pulmonary circulation while
pressure achieved with conventional ventilation.206 The providing cardiac support to the systemic circulation and
recommended frequency range is 3–10 Hz with 5 Hz achieves a higher PaO2 with lower perfusion rates. The
conventionally used to initiate HFOV. Inspiratory time alternative is veno-venous access, used for patients in
is set at 33% and the amplitude setting is determined by respiratory failure with adequate cardiac function as there
adequate CO2 elimination.162 Increased CO2 elimination is no support of systemic circulation. Perfusion rates are
is achieved by lowering the frequency and increasing the higher, the mixed venous PO2 is elevated and the PaO2
amplitude. is lower.214
 CHAPTER 15 VENTILATION AND OXYGENATION MANAGEMENT 495

Nitric oxide when taking into consideration contraindications.223–227

NO is an endothelial smooth muscle relaxant. Inhaled Similarly, interventions to improve compliance failed to
NO is effective for dilation of pulmonary arteries resulting demonstrate adherence to the 45° semirecumbent position
in reduced pulmonary shunting and reduced right that can be sustained by the patient over time. 228,229 Due
ventricular afterload due to reduced pulmonary artery to uncertainty over compliance with 45° semirecum-
tone. Pulmonary shunting refers to failure of uptake of bency in the original trial conducted by Drakulovic,219
alveolar gas by the pulmonary vascular bed due to vascular and the lack of difference in VAP rates despite difficulty
achieving compliance with semirecumbency in the
constriction or interstitial oedema. Inhaled NO has a
van Niewenhoven study,222 new studies are required to
role in the management of pulmonary hypertension and
confirm the equivalence or lack of inferiority of lower
was previously thought to have a role in management of
degrees of backrest elevation to the strict 45° semirecum-
refractory hypoxaemia for patients with ARDS. However,
bent position.
the most recent systematic review and meta-analysis of
NO in ARDS comprising 14 RCTs and 1303 participants Practice tip
reported no effect on overall mortality despite a statisti-
cally significant improvement in oxygenation in the first Backrest elevation is difficult to estimate accurately.
24 hours.215 Use an objective measurement device such as an
inclinometer or protractor.
Positioning
Regular repositioning of critically ill patients is essential
for lung recruitment, prevention of atelectasis and mainte- BOX 15.3
nance of skin integrity (see Chapter 6).
Mechanical ventilation and the bariatric patient
Head-of-bed elevation • Bariatric patients are at increased risk of atelectasis
Supine positioning has been associated with aspiration and have decreased chest wall compliance due to
of abnormally colonised oropharyngeal and gastric the weight of the abdomen.
contents216–218 and increased incidence of VAP compared • Avoid the supine position as this will further
to a semirecumbent position, defined as backrest elevation decrease lung volumes.
at 45°.219 Guidelines and care bundles for VAP prevention • Bariatric patients may require higher airway
recommend semirecumbent positioning for all mechan- pressures to generate adequate tidal volumes.
ically ventilated patients.96,220,221 A more recent trial has,
• Recruitment manoeuvres may improve
however, questioned the feasibility of 45° semirecumbent
oxygenation.230
positioning as this backrest elevation was only achieved for
15% of study observations.222 There was also no difference • Frail elderly may experience difficult weaning due
in VAP incidence between the supine and semirecumbent to the presence of comorbidities such as CHF,
group. Contraindications to backrest elevation include: ischaemic heart disease and COPD.

• suspected or existing spinal injury

• intracranial hypertension (for 45° elevation) Lateral positioning
Patients with unilateral lung disease experience a mismatch
• unstable pelvic fractures of ventilation to perfusion if the consolidated or atelectic
• prone positioning lung is placed in the dependent position.231 Temporary and
• haemodynamic support devices (intra-aortic balloon early positioning of the affected lung in the dependent
pumps, left ventricular assist devices and ECMO) position, amongst other strategies such as avoiding manual
• femoral catheterisation for continuous renal hyperinflation, for patients with unilateral pneumonia or
replacement therapy following aspiration may be beneficial in preventing the
movement of bacteria or acidic gastric contents into the
• large abdominal wounds non-affected lung.232 This theory has been coined ‘prop-
• following femoral sheath removal. agation prevention’. While appealing, as yet there have
As some degree of semirecumbent positioning is been no adequately powered randomised controlled trials
preferable to supine positioning, patients with suspected to support its use. Continuous lateral rotational therapy
or existing spinal injury, pelvic fractures or being managed is a positioning therapy advocated for the prevention
with prone positioning can have the head elevated by and management of respiratory complications associated
tilting the whole bed. Patients with femoral cannulation with immobility.233 The most recently reported multi-
and large abdominal wounds can usually achieve 25–30° centre randomised controlled trial found a significant
positioning. reduction in VAP and shorter durations of ventilation and
Clinical practice audits conducted internationally and ICU stay.234 Continuous lateral rotation therapy requires a
in Australia and New Zealand indicate that compliance special bed system enabling rotation of the upper part of
with a 45° semirecumbent position rarely occurs, even the body to a maximum angle of 90°.
496 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Prone positioning nosocomial infection, including VAP.178,246 Ventilator-

Prone positioning has been shown to improve oxygenation associated lung injury occurs through alveolar over-
and intrapulmonary shunt fraction when compared with distension and cyclic opening and closing of alveoli
rotational turning during the first 72 hours of ARDS235 resulting in diffuse alveolar damage, increased permea-
and in patients with multiorgan failure.236 Prone position- bility, pulmonary oedema, cell contraction and cytokine
ing may also decrease the risk of VAP due to improved production.149,159,165,247–249 VAP substantially increases the
bronchial secretion drainage, limitation of colonisation duration of ICU stay and is associated with an attribut-
of distal lung, decreased atelectasis and increased alveolar able mortality of 5.8–8.5%.250–252 Additional complications
recruitment but may increase the spread of pathogens in associated with mechanical ventilation are listed in
the lung and may increase the risk of aspiration.237–240 Table 15.8. Complications can occur due to inappropriate
Prone positioning results in changes to the distribu- application of mechanical ventilation. This may result in
tion of ventilation and pulmonary blood flow. Pleural extra-alveolar gas causing pneumothoraces or subcutane-
pressures are lower in non-dependent regions and higher ous emphysema due to high peak Pinsp, and alveolar stretch
in dependent regions due to gravitational forces, the and oedema formation as a result of large VT.81
weight of the overlying lung and mismatch between the
local physical structures of the lung and chest wall.241 Weaning from mechanical
The weight of the overlying lung increases in ARDS due
to parenchymal oedema and fluid within the alveoli.242 ventilation
This gradient in pleural pressures means transpulmo- Weaning traditionally occurs via clinician-directed
nary pressure is higher in non-dependent lung regions, adjustments to the level of support provided by the
compared to dependent regions.242 Perfusion also increases ventilator, culminating in a spontaneous breathing trial
from previously non-dependent to dependent lung (SBT) comprising either low level pressure support or a
regions resulting in optimal matching of ventilation and T piece trial.
perfusion to promote gas exchange.
Increased pleural pressure in the dependent dorsal Current recommendations
regions in the supine position can result in airway closure, No ventilation strategy is more lung-protective than the
atelectasis and hypoxaemia.241 The difference in pleural timely and appropriate discontinuation of mechanical
pressures from non-dependent and dependent lung ventilation. Weaning refers to the transition from ventila-
regions is greater in the supine compared to the prone tory support to spontaneous breathing.253 Evidence-based
position. In the supine position, the heart and abdominal consensus guidelines published for weaning in 2001178
contents also compress lung bases and decrease functional and 2007254 emphasise the importance of preventing
residual capacity, whereas in prone positioning, the weights unnecessary delays in the weaning process, early recog-
of these structures are lifted from the lung. nition of a patient’s ability to breathe spontaneously and
The benefits of prone positioning continue to be the use of a systematic method to identify the potential
debated. Although oxygenation improves in 70–80% for extubation.
of patients turned from supine to prone,243 a mortality
benefit has not been shown in all trials. The most recent Weaning predictors
systematic review and meta-analysis that included 11 Clinician judgement regarding prediction of weaning
randomised controlled trials244 found reduced mortality readiness is known to be imperfect, with unnecessary
and improved oxygenation for patients with ARDS prolongation of ventilation255 or high rates of reintubation
managed with protective lung ventilation. Adverse as resultant consequences, both of which are associated
events related to prone positioning were increased risk of with adverse outcomes.256,257 An evidence-based review
decubitus ulcer formation, endotracheal obstruction and evaluating over 50 objective physiological measurements
thoracotomy tube dislodgement. for determining readiness for weaning and extubation
Implementing prone positioning requires forward found most had only a modest relationship with weaning
planning to ensure eye care and protection, mouth care, outcome; no single factor or combination of factors
wound dressings and tracheal suction are attended to before demonstrated superior accuracy.258 Of all predictors
positioning the patient prone. Intravenous lines, electro- studied, the respiratory frequency to tidal volume ratio
cardiogram leads, urinary catheter drainage, chest drains and (f/VT) appears to be most accurate.259 However, inclusion
ostomy bags need to be secured and repositioned appropri- of the f/VT as part of a weaning protocol was found in
ately once the patient is positioned.245 Prone positioning can one randomised study to increase, as opposed to decrease,
be achieved by manual handling of the patient, requiring up the duration of weaning.260 At present, consensus guide-
to five staff, although commercial devices are available that lines254 do not recommend routine inclusion of weaning
facilitate the turning and positioning.245 predictors.
Complications of mechanical ventilation Weaning methods
Physiological complications associated with mechanical Various studies have attempted to identify the best
ventilation include ventilator-associated lung injury and weaning method. Two of the most frequently-cited
 CHAPTER 15 VENTILATION AND OXYGENATION MANAGEMENT 497

TABLE 15.8
Complications of mechanical ventilation

ITEM C O M P L I C AT I O N ( S )
Barotrauma Pneumothorax
Pneumomediastinum
Pneumopericardium
Pulmonary interstitial emphysema
Subcutaneous emphysema
Volutrauma Shearing stress, endothelial and epithelial cell injury, fluid retention and pulmonary oedema,
perivascular and alveolar haemorrhage, alveolar rupture
Biotrauma Activation of systemic and local inflammatory mechanisms
Ventilation/perfusion Alveolar distension causes compression of the adjacent pulmonary capillaries resulting in dead
mismatch space ventilation
↓ Cardiac ouput Resulting in hypotension, ↓ cerebral perfusion pressure (CPP), ↓ renal and hepatic blood flow
↑ Right ventricular afterload Due to ↑ intrathoracic pressure may result in ↓ left ventricular compliance and preload
↓ Urine output Due to ↓ glomerular filtration rate, ↑ sodium reabsorption and activation of the renin–angiotensin–
aldosterone system
Fluid retention Due to above renal factors as well as ↑ antidiuretic hormone and ↓ atrial natriuretic peptide
Impaired hepatic function Due to ↑ pressure in the portal vein, ↓ portal venous blood flow, ↓ hepatic vein blood flow
↑ Intracranial pressure Due to ↓ cerebral venous outflow
Oxygen toxicity Alterations to lung parenchyma similar to those found in ARDS
Pulmonary emboli and deep Due to immobility
vein thrombosis
Ileus, diarrhoea Due to alterations in gastric motility
Gastrointestinal haemorrhage Gastritis and ulceration may occur due to stress, anxiety and critical illness
ICU-acquired weakness Neuropathies and myopathies develop in association with critical illness, corticosteroids and
neuromuscular blockade
Psychological issues Delirium, anxiety, depression, agitation and post-traumatic stress disorder may be experienced by
critically ill ventilated patients in the acute and recovery phases

studies have produced conflicting results. Brochard and Weaning protocols

colleagues261 compared PSV, T piece trials and SIMV, and Implementation of various organisational strategies
concluded that PSV reduced the duration of mechanical such as weaning teams and non-physician-led weaning
ventilation compared with the other methods. Esteban protocols may assist in the timely recognition of weaning
and colleagues262 compared PSV, T piece trials, CPAP and extubation readiness.268–272 Coupling of a sedation
and progressive reduction of SIMV support, and found a and weaning protocol was found to result in a three-day
once-daily T piece trial led to extubation three times more reduction in the duration of ventilation compared to
quickly than SIMV and nearly twice as quickly as PSV. A standard care in four North American hospitals.273 A
recent systematic review comparing trials of PSV and T systematic review and meta-analysis of 11 weaning
piece found no clear evidence of a difference between protocol trials including 1971 patients demonstrated a
these weaning strategies for weaning success.263 Failure to reduction in the duration of mechanical ventilation.274
produce consistent results favouring a single weaning style However, the authors cautioned that the effect of weaning
suggests it is not the mode that is important but rather the protocols may vary according to ICU organisational char-
application of a systematic process.264 acteristics such as an intensivist-led ICU model, high
levels of physician staffing, structured ward rounds, collab-
Spontaneous breathing trials orative discussion and more frequent medical review;
SBTs incorporate a focused assessment of a patient’s all are characteristics reported for ICUs in Australia and
capacity to breathe prior to extubation265 and are recom- New Zealand. 275,276
mended as the major diagnostic test to determine
extubation readiness.254 SBTs can be conducted using Automated weaning
either a T piece or low levels of pressure support266 and Automated computerised systems potentially enable
should need to last only 30 minutes.267 This method of more efficient weaning by providing improved
weaning is less common in Australia and New Zealand, in adaptation of ventilatory support through continuous
contrast to international findings.78,79 monitoring and real-time intervention.277 One such
498 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

system, SmartCare™/PS, monitors three respiratory costs.282,283 A recommendation from the National Asso-
parameters, f, VT and end-tidal carbon dioxide concen- ciation for Medical Direction of Respiratory Care states
tration, every 2 or 5 minutes and periodically adapts that prolonged mechanical ventilation should be defined
PS.277,278 SmartCare™/PS establishes a respiratory status as ‘≥21 consecutive days of ventilation required for
diagnosis, based on evaluation of the three parameters, ≥6 hours per day’.254 Prolonged weaning has been defined
and may either decrease or increase PS, or leave it as >7 days of weaning after the first SBT or more than
unchanged to maintain the patient in a defined ‘respira- three SBTs.254 Little evidence defines the optimal method
tory zone of comfort’.279,280 Once SmartCare™/PS has for managing the difficult-to-wean patient. One trial
successfully minimised the level of PS, a 1-hour obser- found no difference in weaning duration or success when
vation period occurs. For patients who remain within comparing tracheostomy trials to low-level pressure
the respiratory zone of comfort throughout the observa- support in patients with COPD experiencing weaning
tion period, SmartCare™/PS recommends to ‘consider difficulty.284 A recent randomised controlled trial demon-
separation’, indicating the patient’s respiratory status now strated increased weaning success with use of a once daily
suggests the patient will tolerate extubation. progressive tracheostomy mask trial compared to pressure
A recent meta-analysis of automated weaning systems support weaning.285 These patients are most likely to
has shown that SmartCare™/PS may reduce the duration benefit from an individualised and structured approach to
of weaning, total ventilation and ICU length of stay when weaning using progressive lengthening of tracheostomy
compared to protocolised or usual care weaning.281 trials with supportive ventilation in between in combina-
tion with early physical therapy.
The difficult-to-wean patient
International reports indicate patients that require Practice tip
mechanical ventilation for ≥21 days account for less Tachypnoea and decreased VT during weaning are
than 10% of all mechanically ventilated patients, but indicators that a patient is not ready for extubation.
occupy 40% of ICU bed days and accrue 50% of ICU

Summary
Support of oxygenation and ventilation during critical illness are key activities for nurses in ICU. Oxygen therapy
promotes aerobic metabolism but has adverse effects that need to be considered.Various oxygen delivery devices provide
low or variable flows of oxygen.
Strong evidence supports the use of NIV for COPD and CHF, but caution is required when it is used for other
diagnoses such as pneumonia. NIV success is dependent on patient tolerance, with common complications including
pressure ulcers, conjunctival irritations, nasal congestion, insufflation of air into the stomach and claustrophobia.
Airway support can be provided with oro- or nasopharyngeal airways, LMAs and endotracheal intubation; oral
intubation is the preferred method. For a patient with an ETT, the key points for practice are:
• ETT placement should be confirmed with end-tidal CO2 monitoring
• The aim of endotracheal cuff management is to prevent airway contamination and enable positive pressure ventilation
• Closed suctioning reduces alveolar derecruitment compared to open suctioning
• Instillation of normal saline is not recommended during routine tracheal suctioning.
The optimal timing of tracheostomy remains uncertain; however, tracheostomy should be considered for patients
experiencing weaning difficulty.
The goals of mechanical ventilation are to promote gas exchange, minimise lung injury, reduce work of breathing
and promote patient comfort:
• Despite its life-saving potential, mechanical ventilation carries the risk of serious physical and psychological
complications.
• Humidification of dry medical gas is required during mechanical ventilation to prevent drying of secretions,
mucous plugging and airway occlusion.
• The pressure required to deliver a volume of gas into the lungs is determined by elastic and resistive forces.
• Contemporary ventilators now provide a range of modes to facilitate mechanical ventilation.
• Analysis of ventilator graphics provides clinicians with the ability to assess patient–ventilator interaction,
appropriateness of ventilator settings and lung function.
• Semirecumbent positioning at 45° elevation has been shown to reduce VAP but compliance is poor.
• RMs, HFOV, ECMO and prone positioning are strategies that may facilitate management of refractory
hypoxaemia.
 CHAPTER 15 VENTILATION AND OXYGENATION MANAGEMENT 499

Case study
A 60-year-old female, Martha, was admitted to the ICU with acute respiratory failure due to community-
acquired pneumonia. Martha was morbidly obese (190 kg) with extensive central obesity and a body mass
index of 74.2. She had a history of COPD but was not prescribed steroids and had not been investigated
for sleep apnoea.
Martha was commenced on broad spectrum antibiotic cover in the emergency department. On arrival to the
ICU, Martha was placed in an isolation room, and respiratory isolation using droplet precautions for possible
H1N1 were initiated. The patient was commenced on oral oseltamivir at 150 mg twice a day. Martha had a
trial of NIV with FiO2 0.7, PEEP 7 cmH2O (EPAP 7 cmH2O) and pressure support 5 cmH2O (IPAP 12 cmH2O)
to reduce her work of breathing and improve gas exchange. The NIV trial was discontinued as Martha’s
dyspnoea was unrelieved, and hypoxia and hypercapnia persisted. She was intubated with a size 7 oral
ETT and a bronchial alveolar lavage was performed to obtain samples for bacterial and viral screening.
Nasopharyngeal swabs were also obtained. Ventilator settings following intubation were A/C, FiO2 1.0,
respiratory rate 16, Pinsp 30 cmH2O, PEEP 15 cmH2O and inspiratory time of 1.1 seconds. Initial blood gases
were as follows: pH 7.07, PaO2 71 mmHg, PaCO2 71 mmHg, HCO3− 16.4 mmol, base excess −9.5, sodium
123 mmol, chloride 94 mmol, lactate 0.7, SpO2 94% and PaO2/FiO2 (PF) ratio 71. Dynamic compliance was
25.6 mL/cmH2O, resistance was 8.6 cmH2O/(L/s). A chest X-ray showed bilateral pulmonary infiltrates and
a lobular pneumonia. Chest auscultation revealed bilateral crackles, late in the inspiratory phase.
Nursing assessment indicated the following issues:
1 notable audible cuff leak on inspiration despite a cuff pressure of 30 cmH2O
2 atelectasis as evidenced by decreased air entry in lung bases, reduced compliance, diminished gas
exchange and obliteration of costophrenic angles on the chest X-ray.
To address the cuff leak, nursing staff connected rigid manometer tubing between the cuff pressure gauge
and the ETT pilot tube to enable continuous cuff pressure measurement. Cuff pressure did not decrease
over time indicating that the ETT cuff was intact. Therefore, the audible air leak was not caused by a leaking
ETT cuff but was due to an air leak around the cuff. On careful examination of the chest X-ray the ETT cuff
was found to be above the level of the vocal cords and therefore needed repositioning.
To address the atelectasis, Martha was repositioned in a high semi-Fowler position (≥45° HOB elevation).
This change in positioning resulted in an immediate improvement in compliance from a baseline of 25.6
to 38.4 mL/cmH2O. VT also increased from 300 mL to 400 mL. These improvements enabled rapid
downward titration of FiO2 to 0.7 while maintaining SpO2 >90%. An RM using 40 cmH2O for 40 seconds
was performed with further improvement of Martha’s oxygenation indicating her lungs were responsive
to this strategy. The ventilator mode was changed to APRV with a Pinsp of 27 cmH2O for 6 seconds and
an expiratory pressure of 5 cmH2O for 0.4 seconds. Further improvements in oxygenation were noted
(PaO2 180 mmHg and PF ratio 225).

DISCUSSION
A cuff leak may be assumed to be secondary to a hole in either the cuff or pilot tube; however, this is
relatively rare. Audible cuff leaks are more frequently due to a malpositioned ETT. It is important to note
that each time cuff pressure is measured, a small volume of gas leaves the cuff to pressurise the pressure
gauge. Repeated cuff pressure measurement may cause reduced cuff pressure over time, which may be
falsely assumed to indicate the cuff is losing volume due to other causes. Attaching rigid tubing between
the cuff and pressure gauge eliminates this problem and facilitates continuous cuff pressure measurement.
This is a useful strategy for assessing cuff leak problems. In this case scenario, careful troubleshooting
averted the need for ETT replacement and avoided unnecessary risk to the patient.
Patient positioning is extremely important in managing the bariatric patient. Central obesity causes
cephalic displacement of the diaphragm resulting in a positive pleural pressure and subsequent alveolar
collapse. Inspiratory crackles late in the inspiratory phase indicate late alveolar opening and an increased
potential for lung injury due to cyclic alveolar inflation and deflation. Positive pleural pressure decreases
transpulmonary pressure and often necessitates the use of higher levels of PEEP to prevent collapse.
Positioning in the high semi-Fowler position can have a dramatic and positive effect on lung mechanics
for these patients evidenced by the increase in compliance in this case study. RMs typically have a limited
500 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

period of effectiveness, i.e. derecruitment generally occurs following the manoeuvre. APRV maintains the
higher level of pressure for a prolonged time thus sustaining alveolar recruitment. In this case study APRV
and position changes appeared to promote recruitment and improved oxygenation enabling downwards
titration of the FiO2. When considering extubation for the bariatric patient, maintaining PEEP at a high level
prior to extubation and using CPAP following extubation may prevent alveolar derecruitment.

CASE STUDY QUESTIONS

1 In this case study Martha received relatively low levels of PEEP and pressure support prior to intubation.
What are the potential advantages and disadvantages of increasing these parameters for this patient?
2 What is the rationale for using oxygen therapy in patients with COPD and low SpO2?
3 Explain why Martha’s lung compliance increased when positioning was changed from the supine to high
semi-Fowler position.

RESEARCH VIGNETTE

Guérin C, Reignier J, Richard JC, Beuret P, Gacouin A, Boulain T et al. Prone positioning in
severe acute respiratory distress syndrome. N Engl J Med 2013;368(23):2159–68

Abstract
Background: Previous trials involving patients with the ARDS have failed to show a beneficial effect of prone
positioning during mechanical ventilatory support on outcomes. We evaluated the effect of early application of
prone positioning on outcomes in patients with severe ARDS.
Methods: In this multicenter, prospective, randomized, controlled trial, we randomly assigned 466 patients with
severe ARDS to undergo prone-positioning sessions of at least 16 hours or to be left in the supine position. Severe
ARDS was defined as a ratio of the partial pressure of arterial oxygen to the FiO2 of less than 150 mmHg, with a FiO2
of at least 0.6, a positive end-expiratory pressure of at least 5 cmH2O, and a tidal volume close to 6 mL per kilogram
of predicted body weight. The primary outcome was the proportion of patients who died from any cause within
28 days after inclusion.
Results: A total of 237 patients were assigned to the prone group, and 229 patients were assigned to the supine
group. The 28-day mortality was 16.0% in the prone group and 32.8% in the supine group (P<0.001). The hazard ratio
for death with prone positioning was 0.39 (95% confidence interval [CI], 0.25 to 0.63). Unadjusted 90-day mortality
was 23.6% in the prone group versus 41.0% in the supine group (P<0.001), with a hazard ratio of 0.44 (95% CI,
0.29 to 0.67). The incidence of complications did not differ significantly between the groups, except for the incidence
of cardiac arrests, which was higher in the supine group.
Conclusion: In patients with severe ARDS, early application of prolonged prone-positioning sessions significantly
decreased 28-day and 90-day mortality.

Critique
This well conducted randomised controlled trial has a number of strengths. Patients with severe ARDS (defined as
a PF ratio of <150 mmHg, with an FiO2 of ≥0.6, PEEP of ≥5 cmH2O and a VT of approximately 6 mL per kilogram
of predicted body weight) were recruited early (within 36 hours of ventilation) ensuring the intervention was applied
in the early phase of ARDS and not as a rescue measure. Patients were assessed for 12 to 24 hours prior to
randomization, thus confirming the presence of severe ARDS. All patients received standardised protective lung
ventilation thereby removing the style of ventilation as a potential confounder. In the intervention arm, all patients
were proned within 1 hour of randomisation and proning sessions extended for at least 16 consecutive hours,
thereby producing maximal effects of proning. Considerations for translation of this research into practice are as
follows. All participating centres had extensive (greater than 5 years) experience with proning. The study found
no difference in adverse event rates between the prone and supine groups. This finding may not be generalisable
to centres without this level of experience. Additionally, the notable reduction in 28-day mortality found in this
study with proning applies to patients with severe ARDS. Again, the findings are not generalisable to patients with
mild-to-moderate ARDS.
 CHAPTER 15 VENTILATION AND OXYGENATION MANAGEMENT 501

Lear ning a c t iv it ie s
1 Describe how the terms IPAP and EPAP used on some NIV ventilators correlate with the more generic terms of
PEEP and pressure support.
2 Why is it important to consider the patient’s respiratory rate and tidal volume when using a low flow (variable
flow) oxygen delivery device?
3 How do increasing PEEP and recruitment manoeuvres increase oxygenation?
4 Identify some of the potential risks of recruitment manoeuvres and the nursing observations to detect signs of
deterioration.
5 Explain how a reduction in the FiO2 from 1.0 to 0.8 can increase the SpO2.

Online resources
American Association for Respiratory Care, www.aarc.org/resources
American Thoracic Society, www.thoracic.org/statements
Anaesthesia UK, www.frca.co.uk/default.aspx
Australian and New Zealand Intensive Care Society, www.anzics.com.au
ARDS network, www.ardsnet.org/
Canadian Society of Respiratory Therapists, Respiratory Resource, www.respiratoryresource.ca
College of Intensive Care Medicine of Australia and New Zealand (CICM), www.cicm.org.au
Covidien education resources, www.nellcor.com/educ/OnlineEd.aspx
Critical Care Medicine Tutorials, www.ccmtutorials.com
Department of Anaesthesia and Intensive Care, Chinese University of Hong Kong, http://aic-server4.aic.cuhk.edu.hk/web8
Fisher and Paykel Resource Centre, www.fphcare.com/respiratory-acute-care/resource-library.html
Intensive Care Coordination and Monitoring Unit, http://intensivecare.hsnet.nsw.gov.au
NHS Institute for Innovation and Improvement, www.institute.nhs.uk/safer_care/general/human_factors.html
Thoracic Society of Australia and New Zealand, www.thoracic.org.au
Vent World, www.ventworld.com

Further reading
Branson RD, Gomaa D, Rodriquez D Jr. Management of the artificial airway. Respir Care 2014;59(6):974–89.
Canadian Critical Care Trials Group/Canadian Critical Care Society Noninvasive Ventilation Guidelines Group. Clinical practice
guidelines for the use of noninvasive positive-pressure ventilation and noninvasive continuous positive airway pressure in the
acute care setting. CMAJ 2011;183(3):E195–214.
Chatburn RL, Khatib ME, Mireles-Cabodevila E. A taxonomy for mechanical ventilation: 10 fundamental maxims. Respir
Care 2014;59(11):1747–63.
Ferrer M, Sellares J, Torres A. Noninvasive ventilation in withdrawal from mechanical ventilation. Semin Respir Crit Care Med
2014;35(4):507–18.
Jiang JR, Yen SY, Chien JY, Liu HC, Wu YL, Chen CH. Predicting weaning and extubation outcomes in long-term mechanically
ventilated patients using the modified Burns Wean Assessment Program scores. Respirol 2014;19(4):576–82.
Suzumura EA, Figueiró M, Normilio-Silva K, Laranjeira L, Oliveira C, Buehler AM et al. Effects of alveolar recruitment maneuvers
on clinical outcomes in patients with acute respiratory distress syndrome: a systematic review and meta-analysis. Intensive
Care Med 2014;40(9):1227–40.

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170 Meade M, Cook D, Guyatt G, Slutsky A, Arabi Y, Cooper DJ et al.. Ventilation strategy using low tidal volumes, recruitment maneuvers, and
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172 Hess D, Kacmarek R. Essentials of mechanical ventilation. 2nd ed. New York: McGraw-Hill; 2002.
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174 Chatburn R. Classification of ventilator modes: update and proposal for implementation. Respir Care 2007;52(3):301-23.
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178 MacIntyre NR. Evidence-based guidelines for weaning and discontinuing ventilatory support. Chest 2001;120(6):375S-95S.
179 Hormann C, Baum M, Putensen C, Mutz N, Benzer H. Biphasic positive airway pressure (BIPAP) – a new mode of ventilatory support.
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180 McCunn M, Habashi NM. Airway pressure release ventilation in the acute respiratory distress syndrome following traumatic injury. Int
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181 Putensen C, Wrigge H. Airway pressure-release ventilation. In: Tobin M, ed. Principles and practice of mechanical ventilation. 2nd ed.
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182 Rose L, Hawkins M. Airway pressure release ventilation and biphasic positive airway pressure: a systematic review of definitional criteria.
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183 Mols G, von Ungern-Sternberg B, Rohr E, Haberthur C, Geiger K, Guttman J. Respiratory comfort and breathing pattern during volume
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185 Unoki T, Serita A, Grap M. Automatic tube compensation during weaning from mechanical ventilation: evidence and clinical implications.
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186 Fabry B, Haberthur C, Zappe D, Guttmann J, Kuhlen R, Stocker R. Breathing pattern and additional work of breathing in spontaneously
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187 Branson R, Johannigman J. Innovations in mechanical ventilation. Respir Care 2009;54(7):933-47.
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508 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

200 Odenstedt H, Aneman A, Kárason S, Stenqvist O, Lurdin S. Acute hemodynamic changes during lung recruitment in lavage and endotoxin-
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240 Schortgen F, Bouadma L, Joly-Guillou M, Ricard J, Dreyfuss D, Saumon G. Infectious and inflammatory dissemination are affected by
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243 Gattinoni L, Carlesso E, Taccone P, Polli F, Guérin C, Mancebo J. Prone positioning improves survival in severe ARDS: a pathophysiologic
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246 Burns SM, Ryan B, Burns JE. The weaning continuum use of Acute Physiology and Chronic Health Evaluation III, Burns Wean Assessment
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259 Yang KL, Tobin MJ. A prospective study of indexes predicting the outcome of trials of weaning from mechanical ventilation. N Engl J Med
1991;324(21):1445-50.
260 Tanios M, Nevins M, Hendra K, Cardinal P, Allan J, Naumova EN et al. A randomized, controlled trial of the role of weaning predictors in clinical
decision making. Crit Care Med 2006;34(10):2530-5.
261 Brochard L, Rauss A, Benito S, Conti G, Mancebo J, Rekik N et al. Comparison of three methods of gradual withdrawal from ventilatory
support during weaning from mechanical ventilation. Am J Respir Crit Care Med 1994;150(4):896-903.
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 Chapter 16

Neurological assessment
and monitoring
Diane Chamberlain, Leila Kuzmiuk

KEY WORDS Learning objectives

afferent neuron After reading this chapter, you should be able to:
autonomic nervous • describe the anatomy and physiology of the nervous system
system • differentiate between the central and peripheral nervous systems
central nervous
• describe the techniques used for neurological assessment
system
• identify the distinction between normal and abnormal findings
decerebrate
(extensor) • state the determinants of intracranial pressure and describe
compensatory mechanisms
decorticate (flexor)
efferent neuron • explain the importance and process of continuous neurological
assessment in the brain-injured patient
Glasgow Coma
Scale • relate the procedures of selected neurodiagnostic tests to nursing
implications for patient care.
intracranial pressure
neurological
assessment
parasympathetic Introduction
nervous system
The nervous system is the major controlling, regulatory and communicating
post-traumatic
system in the body. It accounts for a mere 3% of total body weight, yet it is
amnesia
the most complex organ system. It is the centre of all mental activity, including
peripheral nervous thought, learning and memory. Together with the endocrine and immune
system systems, the nervous system is responsible for regulating and maintaining
sympathetic homeostasis. Through its receptors, the nervous system keeps in touch with the
nervous system environment, both external and internal. Diseases of the nervous system are
common in the critical care unit, both as primary processes and as complica-
tions of multiple organ failure in the critically ill patient. An understanding of
basic neurophysiology is important if these disorders are to be recognised and
treated. This chapter provides an overview of the anatomy and physiology, and
describes and details neurological assessment.
512 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Neurological anatomy and The CNS is linked to all parts of the body by the
peripheral nervous system (PNS), which transmits signals
physiology to and from the CNS.The PNS is composed of 43 pairs of
spinal nerves that issue in orderly sequence from the spinal
All the sensory details that incorporate a body’s own cord, and 12 pairs of cranial nerves that emerge from the
information systems are related to neurological anatomy base of the brain. All branch and diversify prolifically as
and physiology. Composed of central and peripheral they distribute to the tissues and organs of the body. The
components, with the brain as the command centre, the peripheral nerves carry input to the CNS via their sensory
nervous system is responsible for the body’s most funda- afferent fibres and deliver output from the CNS via the
mental activities. Nerves, which are made up of bundles efferent fibres. Specific physiology of the CNS and PNS
of fibres, deliver impulses to various parts of the body, is discussed in detail later in the chapter. First, however,
including the brain. The brain translates the information neuron cell anatomy and physiology are examined.
delivered by the impulses, which then enables the person
to react. This section discusses the main components of Neurons
the nervous system starting from neurons and nervous Neurons are specialised cells in the nervous system; each
system transmission. Then the central nervous system and is comprised of a dendrite, cell body (soma) and axon.2
the peripheral nervous system are examined and related to Each neuron uses biochemical reactions to receive,
neurological assessment. process and transmit information. Most synaptic contacts
between neurons are either axodendritic (excitatory)
Components of the nervous system or axosomatic (inhibitory). A neuron’s dendritic tree is
The central nervous system (CNS) consists of the spinal connected to many neighbouring neurons and receives
cord and the brain and is responsible for integrating, positive or negative charges from other neurons.The input
processing and coordinating sensory data and motor is then passed to the soma (cell body). The primary role
commands1 (see Figure 16.1). of the soma and the enclosed nucleus is to perform the

FIGURE 16.1 The functional divisions of the nervous system.1

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Adapted from Martini F, Nath J, Bartholomew E. Anatomy and physiology. 9th ed. San Francisco: Pearson Benjamin Cummings; 2011,
with permission.
 CHAPTER 16 NEUROLOGICAL ASSESSMENT AND MONITORING 513

continuous maintenance required to keep the neuron reassembled at the synaptic knob. The synaptic knob also
functional. Most neurons lack centrioles, important receives a continuous supply of neurotransmitter synthesised
organelles involved in the organisation of the cytoskeleton in the cell body, along with enzymes and lysosomes.2 The
and the movement of chromosomes during mitosis. As a movement of materials between the cell body and synaptic
result, typical CNS neurons cannot divide and cannot be knobs is called axoplasmic transport. Some materials travel
replaced if lost to injury or disease. The fuel source for slowly, at rates of a few millimetres per day. This transport
the neuron is glucose; insulin is not required for cellular mechanism is known as the ‘slow stream’. Vesicles containing
uptake in the CNS.2 neurotransmitter move much more rapidly, travelling in the
A myelin sheath, consisting of a lipid-protein casing, ‘fast stream’ at 5–10 mm per hour, which increases synaptic
covers the neuron and provides protection to the axon activity. Axoplasmic transport occurs in both directions. The
and speeds the transmission of impulses along nerve cells flow of materials from the cell body to the synaptic knob
from node to node3 (see Figure 16.2b). Myelin is not a is anterograde flow. At the same time, other substances are
continuous layer but has gaps called nodes of Ranvier (see being transported towards the cell body in retrograde flow
Figure 16.2a). (‘retro’ meaning backward). If debris or unusual chemicals
Each synaptic knob contains mitochondria, portions of appear in the synaptic knob, retrograde flow soon delivers
the endoplasmic reticulum and thousands of vesicles filled them to the cell body. The arriving materials may then alter
with neurotransmitter molecules. Breakdown products of the activity of the cell by turning appropriate genes on or
neurotransmitter released at the synapse are reabsorbed and off. Retrograde flow is the means of transport for viruses,

FIGURE 16.2 A Afferent and B efferent neurons, showing the soma or cell body, dendrites and axon. Arrows indicate
the direction for conduction of action potentials.3

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514 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

pathogenic bacteria, heavy metals and toxins to the CNS, chronically demyelinated axons become vulnerable,
with resulting disease such as tetanus, viral encephalitis and with axon loss being a major cause of disability. In time,
lead intoxication. Defective anterograde transport seems to remyelination may occur, requiring the generation of
be involved in certain neuropathies, including critical illness myelin-competent oligodendrocytes, but most often it
neuropathies.4 does not fully recapitulate developmental myelination.5
Synapses Neurotransmitters
The human brain contains at least 100 billion neurons, each A neurotransmitter is a chemical messenger used by
with the ability to influence many other cells.2 Although neurons to communicate in one direction with other
there are many kinds of synapses within the brain, they can neurons.2 Unidirectional transmission is required for
be divided into two general classes: electrical synapses and multineuronal pathways, for example to and from the
chemical synapses. Electrical synapses permit direct, passive brain. Neurons communicate with each other by recog-
flow of electrical current from one neuron to another nising specific neuroreceptors.
in the form of an action potential; they are described in Chemically, there are four classes of neurotransmitters:
Table 16.1. The current flows through gap junctions, 1 acetylcholine (ACh): the dominant neurotransmitter in
which are specialised membrane channels that connect the the peripheral nervous system, released at neuromuscular
two cells. Chemical synapses, in contrast, enable cell-to- junctions and synapses of the parasympathetic division
cell communication via the secretion of neurotransmitters;
2 biogenic amines: serotonin, histamine and the
the chemical agents released by the presynaptic neurons
catecholamines dopamine and noradrenaline
produce secondary current flow in postsynaptic neurons
by activating specific receptor molecules5 (see Figure 16.3). 3 excitatory amino acids: glutamate and aspartate; and
Myelin increases conduction velocity. Demyelination the inhibitory amino acids: gamma-aminobutyric acid
of peripheral nerves, as occurs in Guillain-Barré syndrome, (GABA), glycine and taurine
slows conduction and may result in conduction block, 4 neuropeptides: over 50 are known, amino acid
which manifests clinically as weakness. Consequently, neurotransmitters being the most numerous.

TABLE 16.1
Generation of action potentials (nervous tissue)

STEP 1: Depolarisation
• A graded depolarisation brings an area of excitable membrane to
threshold (−60 mV)
STEP 2: Activation of sodium channels and rapid depolarisation
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potassium ions diffuse out of the cell − 
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potassium loss continues, and a temporary hyperpolarisation to
approximately −90 mV occurs
• At the end of the relative refractory period, all voltage-regulated
channels have closed, and the membrane is back to its resting state
 CHAPTER 16 NEUROLOGICAL ASSESSMENT AND MONITORING 515

FIGURE 16.3 Sequence of events involved in transmission at a typical chemical synapse.84

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Adapted from Purves D, Augustine G, Hall W, LaMantia A, McNamara J, White L. Neuroscience. 5th ed. New York: Sinauer
Associates; 2012, with permission.

In 2009, it was discovered that there is also more than are an important control point for the effectiveness of
one neurotransmitter per synapse; these are called co- synapses. Neurotransmitters are the common denomina-
transmitters. For example, neuropeptide Y (NPY) and tor between the nervous, endocrine and immune systems.
adenosine triphosphate (ATP) are co-transmitters of Many neurotransmitters are endocrine analogues and
noradrenaline; they are released together and mediate acetylcholine, the main parasympathetic neurotransmitter,
their function by activation of α- and β-adrenoceptors, interacts with immune cells such as macrophages through
and regulate renovascular resistance.6 Similarly, receptors the anti-inflammatory cholinergic pathway.7
516 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Neuroglia neuroglia. Unlike neurons, neuroglia continue to multiply

Neuroglia are the non-neuronal cells of the nervous throughout life. Because of their capacity to reproduce,
system and are 10–50 times more prevalent than neurons.1 most tumours of the nervous system are tumours of
They are divided into macroglia (astrocytes, oligo- neuroglial tissue and not of nervous tissue itself.9
dendroglia and Schwann cells) and microglia, and are
described in Table 16.2. They not only provide physical Central nervous system
support but also respond to injury, regulate the ionic and
chemical composition of the extracellular milieu, partic- The CNS is composed of the brain and spinal cord
ipate in the blood–brain and blood–retina barriers, form (see Figure 16.4).5 The primary purpose is to acquire,
the myelin insulation of nervous pathways, guide neuronal coordinate and disseminate information about the body
migration during development and exchange metab- and its environment. This section describes the anatomy
olites with neurons.8 The CNS has a greater variety of and physiology of the brain and spinal cord.

TABLE 16.2
Neuroglia, their location and role as supporting nervous tissue

CELL TYPE L O C AT I O N MAIN FUNCTION

Astrocytes CNS: the largest and most • Astrocytes are considered as important as the
numerous neuroglial cells in the neuron in communication and brain regulation
brain and spinal cord • They regulate communication, extracellular ionic
and chemical environments between neurons
• They respond to injury and have an important
role in cerebral oedema

Ependymal cells CNS: line the ventricular system of • Transport of CSF and brain homeostasis
the brain and central cord of the • Phagocytotic defence against pathogens
spinal canal • Store glycogen for brain tissue

Microglia CNS: located within the brain • Wander between the peripheral immune system
parenchyma behind the blood– and the CNS as a defence to infection
brain barrier • Displace synaptic input in injured neurons

Oligodendrocytes CNS: spiral around an axon to • Responsible for the formation of myelin sheaths
form a multilayered lipoprotein surrounding axons
coat in both the white and grey • Oligodendrocytes wrap themselves around
matter in the brain and spinal cord numerous axons at once
PNS: Schwann cells are the • Schwann cells wrap themselves around
supporting cells of the PNS peripheral nerve axons
• Unlike oligodendrocytes, a single Schwann cell
makes up a single segment of an axon’s myelin
sheath
 CHAPTER 16 NEUROLOGICAL ASSESSMENT AND MONITORING 517

FIGURE 16.4 The subdivisions and components of the central nervous system.84

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Adapted from Purves D, Augustine G, Hall W, LaMantia A, McNamara J, White L. Neuroscience. 5th ed. New York: Sinauer
Associates; 2012, with permission.

Practice tip Brain

The brain is divided into three regions: forebrain,
The brain consists of three major divisions: 1) the massive midbrain and hindbrain, as described in Table 16.3. The
paired hemispheres of the cerebrum; 2) the brainstem, forebrain, which consists of two hemispheres and is
consisting of the thalamus, hypothalamus, epithalamus, covered by the cerebral cortex, contains central masses
subthalamus, midbrain, pons and medulla oblongata; of grey matter, the basal ganglia, the neural tube and the
and 3) the cerebellum. diencephalon with its adult derivatives: the thalamus and
hypothalamus.1 Midbrain structures include two pairs of
518 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 16.3
Organisation of the brain

DIVISION DESCRIPTION FUNCTIONS

FOREBRAIN
Cerebrum Largest and uppermost portion of the Cortex (outer layer) is the site of conscious thought, memory, reasoning
brain. Divided into two hemispheres, and abstract mental functions, all localised within specific lobes
each subdivided into the frontal,
parietal, temporal and occipital lobes

Diencephalon Between the cerebrum and the Thalamus sorts and redirects sensory input; hypothalamus controls
brainstem. Contains the thalamus and visceral, autonomic, endocrine and emotional function, and the pituitary
hypothalamus gland. Contains some of the centres for coordinated parasympathetic
and sympathetic stimulation, temperature regulation, appetite regulation,
regulation of water balance by antidiuretic hormone (ADH) and regulation
of certain rhythmic psychobiological activities (e.g. sleep)
Brain stem Anterior region below the cerebrum: Connects cerebrum and diencephalon with spinal cord
the medulla, pons and midbrain
compose the brainstem
MIDBRAIN
Midbrain Below the centre of the cerebrum Has reflex centres concerned with vision and hearing; connects
cerebrum with lower portions of the brain. It contains sensory and
motor pathways and serves as the centre for auditory and visual
reflexes

Basal ganglia or The mass of grey matter in the An important role in planning and coordinating motor movements
corpus striatum midbrain beneath the cerebral and posture. Complex neural connections link the basal ganglia to
hemispheres. Borders the lateral the cerebral cortex. The major effect of these structures is to inhibit
ventricles and lies in proximity to the unwanted muscular activity; disorders of the basal ganglia result in
internal capsule exaggerated, uncontrolled movements

Pons Anterior to the cerebellum Connects the cerebellum with other portions of the brain; contains
motor and sensory pathways; helps to regulate respiration; axons from
the cerebellum, basal ganglia, thalamus and hypothalamus; portions of
the pons also control the heart, respiration and blood pressure. Cranial
nerves V–VIII connect the brain in the pons

Hindbrain Contains a portion of the pons, the

medulla oblongata and the cerebellum
Reticular The reticular formation networks run Activity of the cerebral cortex is dependent on both specific sensory
activation through the brainstem core, known as input and non-specific activating impulses from the RAS, and is critical
system (RAS) the tegmentum to the existence of the conscious state, states of alertness and arousal

Medulla Between the pons and the spinal cord The medulla oblongata contains motor fibres from the brain
oblongata to the spinal cord and sensory fibres from the spinal cord to the brain.
Most of these fibres cross at this level. Cranial nerves IX–XII connect to
the brain in the medulla, which has centres for control of vital functions,
such as respiration and the heart rate

Cerebellum Below the posterior portion of Coordinates voluntary muscles; maintains balance and muscle
the cerebellum. Divided into two tone; has both excitatory and inhibitory actions. It also controls fine
hemispheres movement, balance, position sense and integration of sensory input
 CHAPTER 16 NEUROLOGICAL ASSESSMENT AND MONITORING 519

dorsal enlargements, the superior and inferior colliculi. Cerebral cortex

The medulla, pons and midbrain compose the brainstem.1 The forebrain contains the cerebral cortex and the
The hindbrain includes the medulla oblongata, the pons subcortical structures rostral (sideways) to the dienceph-
and its dorsal outgrowth, the cerebellum. alon. The cortex, or outermost surface of the cerebrum,
Nervous tissue has a high rate of metabolism.Although makes up about 80% of the human brain. The cerebral
the brain constitutes only 3% of the body’s weight, it cortex varies in thickness from 2 mm to 4 mm. It contains
receives approximately 15% of the resting cardiac output the cell bodies and dendrites of neurons or grey matter
and consumes 20% of its oxygen.1 Despite its substantial that receive, integrate, store and transmit information.
energy requirements, the brain can neither store oxygen Conscious deliberation and voluntary actions also arise
nor effectively engage in anaerobic metabolism. An from the cerebral cortex. White matter lies beneath the
interruption in the blood or oxygen supply to the brain cerebral cortex and is composed of myelinated nerve fibres.
rapidly leads to clinically observable signs and symptoms. The cortex is involved in the processing of both sensory
Without oxygen, brain cells continue to function for information from the body and the delivery of motor
approximately 10 seconds. Glucose is virtually the commands. These occur in specific areas of the brain and
sole energy substrate for the brain, and it is entirely can be mapped. Topographically, the cerebral cortex is
oxidised.10 The brain can be seen as an almost exclusive divided into areas of specialised functions, including the
glucose-processing machine, producing water (H2O) primary sensory areas for vision (occipital cortex), hearing
and carbon dioxide (CO2). Glucose also provides the (temporal cortex), somatic sensation (postcentral gyrus),
carbon backbone for regeneration of the neuronal pool and primary motor area (precentral gyrus).5 As shown in
of glutamate. This process results from close astrocyte– Figure 16.5,1 these well-defined areas comprise only a
neuron cooperation.11 small fraction of the surface of the cerebral cortex.

FIGURE 16.5 A Major anatomical landmarks on the surface of the left cerebral hemisphere. The lateral sulcus has
been pulled apart to expose the insula. B The left hemisphere generally contains the general interpretive area and the
speech centre. The prefrontal cortex of each hemisphere is involved with conscious intellectual functions. C Regions
of the cerebral cortex as determined by histological analysis. Several of the 47 regions described by Brodmann are
shown for comparison with the results of functional mapping.1

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with permission.
520 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

The majority of the remaining cortical area is known coordinating movements by giving feedback to the motor
as the association cortex, where the processing of extensive cortex, as well as by providing important influences on
and sophisticated neural information is performed.12 The eye movements through brainstem connections, and on
association areas are also sites of long-term memory, and postural activity through projections down the spinal cord.
they control human functions such as language acquisi-
tion, speech, musical ability, mathematical ability, complex Brainstem
motor skills, abstract thought, symbolic thought and other The brainstem is composed of the midbrain, the pons
cognitive functions. Association areas interconnect and and the medulla oblongata.1 These structures connect
integrate information from the primary sensory and motor the cerebrum and diencephalon with the spinal cord.
areas via intra-hemispheric connections.5 The parietal– Brainstem centres are organised into medial, lateral and
temporal–occipital association cortex integrates neural aminergic systems. Collectively, these integrate vestibular,
information contributed by visual, auditory and somatic visual and somatosensory inputs for the control of eye
sensory experiences. The prefrontal association cortex is movements and, through projections to the spinal cord,
extremely important as the coordinator of emotionally provide for postural adjustments. For example, these centres
motivated behaviours, by virtue of its connections with keep the images on matching regions of the retinas when
the limbic system. the head moves by causing conjugate eye movements in
In addition, the prefrontal cortex receives neural input the opposite direction to which the head is turned. This is
from the other association areas and regulates motivated the basis for the ‘doll’s eyes’ test in neurological assessment,
behaviours by direct input to the premotor area, which in which the head is rapidly turned and the eyes move
serves as the association area of the motor cortex. Sensory conjugately in the opposite direction, demonstrating the
and motor functions are controlled by cortical structures integrity of much of the brainstem.15 The sequence of
in the contralateral hemisphere. Particular cognitive sleep states is governed by a group of brainstem nuclei
functions or components of these functions may be later- that project widely throughout the brain and spinal cord.17
alised to one side of the brain.12 The midbrain, inferior to the centre of the cerebrum,
The cerebral cortex receives sensory information from forms the superior part of the brainstem. It contains the
many different sensory organs and processes the informa- reticular formation (which collects input from higher brain
centres and passes it on to motor neurons), the substantia
tion. The two hemispheres receive the information from
nigra (which regulates body movements – damage to the
the opposite sides of the body. Sensory information is
substantia nigra causes Parkinson’s disease) and the ventral
relayed to the cortex by the thalamus. Parts of the cortex
tegmental area (which contains dopamine-releasing
that receive this information are called primary sensory
neurons that are activated by nicotinic acetylcholine
areas and cross at various points in the sensory pathway, receptors).18 White matter at the anterior of the midbrain
because the cerebral cortex operates on a contralateral conducts impulses between the higher centres of the
basis.13 The discriminative touch system crosses high, cerebrum and the lower centres of the pons, medulla,
in the medulla. The pain system crosses low, in the spinal cerebellum and spinal cord. The midbrain contains the
cord.The proprioceptive sensory system that guards balance autonomic reflex centres for pupillary accommodations
and position goes to the cerebellum, which works ipsilat- to light, which constrict the pupil and accommodate the
erally and therefore does not cross. Almost every region of lens.The fibres travel in cranial nerve III, so damage to that
the body is represented by a corresponding region in both nerve will also produce a dilated pupil.3 It also contains the
the primary motor cortex and the somatic sensory cortex.14 ventral tegmental area, packed with dopamine-releasing
The homunculus (see Figure 16.6) visualises the neurons that synapse deep within the forebrain and seem
connection between different areas of the body and to be involved in pleasure: amphetamines and cocaine
areas in brain hemispheres.15 The body on the right side bind to the same receptors that it activates, and this may
is the motor homunculus and on the left the sensory account at least in part for their addictive qualities.
homunculus. Representations of parts of the body that The medulla oblongata lies between the pons and
exhibit fine motor control and sensory capabilities occupy the spinal cord and looks like a swollen tip to the spinal
a greater amount of space than those that exhibit less cord. Running down the ventral aspect of the medulla
precise motor or sensory functions. are the pyramids, which contain corticospinal fibres. The
function of the medulla oblongata is to control automatic
Basal ganglia and cerebellum functions (e.g. breathing and heart rate) and to relay nerve
The basal ganglia play an important role in movement, messages from the brain to the spinal cord. Processing of
as evidenced by the hypokinetic/rigid and hyper- interaural time differences for sound localisation occurs in
kinetic disorders seen with lesions of related nuclei. the olivary nuclei. The neurons controlling breathing have
Their role in the initiation and control of movement mu (μ) receptors, the receptors to which opiates bind.5 This
cannot be isolated from the motor activities of the cortex accounts for the suppressive effect of opiates on breathing.
and brainstem centres discussed previously. Procedural Impairment of any of the vital functions or reflexes
memories for motor and other unconscious skills depend involving these cranial nerves suggests medullary damage.19
on the integrity of the premotor cortex, basal ganglia and The pons Varolii is the part of the brainstem that lies
cerebellum.16 The cerebellum plays a more obvious role in between the medulla oblongata and the mesencephalon.
 CHAPTER 16 NEUROLOGICAL ASSESSMENT AND MONITORING 521

FIGURE 16.6 Somatosensory and motor homunculi. Note that the size of each region of the homunculi is related to
its importance in sensory or motor function, resulting in a distorted-appearing map.15

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Adapted from Blumenfeld H. Neuroanatomy through clinical cases. New York: Sinauer Associates; 2010, with permission.

It contains pneumotaxic and apneustic respiratory centres these areas comprise the limbic system. The hypothalamus
and fibre tracts connecting higher and lower centres, and limbic system, which are closely linked to homeosta-
including the cerebellum.2 The pons seems to serve as sis, act to regulate endocrine secretion and the autonomic
a relay station, carrying signals from various parts of the nervous system, and to influence behaviour through
cerebral cortex to the cerebellum. Nerve impulses coming emotions and drives.1 The hypothalamus integrates
from the eyes, ears and touch receptors are sent on to the information from the forebrain, brainstem, spinal cord
cerebellum. The pons also participates in the reflexes that and various endocrine systems. This area of the brain
regulate breathing.Table 16.4 contains a description of the also contains some of the centres for coordinated para-
cranial nerves including their type of tract, their function sympathetic and sympathetic stimulation, as well as those
and location of origin. for temperature regulation, appetite regulation, regulation
of water balance by antidiuretic hormone (ADH) and
Hypothalamus and limbic system regulation of certain rhythmic psychobiological activities
The hypothalamus, the cingulate gyrus of the cortex, the (e.g. sleep). The release of stored serotonin from axon
amygdala and hippocampus in the temporal lobes and terminals in the diencephalon, medulla, thalamus and a
the septum and interconnecting nerve fibre tracts among small forebrain area (DMTF) results in inactivation of the
522 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 16.4
The cranial nerves, their locations and functions

L O C AT I O N
CRANIAL NERVE TRACT(S) FUNCTION OF ORIGIN
I Olfactory Sensory Sense of smell Diencephalon
II Optic Sensory Vision Diencephalon
III Oculomotor Parasympathetic Muscles that move the eye and lid, pupillary constriction, lens Midbrain
accommodation
Motor Elevation of upper eyelid and four of six extraocular movements
IV Trochlear Motor Downward, inward movement of the eye (superior oblique) Midbrain
V Trigeminal Motor Muscles of mastication and opening jaw Pons
Sensory Tactile sensation to the cornea, nasal and oral mucosa and facial skin
VI Abducens Motor Lateral deviation of eye (lateral rectus) Pons
VII Facial Parasympathetic Secretory for salivation and tears Pons
Motor Movement of the forehead, eyelids, cheeks, lips, ears, nose and neck
to produce facial expression and close eyes
Sensory Tactile sensation to parts of the external ear, auditory canal and
external tympanic membrane
Taste sensation to the anterior two-thirds of the tongue
VIII Vestibulocochlear Sensory Vestibular branch: equilibrium Pons
Cochlear branch: hearing
IX Glossopharyngeal Parasympathetic Salivation Medulla
Motor Voluntary muscles for swallowing and phonation
Sensory Sensation to pharynx, soft palate and posterior one-third of tongue
Stimulation elicits gag reflex
X Vagus Parasympathetic Autonomic activity of viscera of thorax and abdomen Medulla
Motor Voluntary swallowing and phonation
Involuntary activity of visceral muscles of the heart, lungs and
digestive tract
Sensory Sensation to the auditory canal and viscera of the thorax and abdomen
XI Spinal accessory Motor Sternocleidomastoid and trapezius muscle movements Medulla
XII Hypoglossal Motor Tongue movements Medulla

reticular activating system (RAS) and activation of the

DMTF. DMTF activity results in the four stages of sleep.17 Practice tip
The hypothalamus contains a plethora of neurotrans- Openings in the fourth ventricle permit cerebrospinal
mitters. These are found in the terminals of axons that fluid to enter subarachnoid spaces surrounding both
originate from neurons outside the hypothalamus, but the brain and the spinal cord.
most are synthesised within the hypothalamus itself. The
list of putative neurotransmitters includes the ‘classic’
transmitters ACh, GABA, glutamate, serotonin, dopamine Cerebral spinal fluid
and noradrenaline, as well as literally dozens of peptides Cerebral spinal fluid (CSF) is an ultrafiltrate of blood
that have been identified in recent years.20 plasma composed of 99% water with other constituents,
making it close to the composition of the brain extracellu-
Protection and support of the brain lar fluid.1 Approximately 500 mL of CSF is secreted each
The brain occupies the cranial cavity and is covered by day, but only approximately 150 mL is in the ventricular
membranes, fluid and the bones of the skull. The delicate system at any one time, meaning that the CSF is continu-
tissues of the brain are protected from mechanical forces ously being absorbed. The CSF produced in the ventricles
by 1) the bones of the cranium, 2) the cranial meninges must flow through the interventricular foramen, the third
and 3) cerebrospinal fluid. In addition, the neural tissue of ventricle, the cerebral aqueduct and the fourth ventricle to
the brain is biochemically isolated from the general circu- exit from the neural tube.21 Three openings, or foramina,
lation by the blood–brain barrier. allow the CSF to pass into the subarachnoid space
 CHAPTER 16 NEUROLOGICAL ASSESSMENT AND MONITORING 523

(see Figure 16.7).1 Approximately 30% of the CSF passes Blood–brain–cerebral spinal fluid barrier
down into the subarachnoid space that surrounds the spinal The CNS is richly supplied with blood vessels that
cord, mainly on its dorsal surface, and moves back up to
bring oxygen and nutrients to its cells. However, many
the cranial cavity along its ventral surface. Reabsorption
substances cannot easily be exchanged between blood and
of CSF into the vascular system occurs, through a pressure
gradient. The normal CSF pressure is approximately brain because the endothelial cells of the vessels and the
10 mmHg in the lateral recumbent position, although it astrocytes of the CNS form extremely tight junctions,
may be as low as 5 mmHg or as high as 15 mmHg in collectively referred to as the blood–brain barrier (BBB).1
healthy persons. The microstructure of the arachnoid villi In particular, small non-charged, lipid-soluble molecules
is such that, if the CSF pressure falls below approximately can cross the BBB with ease. Evidence suggests that the
3 mmHg, the passageways collapse and reverse flow is BBB maintains the chemical environment for neuronal
blocked. Arachnoid villi function as one-way valves, function and protects the brain from harmful substances.22
permitting CSF outflow into the blood but not allowing Substances in the blood that gain rapid entry to the brain
blood to pass into the arachnoid spaces. The pressure in include glucose, the important source of energy, certain
the CSF manifests as normal intracranial pressure (ICP).3 ions that maintain a proper medium for electrical activity

FIGURE 16.7 Circulation of the cerebrospinal fluid: A sagittal section indicating the sites of formation and routes of
circulation of cerebrospinal fluid (arrows); B orientation of the arachnoid granulations.1

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with permission.
524 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

and oxygen for cellular respiration. Small fat-soluble Cerebral circulation

molecules, like ethanol, pass through the BBB. Some The brain must maintain a constant flow of blood in
water-soluble molecules pass into the brain carried by
order for brain activity to occur. The arterial blood flow
special proteins in the plasma membrane of the endo-
thelial cells. Excluded molecules include proteins, toxins, to the brain consists of approximately 20% of the cardiac
most antibiotics and monoamines (e.g. neurotransmitters). output (see Figure 16.8).5 Normal cerebral blood flow
Some of these unwanted molecules are actively trans- is 750 mL/min. The brain autoregulates blood flow over
ported out of the endothelial cells.When injured (by force a wide range of blood pressure by vasodilation or vaso-
or infection or oxidative processes), the permeability of constriction of the arteries.1 In response to decreased
the BBB is disrupted, allowing a proliferation of various arterial flow, the circle of Willis can act as a protective
chemicals and molecules – even bacteria – into the brain mechanism by shunting blood from one side to the other
parenchyma, with at times devastating consequences.3 or from the anterior to posterior portions of the brain.

FIGURE 16.8 The major arteries of the brain: A ventral view: the enlargement of the boxed area showing the circle
of Willis; B lateral and C mid-sagittal views showing anterior, middle and posterior cerebral arteries; D idealised frontal
section showing the course of middle cerebral artery.84

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Associates; 2012, with permission.
 CHAPTER 16 NEUROLOGICAL ASSESSMENT AND MONITORING 525

This compensatory mechanism delays neurological dete- in perfusion pressure (see Table 16.5). This is important in
rioration in patients.3 protecting the brain from both ischaemia during hypoten-
The cerebral veins drain into large venous sinuses and sion and haemorrhage during hypertension.
then into the right and left internal jugular veins (see
Figure 16.9).23 The venous sinuses are found within the
folds of the dura mater. The veins and sinuses of the brain TABLE 16.5
do not have valves, so the blood flows freely by gravity.1 Changes in cerebrovascular and cerebrometabolic
The face and scalp veins can flow into the brain venous parameters when various cerebral variables are
reduced with and without intact autoregulation
sinuses; therefore, infection can easily be spread into the
dural venous sinuses and then enter the brain. P R I M A RY R E D U C T I O N I N CBV
Patient position can prevent or promote venous drainage T H E S E VA R I A B L E S CBF (ICP) AV D O 2
from the brain. Head turning and tilting may kink the jugular CMRO2 ↑ ↓ –
vein and decrease or stop venous flow from the brain, which CPP (autoregulation intact) – ↑ –
will then raise the pressure inside the cranial vault.
CPP (autoregulation defective) ↓ ↓ ↑
Cerebral blood flow (CBF) is the cerebral perfusion
pressure (CPP) divided by cerebrovascular resistance Blood viscosity – ↓ –
(autoregulation intact)
(CVR). CVR is the amount of resistance created by the
cerebral vessels, and it is controlled by the autoregulatory Blood viscosity ↑ – ↓
mechanisms of the brain. Specifically, vasoconstriction (autoregulation defective)
(and vasospasm) will increase CVR, and vasodilation will PaCO2 ↓ ↓ ↑
decrease CVR.1 It is influenced by the inflow pressure Conductive vessel diameter ↓ ↑ ↑
(systole), outflow pressure (venous pressure), cross-sectional (vasospasm above ischaemic
diameter of cerebral blood vessels and intracranial pressure threshold)
(ICP).1 CVR is similar to systemic vascular resistance AVDO2 = arteriovenous O2 difference; CBF = cerebral blood
but, due to the lack of valves in the venous system of flow; CBV = cerebral blood volume; ICP = intracranial
the brain, cerebral venous pressure also influences the pressure; CMRO2 = cerebral metabolic rate of oxygen;
CVR. An important characteristic of the cerebral circu- CPP = cerebral perfusion pressure; PaCO2 = arterial CO2
lation is its ability to autoregulate, that is, the ability to tension; ↑ = increase; ↓ = decrease; – = no change.
maintain constant cerebral blood flow despite variations

FIGURE 16.9 Cerebral venous drainage.23

Superior sagittal sinus Parietal emissary

Inferior sagittal sinus

Diploic

Superior ophthalmic
Straight sinus Cavernous sinus
Superior petrosal sinus

Transverse sinus Angular

Sigmoid sinus
Mastoid emissary
Inferior petrosal sinus

Retromandibular
Anterior facial
Maxillary

Internal jugular
External jugular
Vertebral

Adapted from Martini F, Nath J, Bartholomew E. Anatomy and physiology. 9th ed. San Francisco: Pearson Benjamin Cummings; 2011,
with permission.
526 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

CBF is affected by extrinsic and intrinsic factors.1 spinal nerve. This information can be used to identify
Extrinsic factors include systemic blood pressure, cardiac the spinal nerve or spinal segment that is involved in an
output, blood viscosity and vascular tone. The body injury. In some areas, the dermatomes are not absolutely
responds to these demands with changes in blood flow. distinct. Some dermatomes may share a nerve supply with
Aerobic metabolism is critically dependent on oxygen in neighbouring regions. For this reason, it is necessary to
order to process glucose for normal energy production, numb several adjacent dermatomes to achieve successful
and the brain does not store energy. Therefore, without a anaesthesia.
constant source of oxygen and energy, its supply from CBF The blood supply to the spinal cord arises from branches
can be exhausted within 3 minutes. Intrinsic factors include of the vertebral arteries and spinal radicular arteries.19 The
PaCO2 (pH), PaO2 and ICP. The vessels dilate with increases mid-thoracic region, at approximately T4–T8, lies between
in PaCO2 (hypercarbia) or low pH (acidosis) and with the lumbar and vertebral arterial supplies and is a vulnerable
decreases in PaO2 (hypoxia). This vasodilation increases CBF. zone of relatively decreased perfusion. This region is most
The vessels constrict with decreases in PaCO2 or high pH susceptible to infarction during periods of hypotension,
and with increases in local PaO2.1 This vasoconstriction will thoracic surgery or other conditions, causing decreased
decrease the CBF. In addition, intrinsic factors can change aortic pressure and potentially leading to ischaemic spinal
the extrinsic factors by altering the metabolic mechanisms. injury with devastating consequences.19
These changes can lead to an alteration in the CBF. For
example, there can be a change from aerobic to anaerobic
metabolism, which increases the concentrations of other
Peripheral nervous system
end-products such as lactic acid, pyruvic acid and carbonic The PNS consists of 12 pairs of cranial nerves and 31 pairs
acid, which causes a localised acidosis. These end-products of spinal nerves, and includes all neural structures lying
result in a high pH that will cause an increase in CBF. outside the spinal cord and brainstem. The cranial nerves
Other factors that can affect CBF include pharmacolog- have previously been discussed regarding their role in
ical agents (anaesthetic agents and some antihypertensive brainstem function. The PNS has both motor and sensory
agents), rapid-eye-movement sleep, arousal, pain, seizures, components. The former includes the motor neuron
elevations in body temperature and cerebral trauma. cell body in the anterior horn of the spinal cord and its
peripheral axonal process travelling through the ventral
Spinal cord root and eventually the peripheral nerve. The motor
The spinal cord is the link between the peripheral nerve terminal, together with the muscle endplate and the
nervous system and the brain. The spinal cord has a small, synapse between the two, comprises the neuromuscular
irregularly shaped internal section of grey matter (unmye- junction. The peripheral sensory axon, beginning at
linated tissue) surrounded by a larger area of white matter receptors in cutaneous and deep structures, as well
(myelinated axons).The internal grey matter is arranged so as muscle and tendon receptors, travels back through
that it extends up and down dorsally in a column, one on peripheral nerves to its cell body located in the dorsal root
each side; another column is found in the ventral region ganglion. Its central process, travelling through the dorsal
on each side (see Figure 16.10).1 root, enters the spinal cord in the region of the dorsal
The spinal cord is an essential component of both horn. All commands for movement, whether reflexive or
the sensory and motor divisions of the nervous system. voluntary, are ultimately conveyed to the muscles by the
The first of the primary functions of the spinal cord activity of the lower motor neurons.
is to transmit sensory impulses along the ascending
tracts to the brain as well as to transmit motor impulses Motor control
down the descending tracts away from the brain.24 The Movements can be divided into three main classes:voluntary
second primary function of the spinal cord is to house activity, rhythmic motor patterns and reflex responses.The
and regulate spinal reflexes. Receipt of sensory impulses highest-order activity is voluntary movement, which allows
may cause a reaction anywhere in the body; alternatively, for expression of the will and a purposeful response to the
the signal might be stored in the memory to be used at environment (e.g. reading, speaking, performing calcula-
some stage in the future. Within the motor division of tions).1 Such activity is goal-directed and largely learned,
the nervous system the spinal cord helps to control the and improves with practice. In rhythmic motor patterns,
various bodily activities, including skeletal muscle activity, the initiation and termination may be voluntary, but the
smooth muscle activity and secretion by both endocrine rhythmic activity itself does not require conscious partic-
and exocrine glands. ipation (e.g. chewing, walking, running). Reflex responses
Sensory neurons from all over the skin, except for the are simple, stereotyped responses that do not involve
skin of the face and scalp, feed information into the spinal voluntary control (e.g. deep tendon reflexes or withdrawal
cord through the spinal nerves. The skin surface can be of a limb from a hot surface). Motor control is carried out
mapped into distinct regions that are supplied by a single in a hierarchical yet parallel fashion in the cerebral cortex,
spinal nerve19 (see Figure 16.11).25 the brainstem and the spinal cord. Modulating influences
Each of these regions is called a dermatome. Sensation are provided by the basal ganglia and cerebellum through
from a given dermatome is carried over its corresponding the thalamus.1
 CHAPTER 16 NEUROLOGICAL ASSESSMENT AND MONITORING 527

FIGURE 16.10 The spinal cord and spinal meninges: A posterior view of the spinal cord, showing the meningeal
layers, superficial landmarks and distribution of grey matter and white matter; B sectional view through the spinal cord
and meninges, showing the peripheral distribution of spinal nerves.1

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528 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

FIGURE 16.11 A Anterior and B posterior distributions of dermatomes on the surface of the skin.25

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2012, with permission.

Sensory control primary somatic sensory cortex in the postcentral gyrus

of the parietal lobe.1 The primary somatic sensory cortex
The somatic sensory system has two major components:
projects in turn to higher-order association cortices in
a subsystem for the detection of mechanical stimuli the parietal lobe, and back to the subcortical structures
(e.g. light touch, vibration, pressure, cutaneous tension) involved in mechanosensory information processing.
and a subsystem for the detection of painful stimuli and
temperature.1 Together, these subsystems provide the Autonomic nervous system
ability to identify the shapes and textures of objects, to The autonomic nervous system, with its three major divisions
monitor the internal and external forces acting on the (sympathetic, parasympathetic and enteric), is largely an
body at any moment and to detect potentially harmful involuntary system and is part of the efferent division, as
circumstances. Mechanosensory processing of external shown in Figure 16.1. It allows the body to adjust to rapidly
stimuli is initiated by the activation of a diverse population changing external events (the ‘flight or fight’ response of
of cutaneous and subcutaneous mechanoreceptors at the the sympathetic division) and to regulate internal activities
body surface that relay information to the central nervous (blood pressure, temperature, airway and breathing, urinary
system for interpretation and ultimately for action. function, digestion by the parasympathetic and enteric
Additional receptors located in muscles, joints and other divisions).1 Whereas the major controlling centres for
deep structures monitor mechanical forces generated by somatic motor activity are the primary and secondary
the musculoskeletal system, and are called proprioceptors. motor cortices in the frontal lobes and a variety of related
Mechanosensory information is carried to the brain by brainstem nuclei, the major locus of central control in the
several ascending pathways that run in parallel through visceral motor system is the hypothalamus and the complex
the spinal cord, brainstem and thalamus to reach the circuitry that it controls in the brainstem tegmentum and
 CHAPTER 16 NEUROLOGICAL ASSESSMENT AND MONITORING 529

spinal cord.1 The status of both divisions of the visceral with few exceptions, act on their effectors by releasing the
motor system is modulated by descending pathways from neurotransmitter adrenaline and the related compound
these centres to preganglionic neurons in the brainstem noradrenaline. This system is therefore described as
and spinal cord, which in turn determine the activity of adrenergic, which means ‘activated by adrenaline’.1 The
the primary visceral motor neurons in autonomic ganglia. autonomic regulation of several organ systems of particular
The postganglionic neurons of the sympathetic system, importance in clinical practice is illustrated in Figure 16.12.15

FIGURE 16.12 (Sympathetic and parasympathetic divisions of the autonomic nervous system. Sympathetic
outputs (left) arise from thoracolumbar spinal cord segments and synapses in paravertebral and prevertebral ganglia.
Parasympathetic outputs (right) arise from craniosacral regions and synapses in ganglia in or near effector organs.15

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Adapted from Blumenfeld H. Neuroanatomy through clinical cases. New York: Sinauer Associates; 2010, with permission.
530 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Neurological assessment and Arousal assessment

The evaluation of arousal focuses on the ability to be
monitoring able to respond to a variety of stimuli and can be described
This section explores the complex issues surrounding using the Awake,Verbal, Pain, Unresponsive (AVPU) scale
cerebral haemodynamics and assessment. The objective or terms such as disorientated, lethargic or obtunded.
of assessment is to determine the extent of neurological The advanced trauma life support course26 recommends
injury, recognise fluctuations in condition and imminent an initial assessment during initial resuscitation based on
deterioration and assist in maintaining cerebral perfusion the response to stimulation: Awake, Verbal, Pain, Unre-
as part of multimodal monitoring. sponsive (AVPU). Observe the patient’s response (verbal
or motor). If there is no response to voice or light touch,
Physical examination painful stimulus is needed to assess neurological status.
The neurological physical exam begins at the onset Central pain should be used first and applied with care.
of patient contact, and the priorities are defined by a Sternal rub, supraorbital pressure (least used), trapezius
primary survey and vital signs. The patient’s history and pinch (most used) or pinching the fleshy portion of the
contact with family can inform the clinical examination upper arm near the axilla are methods for introducing
and should include the patient’s normal baseline status, central pain. Hand grasp is a reflex and is a poor test for
medications and other substance use and past neurological motor strength. If the patient does not respond to verbal
symptoms such as syncope or seizures. stimulus but moves spontaneously in a purposeful manner
Specific areas tested during the initial physical (picks at linen, pulls at tubes), the patient is localising.
exam include level of consciousness, general behaviour, Painful stimulus is not required if spontaneous localisa-
memory, attention and concentration, abstract thought tion has been observed. Watch for symmetry. Localising
and judgement. Not every aspect of the examination is purposeful and intentional movement intended to
will be relevant in all critical care situations and therefore eliminate a noxious stimulus, whereas withdrawal is a
may not be tested. Nevertheless, the clinician should ‘smaller’ movement used to ‘get away from’ noxious
understand how all components are integrated and how stimulus. Abnormal flexion differs from withdrawal in
they influence priority decision making for patient care. that the flexion is rigid and abnormal looking. Abnormal
At change of shift, performing a physical examination with extension is a rigid movement with extension of the limbs.
the incoming nurse ensures clear communication of the
patient’s previous status. The patient’s ability to perform Practice tip
should be taken into consideration, as it may be necessary
to modify assessment techniques. For example, intubated When a patient opens their eyes when you call their
patients who are otherwise awake and aware may gesture name, it is an indication that their reticular activating
or write answers to questions instead of verbalising them. centre (brainstem) functioning is intact but it does not
In addition, when patients are the recipients of very tell you if they are awake or aware.
frequent neurological assessment over an extended period
of time (including arousal and awareness, pupil and motor
response), sleep and sensory rest deprivation is common. Practice tip
Sleep deprivation and sensory overload will confound
assessment accuracy. Therefore, careful consideration Awareness means that the cerebral cortex is working in
needs to be given in regard to the priorities of assessment conjunction with the reticular activating system (arousal)
and rest; a plan needs to implemented to promote rest and that the patient can interact with and interpret their
as neurological injury requires rest and sleep for resto- environment.
ration. See Online resources for links to a full neurological
assessment and physical examination protocol. Assessment of awareness
If arousable, progress to assessment of awareness using
Practice tip the Glasgow Coma Scale (GCS). Teasdale and Jennett27
designed the GCS to establish an objective, quantifiable
Evaluation of the level of consciousness and mentation
measure to describe the prognosis of a patient with a brain
are the most important parts of the neurological
injury and include scoring of separate subscales related
examination. A change in either is usually the first clue
to eye opening, verbal response and motor response
to CNS dysfunction.
(Table 16.6). Originally, the GCS was developed as three
separate response areas and reported as such. Contem-
Conscious state porary use of the GCS automatically adds the three best
Arousal and awareness are the fundamental constituents of response scores and easily loses the information given
consciousness and should be evaluated and documented from the separate response areas. Reporting the GCS
repeatedly for trend analysis. Changes in the conscious as three numbers and then the total gives a broader
state are the first to occur in deterioration. assessment interpretation.
 CHAPTER 16 NEUROLOGICAL ASSESSMENT AND MONITORING 531

all its components can be rated in intubated patients, it

TABLE 16.6 gives all components equal weight and it allows the
Glasgow Coma Scale examiner to localise lesions and diagnose a locked-in
The Glasgow Coma Scale is scored between 3 and 15, 3 being
state.28 The FOUR score assesses four variables: eye
the worst, and 15 the best. It comprises three parameters: best
response, motor response, brainstem reflexes and respir-
eye response, best verbal response and best motor response. ation pattern. This assesses respirations as: 1) spontaneous
The definition of these parameters is given below. regular or irregular, 2) Cheyne-Stokes, 3) intubated but
independently breathing above the ventilator or 4) absent.
PA E D I AT R I C V E R S I O N
THE GLASGOW COMA OF THE GLASGOW COMA
If all four categories are graded at zero, brain death testing
S C A L E F O R A D U LT S SCALE is suggested.29
Best eye response (4) Best eye response (4)
The administration of the FOUR offers a few specific
1 No eye opening 1 No eye opening advantages over utilising the GCS.28 The FOUR adds to
2 Eye opening to pain 2 Eye opening to pain the eye opening of the GCS by testing eye tracking, thus
3 Eye opening to verbal 3 Eye opening to verbal incorporating midbrain and pontine functions. It allows for
command command testing of afferent language processing and remains testable
4 Eyes open spontaneously 4 Eyes open spontaneously regardless of endotracheal intubation, aphasia, aphonia or
Best verbal response (5) Best verbal response (5) trauma to the vocal apparatus. It adds to the motor score of
1 No verbal response 1 No vocal response the GCS, incorporating hand gestures into the evaluation.
2 Incomprehensible 2 Occasionally whimpers The bulk of the motor score is similar to the GCS except
sounds and/or moans that no difference is delineated between flexor posturing
3 Inappropriate words 3 Cries inappropriately and normal flexion to pain. Specific testing of brainstem
4 Confused 4 Less than usual ability
reflexes via pupillary, corneal and cough reflexes further
5 Orientated and/or spontaneous
irritable cry
allows the clinician to localise lesions and track progres-
5 Alert, babbles, coos, sion of cerebral injury, specifically by addressing unilateral
words or sentences to fixed mydriasis, a sign alerting to uncal herniation.29
usual ability
Eye and pupil assessment
Best motor response (6) Best motor response (6)
1 No motor response 1 No motor response to pain
Pupillary responses, including pupil size and reaction
2 Extension to pain 2 Abnormal extension to to light, are important neurological observations and
3 Flexion to pain pain (decerebrate) localise cerebral disease to a specific area of the brain.
4 Withdrawal from pain 3 Abnormal flexion to pain The immediate constriction of the pupil when light is
5 Localising pain (decorticate) shone into the eye is referred to as the direct light reflex.
6 Obeys commands 4 Withdrawal to painful Withdrawal of the light should produce an immediate and
stimuli brisk dilation of the pupil. Introduction of the light into
5 Localises to painful stimuli one eye should cause a similar constriction to occur in the
or withdraws to touch
other pupil (consensual light reaction).30
6 Obeys commands
or performs normal
Other points to consider when conducting pupillary
spontaneous movements observations include the following:31
• Pinpoint non-reactive pupils are associated with
The advantage of the GCS is that it allows rapid serial opiate overdose.
comparisons and categorisation of basic neurological • Non-reactive pupils may also be caused by local
function over time. However, it has several recognised damage.
weaknesses, including poor prediction of outcome beyond • Atropine will cause dilated pupils.
survival, poor inter-rater reliability and inconsistent use in
the prehospital and hospital settings. GCS accuracy will
• One dilated or fixed pupil may be indicative of
an expanding or developing intracranial lesion,
be affected if the patient is receiving anaesthetic agents or compressing the oculomotor nerve on the same side
sedation and noxious stimuli should be avoided. Further- of the brain as the affected pupil.
more, the rare event of a locked-in syndrome, where a patient
is neurologically aware and awake but not responding, is • A sluggish pupil may be difficult to distinguish from
poorly represented by the GCS. Also, interpretation of a fixed pupil and may be an early focal sign of an
response in regard to language used or a previous commu- expanding intracranial lesion and raised intracranial
nication disability is important for assessment accuracy. pressure. A sluggish response to light in a previously
See Online resources for a link to a full GCS procedure. reacting pupil must be reported immediately.
The Full Outline of Unresponsiveness (FOUR) scale Assessment of pupillary function focuses on three
is an accurate predictor of outcome in traumatic brain areas: 1) estimation of pupil size and shape; 2) evaluation
injury (TBI) patients. It is easy to learn, remember and of pupillary reaction to light; and 3) assessment of eye
administer. It has some advantages over GCS: for example, movements. Metabolic disturbances rarely cause pupillary
532 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

changes, so abnormal pupillary findings are usually due The test is repeated with all extremities. Typically, the
to a nervous system lesion.32 Irregular-sized pupils are lower the level of consciousness, the closer to flaccid the
normal for some people and eye prostheses are common; limb(s) will be. An asymmetrical examination may indicate
it is important to establish and document these findings a lesion in the contralateral hemisphere or brainstem.
so a trend can be established to distinguish normal from The next assessment, peripheral reflex response, is
altered states. response to tactile stimuli peripherally and usually elicits
a reflex response rather than a central or brain response.
Practice tip It is important to apply stimuli in a progressive manner,
using the least noxious stimuli necessary to elicit a
Localising is purposeful and intentional movement response. If there is no response to light or firm pressure,
intended to eliminate a noxious stimulus, whereas the clinician must use noxious stimuli. Each extremity is
withdrawal is a ‘smaller’ movement used to ‘get away assessed individually. The typical technique for peripheral
from’ noxious stimulus. noxious stimuli involves pressure on the nail beds for
asserting a peripheral stimulus.The triple-flexion response
Eye and eyelid movements is a withdrawal of the limb in a straight line with flexion
Patients who are comatose will exhibit no eye opening. of the wrist–elbow–shoulder or the ankle–knee–hip.
In patients with bilateral thalamic damage, there may This response is considered a spinal reflex and is not an
be normal consciousness, but an eye opening apraxia indication of brain involvement in the movement. The
(i.e. non-paralytic motor abnormality characterised triple-flexion response is common in patients with severe
by difficulty initiating the act of lid elevation after lid neurological impairment. It is not uncommon in patients
closure) may mimic coma. If the patient’s eyes are closed, who have become brain dead, and great care must be taken
the clinician should gently raise and release the eyelids. to avoid confusion between brain and spinal-mediated
Brisk opening and closing of the eyes indicates that the responses. If the patient has any other motor activity to
pons is grossly intact. If the pons is impaired, one or both peripheral extremity noxious stimuli, it is an indication of
eyelids may close slowly or not at all. In the patient with higher brain function.35
intact frontal lobe and brainstem functioning, the eyes, If a noxious stimulus is applied centrally through a
when opened, should be pointed straight ahead and at sternal rub, trapezius pinch or supraorbital nerve pressure
equal height. If there is awareness, the patient should look and the patient moves an extremity, it is an indication
towards stimuli after eye opening. Eye deviation indicates of brain involvement in the movement and not a spinal
either a unilateral cerebral or brainstem lesion. If the eyes reflex.36 The movement should be noted as normal,
deviate laterally, gently turn the head to see if the eyes decorticate (flexor: either withdrawal or spastic) or decer-
will cross the midline to the other side. A pattern of spon- ebrate (extensor) and documented accordingly. It should
taneous, slow and random movements (usually laterally) be noted that careful consideration should be given to
is termed roving-eye movements. This indicates that the the choice of noxious stimuli with trapezius pinch the
brainstem oculomotor control is intact but awareness is preferred choice as both sternal rub and supraorbital nerve
significantly impaired.33 pressure can be traumatic when applied. In ventilated
patients, endotracheal suction can also be a substitute for a
Limb movement central noxious stimulus, but the choice of stimulus needs
Assessment of extremities and body movement (or motor to be consistent.
response) provides valuable information about the patient
with a decreased level of consciousness.34 The clinician Practice tip
must observe the patient’s spontaneous movements,
The ability to cough with suctioning can be tested in an
muscle tone and response to tactile stimuli. Decorticate
intubated patient and implies an intact cranial nerve X.
(flexor) posturing is seen when there is involvement of a
cerebral hemisphere and the brain stem. It is characterised
by adduction of the shoulder and arm, elbow flexion and Facial symmetry
pronation and flexion of the wrist while the legs extend. In Facial symmetry is often difficult to appreciate in, for
terms of the GCS motor score, the withdrawal flexor scores example, severely ill patients due to oedema, endo-
higher (4/6) than a spastic flexor movement (3/6). Decer- tracheal tube tape and nasogastric tubes. An asymmetric
ebrate (extensor) posturing is seen with severe metabolic response is indicative of a lesion of cranial nerve (CN)
disturbances or upper brainstem lesions. It is characterised VII. Complete hemi-facial involvement is typically seen
by extension and pronation of the arm(s) and extension of in peripheral dysfunction (Bell’s palsy), whereas superior
the legs. Patients may have an asymmetrical response and division (forehead) sparing weakness indicates a pontine/
may posture spontaneously or to stimuli. medullary (central) involvement. It is important to refrain
Motor tone is first assessed by flexing the limbs and from supraorbital pressure until after pupillary responses
noting increased or absent tone.33 If no tone is present, have been assessed because this noxious stimulation may
the hand is lifted approximately 30 cm above the bed and cause alteration in pupillary reactivity (hence one reason
carefully dropped while protecting the limb from injury. for the lack of preference for its use).
 CHAPTER 16 NEUROLOGICAL ASSESSMENT AND MONITORING 533

Corneal reflexes
TABLE 16.7
The corneal reflex is assessed by holding the patient’s eye
PTA scale used to determine severity of brain injury
open and lightly stimulating the cornea.37 The stimuli
should result in a reflexive blink, best seen in the lower P TA S C O R E SEVERITY
eyelid. The traditional assessment technique involves
1–4 hours Mild brain injury
using a wisp of cotton, lightly brushed along the lower
aspect of the cornea. An alternative, and less potentially ≤1 day Moderate brain injury
traumatic, method is to gently instil isotonic eye drops or 2–7 days Severe brain injury
saline irrigation ampoules onto the cornea. This reflex is 1–4 weeks Very severe brain injury
dependent upon CN V for its sensation and CN VII for its
1–6 months Extremely severe brain injury
motor response. Loss of this reflex is indicative of lower
brainstem damage, but it may be absent due to trauma, >6 months Chronic amnesia state
surgery or long-term contact lens usage.
Oropharyngeal reflexes minutes to months. Although the early stages of PTA are
The oropharyngeal reflexes are controlled by CN IX and easily recognised, identifying the end point is difficult and
CN X.38 The gag reflex is elicited by lightly stimulating complex.42
the soft palate with a suction catheter or tongue blade. The duration of PTA is the best indicator of the extent
Clinicians should always avoid stimulating a gag reflex by of cognitive and functional deficits after TBI. The two
wiggling the endotracheal tube because doing so may result most common means of assessing PTA are the Galveston
in an inadvertent extubation. A gag reflex is a forceful, Orientation and Amnesia Test (GOAT) and the Westmead
symmetrical lowering of the soft palate. The cough reflex PTA scale.43 GOAT features ten questions that assess
is usually assessed only in patients with an endotracheal temporal and spatial orientation, biographical recall and
tube. This reflex is elicited by gently passing a suction memory. The test consists of 10 items that involve the
catheter through the tube and stimulating a cough. Loss recall of events that occurred right before and after
of these reflexes is indicative of lower brainstem damage.39 the injury, as well as questions about disorientation. Scores
of 75 or more on this scale (out of a total possible score of
Practice tip 100) correspond to the termination of the PTA episode.
In the Westmead PTA scale, four pictures, one with the
Sluggish pupils are found in conditions that compress examiner’s face and name, are to be recalled by the patient
the third cranial nerve, such as cerebral oedema and on the next day.Those with severe PTA will have difficulty
herniation. completing such short-term memory tasks. Often, patients
will have a GCS of 15 but have moderate-to-severe PTA
Post-traumatic amnesia scale and can be overlooked by inexperienced clinicians who
fail to watch for secondary insults. The duration of PTA
Post-traumatic amnesia (PTA) is a disorder after brain correlates well with the extent of diffuse axonal injury
injury that is classified as a traumatic delirium and may and with functional outcomes. For example, one study
even be found in patients who rate a GCS of 15.40 The found that 80% of patients with PTA duration of less than
incidence of delirium after a brain injury event is high 2 weeks had a good recovery, compared with 46% for
especially with severe injuries and loss of consciousness. those with PTA duration between 4 and 6 weeks.44 A
Delirium is discussed in detail in Chapter 7; however, person is said to be absolved of PTA if they can achieve a
traumatic delirium historically has been referred to in perfect score for three consecutive days.
the literature as post-traumatic amnesia. Post-traumatic
amnesia is defined as the ‘time elapsed from injury until Assessment of the injured brain
recovery of full consciousness and the return of ongoing The primary aim of managing patients with acute brain
memory’.41,p. 841 It is the initial stage of recovery from brain injury in the critical care unit is to maintain cerebral
injury and is characterised by anterograde (formation of perfusion and oxygenation.45 There is little that can
new memory) and retrograde (memory before injury) be done to reverse the primary damage caused by an
amnesia, disorientation and rapid forgetting. Brief periods insult. Secondary insults may be subtle and can remain
of PTA can occur after minor concussion and may be the undetected by routine systemic physiological monitoring.
only clinical sign of any brain injury. This is when PTA is Continuous monitoring of the central nervous system in
useful for defining the severity of injury and alerting the the ICU serves three functions:46
clinician in regard to greater surveillance and investigation
1 determination of the extent of the primary injury
as described in Table 16.7. Patients often progress directly
from coma into delirium without a clearly-defined stupor 2 early detection of secondary cerebral insults so that
stage, so using a tool to measure PTA can be useful to appropriate interventions can be instituted
gauge the actual condition of the patient in the delirium 3 monitoring of therapeutic interventions to provide
state. Duration of PTA is extremely variable, ranging from feedback.
534 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Although serial cranial imaging such as computer- due to the constantly fluctuating magnetic field produced
ised tomography (CT) or functional magnetic resonance by the associated electrons. However, when placed in a
imaging (fMRI) provides useful information, these are superconducting magnet, the magnetic moments of the
neither continuous nor can they be undertaken at the protons will tend to align along the direction of this
bedside. Continuous invasive arterial blood pressure external field. Magnetic resonance imaging (MRI) uses
monitoring in addition to pulse oximetry, tempera- this characteristic of protons to generate images of the
ture, end-tidal carbon dioxide and urine output should brain and body. The advantages of MRI are: 1) it can be
be included as part of standard general monitoring of manipulated to visualise a wide variety of abnormali-
brain-injured patients. In addition, techniques specific to ties within the brain; and 2) it can show a great deal of
the CNS are required. The commonest and most easily detail of the brain in normal and abnormal states.49 The
performed clinical assessment tool is the GCS. Brain- disadvantages of MRI are: 1) it does not show acute or
specific methods of monitoring reflect pressure in subacute haemorrhage into the brain in any detail; 2) the
the cranial cavity, changes in brain oxygenation and time frame and enclosed space required to perform and
metabolism (brain oxygen saturation) and include jugular prepare a patient for the procedure are not advantageous
venous oxygen saturation, near-infrared spectroscopy, brain for neurological emergencies; 3) it is relatively more
tissue monitoring, cerebral haemodynamics (transcranial expensive compared to CT; 4) the loud noise of the
Doppler) and electrical activity of the CNS (EEG). procedure needs to be considered in patient management;
and 5) equipment for life support and monitoring needs
Brain imaging techniques to be non-magnetic due to the magnetic nature of
Computed tomography the procedure.50
CT is the primary neuroimaging technique in the initial
Functional magnetic resonance imaging
evaluation of the acute brain injury patient and uses a
computer to digitally construct an image based upon the Functional magnetic resonance imaging (fMRI) is similar
measurement of the absorption of X-rays through the to MRI but uses deoxyhaemoglobin as an endogenous
brain. Table 16.8 generally summarises the white to black contrast, which serves as the source of the magnetic
intensities seen for selected tissues in CT. The advantages signal for fMRI. It can determine precisely which part of
of CT are: 1) it is rapidly performed, which is especially the brain is handling critical functions such as thought,
important in neurological emergencies; 2) it clearly shows speech, movement and sensation; help assess the effects of
acute and subacute haemorrhages into the meningeal stroke, trauma or degenerative disease on brain function;
spaces and brain; and 3) it is less expensive than an MRI.47 monitor the growth and function of brain tumours; and
Disadvantages include: 1) it does not clearly show acute guide the planning of surgery or radiation therapy for
or subacute infarctions or ischaemia, or brain oedema, but the brain.51
only shows injury; 2) it does not differentiate white from
Cerebral angiography
grey matter as clearly as an MRI; and 3) it exposes the
patient to ionising radiation. Despite these limitations it Cerebral angiography involves cannulation of cerebral
is still the most prevalent form of neurological imaging.48 vessels and the administration of intra-arterial contrast
agents and medications for conditions involving the
Magnetic resonance imaging arterial circulation of the brain. This procedure also has
The tissues of the body contain proportionately large the benefit of using non-invasive CT or MRI with or
amounts of protons (nuclei of hydrogen atoms) that without contrast to guide the accuracy of the procedure.
function like tiny spinning magnets. Normally, these For example, intracranial aneurysms and arteriovenous
protons are arranged randomly in relation to each other malformations can be accurately diagnosed and repaired
without surgical intervention.52
TABLE 16.8 Cerebral perfusion imaging techniques
The brain and related structures in CT Numerous imaging techniques have been developed and
STRUCTURE/FLUID/SPACE GREY SCALE
applied to evaluate brain haemodynamics, perfusion and
blood flow.The main imaging techniques dedicated to brain
Bone, acute blood Very white
haemodynamics are positron emission tomography (PET),
Enhanced tumour Very white single photon emission computed tomography (SPECT),
Subacute blood Light grey xenon-enhanced computed tomography (XeCT), dynamic
Muscle Light grey perfusion computed tomography (PCT), MRI dynamic
susceptibility contrast (DSC) and arterial spin labelling
Grey matter Light grey
(ASL). All of these techniques give similar information
White matter Medium grey about brain haemodynamics in the form of parameters
Cerebrospinal fluid Medium grey to black such as CBF or CBV.53 They use different tracers and have
Air, fat Very black different technical requirements. Some are feasible at the
bedside and others not (see Table 16.9). The duration of
 CHAPTER 16 NEUROLOGICAL ASSESSMENT AND MONITORING 535

TABLE 16.9
A comparison of various imaging techniques for assessing brain structure haemodynamics

S PAT I A L TEMPORAL SCOPE OF EASE OF

IMAGING TECHNIQUE BEDSIDE USE RESOLUTION RESOLUTION USE I N T E R P R E TAT I O N

CEEG excellent good excellent excellent poor

Evoked potentials good fair fair fair poor
Transcranial Doppler good fair fair fair poor
MRI poor excellent poor good fair
Functional MRI poor excellent good poor poor
CT poor excellent poor good fair
Xenon CT poor good poor fair poor
ICP monitoring excellent poor good fair good
CEEG, continuous EEG; CT, computed tomography; ICP, intracranial pressure; MRI, magnetic resonance imaging.

data acquisition and processing varies from one technique microtransducer systems. The reference point for the
to the other. Brain perfusion imaging techniques also transducer is the foramina of Monro (the duct joining
differ in quantitative accuracy, brain coverage and spatial the lateral and third ventricle that is in alignment with
resolution.54 the middle of the ear) although, in practical terms, the
external auditory meatus is often used.
Practice tip For many years ventriculostomy has been recognised
as the most accurate (although the intraparenchymal fibre
The fixed volume of brain parenchyma, CSF and optic system is now similar in accuracy), cost-effective
intravascular blood contained within the rigid, non- and reliable method of monitoring ICP and is associated
expandable cranium determines ICP. Brain tissue with low infection risks if the duration of placement is
accounts for 80% of this volume whereas blood and less than 72 hours.56 The ventriculostomy catheter is part
CSF each account for about 10%. An expansion of any of a system that includes an external drainage system and a
one of these components must occur at the expense of transducer.The drainage system and transducer are primed
another (Monro-Kellie hypothesis). on insertion with preservative-free saline. The transducer
can easily be calibrated or zeroed against a known pressure.
Intracranial pressure monitoring Advantages of using an indwelling ventricular catheter
Invasive measures for monitoring intracranial pressure include allowing CSF drainage to effectively decrease
(ICP) are commonly used in patients with a severe ICP and using the catheter as a way to instil medications.
head injury or after neurological surgery. Normal ICP Access to CSF drainage allows serial laboratory tests of
varies with age, body position and clinical condition. CSF and determination of volume–pressure relation-
The normal ICP is 7–15 mmHg in a supine adult, ships. Disadvantages of ventriculostomy include risk of
3–7 mmHg in children and 1.5–6 mmHg in term infants. infection, which is higher than that associated with other
The definition of intracranial hypertension depends on ICP-monitoring techniques.57 In addition, the catheter
the specific pathology and age, although ICP >15 mmHg may become occluded with blood or tissue debris, inter-
is generally considered to be abnormal. Increased ICP fering with CSF drainage or ICP monitoring. Also, if
causes a critical reduction in CPP and CBF and may significant cerebral oedema is present, locating the lateral
lead to secondary ischaemic cerebral injury. A number of ventricle for insertion of the ventriculostomy catheter
studies have shown that high ICP is strongly associated may be difficult. Importantly, bleeding or ventricular
with poor outcome, particularly if the period of intra- collapse may occur if CSF is drained too rapidly.58 For
cranial hypertension is prolonged.55 ICP is not a static this last reason, many clinicians set the ventriculostomy
pressure and varies with arterial pulsation, with breathing drainage system to drain CSF when the ICP is greater than
and during coughing and straining. Each of the intra- 15–20 mmHg by adjusting the height of the drip chamber.
cranial constituents occupies a certain volume and, In addition, limiting ventricular drainage per hour using
being essentially liquid, is incompressible. ICP cannot gravity and three-way taps to 5–10 mL/h has been used to
be reliably estimated from any specific clinical feature avoid excessively rapid CSF drainage. Using a ventriculo-
or CT finding and must actually be measured. Different stomy may allow life-saving CSF drainage and control of
methods of monitoring ICP have been described but two intracranial hypertension and secondary injury.59
methods are commonly used in clinical practice: intra- While routine ICP monitoring is widely accepted
ventricular catheters and intraparenchymal fibre optic as a mandatory monitoring technique for management
536 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

of patients with severe head injury and is a guideline

suggested by the Brain Trauma Foundation, there is some FIGURE 16.13 The intracranial pressure waveforms.
A Depicts the situation of a compliant system; B a high
debate over its efficacy in improving outcome from pressure wave recorded from a non-compliant system
severe TBI.60 A review of neurocritical care and outcome in which P2 exceeds the level of the P1 waveform,
from TBI suggested that ICP/CPP-guided therapy due to a marked decrease in cerebral compliance.
may benefit patients with severe head injury, including The lower tracing C is an example of an ICP waveform
those presenting with raised ICP in the absence of from a patient monitoring system in which can be
a mass lesion and also patients requiring complex identified the three distinct components, as indicated
interventions.61 in the text.

Pulse waveforms
Interpretation of waveforms that are generated by the P1
cerebral monitoring devices is important in the clinical P2
assessment of intracranial adaptive capacity (the ability of
P3
the brain to compensate for rises in intracranial volume
without raising the ICP).62 Brain tissue pressure and
ICP increase with each cardiac cycle and, thus, the ICP
waveform is a modified arterial pressure wave (see Figure
16.13). The cardiac waves reach the cranial circulation A
via the choroid plexus and resemble the waveforms
transmitted by arterial catheters, although the amplitude
P2
is lower.
There are three distinct peaks seen in the ICP
waveform:63 P3

• P1, the percussion wave, which is sharp and reflects P1

the cardiac pulse as the pressure is transmitted from
the choroid plexus to the ventricle
• P2, the tidal wave, which is more variable in nature
and reflects cerebral compliance and increases in
amplitude as compliance decreases B
• P3, which is due to the closure of the aortic valve and
is known as the dicrotic notch. Of recent importance
is that the elevation of P3 may indicate low global
cerebral perfusion.64
It is important that the waveform be continuously
observed, as changes in mean pressure or in waveform
shape usually require immediate attention. In acute states C
such as head injury and subarachnoid haemorrhage,
the value of ICP depends greatly on the link between
monitoring and therapy, so close inspection of the trend
threshold in adults, especially those who are pressure-
in the ICP and the details derived from the waveform is
active (i.e. ICP varies inversely with mean arterial pressure
extremely important. Simple ongoing visual assessment
[MAP]).63 Higher CPP has been associated with increased
of the ICP waveform for increased amplitude, elevated
lung water and acute respiratory distress syndrome.
P2 and rounding of the waveform provides non-specific
Furthermore, mortality rises approximately 20% for each
information suggestive of decreased intracranial adaptive
10 mmHg loss of CPP. In those studies where CPP was
capacity and altered intracranial dynamics.65
maintained above 70 mmHg, the reduction in mortality
Assessment of cerebral perfusion was as much as 35% for those with severe head injury.66
CPP is calculated as the mean arterial pressure minus the The Brain Trauma Foundation recommends a CPP goal
ICP and represents the pressure gradient across the vessel of 50–70 mmHg despite the lack of definitive data, such
that drives CBF: as from randomised controlled trials and intention-to-
treat clinical trials.67 In the paediatric population a CPP
CPP = MAP – ICP >40 mmHg is the recommended guideline.68,69 Utilising
cerebral oxygenation monitoring in combination with
CPP is a pressure-based indicator of oxygen and pressure has been associated with better outcomes for
metabolite delivery.There is no evidence for the optimum brain-injured patients, and is part of the multimodal
level of CPP, but 70–80 mmHg is probably the critical assessment for brain injury.
 CHAPTER 16 NEUROLOGICAL ASSESSMENT AND MONITORING 537

Assessment of cerebral oxygenation Consequently, brain tissue hypoxaemia is often observed

The three main factors determining cerebral oxygenation during the first 24 hours after injury despite controlled
are cerebral blood flow, arterial oxygen content and cerebral brain pressures. Monitoring partial pressure of oxygen in
metabolic rate of oxygen consumption. In clinical practice brain tissue (PbtO2) can be used to collect more accurate
monitoring of arterial blood gas tensions is routine in most and timely information about cerebral oxygen delivery
critically ill patients. Measurement of cerebral metabolic and demand than ICP allows.74 A tissue oxygen value of
rate of oxygen consumption is not commonplace as it less than 10 mmHg for more than 10 minutes carries a
is technically difficult and cumbersome. Therefore, the higher risk of death. Normal brain oxygen levels (PbtO2
predominant monitoring strategy in clinical practice has between 20 and 25 mmHg) emerge as a critical determi-
relied on measurements of cerebral blood flow and its nant of outcome, with values below 20 mmHg carrying a
surrogates. This section will outline those modalities. higher risk of poor outcomes.71
Regardless of ICP, brain tissue oxygenation falls with
Jugular venous oximetry a decrease in cerebral blood flow below an ischaemic
Jugular venous catheterisation is used for deriving threshold of 18 mL/100 g/min. ICP may respond to the
oxygen-based variables.70 It facilitates the assessment of changes but often several hours later when the damage
jugular venous oxygenation (SjvO2), cerebral oxygen cannot be reversed. Alterations in cerebral metabolic
extraction (CEO2) and arteriovenous difference in rate can also change tissue oxygen levels. Reducing the
oxygen (AVDO2). All of these variables indicate changes patient’s energy consumption via reduced noise and/or
in cerebral metabolism and blood flow, and therefore the distractions, and increasing their protein caloric intake to
catheter generates continuous data that reflect the balance complement their increased stress state, can improve tissue
between supply and demand of cerebral oxygen. oxygenation.73
The catheter is inserted in the right jugular vein, as it
Microdialysis
is slightly larger than the left and provides readings that
are more representative of overall brain function. The Cerebral microdialysis (using a catheter ideally placed in
catheter tip is advanced so that the tip sits in the bulb of the frontal lobe) is a tool for investigating the metabolic
the internal jugular vein. status of the injured brain and is part of multimodal
The normal requirement for cerebral oxygen delivery monitoring. The microdialysis probe is inserted into
is consumption at 35–40% of available oxygen, giving the cerebral tissue where substances in the extracellu-
a normal SjvO2 of 60–65%. Changes in SjvO2 reflect lar fluid surround the semipermeable membrane at the
changes in cerebral metabolic rate and cerebral blood tip of the catheter. Following equilibration of the tissue
flow; however, as it is a global measure, it does not detect metabolites with the perfusion fluid, the dialysate can
regional ischaemia. A high SjvO2 is indicative of increased be analysed for concentrations of products of energy
cerebral blood flow, reduced oxygen consumption and metabolism (glucose, lactate, pyruvate) as indicators of
hyperventilation. Low SjvO2 levels suggest that cerebral hypoxia and ischaemia. In addition, interstitial glycerol
perfusion is reduced, with levels below 40% indicative of can be determined, which is a parameter of lipolysis
global cerebral ischaemia.71 However, caution must be used and/or cell membrane damage. In theory, the micro-
when interpreting values generated using this method, as dialysis catheter acts like a blood capillary.75 Thereby,
high values might also imply an increase in arteriovenous it is proposed that microdialysis provides information
shunting secondary to vasoconstriction, maldistribution regarding events that take place in the tissue before any
of blood flow or lack of oxygen consumption as in brain chemical events are reflected by changes in systemic
death. Because SjvO2 monitoring is a global measure of blood levels of indicator substances.76 These molecules
cerebral oxygenation,72 smaller areas of ischaemia are not diffuse across the membrane part of the catheter and
detected unless these are of sufficient magnitude to affect equilibrate with the perfusion fluid, which is pumped
global brain saturation. SjvO2 requires special care such as through the probe at very low rates of flow. Changes
frequent recalibration to ensure accurate measurements, in the concentration of a substrate in the surround-
observing for catheter migration that interferes with signal ing milieu are reflected by subsequent changes in the
quality and, often, medical intervention to reposition the dialysate.77 Rather than inserting an instrument into the
catheter. The position of the patient also affects signal tissue, microdialysate is extracted and later analysed in
quality and, ideally, the patient should be nursed supine the laboratory or clinically at the patient’s bedside.
with a head elevation of 10–15° and at least a neutral head
alignment. It is important that measurement errors be Non-invasive assessment
excluded when abnormal readings are noted; algorithms Most of the invasive methods of measuring cerebral blood
have been developed to assist nurses when caring for flow and oxygenation can be associated with compli-
patients with jugular bulb oximetry.73 cations. Because of this, many patients with low- or
moderate-grade TBI are not monitored. Patients benefit
Partial brain tissue oxygenation monitoring from noninvasive means of detecting episodes of cerebral
Changes in ICP values alone do not accurately depict poor hypoxia and ischaemia that could lead to poor outcomes,
cerebral blood flow or oxygenation deficits to brain tissue. and these are detailed in the following section.
538 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Transcranial Doppler The EEG becomes substantially abnormal (suppressed)

Transcranial Doppler (TCD) ultrasound has proved to when cerebral blood flow declines to 20–30 mL/100 g/
be a safe, reliable and relatively inexpensive technology min. More subtle abnormalities accompany lesser degrees of
for measuring cerebrovascular blood velocities and hypoperfusion, including initial loss of beta activity, slowing
evaluating cerebral circulation and haemodynamics. Pulses to the theta range and then to the delta range. Irrevers-
of ultrasound are directed using a handheld transducer ible injury to brain tissue occurs at cerebral flows of about
towards the vascular formations in the base of the skull. 10–12 mL/100 g/min. Thus, EEG sensitivity to ischaemia
Velocities from the cerebral arteries, the internal carotids, allows its use in situations where cerebral perfusion is at
the basilar and the vertebral arteries can be sampled by risk.81 Changes over time in these quantitative EEG (qEEG)
altering the transducer location, angle and the instrument’s parameters can trigger remote reading, focused neurologi-
depth setting. The commonest windows in the cranium cal examination, imaging studies and early treatment. Subtle
are located in the orbit (of the eye) and in the temporal EEG changes may be difficult to interpret in isolation, but
and suboccipital regions. TCD measures systolic, diastolic may be better understood when interpreted in concert
and mean middle cerebral artery (MCA) flow velocities with other components of a multimodality monitoring
and a derived value, the pulsatility index (PI). Changes paradigm, which may include microdialysis, brain tissue
in the PI can be used to identify the threshold of auto- oxygen and cerebral perfusion pressure.
regulation or cerebral perfusion pressure break point in Near-infrared spectroscopy
individual patients. In subarachnoid haemorrhage (SAH)
and TBI this may be due to vasospasm or impaired auto- Near-infrared spectroscopy (NIRS) is a non-invasive
regulation or abnormal intracranial compliance. TCD is method of monitoring continuous trends of cerebral
a simple, portable and non-invasive tool, well suited to oxygenated and deoxygenated haemoglobin by utilising
serial monitoring, that can be used at the bedside to detect an infrared light beam transmitted through the skull.
relative changes in CBF in brain-injured patients.78 Oxygenated and deoxygenated haemoglobin moieties have
different absorption spectra, and cerebral oxygenation and
Continuous electroencephalography haemodynamic status can be determined by their relative
Electroencephalography (EEG) is the recording by absorption of near-infrared light. NIRS allows interroga-
sensors along the scalp of electrical activity produced tion of the cerebral cortex using reflectance spectroscopy
by the firing of neurons within the brain. Continuous via optodes, light transmitting and detecting devices,
EEG (cEEG) has the advantage of being continuous and placed on the scalp. Normal saturation is 70%. Because
noninvasive and carries the potential to detect alter- NIRS interrogates arterial, venous and capillary blood
ations in brain physiology at a reversible stage, which within the field of view, the derived saturation represents
may trigger treatment before permanent brain injury regional tissue oxygenation (rSO2) measured from these
occurs. The invention of digital EEG has made cEEG three compartments and can be used to identify tissue
monitoring feasible for ICU patients.79 Currently, the hypoxia and ischaemia in the brain cortex.
main applications of cEEG are diagnosing non-convulsive The clinical and bedside use of NIRS is constrained by
status epilepticus, monitoring and guiding the treatment potential sources of error, which include contamination of
of status epilepticus and detecting delayed cerebral the signal by the extracerebral circulation (such as in the
ischaemia from vasospasm in subarachnoid haemorrhage scalp), extraneous light and the presence of extravascular
patients. Other applications may include monitoring of blood arising from subarachnoid or subdural haemor-
reperfusion after tissue plasminogen activator administra- rhage.82 In a recent study in patients with subarachnoid
tion in acute stroke patients and detection of intracranial haemorrhage, episodes of angiographic cerebral vasospasm
hypertension. Clinically unrecognised electrographic were strongly associated with reduction in trend in the
seizures and periodic epileptiform discharges have been ipsilateral NIRS signal.83 Furthermore, the degree of spasm
shown to be frequent and associated with poor outcome (especially more than 75% vessel diameter reduction) was
in patients with severe brain injury from different aeti- associated with a greater reduction in same-side NIRS
ologies, including TBI, ischaemic and haemorrhagic signal, demonstrating real-time detection of intracerebral
strokes and CNS infection.80 ischaemia.

Summary
This chapter provides an overview of anatomy and physiology in the context of and as applied to neurological assessment
of the critically ill. Priorities of clinical assessment are described. Imaging techniques and assessment incorporate the
therapeutics of intracranial pressure, cerebral perfusion pressure and partial brain tissue oxygenation monitoring, cEEG,
transcranial Doppler and cerebral perfusion imaging.The research vignette reports a systematic review and meta-analysis
of the effectiveness of hypertonic saline in reducing intracranial pressure. The clinical case demonstrates neurologi-
cal assessment priorities in an unstable, traumatic brain injury patient. Clinical, non-invasive and invasive assessment
techniques are described within the context of this patient’s care.
 CHAPTER 16 NEUROLOGICAL ASSESSMENT AND MONITORING 539

Case study
On the 26th April a 68-year-old male, Jonathan, was on the roof of his house cleaning the leaves from
the gutters. He was found some time later by his wife unconscious, lying on his back on the ground. She
immediately called ambulance emergency services. At the scene Jonathan was conscious with a GCS
of 13. He was verbally repetitive with diminished orientation to time and place. His pupils were 3 mm in
diameter and were equal and reacting to light. An occipital scalp haemotoma and contusion was noted. His
lung air entry was equal with diminished rise and fall of the chest. No obvious motor, neural, abdominal or
thorax injures were seen.
Intravenous access was obtained and ondansetron 4 mg administered. Oxygen 8 L via a Hudson mask was
administered and Jonathan was transferred to the nearest trauma tertiary centre by helicopter.

EMERGENCY DEPARTMENT
The transport team arrived 30 minutes later to the emergency department (ED) and bypassed triage.
Jonathan was admitted to the resuscitation area where the trauma team conducted primary and secondary
surveys. On presentation, Jonathan’s vital signs were: heart rate 68 beats/min, respirations 16 breaths/min,
blood pressure 166/78 mmHg, SpO2 97%, temperature 35.3°C, GCS 13.

Primary survey
Jonathon’s primary survey revealed the following details.
• Airway: upper airway cleared. Cervical spine: status unknown, Philadelphia collar in situ.
• Breathing: spontaneously breathing on 6 L/min at 20 breaths/min, equal air entry, decreased bilaterally,
no tracheal deviation.
• Circulation: brief episodes of bradycardia, hypertensive and normovolaemic; pulses present on
palpation, temperature centrally warm, well perfused, skin pink in colour, peripherally cold and pale;
capillary refill >4 seconds.
• Disability: he was alert but agitated and confused, GCS 13; pupils equal and reactive, size 4 mm. Mobile
trauma series performed – chest and pelvis X-ray.

Secondary survey
The secondary survey revealed the following details.
• Head: large posterior occipital haemotoma present. CT revealed extensive acute subdural and
subarachnoid haemorrhages with an occipital communicated fracture and basilar skull fracture into the
carotid canal. Basal cisterns were moderately effaced.
• Face: no oedema, rhinorrhoea or otorrhoea.
• Neck: Philadelphia neck collar left in situ; no obvious lacerations observed around neck area; no
evidence of tracheal deviation. Cervical spine CT reported no bony injury, spine not cleared.
• Chest: abdomen – firm, no abnormal distension. IDC insertion revealed haematuria.
• Pelvis: bruising bilaterally with no obvious deformity.
• Back: marked flank bruising, no lacerations, right perinephric haemotoma on CT; rectal tone present.
• Upper limbs: X-ray revealed right radial and ulna fractures, lacerations and bruising present; pulses
present.
• Lower limbs: all pulses present, no obvious injuries present.

EMERGENCY SURGERY
Jonathan’s GCS decreased to 9 and he was electively intubated. A repeat CT brain scan was performed
and revealed an extension of the left-sided subdural haemorrhage and a new left frontal haemotoma.
Jonathan was transferred to operating theatre within 30 minutes for a craniectomy and evacuation of
the acute subdural and frontal haemorrhages and insertion of an external ventricular drain (EVD). The
EVD insertion was unsuccessful and left as a subdural monitor. A Jackson Pratt drain was inserted and
intraoperatively drained 500 mL.
Following surgery, he was admitted to the intensive care unit (ICU) for further management (Table 16.10).
540 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 16.10
Overview of Jonathan’s clinical parameters and assessment, days 1–6

D AY O F A D M I S S I O N
PA R A M E T E R 1 2 3 4 5 6

Pupils (mm)
Right 3+ 2S 2S 3+ 3+ 3+
Left 3+ 2S 2S 3+ 3+ 3+
GCS 3T 3T 3T 3T 4T 5T
(E1V1(T)M1) (E1V1(T)M1) (E1V1(T)M1) (E1V1(T)M1) (E2V1(T)M1) (E2V1(T)M3)
CSF drainage
(mL/24 h) Nil 26 38 30 25 18*
ICP range 6–25 9–21 16–25 12–26 12–22 11–18
(mmHg)
Sedation Morphine/ Fentanyl/ Fentanyl/ Fentanyl/ Fentanyl/ Fentanyl/
infusion midazolam midazolam midazolam midazolam midazolam midazolam
Propofol Propofol Propofol Propofol
Paralysing agent Vecuronium Vecuronium Vecuronium Vecuronium Vecuronium
intermittent intermittent intermittent intermittent intermittent
Noradrenaline
(mcg/min) 5–18 5–20 2–13 3–10 3–6 Nil
Heart rate range 60–108 58–80 57–88 58–95 60–90 58–88
(bpm)
MAP range 65–100 75–92 72–88 85–98 85–98 78–92
(mmHg)
CPP range 59–92 64–79 61–72 60–78 62–81 63–90*
(mmHg)
CPP = cerebral perfusion pressure; CSF = cerebrospinal fluid; E = eye opening; GCS = Glasgow Coma Scale;
ICP = intracranial pressure; M = motor; MAP = mean arterial pressure; V = verbal; (T) = intubated; * = ICP
external ventricular drain removed.

ICU MANAGEMENT
Day 1
On arrival to the ICU, Jonathan’s condition was critical. His vital signs were: heart rate 115 beats/min;
intubated and mechanically ventilated at 22 breaths/min, Vt 500 mL, FiO2 0.4, PEEP 8 cmH2O; blood
pressure 132/85 mmHg (MAP 100) with noradrenaline support for a CPP of 65; SaO2 98%; temperature
37.5°C; pupils 3/3 mm (R/L), sluggish sequential reaction. He was heavily sedated and unresponsive with a
Glasgow Coma Score (GCS) of 3T (eye opening 1, verbal 1 [T = intubated], motor 1). His subdural monitor
displayed a surrogate ICP of 8 mmHg. He required paralysis with intermittent boluses of vecuronium and
with the need for increasing levels of sedation, noradrenaline and hypertonic saline bolus to control his ICP
and CPP. Normal saline was infused for maintenance fluid. Pain stimulation for neurological assessment
under these conditions was only performed during endotracheal suction.

Days 2–7
Jonathan’s clinical parameters and assessment are depicted in Table 16.10. His condition remained
variable and on day 2 he returned to the operating theatre for insertion of an intraventricular catheter and
external ventricular drainage system. His ICP and CPP were unstable with increasing need for sedation and
intermittent paralysis. Bolus doses of hypertonic saline were administered and increased drainage from
the EVD (38 mL in 24 hours) was noted. Jonathan’s serum sodium levels elevated to hypernatraemic state
with a sodium (Na+) range of 144–154 mmol/L (normal range is 136–144 mmol/L). He was administered free
water boluses of 300 mL by orogastric tube.
 CHAPTER 16 NEUROLOGICAL ASSESSMENT AND MONITORING 541

A repeat CT determined no significant change. The ventricles were effaced but not compressed. After
stabilising on day 5, Jonathan’s noradrenaline and sedation infusions were reduced for neurological
assessment. His GCS was 5 (E2, V1[T], M3) with normal flexion to pain and remained unchanged up until
day 7. Despite an increased GCS it was difficult to assess his verbal response while intubated. The EVD
was removed on day 6 and he remained sedated and ventilated. Jonathan continued to slowly recover.

CASE STUDY QUESTIONS

1 Indicate whether the following factors increase or decrease cerebral blood flow: a) PaCO2 of 30 mmHg;
b) PaO2 of 45 mmHg; c) decreased MAP; d) increased ICP; e) arterial blood pH of 7.
2 Explain the physiological mechanism for dilated (size 5), non-reactive pupils.

RESEARCH VIGNETTE

Lazaridis C, Neyens R, Bodle J, DeSantis S. High-osmolarity saline in neurocritical care: systematic review and
meta-analysis. Crit Care Med 2013;41(5):1353–60

Abstract
Background and purpose: Intracranial hypertension and cerebral edema are known contributors to secondary brain
injury and to poor neurologic outcomes. Small volume solutions of exceedingly high osmolarity, such as 23.4%
saline, have been used for the management of intracranial hypertension crises and as a measure to prevent or reverse
acute brain tissue shifts. We conducted a systematic literature review on the use of 23.4% saline in neurocritically ill
patients and a meta-analysis of the effect of 23.4% saline on intracranial pressure reduction.

Design: We searched computerized databases, reference lists, and personal files to identify all clinical studies in
which 23.4% saline has been used for the treatment of neurocritical care patients. Studies that did not directly
involve either effects on cerebral hemodynamics or the treatment of patients with clinical or radiographic evidence of
intracranial hypertension and/or cerebral swelling were eliminated.

Measurements and main results: We identified 11 clinical studies meeting eligibility criteria. A meta-analysis was
performed to evaluate the percent decrease in intracranial pressure and the 95% confidence intervals, from baseline
to 60 minutes or nadir from the six studies from which this information could be extracted. A fixed effects meta-
analysis estimated that the percent decrease in intracranial pressure from baseline to either 60 minutes or nadir after
administration of 23.4% saline was 55.6% (se 5.90; 95% confidence interval, 43.99–67.12; p < 0.0001).

Conclusions: Highly concentrated hypertonic saline such as 23.4% provides a small volume solution with low cost
and an over 50% reduction effect on raised intracranial pressure. Side effects reported are minor overall in view
of the potentially catastrophic event that is being treated. High quality data are still needed to define the most
appropriate osmotherapeutic agent, the optimal dose, the safest and most effective mode of administration and to
further elucidate the mechanism of action of 23.4% saline and of osmotherapy in general.

Critique
This review found that, across a broad range of acute brain injury syndromes, ICP reduction was greater with hypertonic
saline (HTS) 23.4% compared with mannitol (in most instances), at 60 minutes or nadir. While 11 studies were included
in the systematic review, only six were used in the meta-analysis. Meta-analysis should only be used if studies are
similar in terms of interventions and outcomes, thus it seemed reasonable to not include all studies. However, the
authors do acknowledge that some of the studies they did include in the meta-analysis had differing interventions in
terms of dosing of the saline. This fact may make the results less meaningful. Prior to undertaking a meta-analysis,
it is important to assess the extent to which studies are similar (i.e. homogeneous), to determining if it is reasonable
to pool the data from these studies. If studies are very different, then pooling the data is not appropriate. There are
several statistical tests to determine the extent to which studies are ‘heterogeneous’, but the one used in this study
(Cochran’s Q) has several limitations. Given the small number of studies there may have been a more appropriate test,
542 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

such as the I2 statistic. In terms of the systematic review process, there was no a priori research question published
on a publicly accessible website such as PROSPERO (http://www.crd.york.ac.uk/PROSPERO/), usually in the form of
a protocol. Grey literature was not included in the search strategy, accounting for the lack of inaccessible papers, a
general fault in the systematic process. The flow sheet did not conform to the Preferred Reporting Items for Systematic
Reviews and Meta-Analyses (see http://www.prisma-statement.org) guidance for systematic reviews, and there was
absence of a measure of trial quality for each study. In regard to the studies’ findings, improvements in ICP percent
decrease outcome did not always lead to improvements in patient-oriented outcomes such as symptoms, morbidity,
quality of life or mortality. Further, in many of the studies, equimolar hypertonic comparison was not made, making a
reliable conclusion about the efficacy of HTS difficult. However, the results were encouraging for HTS. ICP reduction
was greatest with HTS, and there were limited but encouraging serious adverse event data.

Lear ning a c t iv it ie s
The first three activities refer to the research vignette.
1 What are the theoretical side effects and complications associated with hypertonic saline therapy administration?
2 Discuss the physiological effects of how hypertonic 23.4% saline reduces ICP.
3 What effect would decreasing the concentration of extracellular potassium ions have on the transmembrane
potential of a neuron?
4 Which brain structure coordinates endocrine and nervous system activities?
5 Which component of the brain controls the cardiac centres, the vasomotor centres and the respiratory rhythm
centre?
6 What information does the GCS provide? What does the GCS predict?
7 During the testing of motor response a noxious stimulus is applied to the nail bed of the middle finger. The
unconscious patient elicits a flexion withdrawal response of the wrist, arm and shoulder. Explain what this
response means in terms of central or peripheral response.
8 What is the pathophysiological basis for the rise in ICP? How would this manifest on the ICP waveform?
9 A patient recovering from a subarachnoid haemorrhage cannot remember events prior to the haemorrhage
event. What type of amnesia is this?

Online resources
Adult Neurological Observation Chart: Education Package, www.aci.health.nsw.gov.au/__data/assets/pdf_file/0018/201753/
AdultChartEdPackage.pdf
American Association of Neuroscience Nurses (AANN), www.aann.org
Australasian Neuroscience Nurses’ Association, www.anna.asn.au
Brain Explorer, www.brainexplorer.org
Brain Injury Association of America, www.biausa.org
FOUR score for Neuro Assessments, http://w3.rn.com/News/clinical_insights_details.aspx?Id=29828
GCS Part 1, www.youtube.com/watch?v=T93Ah9ZkurI&feature=player_detailpage
GCS Part 2, www.youtube.com/watch?v=_jTTPjZ_ruE&feature=player_detailpage
Neurocritical Care Society, www.neurocriticalcare.org
Neurological Exam, www.neuroexam.com/neuroexam
Neurological Foundation of New Zealand, www.neurological.org.nz
Neuroscience tutorials, http://thalamus.wustl.edu/course
Official Journal of the American Academy of Neurology (AAN), http://neurology.org
Physical Examination and Neurological Assessment, www.neurologyexam.com
 CHAPTER 16 NEUROLOGICAL ASSESSMENT AND MONITORING 543

Post-traumatic amnesia protocol, www.psy.mq.edu.au/pta

Rural Neurotrauma Assessment, www.racs.edu.au/media/16138/PUB_090824_-_Neurotrauma_(Standard_Version).pdf
Society for Neuroscience, http://web.sfn.org
The Brain Trauma Foundation, www.braintrauma.org
World Health Organization Neurotrauma, www.who.int/violence_injury_prevention/road_traffic/activities/neurotrauma/en

Further reading
Allen BB, Chiu YL, Gerber LM, Ghajar J, Greenfield JP. Age-specific cerebral perfusion pressure thresholds and survival in
children and adolescents with severe traumatic brain injury. Pediatr Crit Care Med 2014;15(1):62–70.
Crossley S, Reid J, McLatchie R, Hayton J, Clark C, MacDougall M et al. A systematic review of therapeutic hypothermia for
adult patients following traumatic brain injury. Crit Care 2014;18(2):R75.
Kumar R, Singhi S, Singhi P, Jayashree M, Bansal A, Bhatti A. Randomized controlled trial comparing cerebral perfusion
pressure-targeted therapy versus intracranial pressure-targeted therapy for raised intracranial pressure due to acute CNS
infections in children. Crit Care Med 2014;42(8):1775–87.
Lazaridis C, Neyens R, Bodle J, Desantis SM. High-osmolarity saline in neurocritical care: systematic review and meta-
analysis. Crit Care Med 2013;41(5):1353–60.
Le Roux P, Menon D, Citerio G, Vespa P, Bader M, Brophy G et al. Consensus summary statement of the International
Multidisciplinary Consensus Conference on Multimodality Monitoring in Neurocritical Care. Intensive Care Med 2014;
40(9):1189–209.
Manno EM. Update on intracerebral hemorrhage. CONTINUUM Lifelong Learning in Neurology 2012;18(3):598–610.
Sharshar T, Citerio G, Andrews PD, Chieregato A, Latronico N, Menon D et al. Neurological examination of critically ill
patients: a pragmatic approach. Report of an ESICM expert panel. Intensive Care Med 2014;40(4):484–95.

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47 Bremmer R, De Jong BM, Wagemakers M, Regtien JG, Van Der Naalt J. The course of intracranial pressure in traumatic brain injury: relation
with outcome and CT-characteristics. Neurocritical Care 2010;12(3):362–8.
48 Downer JJ, Pretorius PM. Symmetry in computed tomography of the brain: the pitfalls. Clin Radiol 2009;64(3):298–306.
49 Hillary FG, Biswal BB. Automated detection and quantification of brain lesions in acute traumatic brain injury using MRI. Brain Imaging Behavior
2009;3(2):111–22.
50 Mannion RJ, Cross J, Bradley P, Coles JP, Chatfield D, Carpenter A et al. Mechanism-based MRI classification of traumatic brainstem injury and
its relationship to outcome. J Neurotrauma 2007;24(1):128–35.
51 Leitch JK, Figley CR, Stroman PW. Applying functional MRI to the spinal cord and brainstem. Magn Reson Imaging 2010;28(8):1225–33.
52 Greenberg ED, Gold R, Reichman M, John M, Ivanidze J, Edwards AM et al. Diagnostic accuracy of CT angiography and CT perfusion for
cerebral vasospasm: a meta-analysis. Am J Neuroradiol 2010;31(10):1853–60.
53 Vespa PM. Imaging and decision-making in neurocritical care. Neurol Clin 2014;32(1):211-24.
54 Kannan S, Balakrishnan B, Muzik O, Romero R, Chugani D. Positron emission tomography imaging of neuroinflammation. J Child Neurol
2009;24(9):1190–9.
55 Vik A, Nag T, Fredriksli OA, Skandsen T, Moen KG, Schirmer-Mikalsen K et al. Relationship of “dose” of intracranial hypertension to outcome in
severe traumatic brain injury. J Neurosurg 2008;109(4):678–84.
56 Koskinen LO, Olivecrona M. Clinical experience with the intraparenchymal intracranial pressure monitoring Codman MicroSensor system.
Neurosurgery 2005;56(4):693–8.
57 Harrop JS, Sharan AD, Ratliff J, Prasad S, Jabbour P, Evans JJ et al. Impact of a standardized protocol and antibiotic-impregnated catheters on
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58 Adelson PD, Bratton SL, Carney NA, Chesnut RM, du Coudray HE, Goldstein B et al. Guidelines for the acute medical management of severe
traumatic brain injury in infants, children, and adolescents. Chapter 7, Intracranial pressure monitoring technology. Pediatr Crit Care Med
2003;4(3 Suppl):S28-30.
59 Hoffmann J, Goadsby PJ. Update on intracranial hypertension and hypotension. Curr Opin Neurol 2013;26(3):240-7.
60 Brain Trauma Foundation. Guidelines for the management of severe traumatic brain injury. VIII. Intracranial pressure thresholds. J Neurotrauma
2007;24(Supp 1):S55–8.
61 Tzeng Y, Ainslie P. Blood pressure regulation. IX: Cerebral autoregulation under blood pressure challenges. Eur J Appl Physiol 2014;114(3):545-59.
62 Di Ieva A, Schmitz E, Cusimano M. Analysis of intracranial pressure: past, present, and future. Neuroscientist 2013;19(6):592-603.
63 Kasprowicz M, Asgari S, Bergsneider M, Czosnyka M, Hamilton R, Hu X. Pattern recognition of overnight intracranial pressure slow waves using
morphological features of intracranial pressure pulse. J Neurosci Methods 2010;190(2):310–8.
64 Hu X, Glenn T, Scalzo F, Bergsneider M, Sarkiss C, Martin N et al. Intracranial pressure pulse morphological features improved detection of
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65 Howells T, Elf K, Jones PA, Ronne-Engstrom E, Piper I, Nilsson P et al. Pressure reactivity as a guide in the treatment of cerebral perfusion
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66 Johnston AJ, Steiner LA, Coles JP, Chatfield DA, Fryer TD, Smielewski P et al. Effect of cerebral perfusion pressure augmentation on regional
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67 Brain Trauma Foundation Guidelines IX. Cerebral perfusion thresholds. J Neurotrauma 2007;24(Supp 1):S59–64.
68 Brain Trauma Foundation Guidelines, Ch 5. Cerebral perfusion pressure thresholds: Guidelines for the acute medical management of severe
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69 Ragan D, McKinstry R, Benzinger T, Leonard J, Pineda J. Udomphorn Y et al. Alterations in cerebral oxygen metabolism after traumatic brain
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70 Chieregato A, Calzolari F, Trasforini G, Targa L, Latronico N. Normal jugular bulb oxygen saturation. J Neurol Neurosurg Psych 2003;74(6):784–6.
71 Bratton SL, Chestnut RM, Ghajar J, McConnell Hammond FF, Harris OA, Hartl R et al. Guidelines for the management of severe traumatic brain
injury. X. Brain oxygen monitoring and thresholds. J Neurotrauma 2007;24(S1):S65–70.
72 Rabinstein AA. Elucidating the value of continuous brain oxygen monitoring. Neurocritical Care 2010;12(1):144–5.
73 Leal-Noval SR, Cayuela A, Arellano-Orden V, Marín-Caballos A, Padilla V, Ferrándiz-Millón C et al. Invasive and noninvasive assessment of
cerebral oxygenation in patients with severe traumatic brain injury. Intensive Care Med 2010;36(8):1309–17.
74 Maloney-Wilensky E, Gracias V, Itkin A, Hoffman K, Bloom S, Yang W et al. Brain tissue oxygen and outcome after severe traumatic brain injury:
a systematic review. Crit Care Med 2009;37(6):2057–63.
75 Kawai N, Kawakita K, Yano T, Tamiya T, Abe Y, Kuroda Y. Use of intracerebral microdialysis in severe traumatic brain injury. Neurol Surg
2010;38(9):795–809.
76 Chefer VI, Thompson AC, Zapata A, Shippenberg TS. Overview of brain microdialysis. Curr Prot in Neuroscience 2009;7.1.1–7.1.28.
77 Uehara T, Sumiyoshi T, Itoh H, Kurata K. Lactate production and neurotransmitters; evidence from microdialysis studies. Pharm Bio Behav
2008;90(2):273–81.
78 Bouzat, P, Francony G, Fauvage B, Payen J. Transcranial Doppler pulsatility index for initial management of brain-injured patients. Neurosurgery
2010;67(6):E1863–4.
79 White DM, Van Cott AC. EEG artifacts in the intensive care unit setting. Am J Elect Tech 2010;50(1):8–25.
80 Kurtz P, Hanafy KA, Claassen J. Continuous EEG monitoring: is it ready for prime time? Curr Opin Crit Care 2009;15(2):99–109.
81 Guérit J. Neurophysiological testing in neurocritical care. Curr Opin Crit Care 2010;16(2):98–104.
82 Murkin JM, Arango M. Near-infrared spectroscopy as an index of brain and tissue oxygenation. Br J Anaesth 2009;103 (Suppl 1):i3–13.
83 Bhatia R, Hampton T, Malde S, Kandala NB, Muammar M, Deasy N et al The application of near-infrared oximetry to cerebral monitoring during
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Chapter 17

Neurological alterations
and management
Diane Chamberlain, Elaine McGloin

KEY WORDS
Learning objectives
After reading this chapter, you should be able to: cerebral perfusion
• differentiate cerebral hypoxia from cerebral ischaemia and focal from coma
global ischaemia intracranial
• differentiate between primary and secondary brain insults due to brain hypertension
injury meningitis
• relate the procedures of selected neurodiagnostic tests to nursing neuroprotection
implications for patient care
seizures
• discuss the rationale for medical and nursing management in the care of spinal cord injury
the brain-injured patient.
stroke
subarachnoid
haemorrhage
Introduction traumatic brain
Numerous conditions encountered in critical care areas relate to serious neuro- injury
logical dysfunction. While most are associated with critical illness, or are at least
well defined, several others are very infrequent and not addressed extensively
in this chapter. One problem arises in that the onset of an abrupt neurological
complication is frequently obscured by the effects of the primary illness. For
example, a metabolic disorder producing encephalopathy can delay recognition
of an intracerebral haemorrhage, or do so because of its treatment, such as using
sedation to allow better synchrony with a mechanical ventilator. Neurological
alterations are generally defined by problems that derive from the acute aspects
of diseases such as stroke, brain and spinal cord injury and status epilepticus.
This chapter discusses the concepts that underlie neurological abnormalities and
addresses current management techniques and modalities.

Neurological dysfunction
This section discusses the concepts of neurological dysfunction including altered
levels of consciousness, motor and sensory function and cerebral metabolism
and perfusion.
Alterations in consciousness
In critical illness, impaired consciousness is often the first sign of a severe
pathological process. Consciousness is defined as recognition of self and
 CHAPTER 17 NEUROLOGICAL ALTERATIONS AND MANAGEMENT 547

the environment, which requires both arousal and Many of the enzymatic reactions of neurons, glial
awareness. Depressed consciousness can range from mild cells and specialised cerebral capillary endothelium in the
depression to coma, the most severe form of absolute brain must be catalysed by the energy-yielding hydrolysis
unconsciousness. of adenosine triphosphate to adenosine diphosphate and
inorganic phosphate. Without a constant and generous
Altered cognition and coma supply of adenosine triphosphate, cellular synthesis slows
Coma is a state of unresponsiveness from which the patient, or stops, neuronal functions decline or cease, and cell
who appears to be asleep, cannot be aroused by verbal structures quickly fall apart.4 The use of lactate for oxidative
and physical stimuli to produce any meaningful response. metabolism becomes prominent when extracellular brain
Therefore, the diagnosis of coma implies the absence of lactate concentration increases to supraphysiological levels,
both arousal and content of consciousness.1 Coma must inducing a sparing of cerebral glucose. The brain depends
be considered a symptom with numerous causes, different entirely on the process of glycolysis and respiration within
natural modes and several management modes. Stupor is its own cells to provide its energy needs. Even a short
a state of unconsciousness from which the patient can be interruption of blood flow, and thereby of the oxygen and
awakened to produce inadequate responses to verbal and glucose supply, threatens tissue vitality.
physical stimuli. Somnolence is a state of unconsciousness
from which the patient can be fully awakened. Seizures
Although there are many specific causes of uncon- A seizure is an uninhibited, abrupt discharge of ions
sciousness, the sites of cerebral affection are either from a group of neurons resulting in epileptic activity.5
the bilateral cerebral cortex or the brainstem reticular The majority of patients experiencing seizures in the
activating system. The commonest causes of bilateral ICU do not have pre-existing epilepsy, and their chances
cortical disease are deficiencies of oxygen, metabolic of developing epilepsy in the future are usually more
disorders, physical injury, toxins, post-convulsive coma dependent on the cause than on the number or intensity
and infections.2 The reticular activating system maintains of seizures that they experience. However, because of the
the state of wakefulness through continuous stimulation other deleterious neuronal and systemic effects of seizures,
of the cortex. Any interruption may lead to uncon- their rapid diagnosis and suppression during a period of
sciousness. The reticular activating system can be affected critical illness is necessary.
in three principal ways: by supratentorial pressure, Seizures are classified depending on how they start
by infratentorial pressure and by intrinsic brainstem as: 1) partial or focal seizures, 2) generalised or full body
lesions. Supratentorial and infratentorial lesions produce seizures involving both cerebral hemispheres or 3) partial
impaired consciousness by enlarging and displacing seizures with secondary generalisation. Patients may be
tissue. Lesions that affect the brainstem itself damage the conscious during a partial seizure whereas during gener-
reticular activating system directly. alised seizures they are not. As partial seizures may not
always progress to tonic–clonic movement or alteration
Practice tip in consciousness, partial seizure represents one of the
most elusive diagnoses in neurology and is often misdiag-
The first principle of management of a person found nosed. One of the most helpful points in the history of a
unconscious is to keep the patient alive by maintaining partial seizure patient is the pre-epileptic event, the aura.
the airway and the circulation. The patient will describe the aura as a virtually identical
sensation every time.
Recently acquired confusion, severe apathy, stupor or Seizures may either prompt the patient’s admission
coma implies dysfunction of the cerebral hemispheres, the to ICU (because of status epilepticus) or develop as a
diencephalon and/or the upper brainstem.3 Focal lesions complication of another illness.6 Seizures can be due to
in supratentorial structures may damage both hemispheres, vascular, infectious, neoplastic, traumatic, degenerative,
or may produce swelling that compresses the diencephalic metabolic, toxic or idiopathic causes. Factors influenc-
activating system and midbrain, causing transtentorial ing the development of post-traumatic epilepsy include
herniation and brainstem damage. Primary infratentorial an early post-traumatic seizure, depressed skull fracture,
(brainstem or cerebellar) lesions may compress or directly intracranial haematoma, dural penetration, focal neuro-
damage the reticular formation anywhere between the logical deficit and post-traumatic amnesia over 24 hours
level of the mid-pons and (by upward pressure) the dien- with the presence of a skull fracture or haematoma.
cephalon. Metabolic or infectious diseases may depress Seizures in critically ill patients are most commonly due
brain functions by a change in blood composition or the to drug effects; metabolic, infectious or toxic disorders;
presence of a direct toxin. Impaired consciousness may or intracranial mass lesions, although they may be due
also be due to reduced blood flow (as in syncope or severe to trauma or neoplasm.7 Conditions producing seizures
heart failure) or a change in the brain’s electrical activity tend either to increase neuronal excitation or to impair
(as in epilepsy). Concussion, anxiolytic drugs and anaes- neuronal inhibition. A few generalised disorders (e.g.
thetics impair consciousness without producing detectable non-ketotic hyperglycaemia) may produce partial or
structural changes in the brain. focal seizures.
548 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Alterations in motor and sensory parasympathetic branches), the endocrine system and
the immune system, hence ANS dysfunction is related
function to this complex triad.10 Autonomic nerve dysfunction
Alterations in motor and sensory function include skeletal ranges from alterations in the sympathetic–parasympa-
muscle weakness and paralysis. They result from lesions thetic balance to almost complete cessation of activity
in the voluntary motor and sensory pathways, including as occurs in spinal cord injury. As the ANS controls
the upper motor and sensory neurons of the corticospinal organ function autonomic nerve dysfunction is related
and corticobulbar tracts, or the lower motor and sensory to all-organ alteration and failure. The immune system is
neurons that leave the central nervous system (CNS) and connected to the nervous system through the ANS with
travel by way of the peripheral nerves to the muscle and many patients with infections, systemic inflammatory
sensory receptors. response and multi-organ failure exhibiting autonomic
Muscle tone, which is a necessary component of muscle nerve dysfunction. Autonomic nerve dysfunction is
movement, is a function of the muscle spindle (myotatic) assessed by time and spectral domain heart rate variabil-
system and the extrapyramidal system, which monitors ity and is currently being researched as a neurological
and buffers input to the lower motor neurons by way of assessment technique.11
the multisynaptic pathways.8 Upper motor neuron lesions
produce spastic paralysis, and lower motor neuron lesions Alterations in cerebral metabolism
produce flaccid paralysis. Damage to the upper motor and and perfusion
sensory neurons of the corticospinal, corticobulbar and Neuronal cell death occurs in both high and low
spinothalamic tracts is a common component of stroke.9 oxygenated states during injury. Cerebral metabolism and
Polyneuropathies involve multiple peripheral nerves and perfusion are compromised by diverse injury processes
produce symmetrical sensory, motor and mixed sensori- and biochemical patterns of ischaemia and mitochondrial
motor deficits: dysfunction, forming the basis of secondary brain injury
• Lesions of the corticospinal and corticobulbar processes.12
tracts result in weakness or total paralysis of
predominantly distal voluntary movement, Babinski’s Cerebral ischaemia and mitochondrial
sign (i.e. dorsiflexion of the big toe and fanning dysfunction
of the other toes in response to stroking the outer Ischaemia is the inadequate delivery of oxygen, the
border of the foot from heel to toe) and often inadequate removal of carbon dioxide from the cell and
spasticity (increased muscle tone and exaggerated an increase in the production of intracellular lactic acid.
deep tendon reflexes). Ischaemia can be caused by an increase in nutrient util-
• Disorders of the basal ganglia (extrapyramidal isation by the brain in a hyperactive state, a decrease in
disorders) do not cause weakness or reflex changes. delivery related to either cerebral or systemic complica-
Their hallmark is involuntary movement (dyskinesia), tions and/or a mismatch between delivery and demand.13
causing increased movement (hyperkinesias) or The ischaemic cascade is described in Figure 17.1.
decreased movement (hypokinesia) and changes in Inflammation together with oxidative stress, excitotox-
muscle tone and posture. icity, failure of ionic homeostasis including disrupted
• Cerebellar disorders cause abnormalities in the range, calcium, sodium and potassium homeostasis and energy
rate and force of movement. Strength is minimally failure are the key pathological changes in ischaemic brain
affected. damage.14 There is a significant inflammatory response
in the ischaemic brain with significant changes in the
Autonomic nerve dysfunction peripheral immune system.15 When cerebral blood flow
Dysfunctions of the autonomic nervous system (ANS) or (CBF) falls to about 40% of normal, EEG slowing occurs.
autonomic dysreflexia are recognised by the symptoms When CBF falls below 10 mL/100 g/min (20%), the
that result from failure or imbalance of the sympathetic function of ionic pumps fails, which leads to membrane
or parasympathetic components of the ANS such as: 1) depolarisation. Cerebral ischaemia and reperfusion injury
increased (>120/min) or decreased (<50/min) heart rate, contribute to the cascade of physiological events that is
2) increased respiratory rate (>24/min), 3) raised tempera- termed secondary brain injury.16
ture (>38.5°C), 4) increased (>160 mmHg) or decreased Mitochondrial dysfunction occurs in the secondary
(<85 mmHg) systolic blood pressure, 5) increased muscle phase of brain injury and is often associated with normal
tone, 6) decerebrate (extensor) or decorticate (flexor) oxygen levels after reperfusion in the brain. Mitochondria
posturing and 7) profuse sweating. For example, in spinal are sensitive to the high levels of free glutamate that are
injury the presence of a noxious stimulus can be transmit- the product of injury and reperfusion. Free calcium and
ted from the periphery to the spinal cord and activate a nitrous oxide promote excessive production of reactive
dysfunctional sympathetic response. oxygen species and mitochondrial membrane perme-
There are numerous interactions among the CNS, ability. Degradation of deoxyribonucleic acid and essential
peripheral nervous system (both sympathetic and proteins follows and results in neuronal cell death.17
 CHAPTER 17 NEUROLOGICAL ALTERATIONS AND MANAGEMENT 549

FIGURE 17.1 Ischaemic cascade. In cerebral ischaemia, energy failure causes depolarisation of the neuronal
membrane, and excitatory neurotransmitters such as glutamate are released together. A marked influx of Ca2+ into
neurons then occurs, which provokes the enzymatic process leading to irreversible neuronal injury. Inflammation is
also a contributing factor in the development of ischaemic damage.

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Cerebral oedema The cause of cytotoxic oedema, also termed intracellular

Cerebral oedema is defined as increased brain water oedema, is anoxia and ischaemia; it is usually not clinically
content. The brain is particularly susceptible to injury significant, and is reversible in its early phases.
from oedema because of its confined space and limitation Vasogenic oedema
of expansion. There are no lymphatic pathways within
the CNS to carry away the fluid that accumulates. The Vasogenic oedema, sometimes termed extracellular
Monro–Kellie hypothesis states that the contents of the oedema, involves increased capillary permeability, and
cranium, which is about 80% brain tissue, 10% blood and had been termed ‘BBB breakdown’.20 Rises in brain
10% cerebral spinal fluid (CSF), are incompressible and water content with extracellular oedema are often quite
thus an increase in volume in one of the components dramatic because the fluid that results from increased
without a corresponding decrease in another component capillary permeability is usually rich in proteins, resulting
causes a rise in pressure.18 After brain injury, alterations in the spread of oedema and brain ischaemia.This can lead
in ionic gradients lead to a stepwise progression from to cytotoxic oedema, and to the progressive breakdown
what is known as cytotoxic (cellular) oedema to ionic of both astrocytes and neurons.19 While the classifica-
oedema, and finally to vasogenic oedema. Ischaemia tion of oedema is useful to define specific treatments, it
leads to the cessation of primary active transport via is somewhat arbitrary, as cytotoxic and vasogenic oedema
the sodium–potassium pump. As a result co-transporters often occur concurrently. In fact, each of these processes
(secondary active transport) and passive transporters (via may cause the other. Ultimately, these changes can lead to
ion channels) attempt to maintain cellular processes.19 raised intracranial pressure (ICP) and herniation.
By doing so, neurons and neuroglia accumulate active Interstitial oedema
solutes that cause cellular swelling and eventually passage
of fluid into the extracellular space. The primary basis Interstitial oedema occurs as a result of hydrocephalus,
for the formation of cytotoxic oedema is the intracellu- when the pressure within the ventricles is higher than the
lar accumulation of sodium. Eventually, endothelial and capacity of the ependymal cells to confine the CSF within
neuroglial dysfunction impairs the ability to maintain the ventricles. The ventricular ependymal lining ruptures
the integrity of the blood–brain barrier and vasogenic allowing CSF into the extracellular space, most commonly
oedema ensues. Historical conventions that charac- the periventricular white matter. Various causes of inter-
terise oedematous states into ‘cytotoxic’ or ‘vasogenic’ stitial oedema include obstructing masses, meningitis,
categories are fading, as a better understanding of subarachnoid hemorrhage and normal pressure hydro-
the pathophysiological processes that underlie oedema cephalus.21
formation in brain-injured states develop.
Hydrocephalus
Cytotoxic oedema Hydrocephalus is the result of an imbalance between
Cellular swelling, usually of astrocytes in the grey matter, the formation and drainage of CSF. Reduced absorption
is generally seen after cerebral ischaemia caused by cardiac most often occurs when one or more passages connecting
arrest or minor head injury.19 The blood–brain barrier the ventricles become blocked, preventing movement of
(BBB) is intact and capillary permeability is not impaired. CSF to its drainage sites in the subarachnoid space just
550 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

inside the skull.21 This type of hydrocephalus is called surgical shunt for those with chronic conditions. Either is
‘non-communicating’. Reduction in absorption rate, predisposed to blockage and infection.
called ‘communicating hydrocephalus’, can be caused by
damage to the absorptive tissue. Both types lead to an Intracranial hypertension
elevation of the CSF pressure in the brain. A third type of ICP is the pressure exerted by the contents of the brain
hydrocephalus, ‘normal pressure hydrocephalus’, is marked within the confines of the skull and the BBB. ICP incurs
by ventricle enlargement without an apparent rise in CSF changes to the compensatory reserve and pulse amplitude,
pressure, which mainly affects the elderly. The presenting as illustrated in Figure 17.2.23 Normal ICP is 0–10 mmHg,
symptoms are cognitive decline, gait disturbances and and a sustained pressure of >15 mmHg is termed intra-
urinary incontinence. cranial hypertension, with implications for CBF.24 Areas
Hydrocephalus may be caused by congenital brain of reduced CBF and focal ischaemia appear when ICP is
defects, haemorrhage in either the ventricles or the >20 mmHg and global ischaemia occurs at >50 mmHg.
subarachnoid space, CNS infection (syphilis, herpes, The ICP waveform contains valuable information about
meningitis, encephalitis or mumps) or tumours. Irritability the nature of cerebrospinal pathophysiology. Both auto-
is the commonest sign of hydrocephalus in infants and, if regulation of CBF and compliance of the cerebrospinal
untreated, may lead to lethargy. Bulging of the fontanelle, system are reflected in the ICP waveform.25 Waveform
the soft spot between the skull bones, may also be an early analysis of ICP is described in Chapter 16.
sign. Hydrocephalus in infants prevents fusion of the skull Initially, intracranial compliance allows compensation
bones, and causes expansion of the skull. Symptoms of for rises in intracranial volume due to autoregulation.
normal pressure hydrocephalus include dementia, gait During a slow continuous rise in volume, the ICP rises
abnormalities and incontinence.22 Treatment includes to a plateau level at which the increased level of CSF
ventriculostomy drainage of CSF in the short term or a absorption keeps pace with the rise in volume with

FIGURE 17.2 The volume–ICP curve relationship.

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Adapted from McLeod A. Traumatic injuries to the head and spine, 2: nursing considerations. Br J Nurs 2004;13(17):1041–9, with
permission.
 CHAPTER 17 NEUROLOGICAL ALTERATIONS AND MANAGEMENT 551

ample compensatory reserve. This is expressed as an with upper medulla involvement, with ataxic breathing in
index, as shown in Figure 17.3.26 Intermittent expansion the final stages (see Figure 17.4).27
causes only a transient rise in ICP at first.When sufficient Often, neurogenic pulmonary oedema may occur due
CSF has been absorbed to accommodate the volume, the to increased sympathetic activity as a result of the effects
ICP returns to normal. The ICP finally rises to the level of elevated ICP on the hypothalamus, medulla or cervical
of arterial pressure, which itself begins to rise, accom- spinal cord. The causes of intracranial hypertension are
panied by bradycardia or other disturbances of heart classified as acute or chronic. Acute causes include brain
rhythm, termed the Cushing’s response. This is accom- trauma, ischaemic injury and intracerebral haemorrhage.
panied by dilation of the small pial arteries and some Infections such as encephalitis or meningitis may also
slowing of venous flow, which is followed by pulsatile lead to intracranial hypertension. Chronic causes include
venous flow. many intracranial tumours, such as ependymomas, or
The respiratory changes associated with increased ICP subdural bleeding that may gradually impinge on CSF
depend on the level of brainstem involved. A midbrain pathways and interfere with CSF outflow and circula-
involvement results in Cheyne-Stokes respiration. When tion. As the ICP continues to increase, the brain tissue
the midbrain and pons are involved, there is sustained becomes distorted, leading to herniation and additional
hyperventilation. There are rapid and shallow respirations vascular injury.28

FIGURE 17.3 In a simple model, pulse amplitude of intracranial pressure (ICP) (expressed along the y-axis on the
right side of the panel) results from pulsatile changes in cerebral blood volume (expressed along the x-axis) transformed
by the pressure–volume curve. This curve has three zones: a flat zone, expressing good compensatory reserve; an
exponential zone, depicting poor compensatory reserve; and a flat zone again, seen at very high ICP (above the
‘critical’ ICP), depicting derangement of normal cerebrovascular responses. The pulse amplitude of ICP is low and
does not depend on mean ICP in the first zone. The pulse amplitude increases linearly with mean ICP in the zone of
poor compensatory reserve. In the third zone, the pulse amplitude starts to decrease with rising ICP. RAP = index
of compensatory reserve.

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Adapted from Czosnyka M, Pickard J. Monitoring and interpretation of intracranial pressure. J Neurol Neurosurg Psychiat 2004;75(6):
813–21, with permission.
552 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

FIGURE 17.4 Injury to the brainstem can result in various abnormal respiratory patterns.27

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Neurological therapeutic in which secondary brain injury may occur, and some
studies suggest that PbtO2 complements ICP monitoring.
management Episodes of brain hypoxia are common and may occur
even when ICP and cerebral perfusion pressure (CPP) are
This section explores cerebral perfusion, oxygenation and normal,30 emphasising the potential value of multimodal
assessment. The objective of assessment is to identify and monitoring that integrates data from several physiolog-
then initiate strategies in an attempt to prevent secondary ical monitors. A strong relationship is observed between
insults and ischaemia. ICP monitoring is discussed in PbtO2 and several drivers of brain perfusion, such as mean
terms of therapeutic management. arterial pressure, CPP and end-tidal CO2.31 This observa-
Optimising cerebral perfusion and tion can help clinicians to better understand the complex
pathophysiology of the brain after an acute insult, evaluate
oxygenation autoregulation and identify optimal physiological targets
Intracranial hypertension and cerebral ischaemia are the and the utility of therapeutic interventions. The selection
two most important secondary injury processes that can among these forms of oxygenation monitoring is focused
be anticipated, monitored and treated in the ICU. This on the appropriateness of focal or global monitoring, the
applies to all aetiologies of brain injury including trauma. location of the monitor in relation to the injury and the
This section discusses the modalities of neuroprotection, intermittent or continuous nature of the monitoring.
including the management of intracranial hypertension, Jugular venous oxygen saturation (SjO2) is representa-
vasospasm and cerebral ischaemia. Nursing interventions tive of global cerebral oxygen metabolism, but technically
for the prevention of secondary insults and promotion of it is difficult to obtain reproducible results. Cerebral
cerebral perfusion are described in Table 17.1. Importantly, tissue oxygenation values of <20 mmHg are targeted for
the aims of nursing management are based on published intervention based on Brain Trauma Foundation (BTF)
guidelines and are directed at optimising cerebral perfusion guidelines but this is based on lower quality evidence.32
and metabolism by various initiatives. PbtO2 can be increased by increasing the FiO2/PaO2
ratio and by reducing cerebral metabolic requirements for
Management of cerebral oxygenation oxygen (CMRO2) using brain temperature control with
active cooling and metabolic rate control with sedation
and perfusion and adequate feeding. Additional interventions such
Cerebral monitoring in brain-injured patients has focused as volume infusion, transfusion and inotropic support
on the prevention of secondary injury to the brain. There directed at improving cardiac output can also be used to
are currently four techniques that can be used to assess increase oxygen delivery.33
cerebral oxygenation: jugular venous oxygen saturation, Cerebral microdialysis has been used extensively in
positron emission tomography, near-infrared spectroscopy traumatic brain injury, measuring concentrations reflecting
and brain tissue oxygenation (PbtO2) monitoring.29 Brain biochemical changes in the brain after injury.33 Cerebral
oxygen monitoring is useful in a variety of clinical situations microdialysis measurements are focused on metabolites
 CHAPTER 17 NEUROLOGICAL ALTERATIONS AND MANAGEMENT 553

TABLE 17.1
Nursing interventions for the promotion of cerebral perfusion in acute brain injury

AIM GOAL INTERVENTIONS

Maintain oxygenation SaO2 98%, PaO2 100 mmHg, • Maintain airway

PaO2/FiO2 ratio >350 • Use 100% O2 during initial resuscitation phase
PbtO2 >20 • Intubate as soon as possible for Glasgow Coma Scale <8 or
diaphragmatic respiratory insufficiency (C-spine number)
• Obtain arterial blood gas and manipulate set FiO2 to meet parameter
goal
• Suction patient as needed
• Consider need for kinetic therapy, e.g. rotation/percussion therapy
bed within spinal precautions. Use frequent subglottal suctioning,
and maintain head of bed elevation at 30° or more to prevent VAP
• In recovery: assess for upper airway weakness and reflex (prevent
aspiration), sputum retention and atelectasis
Maintain PaCO2 PaCO2 35–40 mmHg • ABG assessment
• Adjust ventilator settings to obtain PaCO2 of 35–40 mmHg
• Ensure optimal PaCO2 for your patient: observe PbtO2 and ICP during
manipulation of PaCO2
• Monitor end-tidal CO2 continuously
• Observe for hypoventilation
Maintain mean MAP 90 mmHg • Maintain euvolaemia
arterial pressure • Give IV volume as prescribed to maintain CVP and PCWP within
(MAP) parameters
• Use noradrenaline once euvolaemic in order to optimise MAP
• Observe PbtO2 for sedation-induced hypotension
• Transfuse to haematocrit of 33% or haemoglobin content 80–100 g/L
• Stroke: thrombolytic, embolic and ICH, MAP 90–120 mmHg with
modest reduction and CPP ≥60 mmHg
Maintain cerebral CPP 50–70 mmHg • Effectively reduce ICP while preserving or improving CPP
perfusion pressure • Position body with neck straight and no knee elevation in order to
50–70 mmHg maintain venous outflow
• Make sure cervical collar and endotracheal tube ties are not too tight,
especially behind the neck
• If patient has a ventriculostomy, drain per prescription
Maintain intracranial ICP <20 mmHg • Elevate head of bed above the level of the heart to obtain optimal
pressure (CP) level of ICP and CPP. Monitor ICP, CPP and PbtO2 to ensure optimal
<20 mmHg level for your patient (15–30°)
• Sedate using propofol, morphine, fentanyl and/or lorazepam/
midazolam
• Hypertonic saline prescription
or
• Mannitol prescription at 0.25–1.0 g/kg IV for ICP sustained at
<20 mmHg (watch serum osmolality and consider holding for values
>320 mOsmol/kg)
• Consider paralytics if positioning, cooling, sedation and mannitol
does not resolve increased ICP
• Maintain the brain temperatures at 36–37°C, using cooling measures;
prevent shivering (increases cerebral metabolic demands)
• Prepare for surgical craniotomy if indicated
Maintain SjO2 50–75% • Group necessary interventions in a timely manner to allow for rest
environment/reduce PbtO2 >20 periods
stimulation • Screen visitors
• Minimise noise and lighting
• Avoid stimulation and prioritise interventions if ICP precarious
• Sedation as prescribed
554 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 17.1 continued

AIM GOAL INTERVENTIONS

Maintain cerebral PbtO2 <20 • Optimise CPP to prescribed levels (60–70 mmHg)
blood flow • Optimise PaCO2 as indicated to increase CBF
• Optimise sedation and consider paralytics
• Consider barbiturate prescription if above measures are not
successful
• PaO2/FiO2 ratio >350
• Maintain CVP of 5–10 mmHg, and a PCWP of 10–15 mmHg
• Administer normal saline and/or colloids as prescribed to maintain
parameters
• Transfuse to haematocrit of 33% or haemoglobin content 80–100 g/L
(prescription to correct coagulopathies)
• Monitor closely for signs and symptoms of neurogenic pulmonary
oedema, especially in patients with cardiac history
• Maintenance of brain temperature at 36–37°C, with active cooling if
necessary
• Transcranial Doppler image to check for vasospasm
• Non-traumatic aSAH, administer IV nimodipine infusion to prevent
vasospasm as prescribed; consider components of HH therapy
• Ischaemic stroke, administer tPA within 3 hours of event
• ICH, prevent rebleeding; administer prescribed haemostatic
medications, reduce hypertension
Maintain nutrition • Ensure early enteric feeding
• Oral enteric feeding tube (nasogastric contradicted in TBI)
• Dietitian referral for metabolic requirements

ABG = arterial blood gas; aSAH = aneurysmal subarachnoid haemorrhage; CBF = cerebral blood flow; CPP = cerebral perfusion
pressure; CVP = central venous pressure; FiO2 = fraction of inspired oxygen; HH = hypervolaemic hypertensive; ICH = intracerebral
haemorrhage; ICP = intracranial pressure; IV = intravenous; MAP = mean arterial pressure; PaCO2 = partial pressure of alveolar
carbon dioxide; PaO2 = partial pressure of alveolar oxygen; PbtO2 = brain tissue oxygenation; PCWP = pulmonary capillary wedge
pressure; SaO2 = arterial oxygen saturation; SjO2 = jugular venous oxygen saturation; TBI = traumatic brain injury; tPa = tissue
plasminogen activator; VAP = ventilator-associated pneumonia.

(glucose, lactate, pyruvate) and neurotransmitters (acetyl- Management of intracranial hypertension

choline, dopamine, glutamate) and certain ions (Ca2+, K+, Raised ICP is treated by removing mass lesions and/or
Na+). Cerebral microdialysis glucose levels are reduced in increasing the volume available for expansion of injured
patients with severe TBI, and consistently low concentra- tissue. This may be achieved by reducing one of the other
tions (<0.66 mmol/L) are associated with poor outcome. available intracranial fluid volumes:
Similarly, reduced cerebral microdialysis glucose, including
1 CSF by ventricular drainage (as discussed previously)
that associated with intensive insulin therapy, is associated
2 cerebral blood volume by hyperventilation, osmotic
with mortality in aneurysmal subarachnoid haemor-
rhage (aSAH). Very low brain glucose may be observed diuretic therapy or hypothermia
during severe hypoxia or ischaemia after TBI and aSAH. 3 brain tissue water content by osmotic diuretic therapy
However, the determinants of cerebral microdialysis 4 removing swollen and irreversibly injured brain
glucose concentration are complex, and in some patients 5 increasing cranial volume by craniotomy
a reduced cerebral microdialysis glucose may result from a decompression.
large increase in glucose consumption rather than reduced The application of these concepts to the following
supply of glucose and oxygen. therapeutic strategies is important in the management of
intracranial hypertension.34
Practice tip
Practice tip
Cerebral perfusion pressure (CPP) = mean arterial
pressure (MAP) − ICP. So, if ICP is increased (common In brain injury, position the patient at 45° head-up to
in moderate/severe TBI), MAP must be increased to maximise the balance between cerebral perfusion and
maintain CPP. minimise cerebral oedema.
 CHAPTER 17 NEUROLOGICAL ALTERATIONS AND MANAGEMENT 555

Hyperventilation in 40–70% of patients with severe TBI or aneurysmal

Hyperventilation reduces PaCO2 and will reduce ICP by subarachnoid haemorrhage. Hyperthermia is inde-
vasoconstriction induced by alkalosis, but it also decreases pendently associated with increased morbidity and
CBF.35 The fall in ICP parallels the fall in cerebral blood mortality after ischaemic and haemorrhagic stroke and, in
volume. Hyperventilation decreases regional blood flow subarachnoid haemorrhage and TBI patients, temperature
to hypoperfused areas of the brain. Thus, generally PaCO2 elevation has been linked to raised intracranial pressure.40
should be maintained in the low normal range of about Temperature elevations as small as 1–2°C above normal
35 mmHg. Hyperventilation should be utilised only when can aggravate ischaemic neuronal injury and exacerbate
ICP elevations are refractory to other methods and when brain oedema.41 Mild hypothermia protects numerous
brain tissue oxygenation is in the normal range.36 The BTF tissues from damage during ischaemic insult. The use
Guidelines recommend hyperventilation therapy only for of paracetamol, cooling blankets, ice packs, evaporative
brief periods when there is no neurological deterioration or cooling and new cooling technologies may be useful in
for longer periods when ICP is refractory to other therapies maintaining normothermia. Hyperaemia (increased blood
and not within the acute phase (i.e. 24–48 hours).32 flow) may occur during rewarming, resulting in acute
brain swelling and rebound intracranial hypertension.42
Osmotherapy Maintenance of body temperature at 35°C may be
Acute administration of an osmotic such as mannitol or optimal.43 Intracranial pressure falls significantly at brain
hypertonic saline produces a potent anti-oedema action, temperatures below 37°C but no difference was observed at
primarily on undamaged brain regions with an intact temperatures below 35°C. Cerebral perfusion pressure peaks
BBB. This treatment causes the movement of water from at 35–36°C and decreases with further falls in temperature.44
the interstitial and extracellular space into the intravascular At temperatures below 35°C, both oxygen delivery and
compartment, thereby improving intracranial compliance oxygen consumption decrease. Cardiac output decreases
or elastance. In addition to causing ‘dehydration’ of the progressively with hypothermia.45 Therefore, cooling to
brain, osmotic agents have been shown to exert beneficial 35°C may reduce intracranial hypertension and maintain
non-osmotic cerebral effects, such as augmentation of sufficient CPP without associated cardiac dysfunction or
CBF (by reducing blood viscosity, resulting in enhanced oxygen debt.46 As the temperature is lowered from 34°C to
oxygen delivery), free radical scavenging and diminishing 31°C, the volume of IV fluid infusion and inotrope require-
CSF formation and enhancing CSF reabsorption.37 ments increase substantially and, despite such interventions,
Intravenous hypertonic saline increases cerebral mean arterial pressure decreases. At 31°C serum potassium,
perfusion and decreases brain swelling and inflammation white blood cell count and platelet counts are diminished.47
more effectively than conventional resuscitation fluids. Thus, it seems that hypothermia to 35°C may be optimal.
Hypertonic saline behaves like 20% mannitol in acute
cerebral oedema but maintains haemodynamic status. Corticosteroids
However, unlike hypertonic saline, mannitol induces a Excessive inflammation has been implicated in the progres-
diuresis, which is relatively contraindicated in patients with sive neurodegeneration that occurs in multiple neurological
both TBI and hypovolaemia as it may worsen intravascu- diseases, including cerebral ischaemia.The efficacy of gluco-
lar volume depletion and decrease cerebral perfusion.38 corticoids is well established in ameliorating oedema
A systemic review found that hypertonic saline given as associated with brain tumours and in improving the
either a bolus or continuous infusion can be more effective outcome in subsets of patients with bacterial meningitis.
than mannitol in reducing episodes of elevated ICP.39 Despite encouraging experimental results, clinical trials of
The BTF has recommended that therapy to reduce glucocorticoids in ischaemic stroke, intracerebral haemor-
ICP should begin at pressures >20 mmHg. The recom- rhage, aneurysmal subarachnoid haemorrhage and traumatic
mendation of the use of hypertonic saline therapy over brain injury have not shown a definite therapeutic effect.
mannitol lies in the fact the hypertonic saline pulls water Furthermore, the CRASH (corticosteroid randomisation
intravascularly, increasing blood pressure and maintain- after significant head injury) trial reported that risk of death
ing cerebral perfusion. Mannitol has the unfortunate was higher in the treatment group than in the control group
result of diuresis and potential decrease in blood pressure, (26% vs 22%; p<0·0001).48 Thus, high-dose steroids are not
decreasing cerebral perfusion pressure. Current BTF indicated for use in severe traumatic brain injury. However,
guidelines show that reasonably good quality evidence anterior pituitary insufficiency is an under-recognised
exists to avoid hypotension (systolic blood pressure [SBP] problem in patients with severe traumatic brain injury,
<90 mmHg). The BTF refers to mannitol as the mainstay particularly in elderly people or those who have diffuse
of treatment in the management of intracranial hyper- axonal injury and skull base fracture. In these instances,
tension, but hypertonic saline is the preferred option since administration of hydrocortisone in physiological doses and
the guidelines were developed. endocrine follow-up are indicated.
Normothermia Barbiturates and sedatives
Hyperthermia occurs in up to 40% of patients with The BTF Guidelines state that high-dose barbiturate therapy
ischaemic stroke and intracerebral haemorrhage and may be considered in haemodynamically-salvageable severe
556 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TBI patients with intracranial hypertension refractory to total score or one of its individual components [eye, motor
maximal medical and surgical interventions.49 The util- on either side, verbal]). This should last for at least 1 hour,
isation of barbiturates for the prophylactic treatment of and is not apparent immediately after aneurysm occlusion
ICP has not been indicated. Barbiturates exert cerebral and cannot be attributed to other causes by means of
protective and ICP-lowering effects through alteration in clinical assessments, cerebral CT or MRI scanning, and
vascular tone, suppression of metabolism and inhibition of appropriate laboratory studies.54 It occurs in about 30% of
free radical-mediated lipid peroxidation. Barbiturates may patients surviving the initial haemorrhage, mostly between
effectively lower CBF and regional metabolic demands. days 4 and 10 after aSAH. The known clinical symptoms,
The lower metabolic requirements decrease CBF and such as decrease in the level of consciousness and focal
cerebral volume. This results in beneficial effects on ICP signs such as aphasia and hemiparesis, may be reversible
and global cerebral perfusion. The BTF Guidelines for or otherwise progress to cerebral infarction resulting in an
barbiturates are included under the heading of ‘Anaesthet- unfavourable outcome or even death. Clinical deteriora-
ics, analgesics and sedatives’. These guidelines recommend tion attributable to delayed cerebral ischaemia is a diagnosis
that barbiturates are beneficial to minimise painful or after exclusion of other causes (such as infection, hypoten-
noxious stimuli as well as agitation as they may poten- sion, hyponatraemia and others), and it is especially difficult
tially contribute to elevations in ICP. Therefore, propofol to diagnose in patients who are comatose or sedated.55
is recommended for the control of ICP, but does not The latter are typically patients with a high grade on the
improve mortality or 6-month outcome.49 World Federation of Neurosurgical Societies scale (grade
4–5), which represent approximately 40–70% of the patient
Surgical interventions population with ruptured aneurysms.56 Early brain injury
The European TBI Guidelines suggest that operative and cell death, blood–brain barrier disruption and initiation
management be considered for large intracerebral lesions of an inflammatory cascade, microvascular spasm, micro-
within the first 4 hours of injury. The use of unilateral thrombosis, cortical spreading depolarisations and failure
craniectomy after the evacuation of a mass lesion, such as of cerebral autoregulation have all been implicated in the
an acute subdural haematoma or traumatic intracerebral pathophysiology of delayed cerebral ischaemia.
haematoma, is accepted practice. Surgery is also recom- Cerebral vasospasm is a self-limited vasculopathy that
mended for open compound depressed skull fractures that develops 4–21 days after aSAH and/or TBI (see Figure
cause a mass effect.50 Mass effect on CT scan is defined 17.6 later). Oxyhaemoglobin, a product of haemoglo-
as distortion, dislocation or obliteration of the fourth bin (Hb) breakdown, probably initiates vasoconstriction,
ventricle; compression or loss of visualisation of the basal leading to smooth-muscle proliferation, collagen remodel-
cisterns or the presence of obstructive hydrocephalus. ling and cellular infiltration of the vessel wall.The resulting
Decompressive craniectomy for refractory intracra- vessel narrowing can lead to delayed cerebral ischaemia.
nial hypertension has been performed since 1977, with a The initial pro-inflammatory effect elicited by Hb and
significant reduction in ICP for both TBI50 and ischaemic Hb-bound cells initiates an inflammatory cascade and
stroke.51 In 2011 a multicentre trial of early decompressive cortical spreading depolarisation involving an increase of
craniectomy in patients with severe TBI, called DECRA, cytokines, leukocytes and cell adhesion molecules charac-
reported that, in adults with severe diffuse traumatic terising the inflammatory process.The symptoms are poorly
brain injury and refractory intracranial hypertension, an localised and develop gradually over hours, suggesting a
early bifrontotemporoparietal decompressive craniectomy progressing, global disease process. aSAH patients develop
decreased ICP and the length of stay in the ICU but was cerebral vasospasm, and about one-third develop symptom-
associated with more unfavorable outcomes at both 6 atic vasospasm, which is associated with neurological signs
and 12 months.52 This finding has resulted in controversy and symptoms of ischaemia. Post TBI cerebral vasospasm
about the technique, timing and selection of patients for occurs in approximately 10–15% of patients.
decompressive craniectomy. The randomised evaluation Calcium antagonists, such as nimodipine, have not
of surgery with craniectomy for uncontrollable elevation been effective in TBI subarachnoid haemorrhage with
of intracranial pressure (RESCUEicp) trial is a continuing vasospasm, and studies have suggested that calcium antag-
randomised trial of decompressive craniectomy.53 This onists even prevent neurogenesis after TBI. Nimodipine has
trial has a higher intracranial pressure threshold for demonstrated effectiveness in the treatment of vasospasm
decompressive craniectomy than did the DECRA trial, in aSAH and is now the only drug for which high quality
and includes patients with mass lesions and unilateral or evidence exists, reducing the incidence of delayed cerebral
bilateral decompressive craniectomy. ischaemia and poor outcome by 40%, without ameliorat-
ing vasospasm. An initial study of nimodipine in patients
Prevention of delayed cerebral with TBI demonstrated no difference in outcome, and a
ischaemia and cerebral vasospasm Cochrane systematic review supports this conclusion.57
Delayed cerebral ischaemia is defined as the occurrence of In aSAH, the outdated ‘Triple H’ therapy (hypervolae-
focal neurological impairment (such as hemiparesis, aphasia, mia, hypertension, haemodilution) was aimed at increasing
apraxia, hemianopia or neglect) or a decrease of at least cerebral perfusion. Despite its widespread use as a mainstay
2 points on the Glasgow Coma Scale (GCS) (either on the therapy for cerebral vasospasm, there are no randomised
 CHAPTER 17 NEUROLOGICAL ALTERATIONS AND MANAGEMENT 557

controlled trials to support the intervention. While no are 13 million people living with TBI-related disability in
benefit was shown for cerebral vasospasm, CBF or clinical the USA and the European Union.59 An Australian and
outcome, clinical studies revealed that hypervolaemia New Zealand epidemiological study of TBI67 found that
resulted in pulmonary oedema, as well as haemodilu- the mean age was 41.6 years; 74% were men; 61% were
tion, and with it a decrease in arterial oxygen and oxygen due to vehicular trauma, 24% were falls in elderly patients
carrying capacity. Anaemia has been associated with a and 57% had severe TBI (Glasgow Coma Scale score ≤8).
worse outcome after aSAH. These studies achieved the Twelve-month mortality was 26% in all patients and 35%
elimination of haemodilution from ‘Triple-H’ therapy and in patients with severe TBI.
a change from hypervolaemia target to euvolaemia. These
changes, along with the established hypertensive therapy, Aetiology of TBI
are the mainstays in clinical practice as recommended in Falls are the leading cause of TBI among all age groups
the Neurocritical Care Society aSAH guidelines.58 (35.2%), followed by motor vehicle collisions or traffic
In aSAH, endovascular therapies should be considered accidents (17.3%), being struck by/against an object
in patients at risk for vasospasm-related ischaemia prior (16.5%) and assaults (10%).64,68 However, causes of TBI
to the development of delayed cerebral ischaemia. The fatalities are slightly different. Among all causes of injury,
literature on this intervention is limited to only a few road traffic accidents lead to the most TBI fatalities
prospective studies. Prophylactic angioplasty done without (31.6%). As another example, the lethality of gunshot
the presence of angiographic arterial narrowing exposes wounds to the head is approximately 90%. Because of
patients to risk of vessel rupture and death without clear this, gunshot wounds are a much higher percentage of
benefit in outcome.58 Thus, routine prophylactic cerebral TBI fatalities than the overall incidence would suggest.69
angioplasty is not recommended in the Neurocritical Sporting accidents and falls account for a far greater
Care Society aSAH guidelines. percentage of mild injuries. Infants and toddlers up to
4 years of age, older adolescents aged 15–19 years and adults
older than 65 years of age are the highest risk age groups
Central nervous system for TBI.70 This trimodal distribution has been demon-
disorders strated for most ethnic and racial groups studied, as well as
in global studies of TBI.64 Most studies have found that the
CNS disorders include brain and/or spinal injury from highest age-specific incidence is in the young adult years.
trauma, infection or immune conditions. The pathophys- Injury and debility in this age group also carries signif-
iology and aetiology of these disorders are discussed here, icant morbidity, with many more years of potential life
including management of these conditions. lost and lost productivity for injuries incurred in young
people. For every age group studied, males are more likely
Traumatic brain injury to suffer TBI than females. Among young people, males
Head injury is a broad classification that includes injury are up to seven times more likely to suffer a TBI. People of
to the scalp, skull or brain. TBI is the most serious form colour and those of lower socioeconomic strata also suffer
of head injury. The range of severity of TBI is broad, from rates of TBI 30% to 50% higher than majority individuals.
concussion through to post coma unresponsiveness. The Alcohol is involved in 50% of cases of TBI, either because
incidence rates of TBI are increasing worldwide, though of intoxicated drivers or pedestrians, increased risk of falls,
estimates vary considerably between countries.59 In the suicide attempts or interpersonal violence.64,67
USA, rates of TBI-related hospitalisations and emergency The transfer of energy to the brain tissue actually
department visits were approximately 90 per 100,000 causes the damage and is a significant determinant in the
population and 715 per 100,000 population, respectively, severity of injury. In the past 10 years, the introduction of
in 2010.60 A systematic review of studies from 23 European safer car designs, airbags and other road traffic initiatives
countries reported an overall average TBI incidence (e.g. redesigning hazardous intersections, driver education
rate range of 150–300 per 100,000 population.61 This is campaigns, random breath testing and reducing speed
comparable to the 2004/5 Australian age-standardised limits) have decreased the overall number of road fatalities;
incidence rate of about 150 per 100,000 population.62,63 improvements in retrieval, neurosurgery and intensive
Reviewers of the global literature agree that the incidence care in the past few decades have enabled many people to
of TBI is highest in countries of low to middle income.59, 64 survive injuries that would previously have been fatal.66,67
Males have a higher incidence of TBI across all age groups
in all regions61,65,66 with the highest rates reported in those Pathophysiology of TBI
aged 15–25 years. Rates in older populations (over 65 TBI is a heterogeneous pathophysiological process (see
years) are increasing65,66 and this group is at highest risk of Figure 17.5). The mechanisms of injury forces inflicted
TBI. In the very young (0–4 years),TBI rates have declined on the head in TBI produce a complex mixture of
significantly over the past decade. Quality outcome data diffuse and focal lesions within the brain.71 Damage
from long-term follow-up of TBI cohorts are limited but resulting from an injury can be immediate (primary)
physical complaints, disabilities and neuropsychological or secondary in nature. Secondary injury results from
difficulties appear common and it is estimated that there disordered autoregulation and other pathophysiological
558 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

changes within the brain in the days immediately after dysfunction characterised by episodes of increased heart
injury. Urgent neurosurgical intervention for intracere- rate, respiratory rate, temperature, blood pressure, muscle
bral, subdural or extradural haemorrhages can mitigate tone, decorticate or decerebrate posturing and profuse
the extent of secondary injury. Scalp lesions can bleed sweating.74 Lack of insight into these processes and imple-
profusely and quickly lead to hypovolaemic shock and menting early weaning of supportive therapies can lead to
brain ischaemia. Cerebral oedema, haemorrhage and significant secondary insults.
biochemical response to injury, infection and increased
ICP are among the commonest physiological responses Focal injury
that can cause secondary injury. Tissue hypoxia is also of Because of the shape of the inner surface of the skull,
major concern and airway obstruction immediately after focal injuries are most commonly seen in the frontal
injury contributes significantly to secondary injury. Poor and temporal lobes, but they can occur anywhere.
CBF, as a result of direct (primary) vascular changes or Contact phenomena or a local blow to the head or
damage, can lead to ischaemic brain tissue, and eventually the head coming into contact with another item with
neuronal cell death.72 Systemic changes in temperature, force are commonly superficial and can generate contu-
haemodynamics and pulmonary status can also lead to sional haemorrhages through coup and contrecoup
secondary brain injury (Figure 17.6). In moderate-to-se- mechanisms.75 Cerebral contusions are readily identifi-
vere, and occasionally in mild, injury CBF is altered in able on CT scans, but may not be evident on day 1 scans,
the initial 2–3 days, followed by a rebound hyperaemic becoming visible only on days 2 or 3. Deep intracere-
stage (days 4–7) leading to a precarious state (days 8–14) bral haemorrhages can result from either focal or diffuse
of cerebral vessel unpredictability and vasospasm.73 damage to the arteries.
More than 30% of TBI patients have autonomic nerve

FIGURE 17.5 Pathophysiology of traumatic brain injury.

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 CHAPTER 17 NEUROLOGICAL ALTERATIONS AND MANAGEMENT 559

FIGURE 17.6 Conceptual changes in cerebral blood flow and intracranial pressure (ICP) over time following traumatic
brain injury: (A) cytotoxic oedema; (B) vasogenic oedema; (C) cerebral blood flow. CPP = cerebral perfusion pressure;
MAP = mean arterial pressure.

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Diffuse injury
FIGURE 17.7 Extradural haematoma and a subtle
Diffuse (axonal) injury refers to the shearing of axons and subdural haematoma (left), subdural haematoma
supporting neuroglia; it may also traumatise blood vessels (middle left), diffuse axonal injury (middle right) and
and can cause petechial haemorrhages, deep intracerebral combination injuries (right).
haematomas and brain swelling.75 Diffuse injury results from
the shaking,shearing and inertial effects of a traumatic impact.
Mechanical damage to small venules as part of the BBB
can also trigger the for mation of haemorrhagic contusions.
This vascular damage may increase neuronal vulnerability,
causing post-traumatising perfusion deficits and the extra-
vasation of potentially neurotoxic blood-borne substances.
The most consistent effect of diffuse brain damage, even
when mild, is the presence of altered consciousness. The
depth and duration of coma provide the best guide to the dizziness, facial and skull fractures, including the loss
severity of the diffuse damage.The majority of patients with of CSF from the nose or the ear, will categorise those
diffuse injury will not have any CT evidence to support the needing further surveillance. Routine head CT and
diagnosis. Other clinical markers of diffuse injury include assessment of post-traumatic amnesia are recommended to
the high speed or force strength of injury, absence of a lucid exclude mass lesions and diffuse axonal injury. Diagnosis
interval and prolonged retrograde and anterograde amnesia. and management in the acute phase of mild TBI are as
Figure 17.7 contrasts CT scans with haematoma formation crucial to functional outcome and rehabilitation as in
and diffuse axonal injury. moderate-to-severe TBI.76
Mild TBI Skull fractures
Mild TBI often presents as a component of multitrauma Skull fractures are present on CT scans in about two-thirds
or sports injury and can be overlooked at the expense of of patients after TBI. Skull fractures can be linear, depressed
other peripheral injuries. Risk factors such as vomiting, or diastatic, and may involve the cranial vault or skull base.
560 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

In depressed skull fractures the bone fragment may cause (see Table 17.1). Interventions are targeted at maintain-
a laceration of the dura mater, resulting in a cerebrospinal ing adequate CBF and minimising oxygen consumption
fluid leak.73 Basal skull fractures include fractures of the by the brain in order to prevent ischaemia. In a post hoc
cribriform plate, frontal bones, sphenoid bones, temporal analysis of the use of saline in critically ill patients with
bone and occipital bones. The clinical signs of a basal skull TBI, fluid resuscitation with albumin was associated with
fracture may include: CSF otorrhoea or rhinorrhoea, higher mortality rates than was resuscitation with saline.77
haemotympanum or presence of blood in the tympanic The anticipation and prevention of systemic complications
cavity of the middle ear, postauricular ecchymoses, peri- are also crucial. Assessment is vital to establish priorities in
orbital ecchymoses and injury to the cranial nerves – VII care and is discussed in Chapter 16.
(weakness of the face),VIII (loss of hearing), olfactory (loss Nursing management of the neurologically impaired,
of smell), optic (vision loss) and VI (double vision). immobilised, mechanically ventilated patient is described
in Table 17.2 and is an adaptation of the current
Patient management guidelines32 (see Table 17.3) to clinical practice (see Online
The surveillance and prevention of secondary injury is resources for TBI-related protocols). In all TBI multi-
the key to improving morbidity and mortality outcomes73 trauma patients, disability and exposure/environmental

TABLE 17.2
Nursing management of the neurologically impaired, immobilised, mechanically-ventilated patient

NURSING DOMAIN NURSING OUTCOME NURSING INTERVENTIONS

Ventilation and • Airway patent • Assess ventilation parameters: ensure ET patency and position
oxygenation • Arterial pH, PaO2, PbtO2, SaO2 • Assess bilateral chest movement: listen for airway obstruction or
within normal range ET cuff leak; auscultate for air entry.
• PaCO2 and ETCO2 within normal • Assess chest X-ray
range • Adequate sedation and ventilation to maintain PbtO2, ICP, CPP
• Lungs clear to auscultation • Suction only as necessary: preoxygenate, avoid prolonged
• No evidence of atelectasis or coughing; effective technique.
aspiration • Avoid ICP complications of PEEP
• Chest X-ray clear of pathology • Position to avoid aspiration
• Provide meticulous oral hygiene
Mobility/safety • Cerebral blood flow • Haemodynamic stability maintained. Brain ischaemia and
uncompromised intracranial hypertension controlled
• Minimal and transient changes • Nursing interventions planned for minimal disturbance; efficient
in PbtO2–ICP–CPP and return to intervention
desired parameters within 5 min • Pressure-relieving mattress: allows minimal position changes
of nursing intervention for integument protection, with minimal cerebral oxygen
• Patient integument maintained consumption, sequential compression device for venous return
and infection free: skin, mucous • Hygiene maintained: assess integument, assess cornea, assess
membranes, cornea, wounds, mucous membranes
invasive lines • Maintain infection control interventions with invasive devices and
• Complications of immobility wounds
prevented: deep vein thrombosis, • Administer preventive plan of treatment with vigilance and
pneumonia, muscle strength prediction
• Patient safety enabled, • Enable communication with other health professionals
preventing nosocomial infection, • Chemical and physical restraint applied per assessment and
secondary brain injury, self-harm prescription, within institutional policy
• Nutrition prescribed according to
patient need
• Healing defined and uneventful
Psychological/family • Family and significant others • Refer and coordinate information and service provision from
informed and supported other health professionals
• Psychological wellbeing of • The provision of quality, informed and inclusive care to the
patient in recovery patient provides family and significant others with the confidence
• The patient will feel safe that the nurse advocates for the patient in their place
• Ensure psychological assessment and administer prescribed
therapy for delirium and post-traumatic stress
• Nursing interventions planned to allow for rest and recovery
• Administer coordinated rehabilitation strategies
CPP = cerebral perfusion pressure; ETCO2 = end tidal carbon dioxide; ICP = intracranial pressure; PaCO2 = partial pressure
of alveolar carbon dioxide; PaO2 = partial pressure of alveolar oxygen; PbtO2 = brain tissue oxygenation; PEEP = positive
end-expiratory pressure; SaO2 = arterial oxygen saturation.
 CHAPTER 17 NEUROLOGICAL ALTERATIONS AND MANAGEMENT 561

TABLE 17.3
Summary of guidelines of the management of severe traumatic brain injury from the Brain Trauma Foundation

ITEM LEVEL I LEVEL II LEVEL III

Blood pressure None Blood pressure should be monitored and Oxygenation should be monitored and hypoxia
and oxygenation hypotension (SBP <90 mmHg) avoided (PaO2 <60 mmHg or O2 saturation <90%) avoided
Hyperosmolar None Mannitol is effective for control of raised Restrict mannitol use prior to ICP monitoring to
therapy intracranial pressure at doses of 0.25 gm/kg patients with signs of transtentorial herniation
to 1 g/kg body weight. Arterial hypotension or progressive neurological deterioration not
(SBP <90 mmHg) should be avoided attributable to extracranial causes
Hypertonic saline evidence is limited
on the use, concentration and method
of administration for the treatment of
traumatic intracranial hypertension
Prophylactic Insufficient Insufficient data Prophylactic hypothermia is not significantly
hypothermia data associated with decreased mortality
Prophylactic hypothermia is associated with
significant higher Glasgow Outcome Scale scores
Infection Insufficient Periprocedural antibiotics for intubation Routine ventricular catheter or prophylactic
prophylaxis data should be administered to reduce the antibiotic use for ventricular catheter placement is
incidence of pneumonia – but does not not recommended to reduce infection
change length of stay or mortality
Early tracheostomy – reduces mechanical Early extubation in qualified patients, without
ventilation days increased risk of pneumonia
Deep vein Insufficient Insufficient data Graduated compression stockings or intermittent
thrombosis data pneumatic compression stockings until ambulatory
prophylaxis Low-molecular-weight heparin or low
unfractionated heparin in combination with above.
Risk of expansion of intracranial haemorrhage
Indications for Insufficient ICP monitoring recommended for patients Normal CT with 2 or more of the following:
ICP monitoring data with GCS score of 3–8 with abnormal CT • Age 40+ years
• Motor posturing
• SBP <90 mmHg
• GCS score 9–15 with abnormal CT at
prescription discretion
ICP monitoring Insufficient Insufficient data Insufficient data
technology data The ventricular catheter with external strain gauge,
most accurate low-cost, reliable ICP device
Can also be recalibrated in situ
Parenchymal ICP cannot be recalibrated. Negligible
drift
ICP treatment Insufficient Treatment initiated ICP above 20 mmHg A combination of ICP values, clinical and brain CT
threshold data should be used to determine the need for treatment
Cerebral Insufficient Aggressive attempts to maintain CPP CPP of <50 mmHg should be avoided
perfusion data above 70 mmHg with fluids and pressors The CPP value to target lies within the range of
due to risk of ARDS 50–70 mmHg
Patients with intact pressure autoregulation tolerate
higher CPP values
Ancillary monitoring of cerebral parameters that
include blood flow, oxygenation or metabolism
facilitates CPP management
Brain oxygen Insufficient Insufficient data Jugular venous oxygenation (<50%) or brain
monitoring and data tissue oxygen tension (<15 mmHg) are treatment
thresholds thresholds and are to be avoided
Anaesthetics, Insufficient Manage pain and agitation None advised
analgesics and data High-dose barbiturate may be used in
sedatives haemodyamically stable patients refractory
to other ICP treatments.
Propofol for the control of ICP. High-dose
propofol can produce significant morbidity
562 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 17.3 continued

ITEM LEVEL I LEVEL II LEVEL III

Nutrition Insufficient Full caloric replacement by day 7 post injury None advised
data
Antiseizure Insufficient Phenytoin or valproate is not None advised
prophylaxis data recommended for preventing late post-
traumatic seizures
Anticonvulsants are indicated to decrease
the incidence of early post-traumatic
seizures
Hyperventilation Insufficient Prophylactic hyperventilation (PaCO2 Use hyperventilation for temporary reduction of
data <25 mmHg) is not recommended elevated ICP
Hyperventilation should be avoided during the first
24 hours after injury when CBF is often critically
reduced
If hyperventilation used; SjO2 or PbrO2 measures
recommended to monitor oxygen delivery
Steroids Not recom- None advised None advised
mended
ARDS = acute respiratory distress syndrome; CBF = cerebral blood flow; CPP = cerebral perfusion pressure; CT = computerised
tomography (scan); GCS = Glasgow Coma Scale; ICP = intracranial pressure; PaCO2 = partial pressure of alveolar carbon dioxide;
PaO2 = partial pressure of alveolar oxygen; PbrO2 = brain tissue oxygenation; SBP = systolic blood pressure; SjO2 = jugular venous
oxygen saturation.
Adapted from Brain Trauma Foundation, American Association of Neurological Surgeons, Joint Section on Neurotrauma and Critical
Care. Guidelines for management of severe head injury. New York: Brain Trauma Foundation; 2007, with permission.

control assessment includes further investigations with involved in SCI are the 5th, 6th and 7th cervical (neck),
complete CT scans. The management of TBI should the 12th thoracic and the 1st lumbar. These vertebrae
include spinal precautions until spinal injury is defini- are the most susceptible because there is a greater range
tively excluded. of mobility in the vertebral column in these areas.83
Damage to the spinal cord ranges from transient
Spinal cord trauma concussion or stunning (from which the patient fully
A 2014 report summarising the epidemiology of traumatic recovers) to contusion, laceration and compression of
spinal cord injury (SCI) estimated a global-incident rate of the cord substance (either alone or in combination) to
23 cases per million of the population.78,79 This translates to complete transection of the cord (which renders the
almost 180,000 cases per year. Traffic-related accidents are patient paralysed below the level of the injury).
the leading cause of traumatic SCI in developed countries,
accounting for one-third to one-half of cases.80 Falls are Mechanisms of injury
the next most common cause of traumatic SCI, with Cervical injury can occur from both blunt and penetrat-
rates increasing in the elderly in particular. In developing ing trauma but, in reality, is a combination of different
countries, traumatic SCI is most often caused by falls at mechanisms of acceleration and deceleration with and
home or in the workplace, with rates as high as 63%.79 without rotational forces and axial loading.78 An illus-
The highest proportion of violence-related traumatic SCI trative example is a diving injury, caused by a direct load
occurs in areas of armed conflict or high availability of through the head and cervical spine. Cervical trauma is
weapons. Recreational injuries occur most often with produced by a combination of the mechanisms listed
snowboarding, rugby and diving accidents. A systematic below.
review of 13 studies from around the world indicated that • Hyperflexion: usually results from forceful
in most regions there are peak rates of traumatic SCI in deceleration and is often seen in patients who have
young adults (15–29 years) and that in older age groups sustained trauma from a head-on motor vehicle
the incidence rate increased steadily with increasing age. collision or diving accident. The cervical region is
A predominance of males is also evident in cases from all most often involved, especially at the C5–C6 level.
regions.81,82 • Vertical compression or axial loading: typically
Of all SCI cases, 51% resulted in complete tetraplegia occurs when a person lands on the feet or buttocks
(loss of function in the arms, legs, trunk and pelvic organs). after falling or jumping from a height. The vertebral
The predominant risk factors for SCI include age, gender, column is compressed, causing a fracture that results
and alcohol and drug use. The vertebrae most often in damage to the spinal cord.
 CHAPTER 17 NEUROLOGICAL ALTERATIONS AND MANAGEMENT 563

• Hyperextension: is the most common type of injury. the patient has either increased or decreased cutaneous
Hyperextension injuries can be caused by a fall, a sensation of pain, temperature and touch on the
rear-end motor vehicle collision or hit on the head same side of the spinal cord at the level of the lesion.
(e.g. during a boxing match). Hyperextension of the Below the level of the lesion on the same side, there
head and neck may cause contusion and ischaemia is complete motor paralysis. On the patient’s opposite
of the spinal cord without vertebral column damage. side, below the level of the lesion, there is loss of pain,
Whiplash injuries are the result of hyperextension. temperature and touch because the spinothalamic
Violent hyperextension with fracture of the pedicles tracts cross soon after entering the cord.
of C2 and forward movement of C2 on C3 produces
the ‘Hangman’s fracture’. Pathophysiology
• Extension–rotation: rotational injuries result from SCIs can be separated into two categories: primary
forces that cause extreme twisting or lateral flexion injuries and secondary injuries. Primary injuries are
of the head and neck. Fracture or dislocation of the result of the initial insult or trauma, and are usually
vertebrae may also occur. The spinal canal is narrower permanent. The force of the primary insult produces
in the thoracic segment relative to the width of the its initial damage in the central grey matter of the cord.
cord so, when vertebral displacement occurs, it is Secondary injuries are usually the result of a contusion or
more likely to damage the cord. Until the age of 10, tear injury, in which the nerve fibres begin to swell and
disintegrate. Secondary neural injury mechanisms include
the spine has increased physiological mobility due to
ischaemia, hypoxia and oedema, cellular and molecular
lax ligaments, which affords some protection against
inflammatory injury and cell death. Ischaemia, the most
acute SCI. Elderly patients are at a higher risk due to
prominent post SCI event, may occur up to 2 hours post
osteophytes and narrowing of the spinal canal.
injury and is intensified by the loss of autoregulation
of the spinal cord microcirculation.84 This will decrease
Classification of spinal cord injuries
blood flow, which is then dependent on the systemic
SCIs can be broadly classified as complete or incomplete.78 arterial pressure in the presence of hypotension or
The diagnosis of complete SCI cannot be made until vasogenic spinal shock. Oedema develops at the injured
spinal cord shock resolves. There are four incomplete SCI site and spreads into adjacent areas. Hypoxia may occur
syndromes as follows: as a result of inadequate airway maintenance and venti-
• Anterior cord syndrome: injury to the motor and lation. Immune cells, which normally do not enter the
sensory pathways in the anterior parts of the spine; spinal cord, engulf the area after a spinal cord injury and
thus patients are able to feel crude sensation, but release regulatory chemicals, some of which are harmful
movement and detailed sensation are lost in the to the spinal cord. Highly reactive oxidising agents (free
posterior part of the spinal cord. Clinically, the radicals) are produced, which damage the cell membrane
patient usually has complete motor paralysis below and disrupt the sodium–potassium pump.
the level of injury (corticospinal tracts) and loss Free radical production and the formation of reactive
of pain, temperature and touch sensation oxygen and nitrogen species or lipid peroxidation lead to
(spinothalamic tracts), with preservation of light vasoconstriction, increased endothelial permeability and
touch, proprioception and position sense. The increased platelet activation. A secondary chain of events
prognosis for anterior cord syndrome is the worst produces ischaemia, hypoxia, oedema and haemorrhagic
of all the incomplete syndrome prognoses. lesions, which in turn result in the destruction of myelin
and axons. Autoregulation of spinal cord blood flow may
• Posterior cord syndrome: this is usually the result of be impaired in patients with severe lesions or substantial
a hyperextension injury at the cervical level and is
not commonly seen. Position sense, light touch and oedema formation. These secondary reactions, believed
vibratory sense are lost below the level of the injury. to be the principal causes of spinal cord degeneration
at the level of injury, are now thought to be reversible
• Central cord syndrome: injury to the centre of the 4–6 hours after injury. Therefore, if the cord has not
cervical spinal cord, producing weakness, paralysis suffered irreparable damage, early intervention is needed
and sensory deficits in the arms but not the legs. to prevent partial damage from developing into total and
Hyperextension of the cervical spine is often the permanent damage.85
mechanism of injury, and the damage is greatest to Spinal shock occurs with physiological or anatomical
the cervical tracts supplying the arms. Clinically, the transection or near-transection of the spinal cord; it occurs
patient may present with paralysed arms but with no immediately or within several hours of a spinal cord injury
deficit in the legs or bladder. and is caused by the sudden cessation of impulses from
• Brown-Séquard syndrome: this involves injury to the the higher brain centres.86 It is characterised by the loss
left or right side of the spinal cord. Movements are lost of motor, sensory, reflex and autonomic function below
below the level of injury on the injured side, but pain the level of the injury, with resultant flaccid paralysis.
and temperature sensation are lost on the side opposite Loss of bowel and bladder function also occurs. In
the injury. The clinical presentation is one in which addition, the body’s ability to control temperature is lost
564 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

(i.e. poikilothermia) and the patient’s temperature tends to Spinal shock is associated with decreases in systemic
equilibrate with that of the external environment. vascular resistance, arterial hypotension, venous pooling,
Neurogenic spinal shock occurs as a result of mid- to severe bradycardia and decreased myocardial contractility.
upper-level cervical injuries and is the result of sympa- Consequently, treatment of neurogenic shock includes
thetic vascular denervation and peripheral vasodilation. fluid replacement using crystalloid solutions to maintain
The loss of spinal cord vasculature autoregulation occurs, arterial blood pressure, circulatory volume, renal function
causing the blood flow to the spinal cord to be dependent and tissue oxygenation. Lower-limb compression assists
on the systemic blood pressure. Signs and symptoms with venous return. Infusion of free water must be
include hypotension, severe bradycardia and loss of the avoided, as this decreases plasma osmolarity and promotes
ability to sweat below the level of injury.The same clinical spinal cord oedema. Atropine may be administered to
findings pertaining to disruption of the sympathetic trans- reverse bradycardia and increase cardiac output. Admin-
missions in spinal shock occur in neurogenic shock.78 istration of vasopressors (e.g. noradrenaline) prior to
correction of the intravascular volume status may increase
Systemic effects of spinal cord injury systemic vascular resistance (left ventricular afterload) and
The traumatic insult causing the spinal cord injury is further impair myocardial contractility. Therefore, careful
associated with an immediate stimulation of central and volume replacement is the first step, and administration of
peripheral sympathetic tone. Initially, the elevated sympa- vasopressors the second step, in the treatment of arterial
thetic activity raises systemic arterial blood pressure hypotension and low cardiac output after acute cervical
and induces cardiac arrhythmias. At the stage of spinal spinal cord injury.8
shock with loss of neuronal conduction, the sympathetic The major early cause of death in patients with acute
excitation is closely followed by decreases in systemic cervical SCI is respiratory failure. Tracheal intubation may
vascular resistance, arterial hypotension and venous be indicated in unconscious patients, during shock, in
pooling. Lesions above the level of T5 additionally present patients with other major associated injuries and during
with severe bradycardia and cardiac dysfunction. The cardiovascular and respiratory distress. It is also indicated in
decreases in cardiac output combined with systemic hypo- conscious patients presenting with the following criteria:
tension further aggravate spinal cord ischaemia in tissues maximum expiratory force below +20 cmH2O, maximum
with defective autoregulation.85 inspiratory force below −20 cmH2O, vital capacity below
Spinal cord injury may produce respiratory failure.The 1000 mL and presence of atelectasis, contusion and
extent of respiratory complications is related to the level infiltrate.85
of the injured segments. Injuries above the level of C4–C5
produce complete paralysis of the diaphragm, with sub- Investigations and alignment
stantial decreases in tidal volume and consecutive hypoxia. Following the initial assessment of the patient, detailed
With lesions below C6, the function of the diaphragm is CT diagnostic radiography defines the bone damage and
maintained and there is incomplete respiratory failure due compression of the spinal cord. Cervical spine fractures
to paralysed intercostal and abdominal musculature. As a occur predominantly at two levels, at the level of C2
consequence, arterial hypoxia and hypercapnia occur, both and at the level of C6 or C7. Unfortunately, 20–30%
of which promote neuronal and glial acidosis, oedema and of these fractures can be missed on plain radiographs.
neuroexcitation.86 Current data and the American College of Radiology
Appropriateness Criteria recommend use of multidetec-
Patient management tor-row computed tomography as the initial screening
Spinal cord injury should be suspected in patients with examination in suspected cervical trauma instead of
neck pain, sensory and motor deficits, unconsciousness, radiographs. Specific radiological procedures such
intoxication, spondylitis or rheumatoid arthritis, all major as cervical myelography, high-resolution CT scan or
trauma, distracting injuries, head injury and facial fractures. magnetic resonance imaging will identify fractures, dis-
Prior to admission, if spinal cord injury is suspected or location of bony fragments and spinal cord contusion.83
cannot be excluded, the patient must be placed on a spine In patients with a dislocated cervical fracture, decompres-
board with the head and neck immobilised in a neutral sion and anatomical bony realignment may be achieved
position using a rigid collar to reduce the risk of neuro- with traction forces applied manually, or with halo or
logical deterioration from repeated mechanical insults. Gardner–Wells systems under radiological control. If
Spinal injury patients are susceptible to pressure injuries the anatomical bony alignment procedures and traction
(see Chapter 6), so time must be considered when hard forces fail to decompress the cord, surgical intervention
surfaces are used for immobilisation. Total neck immobili- to remove the lesion is required. The timing of surgical
sation should not interfere with maintenance of the airway, intervention remains controversial. While urgent surgical
and inadequate respiratory function must be avoided.82 decompression or internal stabilisation should be
performed in all patients with deteriorating neurological
Resuscitation status, some centres tend to defer surgical treatment in
Initial treatment aims for decompression of the spinal cord patients with spinal cord injury who have stable neuro-
and reversal of neurogenic shock and respiratory failure. logical deficits.87
 CHAPTER 17 NEUROLOGICAL ALTERATIONS AND MANAGEMENT 565

Neuroprotection and regeneration Cerebrovascular disorders

There is robust experimental and some clinical evidence Cerebral vascular disorders include cerebrovascular disease
that hypothermia may be beneficial in acute SCI.88 Most and cerebral vascular accidents (stroke). A stroke (acute
other neuroprotective agents have not been successful, brain injury of vascular origin) may be either ischaemic
which has been attributed to attempting to block only one or haemorrhagic and is defined as an interruption of the
molecular pathway of a complex range of SCI molecular blood supply to any part of the brain, resulting in damaged
mechanisms. There has been renewed interest in regener- brain tissue.
ation, which involves stem cell transplantation or similar
restorative approaches designed to optimise spontaneous Stroke
axonal growth and myelination, but it is still in its infancy According to World Health Organization (WHO)
in some countries due to limiting legislation in regard to estimates, one in every 10 deaths is caused by stroke; thus,
stem cell research. it is the third most common cause of death in developed
countries, exceeded only by coronary heart disease and
Collaborative management cancer.89 Worldwide, 15 million people suffer a stroke each
Patients with acute cervical spinal cord injury require year; one-third die and one-third are left permanently
ICU monitoring, observation and support of ventilation, disabled. The prevalence of stroke in the USA is about
a nasogastric tube to reduce abdominal distension and risk 7 million (3.0%).90 China has one of the highest rates of
of aspiration, a urinary catheter and thermal maintenance. mortality (19.9% of all deaths in China), along with Africa
• Tracheostomy is indicated in high cervical spine and parts of South America. In Europe, the incidence of
injury and ischaemia, sometimes only while the early stroke varies from 101.1 to 239.3 per 100,000 in men
oedema is resolving. and 63.0 to 158.7 per 100,000 in women.91 Stroke is the
• Spinal alignment and immobilisation requires primary cerebrovascular disorder in Australia and New
careful positioning with dedicated neck support by Zealand and is still the third-leading cause of death. Every
experienced clinicians. year approximately 40,000 people in Australia are admitted
to hospital with a diagnosis of stroke.92 The prevalence of
• Shoulder and lumbar support pillows are often stroke is higher among men than women. Almost 60%
prescribed. Pressure-relief mattresses must be suitably
of people who have had a stroke are aged 65 years and
designed for spine immobilisation and, when
over, while 18% are under the age of 55 years. Stroke can
prescribed, can be tilted to facilitate ventilation.
be divided into two major categories: ischaemic (85%),
• Meticulous integument and bowel care is indicated in which vascular occlusion and significant hypoperfusion
with daily protocols for regular stool softeners and occur; and haemorrhagic (15%), in which there is extra-
peristaltic stimulants essential for the prevention of vasation of blood into the brain. Although there are some
autonomic dysreflexia (i.e. strong sensory input from similarities between the two broad types of stroke, the
the bowel to the spinal cord that evokes a massive reflex aetiology, pathophysiology, medical management, surgical
sympathetic surge) and autonomic nerve dysfunction. management and nursing care differ.
• Early nutritious feeding is essential, whether oral Aetiology
or enteric; however, aspiration must be prevented.
The supplementation of feeding with high-energy Hypertension is the leading risk factor for stroke. Other
protein fluids to match the catabolic state assists with risk factors include diabetes, cardiac disease, previous
recovery (see Chapter 19). cerebrovascular disease (transient ischaemic attack or
• Hyperglycaemia is associated with increased stroke or myocardial infarction), age, sex, lipid disorders,
inflammation and must be controlled to less than excessive ethanol ingestion, elevated hematocrit, elevated
10 mmol/L, avoiding hypoglycaemia.89 fibrinogen and cigarette smoking. Cerebral arteriosclerosis
predisposes individuals to both ischaemic and haemor-
• The concepts of pain relief and sedation in patients rhagic stroke. Smoking is the strongest risk factor for aSAH.
with spinal cord injury are based on the maintenance
of coupling between metabolism and spinal cord Atrial fibrillation, endocarditis and medications containing
blood flow while achieving hypnosis, analgesia and a supplemental oestrogen are risk factors for embolic stroke.
‘relaxed cord’. These concepts include maintenance Seizures develop in approximately 10% of cases, usually
of normal to high systemic perfusion pressures, appearing in the first 24 hours and more likely to be focal
normoxia and normocapnia. than generalised. Occurrence of seizures within 24 hours
of stroke is associated with higher 30-day mortality, which
• Psychological and empathetic support is essential may be a reflection of severe neuronal damage.93
and appropriate referral for grieving and stress is
paramount. Rehabilitation counselling and planning Ischaemic stroke
starts at the acute stage in order to give the family Ischemic stroke compromises blood flow and energy
unit some future focus and hope. supply to the brain, which triggers mechanisms that lead
See Online resources for specific protocols related to to cell death. Infarction occurs rapidly in the region of
spinal injury. most severe ischaemia (termed ischaemic penumbra) and
566 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

expands at the expense of the surrounding hypoxic tissue,

from the centre to the periphery. Therapeutic strategies in TABLE 17.4
acute ischaemic stroke are based on the concept of arresting Classification and type of ischaemic stroke and
the transition of the penumbral region into infarction, treatment options
thereby limiting ultimate infarct size and improving neuro- C L A S S I F I C AT I O N T R E AT M E N T O P T I O N S
logical and functional outcome. Ischaemic stroke can be
Middle cerebral Intravenous or intra-arterial tissue
further categorised as middle cerebral artery occlusion,
artery occlusion plasminogen activator (tPA)
acute basilar occlusion and cerebellar infarcts.94
Exclusion criteria: >3 hours elapsed
from stroke onset and widespread
Practice tip early infarct changes on CT scan
Tolerate autoprotective hypertension
For consideration of ischaemic stroke lysis, the timing
for perfusion of the ischaemic
of the onset of symptoms needs to be very clearly
penumbra
defined. In particular, if a patient wakes from sleep with
stroke symptoms, the timing of onset must be assumed Acute basilar Anticoagulation with intravenous
occlusion heparin
to be when they were last well – that is, the time when
Thrombolysis up to 12 hours after
they went to sleep.
onset
The management of an ischaemic stroke comprises Cerebellar infarcts May be difficult to recognise
four primary goals: restoration of CBF (reperfusion), because of the slow evolution of
prevention of recurrent thrombosis, neuroprotection and brainstem and cerebellar signs
supportive care. The timing of each element of clinical Aspirin, antihypertensives and
management needs to be implemented in a decisive conventional cerebral oedema
strategies
manner.
For eligible patients, IV tissue plasminogen activator
should be administered intravenously with a dose of airway and haemodynamic management proceeds in a
0.9 mg/kg (maximum of 90 mg), with 10% of the total common pathway with other stroke subtypes. Because
dose administered as an initial bolus and the remainder many ICH patients are obtunded or comatose, airway
infused over 60 minutes, provided that treatment is initiated management (specifically the need for intubation for
within 4.5 hours of clearly defined symptom onset.95 The airway protection) should be considered throughout the
recommendation assumed a relatively higher value on early treatment course. Following the diagnosis of ICH,
long-term functional improvement and a relatively lower immediate consideration should be given to the need for
value on minimising the risk of intracerebral hemorrhage 1) acute control of elevated blood pressure, 2) correction
in the immediate peristroke period.96 of coagulopathy because of medications or underlying
Table 17.4 shows the classification and treatment medical conditions and 3) the need for urgent surgical
strategies, and the Online resources reflect specific ischaemic haematoma evacuation.
stroke protocols. Over 90% of patients have acute hypertension
exceeding 160/100 mmHg, whether or not there is a
Intracerebral haemorrhage history of pre-existing hypertension. It remains unclear
Intracerebral haemorrhage (ICH) comprises 10–15% of whether this response is adaptive (to maintain perfusion
all strokes with an incidence of 24.6 per 100,000 person- to an ischemic penumbra surrounding the haematoma)
years, with a growing incidence associated with the use or potentially harmful (resulting in rebleeding, peri-
of anticoagulation, antiplatelet agents and an ageing haematoma oedema expansion, or both).100 Presently,
population.97 Despite this, ICH remains the last stroke based on the existing incomplete evidence, American
type without a definitive treatment and contributes to Heart Association/American Stroke Association guidelines
significant morbidity and mortality. Up to half of patients recommend that, for patients with SBP of >200 mmHg or
die within 30 days, often despite extensive stays in the mean arterial pressure (MAP) of >150 mmHg, continuous
ICU. Moreover, those who survive have a high degree intravenous infusion to reduce the blood pressure should
of long-term disability.98 Ideally, patients with acute ICH be applied, with monitoring every 5 minutes. For SBP of
should be admitted to an ICU based on the need for close >180 mmHg or MAP of >130 mmHg in patients with a
monitoring of neurological and haemodynamic condition likelihood of ICP elevation, reducing blood pressure while
and the risk for early deterioration from haematoma simultaneously maintaining a cerebral perfusion pressure
expansion, cerebral oedema, hydrocephalus or airway of ≥60 mmHg is recommended. If there is no evidence of
compromise. Many ICHs continue to grow and expand elevated ICP, a modest reduction of blood pressure (e.g.,
over several hours after onset of symptoms.99 MAP of 110 mmHg or a target BP of 160/90 mmHg) with
As with all emergency management, initial assessment a re-examination every 15 minutes is recommended.101
of airway, breathing and circulation is critical. Until the Antithrombotic medications are a risk factor for the
diagnosis of ICH is made from neuroimaging, overall occurrence of ICH, as well as for haematoma expansion
 CHAPTER 17 NEUROLOGICAL ALTERATIONS AND MANAGEMENT 567

if an ICH occurs. As there is a broad range of antithrom-

Practice tip
botic medications, including warfarin, heparin, antiplatelet
agents such as aspirin and clopidogrel and newer agents Fever is the most common medical complication in
such as dabigatran and rivaroxaban, the specific risks and patients suffering from aSAH and is associated with
interventions to reverse coagulopathy vary. Also, coagulop- neurological deterioration.
athies may be due to underlying medical conditions, such
as liver disease or haematological malignances.102 Most of Other aspects of management in the acute stages
the brain injury and swelling that happens in the days after include suitable analgesia, seizure control and treatment
ICH is the result of inflammation caused by thrombin and with nimodipine to prevent delayed cerebral ischaemia and
other coagulation end-products. Dysautonomia, in the vasospasm. Vasospasm often occurs 4–21 days after initial
form of central fever, hyperventilation, hyperglycaemia haemorrhage when the clot undergoes lysis (dissolution),
and tachycardia or bradycardia, is also common. Hyper- increasing the chances of rebleeding. It is believed that
glycaemia at the time of hospital admission is associated early open surgical clipping or wrapping and endovascular
with early mortality and poor outcome in ICH patients.103 coil embolisation prevent rebleeding and that removal of
blood from the basal cisterns around the major cerebral
Subarachnoid haemorrhage arteries may prevent vasospasm.108 (See previous section on
Admission to the ICU is indicated for aSAH Hunt Prevention of delayed cerebral ischaemia and cerebral vasospasm.)
Hess Severity Scale III (see Table 17.5) or the World The management of acute hydrocephalus secondary to
Federation of Neurosurgical Societies Scale grade 4. This aSAH is usually managed by external ventricular drainage
level of severity is at greater risk of systemic compli- (EVD) and is associated with neurological improvement.
cations and clinical deterioration.104 Resuscitation is ICP monitoring and drainage of CSF via ventriculostomy
directed towards maintaining cerebral perfusion pressure is indicated in aSAH.109
by ensuring adequate arterial blood pressure (often with Increased sympathetic activation from the presence of
haemoglobin in the subarachnoid space results in elevated
the use of inotropes to produce relative hypertension
catecholamine levels.This is characterised by hypothalam-
although reactive hypertension is often present), ensuring
ically mediated changes including increased sympathetic
euvolaemia and producing relative haemodilution.105 and parasympathetic activity that causes cardiac and
Hypovolaemia occurs in 30–50% of patients, as does pulmonary complications (neurogenic pulmonary
hyponatraemia in 30% of patients. In the first 6 days, oedema).110 Manifestations include electrocardiographic
plasma volume decreases of greater than 10% can occur changes, arrhythmias, impaired cardiac contractility,
following aSAH, thus increasing the risk of delayed elevated troponin levels and myocardial necrosis. Cardiac
cerebral ischaemia and vasospasm.106 Women have been and pulmonary complications are associated with delayed
found to have more significant drops in blood volume cerebral ischaemia and poor outcome after aSAH. As
than men following aSAH. ‘Third space’ loss, insensible cardiac function is one of the determinants for adequate
losses and blood loss account for this drop in fluid volume, CBF, it is essential to identify such occurrences early and
as well as electrolyte disturbances.107 treat them accordingly.
Hyponatraemia occurs from alterations in atrial natri-
uretic factor in response to sympathetic nervous system
TABLE 17.5 activation. The syndrome of inappropriate secretion of
Hunt-Hess scale for aneurysmal subarachnoid antidiuretic hormone is primarily responsible for hypo-
haemorrhage (aSAH) natraemia in those with aSAH, as is cerebral salt-wasting
syndrome; however, both mechanisms are still relatively
SCORE DESCRIPTION
misunderstood.109
0 Unruptured; asymptomatic discovery
I Asymptomatic or minimal headache with slight
Cerebral venous thrombosis
nuchal rigidity Compared to cerebral infarctions from arterial sources,
cerebral venous infarctions are less common. The ratio
II Moderate-to-severe headache, nuchal rigidity;
no neurological deficit other than cranial nerve
of venous strokes to arterial stroke is reported as 1:62.5.
deficit
Cerebral venous thrombosis is particularly important to
recognise because there is general consensus that early
III Drowsiness, confusion or mild focal deficit anticoagulation can result in good clinical outcomes.111
(e.g. hemiparesis), or a combination of these
Magnetic resonance and CT vascular imaging has made
findings
it easier to establish the diagnosis, but close monitoring
IV Stupor, moderate-to-severe deficit, possibly of the patient is essential, as late deterioration can occur.
early decerebrate rigidity and vegetative
disturbances Patient management
V Deep coma, decerebrate rigidity, moribund Expected outcomes for patients with acute ischaemic and
appearance haemorrhagic stroke include prevention of secondary
injury and of airway and respiratory complications, and
568 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

maintenance of haemodynamic stability.Timely assessment Meningitis

and intervention are paramount in the management of Meningitis is inflammation of the pia and arachnoid layers
ischaemic stroke, especially regarding interventional phar- of the meninges. Acute community-acquired meningitis
macology and prevention of cerebral haemorrhage.104 See can develop within hours to days and is usually viral or
Online resources for specific protocols related to stroke. bacterial. Viral meningitis usually has a good prognosis,
Atrial fibrillation and deep vein thrombosis prevention whereas bacterial meningitis is associated with significant
(in ischaemic stroke) requires anticoagulation control. In rates of morbidity and death, so it is critical to recognise
haemorrhagic stroke, a sequential compression device and
and differentiate them promptly.112 The incidence,
stockings are indicated for deep vein thrombosis prophy-
mortality and morbidity from acute community-
laxis as anticoagulants are a risk factor for rebleeding.102
acquired meningitis have decreased significantly, especially
Maintenance of bowel and bladder function and
in high-income countries, probably as a result of vacci-
prevention of integument complications, malnutrition,
nation and better antimicrobial and adjuvant therapy, but
seizures and increasing neurological deficits are important
the disease still has a high toll. The incidence of bacterial
goals. Environmental precautions are implemented to
provide a non-stimulating environment, preventing rises meningitis has declined from 3–5 per 100,000 per year a
in ICP and further bleeding. few decades ago to 1.3–2 per 100,000 per year currently.112
Sensory perceptual and motor alterations need to be The incidence of disease caused by Neisseria meningit-
assessed in regard to effective communication and pain idis remains an issue of public health concern in Australia
management. Rehabilitation and psychological support and New Zealand. The introduction of a publicly funded
for the patient and significant others are integrated into program of selective vaccination with conjugate serogroup
the acute care phase for a smooth transition.104 C meningococcal vaccine in 2004 has resulted in a signif-
icant reduction in the number of cases of meningococcal
Infection and inflammation disease.113 The policy of giving antibiotics prior to hospital
The CNS infections of major interest in the ICU are admission in Australia, implemented in 1995, reduced
divided into those that affect the meninges (meningitis) the case-fatality rate for those receiving antibiotics. The
and those that affect the brain parenchyma (encephalitis). onset of meningococcal disease varies seasonally, rising in
They may be viral or bacterial in aetiology. There are June and peaking in late spring each year.114 The highest
also numerous medical conditions that may produce an incidence of meningococcal disease is for children aged
encephalopathic illness that may mimic viral encephal- 4 years and under. A secondary peak in the incidence of
itis. In patients recently returning from abroad, particular meningococcal disease is seen in adolescents and young
vigilance must be paid to the possibility of such non-viral adults. During the 2009 H1N1 influenza epidemic there
infections as cerebral malaria, which may be rapidly fatal were several cases of H1N1 influenza-related meningitis.
if not treated early. A number of metabolic conditions, Table 17.6 has the CSF profiles for acute meningitis and
including liver and renal failure and diabetic complica- encephalitis and Table 17.7 has the classification, treatment
tions, may also cause confusion due to the manifestation and clinical presentation of meningitis.
of cerebral oedema. The possible role of alcohol and drug Complications of meningitis vary according to the
ingestion must always be considered. aetiological organism, the duration of symptoms prior to

TABLE 17.6
Typical profiles of cerebrospinal fluid in acute meningitis and encephalitis

MENINGITIS ENCEPHALITIS

I N V E S T I G AT I O N REFERENCE RANGE BACTERIAL VIRAL BACTERIAL/VIRAL

Opening pressure <30 mmH2O Raised Normal Raised

White cells
Total count <5 ⫻ 106/L Greatly raised Moderately raised Moderately raised
Differential Lymphocytes Neutrophils Lymphocytes Lymphocytes
(60–70%), monocytes predominate predominate predominate
(30–50%), no neutrophils
or red blood cells
Glucose concentration 2.8–4.4 mmol/L Lowered Normal Normal
CSF: serum glucose >60% Lowered Normal Normal
ratio
Protein concentration <0.45 g/L Raised Normal or slightly Normal or slightly
raised raised
 CHAPTER 17 NEUROLOGICAL ALTERATIONS AND MANAGEMENT 569

TABLE 17.7
Classification of acute meningitis

ACUTE MENINGITIS BACTERIAL – NOTIFIABLE DISEASE VIRAL

Aetiology Neisseria meningitis Enteroviruses: 85–95% of cases

• Serogroups A, B, C – 90% invasive isolates Herpes simplex 1 and 2
• Serogroup B – most disease Varicella zoster
• Serogroup A – epidemic disease and indigenous Cytomegalovirus
haemophilus influenzae type B streptococcus Epstein–Barr
pneumoniae listeria monocytogenes HIV infection can also present as aseptic
meningitis
Post infectious encephalomyelitis: may
occur following a variety of viral infections,
usually of the respiratory tract.
Cryptococcus neoformans
Fungal isolates

Pathophysiology Rapid recognition and diagnosis of meningitis is The physical signs are not so marked and
imperative the illness is not as severe and prolonged
Quick and insidious progress of disease as bacterial meningitis
Colonisation of mucosal surfaces (nasopharynx) Viral infection of mucosal surfaces of
Haematogenous or contiguous spread respiratory or gastrointestinal tract
Specific antibodies important defence Virus replication in tonsillar or gut lymphatics
Bacterial invasion of meninges: inflammatory response, Viraemia with haematogenous
breakdown of the BBB, cerebral oedema, intracranial dissemination to the CNS
hypertension Meningeal inflammation, BBB breakdown,
Vasculitis, spasm and thrombosis in cerebral blood vessels cerebral oedema, vasculitis and spasm

Clinical presentation Presents with sepsis: headache, fever, photophobia, Presents with non-specific symptoms,
and progression vomiting, neck stiffness, alteration of mental status viral respiratory illness, diarrhoea, fever,
Meningococcaemia is characterised by an abrupt onset headache, photophobia, vomiting,
of fever (with petechial or purpuric rash) anorexia, rash, cough and myalgia
Progresses to purpura fulminans, associated with the Occurs in summer or late autumn
rapid onset of hypotension, acute adrenal haemorrhage Enteroviral, pleurodynia, chest pain,
syndrome and multi-organ failure hand-foot-mouth disease
Kernig’s sign HSV-2: acute genital herpes
Brudzinski’s sign
Cranial nerve palsy (III, IV, VI, VII) uncommon and develop
after several days
Focal neurological signs in 10–20% cases
Seizures in 30% of cases
Signs of intracranial hypertension: coma, altered
respiratory status
Leads to hypertension and bradycardia before herniation,
or brain death, leads to irreversible septic shock

Treatment If meningococcal infection is suspected, the best way Administer intravenous aciclovir
to reduce mortality is to administer empirical IV therapy Dexamethasone may be prescribed:
immediately reduces BBB permeability
Ceftriaxone 2 g IV 12-hourly or cefatoxime 2 g IV Supportive treatment and resuscitation
6-hourly or immediately Management of intracranial hypertension/
Consequent dose, times and type of antibiotic need ischaemia
to be modified after full investigation and a detailed
examination have taken place
Dexamethasone may be prescribed: needs to be at same
time as antibiotic as outcome neurologically is reduced if
given after antibiotic. Reduces BBB permeability
Supportive treatment and resuscitation
Management of intracranial hypertension/ischaemia

BBB = blood–brain barrier; CNS = central nervous system

570 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

initiation of appropriate therapy and the age and immune • Mycobacterium tuberculosis, the yeast Cryptococcus
status of the patient.114 Temporary problems include devel- neoformans and Treponema pallidum (syphilis) may also
opment of haemodynamic instability and disseminated affect the brain parenchyma but usually produce
intravascular coagulopathy, particularly in meningo- chronic or subacute meningitis in such circumstances.
coccal infection, syndrome of inappropriate secretion of
In the majority of encephalitis cases, the offending
antidiuretic hormone or other dysregulation of the hypo-
organism finds access to the brain via the nasopharyngeal
thalamic–pituitary axis (e.g. diabetes insipidus), and an
epithelium and the olfactory nerve system. Arboviruses
acute rise in ICP.
are transmitted from infected animals to humans through
bite of infected animals.117 The cytokine storm results in
Practice tip
neural cell damage, as well as the apoptosis of astrocytes.
CSF concentrations of most antimicrobial drugs The disruption of the blood–brain barrier progresses to
are considerably less than in the serum due to poor septic shock, disseminated intravascular coagulopathy and
penetration of the blood–CSF barrier. Thus, the dose multi-organ failure. Encephalitis may present with progres-
for treating meningitis is usually higher than the regular sive headache, fever and alterations in cognitive state
dose. (confusion, behavioural change, dysphasia) or conscious-
ness. Focal neurological signs (paresis) or seizures (focal or
Focal neurological signs may develop in the early stages generalised) may also occur. Upper motor signs (hyper-
of meningitis, but are more common later. The devel- reflexia and extensor–plantar responses) are often present,
opment of subdural empyema, brain abscess and acute but flaccid paralysis and bladder symptoms may occur
hydrocephalus may require surgical intervention. Bacterial if the spinal cord is involved.118 Associated movement
meningitis with accompanying bacteraemia can lead to a disorders or the inappropriate secretion of antidiuretic
marked systemic inflammatory response with septic shock hormone may be seen.The most sensitive type of imaging
and acute respiratory distress syndrome. for diagnosis of encephalitis is MRI; in HSV encephalitis,
CT scans may initially appear normal, but MRI usually
Encephalitis shows involvement of the temporal lobes and thalamus.119
Encephalitis implies inflammation of the brain substance Examination of CSF can assist in differential diagnosis.
(parenchyma), which may coexist with inflammation of the Refer to Table 17.6 for CSF profiles. Electroencephal-
meninges (meningoencephalitis) or spinal cord (enceph- ography is less sensitive but may be helpful if it shows
alomyelitis). Encephalitis may be mild and self-limited, or characteristic features (e.g. lateralising periodic sharp and
may produce devastating illness. slow-wave patterns).
Herpes simplex virus encephalitis is the most common
sporadic viral encephalitis worldwide, with an annual Patient management
incidence of 1 in 250,000–500,000.115 It is the commonest Neurological derangement often coexists with circulatory
cause of non-seasonal encephalitis in Australia. Without insufficiency, impaired respiration, metabolic derangement
treatment, herpes simplex virus encephalitis is fatal in up and seizures. Protecting the patient from injury secondary
to 80% of cases, and leaves up to 50% of survivors with to raised ICP and seizure activity is essential. Prevention
long-term sequelae.116 of complications associated with immobility, such as
decubitus and pneumonia, is required. It is important to
• In the absence of particular risk factors, other institute droplet infection control precautions in those
common causes are enteroviruses, influenza virus
and Mycoplasma pneumoniae. However, the likely attending the patient until 24 hours after the initiation of
antibiotic therapy (oral and nasal discharge is considered
pathogens in encephalitis are dramatically influenced
infectious). See Online resources for infection control
by geographical location, history of travel and animal
protocols relating specifically to meningitis.
exposure and vaccination.
Support in an ICU is often required in encephalitis
• Murray Valley encephalitis virus causes seasonal to maintain ventilation, protect the airway and manage
epidemics of encephalitis at times of high regional complications, such as cerebral oedema. The management
rainfall. This arthropod-borne virus is the commonest of acute viral encephalitis includes aggressive airway,
flavivirus to cause encephalitis in Australia. ventilation, sedation, seizure, haemodynamic and fluid
• Since 2005, the distribution of Japanese B and nutritional support. Clinical deterioration is usually
encephalitis virus has expanded into Australia via the result of severe cerebral oedema with diencephalic
the Torres Strait Islands.117 It causes disease clinically herniation or systemic complications, including gener-
similar to Murray Valley encephalitis. In addition, two alised sepsis and multiple organ failure. The use of ICP
novel encephalitis viruses were recently identified monitoring in acute encephalitis remains controversial but
in Australia, the Hendra virus and Australian bat should be considered if there is a rapid deterioration in
lyssavirus. These should be considered if there is a the level of consciousness, and if imaging suggests raised
history of animal exposure, or if no other pathogen ICP. Prolonged sedation may be necessary. Decompres-
can be implicated. sive craniotomy may be successful in cases where there is
 CHAPTER 17 NEUROLOGICAL ALTERATIONS AND MANAGEMENT 571

rapid swelling of a non-dominant temporal lobe, as poor that attack myelin, cause inflammation and destruction
outcome is otherwise likely.119 and leave the axon unable to support nerve conduction.
This demyelination may be discrete or diffuse, and may
Neuromuscular alterations affect the peripheral nerves and their roots at any point
Generalised muscle weakness can manifest in several from their origin in the spinal cord to the neuromuscular
disorders that require ICU admission or complicate the junction. The weakness of GBS results from conduction
clinical course of patients. These may involve motor block and concomitant or primary axonal injury in the
neuron disease, disorders of the neuromuscular junction, affected motor nerves. Pain and paraesthesias are the
peripheral nerve conduction and muscular contraction. clinical correlates of sensory nerve involvement.
These disorders manifest as Guillain–Barré syndrome,
myasthenia gravis and critical illness polyneuropathy and Clinical manifestations
myopathy. Onset is rapid, and approximately 20% of cases lead to
total paralysis, requiring prolonged intensive therapy
Guillain–Barré syndrome with mechanical ventilation. The therapeutic window
Guillain–Barré syndrome (GBS) is an immune-medi- for GBS is short, and the current optimal treatment with
ated disorder resulting from generation of autoimmune whole plasma exchange or immunoglobulin therapy lacks
antibodies and/or inflammatory cells that cross-react with immunological specificity and only halves the severity of
epitopes on peripheral nerves and roots, leading to demye- the disease.120 GBS has three phases – acute, plateau and
lination or axonal damage or both, and autoimmune insult recovery – each stage lasting from days to weeks and in
to peripheral nerve myelin. Estimates of GBS incidence recovery to months and years. The patient presents with:
range from 0.8 to 1.9 cases per 100,000 person-years, • symmetrical weakness, diminished reflexes and
are higher in males and increase with age.120 In Australia, upward progression of motor weakness; a history of
Guillain–Barré has an average incidence of about 1.5 per a viral illness in the previous few weeks suggests the
100,000, in men slightly higher than in women.120 Of all diagnosis
patients, 85% recover with minimal residual symptoms; • changes in vital capacity and negative inspiratory
severe residual deficits occur in up to 10%. Residual deficits force, which are assessed to identify impending
are most likely in patients with rapid disease progres- neuromuscular respiratory failure.
sion, those who require mechanical ventilation or those
Indications for ICU admission include the following:
60 years of age or over. Death occurs in 3–8% of cases,
ventilatory insufficiency, severe bulbar weakness threat-
resulting from respiratory failure, autonomic dysfunction, ening pulmonary aspiration, autonomic instability or
sepsis or pulmonary emboli.121 coexisting general medical factors,122 and often a combi-
Aetiology nation of factors, are present. About 30% of patients have
The diagnosis of GBS is confirmed by the findings of respiratory failure that requires mechanical ventilation.
cytoalbuminological dissociation (elevation of the CSF
Practice tip
protein without concomitant CSF pleocytosis), and
by neurophysiological findings suggestive of an acute In Guillian–Barré syndrome vital capacity less than
(usually demyelinating) neuropathy. These abnormalities 20 mL/kg is a sign of respiratory fatigue requiring early
may not be present in the early stages of the illness.120 intubation and leads to earlier extubation and a better
There are two forms of GBS. The demyelinating form, prognosis.
the more common one, is characterised by demyelin-
ation and inflammatory infiltrates of the peripheral nerves Ventilatory failure is primarily caused by inspiratory
and roots. In the axonal form the nerves show Wallerian muscle weakness, although weakness of the abdominal and
degeneration (the fatty degeneration of a nerve fiber after accessory muscles of respiration, retained airway secretions
it has been severed from its cell body) with an absence leading to pulmonary aspiration and atelectasis are all
of inflammation. Discrimination between the axonal and contributory factors. The associated bulbar weakness and
demyelinating forms relies mainly on electrophysiological autonomic instability reinforce the need for control of the
methods. There is a close association between GBS and a airway and ventilation.
preceding infection, suggesting an immune basis for the Acute motor and sensory axonal neuropathy, the
syndrome.The commonest infections are due to Campylo- acute axonal form of GBS, usually presents with a rapidly
bacter jejuni, cytomegalovirus and Epstein–Barr virus. developing paralysis developing over hours and a rapid
development of respiratory failure requiring tracheal
Pathophysiology intubation and ventilation. PaCO2 may remain constant
GBS is the result of a cell-mediated immune attack on until just before intubation, emphasising the importance
peripheral nerve myelin proteins. The Schwann cell is of not relying purely on arterial blood gas analysis to make
spared, allowing for remyelination in the recovery phase of decisions regarding intubation.
the disease. With the autoimmune attack there is an influx Recently, sensory involvement in relation to pain has
of macrophages and other immune-mediated agents been studied asserting the clinical observation of pain
572 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

ranging from mild to severe in the acute and rehabilitant • Routine daily gentle exercise as part of a flexible
phases. Chronic pain is often present in survivors of GBS.123 program improves wellbeing and strength.
There may be total paralysis of all voluntary muscles
of the body, including the cranial musculature, the • Fatigue must be avoided, as autonomic nerve
dysfunction, deafferent pain syndromes, muscle pain
ocular muscles and the pupils. Prolonged paralysis and
and depression can be exacerbated.
incomplete recovery are more likely, and prolonged venti-
latory support may be necessary. Walgaard and colleagues • Suctioning, coughing, bladder distension, constipation
found that GBS patients who experience rapid disease and the Valsalva manoeuvre can also aggravate
progression, bulbar dysfunction, bilateral facial weakness autonomic nerve dysfunction instability.
or autonomic nerve dysfunction were more likely to • Therapeutic massage, warm and cold packs and
require mechanical ventilation.124 Tracheostomy is usually careful positioning contribute to comfort and pain
performed within 2 weeks, and mechanical ventilation is management.
delivered in a supportive mode with minimal yet adequate
sedation and pain management.
• The patient’s surroundings should be pleasant and
presentable, especially during long recovery.
Patient management • Communication techniques need to be refined to
Assessment and understanding of neuromuscular weakness prevent fatigue and frustration.
through motor and sensory neurological assessment is vital • Patience, tolerance, empathy, humour and family
in the acute care and rehabilitation of GBS patients: involvement assist the patient in psychological
• Comprehensive respiratory assessment (level of resilience and recovery.
overall patient comfort, frequency and depth of In the acute phase, accurate diagnosis and timely venti-
breathing, forced vital capacity, use of accessory latory support are provided by effective communication
muscles, presence of paradoxical respiration and between primary and in-hospital care providers. Patients
integrity of upper airway reflexes), ABG data and who require mechanical ventilation typically present with
chest radiography determine levels of fatigue in both rapidly progressive weakness and fatigue.
the acute stage (for intubation and ventilation) and The side effects of intravenous immunoglobulin
rehabilitation (weaning) stage. Long-term ventilation administration include low-grade fever, chills, myalgia,
increases the risk of ventilator-associated pneumonia diaphoresis, fluid imbalance, neutropenia, nausea and
(VAP), and routine surveillance for VAP is vital. headaches, and at times acute tubular necrosis. Adminis-
• Cardiovascular assessment is important, as serious tration and assessment require adherence to transfusion
tachyarrhythmias and bradyarrhythmias and protocols. Plasmapheresis is performed by transfusion
destabilising fluctuations in blood pressure caused nurse specialists in collaboration with the patient care
by autonomic impairment are prevalent. This nurse. Multidisciplinary case management is utilised after
feature is common during fatigue, sleep and states of stabilisation in the acute phase, especially when the level
dehydration. Often, autonomic dysfunction is worst of severity is determined. Recovery and rehabilitation
in the early stages of a nosocomial infection.125 process information is provided to the patient and family
so that consultation and communication are effective
• Cranial nerve assessment and dermatome (for in recovery.
sensory) and muscle strength assessment assist in
mapping the progression, severity and rehabilitation Myasthenia gravis
of the disease and determining the risk of aspiration.
Myasthenia gravis is an autoimmune disorder caused by
Pain (especially neuropathic) is particularly common
autoantibodies against the nicotinic acetylcholine receptor
in GBS during changes in myelination, and can be
difficult to treat.126 Assessment will include all aspects on the postsynaptic membrane at the neuromuscular
as indicated for the long-term immobile, intubated, junction. It is characterised by weakness and fatigability
ventilated and neuromuscular-impaired patient. of the voluntary muscles. It peaks in the third and sixth
decades of life. Its prevalence in Western countries is
When caring for a neuromuscular-impaired patient, a 14.2/100,000.127 Prevalence rates have been rising steadily
structured care plan is essential for continuity of care and over recent decades, probably due to decreased mortality,
should involve the patient and family. This is of particular longer survival and higher rates of diagnosis. The devel-
importance in the long-term recovery phase, where the opment of respiratory failure, progressive bulbar weakness
provision of sleep, good nutrition and prevention of the leading to failure of airway protection and severe limb
complications of immobility (nosocomial infections, deep and truncal weakness causing extensive paralysis, as in a
vein thrombosis, integument and muscular weakening, myasthenic crisis, all may result in admission to ICU.
adequate nutrition and constipation) are important:
• Endotracheal and pharyngeal suction can be Aetiology
demanding (weakened upper airway reflexes), and Myasthenic crisis occurs when weakness from acquired
sputum plugging and retention requires frequent myasthenia gravis becomes severe enough to necessitate
repositioning and physiotherapy. intubation for ventilatory support or airway protection.
 CHAPTER 17 NEUROLOGICAL ALTERATIONS AND MANAGEMENT 573

At some point in their illness, usually within 2–3 years the underlying myasthenia gravis. An experienced neurol-
after diagnosis, 12–16% of myasthenic patients experience ogist, who will ultimately provide the patient’s care outside
crisis. This occurrence is most likely in patients whose the ICU, should be part of the care team. Options for
history includes previous crisis, oropharyngeal weak- treatment during crisis include: use of acetylcholinester-
ness or thymoma. Possible triggers include infections, ase inhibitors, plasma exchange, IV immunoglobulins and
aspiration, physical and emotional stress and changes in immunosuppressive drugs, including corticosteroids.131
medications.128 Most antibiotics have a trigger effect and
should be carefully prescribed by an informed doctor. Patient management
Median duration of hospitalisation for crisis is 1 month. Careful and accurate assessment by the nurse in the
The patient usually spends half of this time intubated in presenting myasthenic crisis patient determines the
the ICU. About 25% of patients are extubated on hospi- triggers of the event and incorporates a history, including
tal day 7, 50% by hospital day 13, and 75% by hospital infections and prescribed medications. These medica-
day 31. The mortality rate during hospitalisation for crisis tions can exacerbate acetylcholine receptor blockade, and
has fallen from nearly 50% in the early 1960s to between respiratory demand proves too much for the myasthenic
3% and 10% today. With the incidence of crisis remain- patient. Awareness by the nurse of trigger medications
ing stable over the past 30 years, this fall in mortality ensures advocacy for the patient when the prescription
rates probably reflects improvements in the intensive care is uncertain.128
assessment and management of these patients.129 • Respiratory and cardiovascular assessment incorporates
upper and lower airway muscle weakness. ABGs are
Pathophysiology a poor marker for intubation and ventilation because
In myasthenia gravis both structural changes in the archi- these values change late in the decompensation cycle.
tecture of the neuromuscular junction and dynamic Being able to recognise fatigue (inability to speak,
alterations in the turnover of acetylcholine receptors erode poor lung expansion,VC below 1 L, shoulder and arm
the safety margin and efficiency of neuromuscular trans- weakness) in patients with neuromuscular weakness
mission. Of all patients with myasthenia gravis, 80–85% and air hunger is important.130
have an identifiable and quantifiable antibody found in the
immunoglogulin G fraction of plasma, which is responsi- • Non-invasive ventilation can be difficult to administer
safely, with the potential for aspiration due to insidious
ble for blocking receptors to the action of acetylcholine upper airway weakness; however, the option should be
at the neuromuscular junction.128 Therefore, successful considered with careful assessment of gag, swallow and
neuromuscular transmission is markedly affected by small cough reflexes in order to prevent intubation.129
and subtle changes in acetylcholine release and other
triggers (as above), and this gives rise to the decrement • Neuromuscular blockade should be avoided (residual
in transmission with repetitive stimulation and the char- long-term paralysis), with the use of glottal local
acteristic fatigable muscle weakness. Pharmacological anaesthetic spray for emergency intubation and
management for myasthenia gravis includes the use of ventilation.
anticholinesterases (pyridostigmine), steroids, azathio- • Placement of small-bore duodenal tubes decreases the
prine and cyclophosphamide. Thymectomy reduces the risk of aspiration and may be more comfortable than
antibodies responsible for acetylcholine blockade and is regular nasogastric tubes for the patient.
often performed early in the disease.129 Plasmapheresis • Tracheostomy is generally not needed, as the duration
and intravenous immunoglobulin are used in the short of intubation is often less than 2 weeks.
term for myasthenic crisis and are especially useful for
preventing respiratory collapse or assisting with weaning. • Cardiac assessment needs to include assessment for
arrhythmias of both atrial and ventricular origin due
Clinical manifestations to autonomic nerve dysfunction.128 These can be
insidious and can be provoked by subtle changes in
In a myasthenic crisis, vital capacity falls, cough and
electrolytes.
sigh mechanisms deteriorate, atelectasis develops and
hypoxaemia results.130 Ultimately, fatigue, hypercarbia • Nursing care will relate to the needs of long-term
and ventilatory collapse occur. Commonly, superimposed immobilised, intubated, ventilated patients with
pulmonary infections lead to increased morbidity and neuromuscular alterations.
mortality. Assessment for triggers begins with a careful Myasthenia gravis patients have similar care needs to
review of systems, with attention to recent fevers, chills, those of patients with GBS (refer to Patient management
cough, chest pain, dysphagia, nasal regurgitation of liquids for GBS). Fatigue and the structure and timing of care
and dysuria. Detailed history taking should note any are very important. Flexibility of care is important, as
trauma, surgical procedures and medication use. General energy fluctuates on an hourly basis.130 Despite having a
assessment includes vital signs; ear, nose and throat shorter recovery time than GBS, weaning and recovery
inspection; chest auscultation; and abdominal check. In in myasthenia gravis is still a slow process and impulsive
addition to supportive care and the removal of triggers, extubation is discouraged.131 Therapy should be tailored
management of myasthenic crisis includes treatment of on an individual basis using best clinical judgement.
574 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Status epilepticus blood pressure; a loss of cerebral autoregulation, resulting

Status epilepticus (SE) has been generally defined as in the dependence of CBF on systemic blood pressure;
enduring seizure activity that is not likely to stop spon- and hypoglycaemia due to the exhaustion of glycogen
taneously. The traditional SE definition is 30 minutes of stores and increased neurogenic insulin secretion. Intra-
continuous seizure activity (which has been updated due to cranial pressure can rise precipitously in SE.The combined
neurological alteration to 5 minutes only) or two or more effects of systemic hypotension and intracranial hyper-
seizures without full recovery of consciousness between tension may result in a compromised cerebral circulation
the seizures.132 There are as many types of SE as there are and cerebral oedema. Intracranial pressure monitoring is
types of seizures. The distinction between convulsive and advisable in prolonged severe SE when raised intracranial
non-convulsive SE depends on clinical observation and pressure is suspected. Further complications that can occur
on a clear understanding of several SE types. Estimates include rhabdomyolysis leading to acute tubular necrosis,
of the overall incidence of SE have varied from 10 to 60 hyperkalaemia and hyponatraemia.135
per 100,000 person-years, depending on the population Patient management
studied and the definitions used.133 Over half the cases of
SE are acute symptomatic, emphasising the importance in The following patient management should be considered.
management of identifying an acute precipitant. Infections Resuscitation
with fever are the major cause of SE, accounting for 52%
of cases, while in adults low antiepileptic drug levels, SE requires control of the seizure and then investigation
cerebrovascular accident, hypoxia, metabolic causes and regarding the cause. Airway protection is often difficult in
alcohol represent the main acute causes. The mortality in the seizing patient, so the first line of treatment includes
status epilepticus is about 20%; most patients die of the basic life-support measures followed by the administra-
underlying condition rather than the status epilepticus tion of IV propofol, midazolam or, in refractory cases,
itself. SE can result in permanent neurological and mental phenytoin. Neuromuscular blockade will be required to
deterioration, particularly in young children; the risks of facilitate intubation in patients who continue to have
morbidity greatly increase with longer duration of the tonic–clonic seizure activity despite these pharmacolog-
status epilepticus episode. SE in the intensive care setting ical interventions. Rocuronium (1 mg/kg), a short-acting,
falls into two main groups: those transferred to the ICU non-depolarising muscle relaxant that is devoid of signifi-
because of uncontrolled SE (refractory SE) and those who cant haemodynamic effects and does not raise intracranial
are admitted to the ICU for another reason and have SE pressure, is the preferred agent. Succinylcholine should be
as an additional finding.134 avoided if possible, as the patient may be hyperkalaemic
as a consequence of possible rhabdomyolysis. Prolonged
Pathophysiology neuromuscular blockade should be avoided as it only stops
At a cellular level, status epilepticus results from a failure the motor response, hence masking the altered neuronal
of normal inhibitory pathways, primarily mediated activity.131 Once the seizures are controlled, intubation and
by gamma-aminobutyric acid acting via gamma- ventilation can protect the airway and potentially reverse
aminobutyric acid A receptors. This loss of inhibitory the acidosis. In the patient who already has an airway
drive allows the activation of excitatory feedback loops, secured, urgent IV administration of propofol, midazolam
leading to repetitive, synchronous firing of large groups or phenytoin is indicated.132
of neurons. As seizure activity continues, there is further
decline in gamma-aminobutergic inhibitory tone that Practice tip
counterbalances neuronal excitation function. Continued
The three most crucial factors determining the outcome
excitatory input mediated primarily by glutamate leads
from status epilepticus are the underlying aetiology,
to neuronal cell death.134
the speed of anti-seizure treatment and the age of the
Clinical manifestations person. Older aged individuals with status epilepticus
Convulsive SE is a medical emergency. The initial conse- frequently have a symptomatic cause, possess a more
quence of a prolonged convulsion is a massive release of limited reserve to recover due to comorbidities and
plasma catecholamines, which results in a rise in heart have a higher mortality rate.
rate, blood pressure and plasma glucose. During this stage
cardiac arrhythmias are often seen, and may be fatal. CBF Specific post SE patient assessment
is greatly increased, and thus glucose delivery to active Post SE, the patient remains intubated, ventilated and
cerebral tissue is maintained. As the seizure continues, sedated. Neurological assessment is limited in the sedated
hyperthermia above 40°C with lactic and respiratory patient. Pupillary response is usually sluggish and reflects
acidosis continues to intensify, especially without adequate the medication prescribed. Routine monitoring in an ICU
resuscitation and control of the seizure.135 is essential, with CT and MRI to exclude mass lesions.
The SE may then enter a second, late phase in which Blood glucose level should be checked immediately by
cerebral and systemic protective measures progressively bedside testing. Blood should be tested for electrolytes,
fail. The main characteristics of this phase are: a fall in magnesium, phosphate, calcium, liver and renal function,
 CHAPTER 17 NEUROLOGICAL ALTERATIONS AND MANAGEMENT 575

haematocrit, white blood cell count, platelet count, antie- duration.The goal of pharmacological therapy is to achieve
pileptic drug levels, toxic drugs and substances (particularly the rapid and safe termination of the seizure, and to prevent
salicylates) and alcohol. its recurrence without adverse effects on the cardiovascu-
EEG monitoring in the ICU for refractory SE is lar and respiratory systems or without altering the level of
essential, as a patient may enter a drug-induced coma consciousness. Diazepam, lorazepam, midazolam, phenytoin
with little outward sign of convulsions yet have ongoing and phenobarbitone have all been used as first-line therapy
electrographic epileptic activity. Furthermore, continuous for the termination of SE.102 The antiseizure activity of
recording will give an indication of worsening of gener- phenytoin is complex; however, its major action appears to
alised convulsive status epilepticus regardless of the presence block the voltage-sensitive, use-dependent sodium channels.
or absence of sedating drugs or paralysing agents. This can Once SE is controlled, attention turns to preventing its
be monitored only by EEG and manifests as bilateral EEG recurrence. The best regimen for an individual patient will
ictal discharges. Deeper sedation and anaesthesia is then depend on the cause of the seizure and any history of anti-
indicated and can be titrated to EEG results.136 epileptic drug therapy. A patient who develops SE in the
course of alcohol withdrawal may not need antiepileptic
Pharmacological patient management drug therapy once the withdrawal has run its course. In
Because only a small fraction of seizures go on to become contrast, patients with new, ongoing epileptogenic stimuli
SE, the probability that a given seizure will proceed to SE (e.g. encephalitis or trauma) may require high doses of
is small at the start of the seizure and increases with seizure antiepileptic medication to control their seizures.

Summary
This chapter provides a description and application of neurological alterations and their management. The chapter
launches with an overview of neurological dysfunction, specifically pathophysiological alterations of consciousness, alter-
ations in motor and sensory function and alterations in cerebral perfusion and metabolism. Cerebral oedema is related to
intracranial pressure preceding the therapeutic management of these conditions. Intracranial hypertension is discussed in
association with cerebral perfusion and metabolic events. Delayed cerebral ischaemia and vasospasm are applied to brain
injury in general but, more specifically, aneurysmal subarachnoid haemorrhage. Central nervous system disorders include
traumatic brain and spinal injury, their aetiology, clinical pathophysiology and management. Cerebrovascular disorders
focus on ischaemic stroke, intracerebral haemorrhage and aneurysmal subarachnoid haemorrhage. The research vignette
reports on a randomised controlled trial of blood pressure reduction in ischaemic stroke in a highly prevalent Chinese
population. Meningitis and encephalitis are included in the section on infection and inflammation with Guillain–Barré
syndrome, myasthenic crisis and status epilepticus in the neuromuscular alterations component. A traumatic brain injury
case is presented with learning activities.

Case study
Luke, a 25-year-old male, was standing outside a pub on a Friday night and became involved in a verbal
altercation with another man. Without warning Luke was punched in the left side of his head, causing him
to fall backwards and strike his head on the concrete pavement. As the attack was sudden, Luke did not
have time to break his fall with his hands and his head took the full impact. It was about 10 minutes before
a passerby recognised that Luke was unconsciousness.
An ambulance was called and arrived approximately 6 minutes later. On initial assessment Luke’s GCS
was 7: eye opening response = 2, verbal response = 2 and motor response = 3. His limbs: extension
in the right and abnormal flexion in the left to pain. His vital signs: heart rate 85 beats per minute and
regular, respirations 12 per minute and regular. Blood pressure was 135/89 mmHg. A hard C spine collar
was applied and spinal precautions were applied. As the officers were carrying out this initial assessment,
Luke’s GCS dropped to 4 (eye opening response = 1, verbal response = 1 and motor response = 2). His
pupils were unequal, the left pupil was noted to be unresponsive and size 6 and his right pupil was
briskly reactive and size 3. At the same time his breath rate dropped to 8 per minute and his blood
pressure rose to 168/98 mmHg. The ambulance officers inserted a wide bore antecubital fossa cannula
and administered mannitol 100 mL immediately stat. Luke was intubated and hand ventilated with a
size 7.5 endotracheal tube and transferred to a major tertiary hospital approximately 500 metres away.
The time from the 000 phone call being logged to ‘time off stretcher’ in the emergency department was
37 minutes.
576 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

On arrival into the emergency department Luke was attached to a ventilator. His GCS remained as 4,
but his vital signs were unremarkable. A full primary trauma survey was performed together with a CT
scan of his head and cervical spine. The CT scan of his head indicated an acute left-sided extradural
haematoma, 13 mm in depth overlying the left temporal lobe with effacement of the left lateral ventricle
and 3 mm midline shift to the right. The CT of the cervical spine confirmed no abnormality. Luke was
transferred to the operating theatre where a left-sided craniotomy and evacuation of a large extradural
haematoma was performed. An EVD was inserted into the right lateral ventricle. There was significant
swelling of the brain tissue during surgery, so that the bone flap was unable to be replaced at the end of
surgery. The neurosurgeons prescribed an ICP below 20 mmHg and CPP greater than 65 mmHg. Luke was
then transferred to the ICU.

INTENSIVE CARE
In the ICU Luke was connected to the ventilator and monitor. EtCO2 continuous monitoring was in progress.
At that time his ICP increased to 28 mmHg. In response, the EVD system was opened to drain CSF and
Luke was placed in a reverse Trendelenburg position with neutral alignment while maintaining spinal
precautions. IV propofol and fentanyl infusions were commenced. Luke’s vital signs on admission to the
ICU were: GCS 3; left pupil remained fixed and dilated, size 6, right pupil size 3 and sluggishly reactive; core
temperature 37.9°C; heart rate 62 beats per minute; sinus rhythm; blood pressure 117/54, MAP 69 mmHg.
Noradrenaline infusion was commenced through a central venous catheter commencing at 0.567 mcg/kg/
min to maintain a CPP greater than 65 mmHg.

Luke’s core body temperature was actively cooled to between 35°C and 36°C. To prevent shivering, an
IV cisaturcurium infusion was commenced. In response to a high PaCO2 of 43 mmHg his respiratory rate
on the ventilator was increased to 16 breaths per minute. After these interventions Luke’s ICP reduced to
19 mmHg.

Luke’s parents finally arrived and a meeting was arranged for them to speak with the neurosurgeons and
the intensive care specialist. During this meeting Luke’s prognosis was described as very poor due to the
nature of his injury. Also, the pupillary changes, changes in vital signs and fact that his brain appeared to be
non-pulsatile at the end of surgery were indicators of a very poor prognosis.

DAY 2
Over the next 24 hours, Luke’s condition remained critical. A progress CT scan was performed and showed
evolving petechial haemorrhages in the pons located in the brain stem. He remained heavily sedated and
neuromuscular blockade was continued. The ICP continued to fluctuate, ranging between 17 mmHg and
26 mmHg. The spikes in ICP were treated with IV boluses of propofol and fentanyl. At one occasion in
response to rising ICP, a Cushing’s triad response was noted. The heart rate dropped to 48 beats per
minute, and the systolic blood pressure increased to 187 mmHg despite the noradrenaline infusion being
titrated to 0 mL/hour. In response, IV mannitol 100 mL was administered. The prescribed CPP of greater
than 65 mmHg was maintained by titrating high doses of IV noradrenaline with regular IV fluid boluses. The
EVD height was initially set at 15 cmH2O and on free drainage but, with the rises in ICP, this was lowered to
10 cmH2O. This was to allow for a greater drainage of CSF to reduce the pressure and volume within the
brain. The ventilator settings were adjusted to maintain a PaCO2 between 35 and 40 mmHg. Active cooling
continued, maintaining core temperature between 35°C and 36°C. Heart rate ranged from 63–72 beats per
minute. Central venous pressure varied from 6 to 13 mmHg.

Luke’s IV fluid intake included IV infusions of 0.9% normal saline, propofol, fentanyl, cisaturcurium infusions
and noradrenaline. An IV crystalloid fluid bolus of 250 mL was administered on two occasions due to
increasing noradrenaline requirements, large urinary output and low central venous pressure measurements.
Luke was also commenced on enteral feeding via a nasogastric tube. Luke’s hourly urinary output varied
between 40 and 195 mL/hour. Given the seriousness of Luke’s condition, his parents, siblings and close
friends were in attendance throughout the day and night and they were given regular updates in regard to
Luke’s progress and condition by the nursing and medical teams.

DAY 3
At 04:26 Luke’s ICP increased suddenly to 31 mmHg. His core temperature and PaCO2 were within the
prescribed target limits. Luke’s heart rate initially increased to 145 beats per minute and then slowed to
39 beats per minute and his blood pressure rose to 194 mmHg. During this time his right pupil had become
 CHAPTER 17 NEUROLOGICAL ALTERATIONS AND MANAGEMENT 577

unreactive and increased to size 5. A further bolus of mannitol 100 mL was given immediately stat and
the EVD height was lowered to 5 cmH20. Over the next 20 minutes Luke’s ICP fell to 22 mmHg. Despite
this, Luke remained bradycardic (rate 48 beats per minute) and noradrenaline requirements increased to
1.11 mcg/kg/min. Soon after, Luke’s hourly urinary output measure increased to 480 mL of dilute urine,
which was attributed to the mannitol. In the subsequent hour the urinary output increased to 680 mL
and serum and urine osmolality samples were sent to the laboratory. The results were consistent with
diabetes insipidus. A fluid bolus was administered to counteract the diuresis and 1 mcg of desmopressin
intravenously was prescribed and administered with effect.
Later that morning the neurosurgeons and intensive care staff specialist requested to meet with Luke’s
family. As with all meetings between the medical teams and family, the bedside nurse was in attendance.
They were informed that Luke was showing signs consistent with severe brain damage and possibly even
brain death. The decision was made to reduce the sedation and the neuromuscular blockade and, if the
ICP remained at 20 mmHg or below, to cease it altogether to allow the medical team to assess Luke’s
neurological condition and to carry out cranial nerve testing. Although devastated by the outcome of the
meeting, the family appeared to understand the progression of Luke’s condition. During the course of the
afternoon, sedation and neuromuscular blockade were reduced and finally ceased altogether without a
correlating rise in ICP. Overnight, haemodynamics were maintained within acceptable parameters with
the support of noradrenaline, fluid bolus and further desmopressin administration. The family stayed with
Luke overnight. The next day Luke was declared brain dead after extensive brain death tests. The medical
and nursing team met with the family to inform them that Luke had died. At this stage the family broached
the topic of organ donation as they had discussed this amongst themselves overnight. They felt that Luke
would have wanted to donate his organs. A meeting was set up with the organ donation coordinator
who then started the process. Following the donation of his organs, Luke’s family, in a follow-up with the
coordinator, stated that they found much solace from the fact that he had donated his organs and so had
improved the lives of others.

CASE STUDY QUESTIONS

1 With a brain injury to the left side of the brain, what deficits would you expect to see in your patient?
What potential communication problems may be encountered and why?
2 From your reading of the Case study, explain the rationale for why pupil dysfunction is ipsilateral while
limb movement is contralateral.
3 What clinical signs are indicative of a fractured base of skull?
4 Explain the compensatory mechanisms used by the body to help control intracranial pressure.
5 What is the basis for PaCO2 control in a patient with a traumatic brain injury?

R E S E A R C H V I G N E T T E 137

He J, Zhang Y, Xu T, Zhao Q, Wang D, Chen CS et al; CATIS Investigators. Effects of immediate blood pressure
reduction on death and major disability in patients with acute ischemic stroke: the CATIS randomized clinical trial.
JAMA 2014;311(5):479–89

Abstract
Importance: Although the benefit of reducing blood pressure for primary and secondary prevention of stroke has
been established, the effect of antihypertensive treatment in patients with acute ischemic stroke is uncertain.

Objective: To evaluate whether immediate blood pressure reduction in patients with acute ischemic stroke would
reduce death and major disability at 14 days or hospital discharge.

Design, setting, and participants: The China Antihypertensive Trial in Acute Ischemic Stroke, a single-blind, blinded
end-points randomized clinical trial, conducted among 4071 patients with nonthrombolysed ischemic stroke within
578 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

48 hours of onset and elevated systolic blood pressure. Patients were recruited from 26 hospitals across China
between August 2009 and May 2013.

Interventions: Patients (n = 2038) were randomly assigned to receive antihypertensive treatment (aimed at lowering
systolic blood pressure by 10% to 25% within the first 24 hours after randomization, achieving blood pressure less than
140/90 mmHg within 7 days, and maintaining this level during hospitalization) or to discontinue all antihypertensive
medications (control) during hospitalization (n = 2033).

Main outcomes and measures: Primary outcome was a combination of death and major disability (modified Rankin
Scale score ≥3) at 14 days or hospital discharge.

Results: Mean systolic blood pressure was reduced from 166.7 mmHg to 144.7 mmHg (−12.7%) within 24 hours
in the antihypertensive treatment group and from 165.6 mmHg to 152.9 mmHg (−7.2%) in the control group within
24 hours after randomization (difference, −5.5% [95% CI, −4.9 to −6.1%]; absolute difference, −9.1 mmHg [95% CI,
−10.2 to −8.1]; P < 0.001). Mean systolic blood pressure was 137.3 mmHg in the antihypertensive treatment group
and 146.5 mmHg in the control group at day 7 after randomization (difference, −9.3 mm Hg [95% CI, −10.1 to −8.4];
P <0 .001). The primary outcome did not differ between treatment groups (683 events [antihypertensive treatment]
vs 681 events [control]; odds ratio, 1.00 [95% CI, 0.88 to 1.14]; P = 0.98) at 14 days or hospital discharge. The
secondary composite outcome of death and major disability at 3-month posttreatment follow-up did not differ
between treatment groups (500 events [antihypertensive treatment] vs 502 events [control]; odds ratio, 0.99 [95%
CI, 0.86 to 1.15]; P = 0.93).

Conclusion and relevance: Among patients with acute ischemic stroke, blood pressure reduction with anti-
hypertensive medications, compared with the absence of hypertensive medication, did not reduce the likelihood of
death and major disability at 14 days or hospital discharge.

Critique
This is the first randomised trial with sufficient statistical power to test the effect of immediate blood pressure
reduction on adverse clinical outcomes in patients with acute ischaemic stroke. One of the major unresolved
management issues in stroke care is how to manage this early elevation of blood pressure in patients with cerebral
ischaemia. Despite the large sample size, blood pressure reduction with antihypertensive medications, compared
with the absence of hypertensive medication, did not reduce the likelihood of death and major disability at 14 days
or hospital discharge.

This study reflects the population and clinical practice of China. Compared with white populations, Chinese have
a higher age-adjusted incidence of stroke, a lower mean age of stroke onset and a higher proportion of strokes
attributable to ICH.138 Enrolled patients were substantially younger, smoked more often and received concomitant
acute anticoagulation therapy more often than typical Western stroke cohorts.

The CATIS design and implementation has some limitations. The open-label intervention where both the researchers
and participants know which treatment is being administered left outcome assessments vulnerable to rater bias
and may have influenced the results. Also, the entry stroke severity was relatively mild, with a median National
Institutes of Health Stroke Scale score of 4. This degree of severity parallels the average severity of ischaemic
stroke in clinical practice but is substantially less than other clinical trials because of the high rate of good outcomes
expected with mild deficits at presentation. As a result, two-thirds of enrolled patients in the control group achieved
the primary outcome (alive and not disabled), reducing opportunities for the intervention to demonstrate benefit.
As well, patients treated with intravenous thrombolytic therapy at baseline were excluded because of different
requirements for blood pressure reduction, excluding another group of greater severity. The remaining unanswered
question in blood pressure management in early ischaemic stroke involves the acute period, within the first few
hours after stroke onset, when there is still substantial penumbral, at-risk tissue and if blood pressure modification
has a role in improving outcome.
 CHAPTER 17 NEUROLOGICAL ALTERATIONS AND MANAGEMENT 579

Lear ning a c t iv it ie s
1 What are the different types of cerebral oedema that can occur?
2 What are the main therapeutic management strategies used to minimise vasospasm post clipping of a ruptured
aneurysm?
3 A child is taken to the emergency room with lethargy, fever and a stiff neck on examination.
a) What findings on initial lumbar puncture indicate bacterial versus viral meningitis? b) In the case of bacterial
meningitis, what are the most likely organisms?
4 Your patient had symptoms of an ischaemic stroke approximately 2 hours ago and is undergoing a confirmatory
CT scan in 30 minutes. You know tPA must be administered within 3 hours of the symptoms. What actions
would you take? What is your rationale for these actions?

Online resources
Academy Spinal Cord Injury Nurses (ASCIP), www.academyscipro.org
Australian Institute of Health and Welfare publication: Stroke and its management in Australia: an update, www.aihw.gov.au/
publication-detail/?id=60129543613
Brain Injury Association of America, www.biausa.org
Brain Trauma Foundation, www.braintrauma.org
Centers for Disease Control: Traumatic Brain Injury, www.cdc.gov/traumaticbraininjury
Cervical collars, www.youtube.com/watch?v=cYxnp6ml8mE
Cervical traction, www.alfredhealth.org.au/Assets/Files/SpinalClearanceManagementProtocol_External.pdf
CSF drainage and ICP monitoring system, www.youtube.com/watch?v=MPpH8MnXhb8&list=PLH9gpVKlHL6p09M1Pz8Upo
qggfwLsfxzA
Ethical guidelines for the care of people in post-coma unresponsiveness, www.nhmrc.gov.au/_files_nhmrc/file/publications/
synopses/e81.pdf
External ventricular drain, www.aann.org/uploads/AANN11_ICPEVDnew.pdf
Hypertonic Saline Protocol, https://ambulance.qld.gov.au/docs/cpm_dtp_combined_040514_b.pdf
Meningitis, http://netsvic.org.au/clinicalguide/cpg.cfm?doc_id=5179
Model of Stroke Care Western Australia, www.healthnetworks.health.wa.gov.au/modelsofcare/docs/Stroke_Model_of_Care.pdf
National Resource Centre for Traumatic Brain Injury, www.brainlink.org.au
National Stroke Foundation of Australia publication, www.strokefoundation.com.au
Sports injuries: head and spine, www.injuryupdate.com.au/injury-head-neck-spinal.php
Stroke Management Guidelines, http://strokefoundation.com.au/site/media/clinical_guidelines_stroke_managment_2010_
interactive.pdf
Stroke Thrombolytic Protocol, www.health.wa.gov.au/circularsNew/attachments/556.pdf
Traumatic Brain Injury National Data Centre, www.tbindc.org
World Health Organization Neurological Disorders, www.who.int/mental_health/.../neurological_disorders_report_web.pdf

Further reading
Anaesth Intensive Care Med 2014;15(4):141–208. Special edition on neurosurgical anaesthesia and physiology, <http://www.
sciencedirect.com/science/journal/14720299/15/4>; [accessed 11.14].
Crit Care Clin 2014;30(4):657–842. Special edition on neurocritical care, <http://www.sciencedirect.com/science/ journal/
07490704/30/4>; [accessed 11.14].
Gibson CL. Cerebral ischemic stroke: is gender important? J Cereb Blood Flow Metab 2013;33(9):1355–61. Open Access,
<http://www.nature.com/jcbfm/journal/v33/n9/full/jcbfm2013102a.html>; [accessed 11.14].
Schweizer S, Meisel A, Marschenz S. Epigenetic mechanisms in cerebral ischemia. J Cereb Blood Flow Metab 2013;
33(9):1335–46. Open Access, <http://www.nature.com/jcbfm/journal/v33/n9/full/jcbfm201393a.html>; [accessed 11.14].
580 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

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32 Brain Trauma Foundation, American Association of Neurological Surgeons, Joint Section on Neurotrauma and Critical Care. Guidelines for
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34 Stocchetti N, Maas AI. Traumatic intracranial hypertension. N Engl J Med 2014;370(22):2121-30.
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 CHAPTER 17 NEUROLOGICAL ALTERATIONS AND MANAGEMENT 581

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96 Ciccone A, Valvassori L, Nichelatti M, Sgoifo A, Ponzio M, Sterzi R. Endovascular treatment for acute ischemic stroke. N Engl J Med
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102 Steiner T, Al-Shahi Salman R, Beer R, Christensen H, Cordonnier C, Csiba L et al. European Stroke Organisation guidelines for the
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104 Helbok R, Kurtz P, Vibbert M, Schmidt MJ, Fernandez L, Lantigua H et al. Early neurological deterioration after subarachnoid haemorrhage:
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107 Hamdan A, Barnes J, Mitchell P. Subarachnoid hemorrhage and the female sex: analysis of risk factors, aneurysm characteristics, and
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108 Sandström N, Yan B, Dowling R, Laidlaw J, Mitchell P. Comparison of microsurgery and endovascular treatment on clinical outcome following
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109 Wang X, Chen J-X, Mao Q, Liu Y-H, You C. Relationship between intracranial pressure and aneurysmal subarachnoid hemorrhage grades.
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Chapter 18

Support of renal function

Ian Baldwin, Gavin Leslie

KEY WORDS
Learning objectives
After reading this chapter, you should be able to: acute kidney injury
• summarise the physiology of urine production acute renal failure
• describe the most likely causes of kidney injury in the critically ill adult continuous renal
replacement
• differentiate between acute and chronic renal failure therapy
• outline treatment approaches in managing acute kidney injury in critical dialysis history
illness
urine production
• appreciate historical developments in dialysis
• describe the indications for renal replacement therapy in critical care
• understand the principles and challenges associated with nursing
management of continuous renal replacement therapy in critical care.

Introduction
Sudden deterioration of kidney function as a result of physiological injury, to the
point where there is retention of nitrogenous wastes, referred to as acute renal
failure (ARF), is a common manifestation of critical illness and is often associated
with failure of other organs. Acute renal failure is a syndrome with numerous
causes, including glomerulonephritis, prerenal azotaemia, urinary tract obstruc-
tion and vasculitis. Acute tubular necrosis (ATN) is a collective term commonly
used in the past to describe acutely deteriorating renal function, reflecting
pathological changes from various renal insults of a nephrotoxic or ischaemic
origin. Factors that cause renal function to deteriorate are not, however, always
ischaemic or necrotic in origin, and a syndrome with degrees of deterioration
prior to failure is often evident. Therefore, a consensus definition and classifica-
tion system has been established that focuses on incremental organ injury rather
than end-stage organ failure.1 This approach describes staging of ARF severity
and embraces the concept of acute kidney injury (AKI) where, like other organs
of the body, a dynamic spectrum is found, from small indiscrete changes in
function that are immediately reversible through to gross signs and irreversible
organ failure.2 With this change of conceptual focus in recent years new consensus
guidelines have been released in an effort to better guide clinical understanding
and decision making, the most comprehensive being from the Kidney Disease:
Improving Global Outcomes (K-DIGO) group.3 Acute kidney injury is defined
 CHAPTER 18 SUPPORT OF RENAL FUNCTION 585

by a rapid deterioration in renal function (hours to days), Anatomy of the kidney, nephron and
which is easily detected by commonly measured markers
of kidney performance, including blood urea nitrogen and urinary drainage system
serum creatinine, with inability to adequately regulate The functional anatomy of the renal system includes the
electrolytes, sodium and water balance.4,5 While generally two kidneys, ureters, bladder and urethra (see Figure 18.1).
reversible, AKI can be life-threatening in the critically ill The ureters, bladder and urethra collect, drain and
patient if acid–base imbalance, abnormal electrolyte levels
(particularly potassium) or fluid overloads are not effec-
tively diagnosed and managed. FIGURE 18.1 Kidney and urinary drainage system.
The preferred serum marker of renal function is the
serum creatinine level.3 The exact level of serum creatinine 2UJDQVDQGVWUXFWXUHVRIWKHXULQDU\V\VWHP
that is considered excessive is disputed; however, an
increase in magnitude of 1.5 or more of the baseline serum $GUHQDO
creatinine is commonly agreed on as being indicative of JODQGV
AKI.3 Urine output is also a key factor in determining the 5LJKW .LGQH\
severity of ARF. It is well established that oliguric renal UHQDO
failure, that is, a urine output of less than 0.5 mL/kg/h in DUWHU\
adults and 1 mL/kg/h in infants, is associated with poorer
patient outcome than the non-oliguric form.6
AKI is reported to occur in more than 60% of
intensive care patient admissions, much higher than 5LJKW
the broader hospital rate of 5%.7,8 In critical care, AKI UHQDO
often forms part of the multiple organ dysfunction YHLQ $RUWD
syndrome, whose cause has often been associated with 9HQDFDYD 8UHWHU
sepsis, trauma, pneumonia or cardiovascular dysfunction
(see Chapter 22). Mortality in intensive care AKI is high,
with those patients requiring renal replacement therapy
(RRT) having worse outcomes than patients who can be %ODGGHU
managed without this intervention.9
This chapter focuses on the underlying causes and
management of AKI in critical care, with particular
emphasis on nursing perspectives for managing patients
with this life-threatening organ system dysfunction.

Related anatomy and physiology

The renal system has a number of functions, including
regulation and maintenance of fluid and electrolyte
balance, clearance of metabolic and other waste products, $
an indirect role in the maintenance of blood pressure, 8UHWKUD
acid–base balance and an endocrine function. In critical
care, an appreciation of renal function in relation to fluid )URQWDOVHFWLRQRINLGQH\
management, blood pressure, electrolyte and acid–base
functions is essential. 3\UDPLG
Regulation and maintenance of the extracellular fluid )LEURXV
3DSLOOD FDSVXOH
and electrolyte constituents occur principally via the
process of filtration and reabsorption. The kidneys receive 0LQRU
approximately 25% of the cardiac output each minute, and FDO\[
excrete approximately 180 L/day of glomerular filtrate. 5HQDO
SHOYLV 0DMRU
Fortunately, tubular reabsorption accounts for approx- FDO\[
imately 178.5 L/day of the original filtrate, allowing 0HGXOOD
for a modest daily fluid intake of 1.5 L to achieve fluid 8UHWHU
balance. During this process of filtration and reabsorption, &RUWH[
metabolic byproducts and electrolyte and other wastes
(including many drugs) are also excreted and maintained in
balance. As with all body organ systems, an adequate blood
pressure and supply of oxygen to the kidneys is paramount %
in maintaining the fluid and electrolyte regulatory role.
586 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

temporarily store the urine produced from each kidney.10 Urine production, regulation of
While important in providing the conduit for the final
excretion of urine, the kidney is the primary organ of GFR and filtrate reabsorption in the
interest in the renal system, particularly in critical care nephron
practice, and hence will be described in more detail from Urine production consists of a three-stage process, which
the anatomical and physiological perspectives. occurs in the nephron: glomerular filtration, tubular
The kidneys are located in the retroperitoneal space reabsorption and tubular secretion (see Figure 18.3).
on the posterior wall of the abdominal cavity, encased in a As previously noted, the production of urine is highly
protective combination of the ribs, muscle, fat, tendon and dependent on delivery of blood under pressure to the
the renal capsule. Each adult kidney weighs approximately glomerulus. This results in the first step of the urine
140 g. The kidneys may develop a different anatomical production process, glomerular filtration. The glomerular
appearance, or vary in number and location from the filtration rate (GFR) is about 125 mL/min under normal
classic description provided here. The functional unit of conditions. Changes in the diameter of the afferent and
the kidney is the nephron, which consists of a filtrate- efferent arteriole help regulate glomerular blood flow,
collecting device (the Bowman’s capsule), a convoluted but this is unable to compensate for large variations of
tubule that varies in length and diameter, finally attaching mean blood pressure; hence, filtration rates may rise or fall
to a common filtrate-collecting tubule and duct (see markedly over the course of a day.11
Figure 18.2). Within the Bowman’s capsule rests the As the filtrate transgresses the glomerulus it is collected
glomerulus, a tuft of interlaced capillaries that arise from into the Bowman’s capsule and delivered into the proximal
the afferent arteriole. The efferent arteriole then drains convoluted tubule, loop of Henle and then the distal
from the glomerulus, via a closely entwined network convoluted tubule, where a number of processes result in
called the peritubular capillaries, until these collect in the the reabsorption of about 99% of the glomerular filtrate.
venous network of the kidney. The remaining fluid within the tubule drains into the
The glomeruli and nephrons lie in the cortical area of collecting tubule to form urine.This fluid has substantially
the kidney, while the collecting ducts gather together into different properties from the original glomerular filtrate, as
the renal pyramids, which lie in the medulla of the kidney. fluid and many electrolytes and glucose are reabsorbed by
The pyramids drain into the calyces of the kidney, which the peritubular capillaries.11
then drain into the renal pelvis where urine is gathered Along with blood pressure, the sodium content of the
to drain into the ureter. The major blood vessels of the extracellular fluid is critical in maintaining fluid balance,
kidney, the renal artery and veins also enter the renal as it constitutes the major electrolyte and osmotic agent of
capsule through the pelvis of the kidney.10 the glomerular filtrate. It is imperative that sodium intake
and loss are equally balanced, as excessive losses will result
in associated fluid loss and excessive intake will result
FIGURE 18.2 Nephron and glomerulus. in fluid retention. If sodium balance is not maintained,
other compensations such as a rise in blood pressure may
result to restore fluid balance. As blood pressure rises, the
excretion of sodium also increases by way of additional
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renal function
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adjusting the final amount of fluid and electrolyte to be
excreted from the kidney. These include the sympathetic
&ROOHFWLRQ nervous system response, angiotension II, aldosterone,
WXEH antidiuretic hormone and atrial natriuretic peptide. All
these mechanisms work in synchrony with blood pressure
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 CHAPTER 18 SUPPORT OF RENAL FUNCTION 587

FIGURE 18.3 Urine formation: filtration, reabsorption and excretion.

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the kidney and is able to reduce the filtration rate by (see Figure 18.4). Renin is produced and released from
constricting the afferent arteriole of the glomerulus, thus the juxtaglomerular apparatus, a collection of cells in the
inhibiting blood flow and pressure necessary to create the macula densa of the distal tubule, and the adjacent afferent
glomerular filtration rate. This stimulation of the sympa- arteriole next to the glomerulus, which monitors blood
thetic nervous system also increases the reabsorption of sodium concentration.When released, renin stimulates the
salt and water in the tubule and stimulates the release activation of angiotensin I from angiotensinogen. Under
of renin. the influence of coenzyme A, angiotensin I converts to
Antidiuretic hormone angiotensin II, a potent vasoconstrictor and stimulus
to reabsorb sodium and water. The vasoconstrictor effect
The antidiuretic hormone is excreted from the pituitary raises blood pressure and flow to the glomerulus, inhibiting
gland under regulation of hypothalamic osmoreceptors
further renin release (a negative feedback mechanism) as
(thirst centre), and reduces kidney diuresis (the excretion
perfusion pressure normalises. This allows the return of
of water). By enhancing the kidney’s ability to concen-
trate urine, it ensures that the excretory functions of waste natriuresis (sodium excretion) and diuresis. This response
products and electrolytes continue while limiting fluid is essential in assisting with retaining fluid in the event
loss. Antidiuretic hormone is essential to surviving limited of falling blood pressure, or boosting fluid excretion as
periods of fluid deprivation and fine-tuning the urine blood pressure rises. It also responds effectively to a rise
volume production on a continuous basis. in sodium intake by reducing angiotensin II formation
and allowing a larger natriuresis, resulting in mainte-
Renin–angiotensin–aldosterone system nance of sodium balance, a key to tissue fluid distribution
Renin is the chemical trigger that initiates a cascade system and balance.11
resulting in two powerful hormones acting on the kidney Aldosterone is a mineralocorticoid excreted from the
to significantly influence sodium and water excretion adrenal cortex in response to angiotensin II. Aldosterone
588 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

FIGURE 18.4 Renin–angiotensin–aldosterone system (RAAS).

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increases the reabsorption of sodium, and hence water, in

the cortical collecting tubules and increases the rate of FIGURE 18.5 Hydrogen ion regulation in the kidney.
potassium excretion. This has a dual effect of regulating
sodium balance and extracellular fluid volume. As fluid
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periods of increased circulating fluid volume. Atrial natri- + +
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antagonising effect to the renin–angiotensin–aldosterone 1+
system (which acts primarily to preserve sodium and 1+
water). These natriuretic, and hence diuretic, effects are
mild and self-limiting, and occur in response to mild rises 1+
in GFR and reductions in sodium reabsorption. As blood
pressure falls, the drop in GFR compensates for the effect
of atrial natriuretic peptide, ensuring that excessive loss of 7XEXODUHSLWKHOLXP
sodium and water does not occur.11
Regulation of acid–base and electrolyte acidosis the kidney raises H+ secretion by active transport
balance to combine with ammonia in the renal tubule to form
The kidney assists in the management of body pH by ammonium, which is unable to be reabsorbed. Coinci-
regulation of the excretion of hydrogen (H+) and bicar- dentally, raised H+ excretion increases the reabsorption
bonate (HCO3−) ions.While the renal response to alkalosis of sodium, which increases the alkalotic ion, bicarbonate
or acidosis is slow in comparison with plasma buffers and (HCO3−). Conversely, during alkalosis the reabsorption
respiratory regulation (see Chapter 13), it does result in a of hydrogen ions is increased. These changes in hydrogen
net loss of H+ ions or recovery of HCO3− ions, which are ion concentration in the renal filtrate alter the pH of the
the basis of human pH balance (see Figure 18.5). During urine down to a maximum level of four.6 The buffering
 CHAPTER 18 SUPPORT OF RENAL FUNCTION 589

of H+ with ammonia reduces the acidifying effect of the may result in failure can be averted. This concept is more
hydrogen ions, particularly as some ammonium combines clearly described in the later section on ATN and AKI,
with chloride to form ammonium chloride.11 which includes the RIFLE Criteria (see Figure 18.6).1,2
The conventional classification of ARF is based on the
Role as an endocrine organ perceived causative mechanisms:5,13
The kidney has two homeostatic roles as an endocrine
organ. Although neither has effects relevant to acute • prerenal
illness, patients with chronic renal dysfunction often need • intrarenal (intrinsic)
supplementation to overcome the loss of renal endocrine • postrenal.
support. Erythropoietin is important in stimulating the However, irrespective of causative mechanism, should
generation of new red blood cells and is released from the kidney injury progress to failure the same renal replace-
kidney in response to a sustained drop in arterial blood ment therapies are suitable to treat this.
oxygen levels. Calcitriol helps regulate the absorption Prior to considering whether a critically ill patient has
of calcium from the gut, which in turn promotes bone suffered acute injury, it has been recommended the effects
resorption of calcium and the reabsorption of calcium in of intra-abdominal hypertension be considered.14 As it is
the kidney. The kidney also acts to convert vitamin D to possible up to half of mechanically ventilated patients will
its active form, which is necessary for the maintenance of have this to some degree, measures to relieve the pressure
body calcium levels.11 should be considered as changes in renal function can
result due to either direct pressure on the kidney and/or
Pathophysiology and drainage system or increased pressure within the venous
circulation of the kidney. Intra-abdominal hypertension
classification of renal failure also clouds the assessment of haemodynamic parameters
Diseases of the kidneys affect the structure and therefore and cardiovascular performance, making it difficult to
the function of the nephrons in some way. Pathology assess fluid needs and responsiveness to fluid resuscita-
such as this, if untreated, may not cause complete loss of tion.15 For a more detailed discussion of intra-abdominal
renal function (i.e. ARF), but is dependent on the amount hypertension, please refer to Chapter 20.
of nephron damage or ‘injury’ occurring at the time of
the illness, and whether the patient has had any previous Prerenal causes
illness that resulted in undetected kidney damage.12 By Prerenal factors affecting blood supply to the kidneys,
focusing on factors that resulted in kidney injury, both such as hypovolaemia, cardiac failure or hypotension/
individually and collectively, more serious damage that shock, can cause AKI. The mechanism and outcome are

FIGURE 18.6 Criteria for diagnosis of acute renal failure: the risk, injury and failure criteria with outcomes of loss and
end-stage renal disease (RIFLE).32

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590 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

easily related. As blood flow to the kidneys is reduced, less loss of perfusion has occurred, and there is no obstruc-
glomerulofiltration occurs, urine production diminishes tion to urine flow.16 Diagnosis is made by exclusion of
and wastes accumulate.This state can be reversed by resto- other causes. The common causes of this type of ARF,
ration of blood volume or blood pressure. In the short glomerulonephritis, nephrotoxicity and chronic vascular
term (1–2 hours), nephrons remain structurally normal and insufficiency, are discussed below.
respond by limiting fluid lost by urine production while
concentrating the excretion of waste products. The phys- Glomerulonephritis
iological process combines the neuroendocrine control This condition is caused by either an infective or a non-
of the hypothalamus and the sympathomimetic response, infective inflammatory process damaging the glomerular
which then regulates both antidiuretic hormone secretion membrane or a systemic autoimmune illness attacking the
and the stimulation of the renin–angiotensin–aldosterone membrane.16 Either cause results in a loss of glomerular
system (see Figure 18.7). This process is highly influenced membrane integrity, allowing larger blood components
by any pre-existing illness or concurrent factors such as such as plasma proteins and white blood cells to cross
diabetes and systemic infection.13 the glomerular basement membrane. This causes a loss of
blood protein, tubular congestion and failure of normal
Intrarenal (intrinsic) causes nephron activity. Resolution is based on treating the cause,
Intrinsic damage to the nephron structure and function such as an infection or autoimmune inflammatory illness.17
can be due to infective or inflammatory illness, toxic drugs,
toxic wastes from systemic inflammation in sepsis, vascular Nephrotoxicity
obstructive thrombus or emboli. In differentiating this Nephrotoxicity occurs as a result of damage to nephron
type of ARF, a process of elimination has been suggested cells from a wide range of agents, including many drugs
where failure of kidney function persists after the resto- used in critical care (e.g. antibiotics, anti-inflammatory
ration of adequate perfusion (blood flow), or where no agents, cancer drugs, radio-opaque dyes).Toxic products of

FIGURE 18.7 Neuroendocrine response to shock, resulting in oliguria.

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 CHAPTER 18 SUPPORT OF RENAL FUNCTION 591

muscle breakdown in severe illness and trauma, commonly structural derangement, more likely explained through
called rhabdomyolysis (see Chapter 23),6,13 blood product an imbalance in energy generation sufficient to support
administration reactions and blood cell damage associated renal function combined with a renal protective ‘shut-
with major surgery are also causative agents.18 As these down’ at a cellular level.5,21
agents may often be given concurrently, a cumulative ATN describes damage to the tubular portion of the
effect, along with intermittent falls in renal perfusion, may nephron and may range from subtle metabolic changes to
result in the development of intrinsic ARF. total dissolution of cell structure, with tubular cells ‘defoli-
ating’ or detaching from the tubule basement membrane.22
Vascular insufficiency Most AKI in ICU patients is multifactorial in origin and
One-third of patients who develop ARF in the intensive may involve more than one causative mechanism and is
care unit (ICU) have chronic renal dysfunction.19 not always an ischaemic or necrotic event.16 In critical
This chronic dysfunction may be undiagnosed prior to illness, the most common combination causing ARF is
the critical illness, and may be related to diabetes, the the administration of nephrotoxic agents in association
ageing process and/or long-term hypertension. These with prolonged hypoperfusion or ischaemia.22 This type
factors create a reduction in both large and microvascu- of tubular necrosis can be further mediated by infection,
lature blood flow into and within the kidney, therefore blood transfusion reactions, drugs, ingested toxins and
reducing glomerular filtration activity and affecting the poisons, or be a complication of heart failure or major
reabsorption and diffusive process of the nephron. This cardiovascular surgery. The initial insult can also be
reduction in blood flow is exacerbated by degenerative compounded by metabolic disturbances and subsequent
vessel obstruction with atheromatous plaque, particularly systemic infection.
pronounced in diabetic patients due to ineffective glucose While ATN is reported as the causative mechanism
metabolism. Diabetic patients are more likely to develop for up to 30% of acute kidney failure in the intensive
ARF associated with medical care in hospital from what care setting, the precise causative pathology is not easily
may otherwise seem to be a relatively trivial insult to the identifiable in critically ill patients with multiple comor-
kidneys in a younger, healthy patient. The event may be bidities, for example diabetes, advanced age, investigations
enough to move the patient from kidney injury to ARF, requiring radio-opaque dye administration, potent and
as they lack any degree of ‘renal reserve’ or tolerance to nephrotoxic drug administration or major surgery with
events such as low blood pressure or administration of an inflammatory state due to an underlying infection.This
nephrotoxic drugs normally filtered by the kidneys.13 is the context of critical illness and AKI where, despite
modulation of the cause and support with artificial renal
Postrenal causes replacement therapies, mortality ranges from 28–90%
Urinary tract obstruction is the primary postrenal cause of depending on diagnostic criteria or definition.4,23
ARF, and is uncommon in the critical care setting as it is This type of kidney damage is of particular importance,
rarely associated with acute onset renal failure.13 Postrenal as it is abrupt in onset and causes a rapid cessation of
obstruction is more common in the community and is normal nephron function, a picture typical of any critical
associated with urological disorders such as prostate gland illness and failure of other body organs.4 As this failure is
enlargement in males, urinary tract tumours and renal commonly mediated by a loss in total or regional blood
calculi formation impairing urine outflow. It is essential flow to the kidney,24 it is more pronounced in the kidney
that blockage of any urinary drainage device be excluded medulla or outer regions sensitive to reduced blood flow.
in the critically ill patient when undertaking an assessment The cause of this loss in blood flow may be multifactorial
of apparent oliguria. but is commonly associated with shock and consequent
Acute tubular necrosis and acute low blood pressure (see Figure 18.7). Tubular cells suffer
an ischaemic insult, causing a shedding of the cells from
kidney injury the nephron basement membrane. This shedding of cells
Intrinsic ARF (described above) is often associated has an initial loss of cell polarity, and then cell death,
with typical microscopic changes on pathology exam- with a ‘patchy’ occurrence along the tubule basement
ination of kidney tissue. This pathology is termed ATN, membrane.22 In addition, some cells detach themselves
and possibly explains how and why, in the acute setting, before death in a response known as apoptosis (cell self-
kidneys can fail abruptly to minimal to no function (no death)22 (see Chapter 22). The response is aimed at organ
urine output and therefore no waste clearance), and survival, with some individual cells ‘sacrificing’ themselves
can then after a period of time, with artificial support, during a period of crisis. This protective response reduces
recover to normal function in many patients.20 This is oxygen demand by initiating cell death in some tubules,
now a contentious issue amongst leading researchers while others differentiate and/or proliferate for repair,
who are cautioning against the widespread adoption of and allows continuation of some normal function. If the
the term ATN to explain the pathophysiological changes causative process abates, remaining cells regenerate by
and disruption of kidney function seen as kidney injury differentiation and proliferation, tissue repair occurs with
develops.3,5 Current opinion suggests renal dysfunc- restoration of normal epithelium in some tubules and
tion is possibly attributable to a functional rather than nephron function returns.
592 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

During this period cellular ‘debris’ collects in the assessment of fluid and electrolyte balance, as described in
tubule loops, causing obstruction of tubular flow, with Chapters 9 and 21.
backleak of filtrate occurring through the ‘patchy’ exposed
tubular membrane surface. An inflammatory process Uraemic complications
is also stimulated due to release of cell adhesion factors Uraemic complications are influenced by the rate of urea
and leucocyte activation,25 which in turn causes further accumulation and vary from patient to patient. As serum
vasoconstriction and ischaemia26 in the acute stage. The urea levels rise rapidly (i.e. over the course of a few days),
backleakage and static tubular fluid creates a concentrate above 20 mmol/L blood coagulation can be affected.
that, by diffusion, raises blood levels of wastes such as urea, A rash and related itchiness can occur. As blood levels
creatinine and other toxins. Along with the cessation of continue to rise, neurological function can be affected and
urine flow, toxicity occurs due to high serum levels of level of consciousness will deteriorate. In some cases high
wastes such as urea, creatinine, potassium and undefined levels of urea can result in encephalopathy.30
toxins.25 This is the clinical state associated with the
pathology of AKI that better describes the total ‘picture’ of Cardiovascular alterations
pre-illness status, immediate causative events and degree Cardiovascular alterations can occur as a result of
of injury determined by patient serum creatinine or urine acute kidney injury31 as a result of direct effects on the
output.1,2 myocardium but also because of fluid accumulation and
In the past authors have often employed the term electrolyte disturbance. The greatest concern is fluid
ATN to describe ARF,11 using it as a surrogate for ARF overload as a consequence of failure to excrete the excess
in the acute setting, as it focuses on the pathophysiol- quantities of fluid used in resuscitating critically ill patients
ogy of tubular damage, recognising this damage as a final and the necessity to provide adequate nutrition in the
outcome of all causative factors. However, more recently, form of parenteral or enteral nutrition.32 Without appro-
with the development of a consensus definition for priate management heart failure and pulmonary oedema
ARF describing stages of illness severity, the term AKI can develop. Electrolyte disturbances are numerous in the
is now used reflecting pathophysiology, the outcome of patient with severe AKI, but of paramount concern is
many causative factors and the clinical context where hyperkalaemia to the extent that cardiac rhythm disturb-
small derangements may be evident with reversibility of ance can occur. As potassium levels rise the cardio-electric
dysfunction and recovery, through to irreversible damage cycle becomes ‘dampened’, eventually deteriorating to a
with kidney failure.1–3 sign wave with no concurrent cardiac pumping action.
The kidneys are vital human body organs essential Please refer to Chapter 11 for a more detailed discussion
to sustaining life. An important interrelationship of the of cardiac arrhythmias associated with electrolyte
kidneys and other body organs exists, with the brain, disturbances.
heart, liver and lungs dependent on receiving ‘clean’
blood to function. As toxins and fluid rapidly accumulate Respiratory alteration
due to AKI during critical illness these changes As noted earlier, fluid accumulation will invariably result
contribute to organ dysfunction,27,28 although many of in inadequate clearance of the pulmonary interstitial space
these interrelationships (e.g. with the liver) are poorly by the pulmonary lymphatics, resulting firstly in interstitial
understood.29 oedema and moving on to overt pulmonary oedema and
serious impairment of pulmonary gas exchange. Respir-
Acute kidney injury: Clinical atory rate may also increase as patients develop metabolic
acidosis both through renal injury and associated critical
and diagnostic criteria for illness.
classification Haematological alterations
Clinical assessment The primary haematological concern in AKI is related to
Clinical assessment of the patient with impending renal the anti-coagulatory effects of rapidly increasing serum
failure can involve myriad tests and investigations; however, urea. While the kidney accounts for 90% of circulating
the majority of these are not used to assess the critically ill erythropoietin production,12 the acute nature of severe
patient. The clinical history is important in differentiating AKI does not influence anaemia to the extent of more
pre-existing renal disease and cataloguing the numerous common causes such as haemorrhage related to trauma or
factors already discussed that can contribute to AKI. The surgery or even iatrogenic blood loss.
key assessments used in monitoring renal function are
urine output, serum creatinine and urea levels, combined Neurological alterations
with more general measures including heart rate, blood Changes to central nervous system function can be related
pressure, fluid balance and daily weight. These measures to accumulating urea, fluid and disruption of sodium
are essential for the critically ill patient, and alterations balance. In the most severe form these can result in loss of
provide the diagnostic key. They also link into the wider consciousness and fitting.
 CHAPTER 18 SUPPORT OF RENAL FUNCTION 593

Diagnosis In the event that urine output decreases further, or was

worse than this when first identified, to less than 0.5 mL/
The management of AKI begins with the diagnosis,
kg/h or a creatinine increase of twice the normal value
based on the patient’s presenting signs and symptoms
occurs, renal injury is likely, with these clinical changes
linked to a patient history. A long-term history of renal
proposed as being highly sensitive towards injury having
disease involving urinary tract infections, diabetes, cardiac
occurred. At this stage the above measures would be
failure and systemic inflammatory illnesses are all highly
appropriate and further investigation as to possible causes
relevant.12 Immediate history of presentation to a hospital
is warranted.With treatment of the underlying cause, close
involving surgery or any life-threatening illness with
monitoring, support of haemodynamics and fluid admin-
associated shock is also highly relevant in association with
istration, most patients should not progress further in the
reduced urine output volumes over time.
failure continuum.
Nurses in the critical care setting, who measure
The next progression in clinical deterioration is
urine output hourly, readily recognise a key sign of
oliguria, or urine output being less than 0.5 mL/kg/h for
impending renal dysfunction. Oliguria in the absence of
24 hours or anuria for 12 hours. The creatinine increase
catheter obstruction should be responded to quickly, as
is now proposed as being three times the normal level
this suggests inadequate kidney blood flow and, to some
and, with minimal to no urine output, renal ‘failure’ is
extent, is a delayed observation considering the continual
proposed as a clinical diagnosis using this criterion. It is
moderation of kidney function producing urine output.
at this stage when renal replacement therapy would need
Persisting oliguria or the onset of anuria with associated
to be considered and, if not already attended to, patients
rises in blood creatinine defines the injury phase of AKI.
should be transferred to ICU. A continuous therapy, or
This sequence of events can be identified in the collective
continuous renal replacement therapy (CRRT), is recom-
criteria known as the ‘RIFLE’ criteria – risk, injury,
mended. This term is more specific for the modes of
failure, and outcome criteria of loss and end-stage disease
treatment commonly applied in the ICU. Renal replace-
– which provides the basis for a widely-accepted approach
ment therapy (RRT) refers to any treatment that replaces
to diagnosing and classifying AKI.3
renal function and includes intermittent haemodialysis
and peritoneal dialysis (PD). It is also important to
Consensus definition: the RIFLE understand that, in the setting of an acute illness, many
criteria patients progress through these stages of renal dysfunction
The RIFLE criteria are shown in Figure 18.6, and use to the failure stage quickly or the problem is unidenti-
rising creatinine and falling urine output as highly fied until the failure stage is met. The timing for taking
sensitive and specific indicators for a continuum of renal a blood sample to measure creatinine or when a urine
failure. This is a useful classification system to grade loss catheter is passed to measure urine output also influences
of kidney function, reflecting stages of injury to the this identification. The diagnosis may be made only at
kidney before failure occurs. Without this, the small but the failure stage, without any identifiable period of risk
important losses of kidney function before the failure state or injury as proposed by the RIFLE criteria. With a
are not adequately considered.1 This approach provides critical illness, serum values of creatinine, urea, pH and
a consensus definition for loss of kidney function that is potassium are readily available in the ICU and are used for
useful for clinical practice and research into this area, with diagnosis in association with the RIFLE definition. Daily
clinicians all talking the same ‘language’ when comparing monitoring of these values as a minimum is necessary for
patients and/or results from clinical trials.The shape of the diagnosis and monitoring during CRRT in the ICU. The
diagram indicates that more people will develop symptoms normal laboratory values for these biochemical markers
of ARF linked to kidney ‘injury’ and be considered ‘at are essential knowledge for nurses to understand AKI and
risk’ (high sensitivity) than those at the bottom of the management.
definition, who are fewer in number but need to fulfil Treatment with CRRT may not be implemented
strict criteria (high specificity). until failure is evident, by anuria and uraemia, or until
To better understand the RIFLE criteria in a clinical patients meet the RIFLE definition criteria. However,
care context, the following discussion is useful to consider in some patients, CRRT may be commenced earlier, in
in association with a review of Figure 18.6. In a hospital anticipation of failure and as a strategy to prevent further
setting, those patients with a risk of renal injury would kidney damage or complications of functional renal
be identified by a low urine output of less than 0.5 mL/ deterioration.
kg/h for 6 hours. In this situation their creatinine would
be expected to rise, indicating a concurrent reduction in
Practice tip
glomerular filtration rate. Reducing renal risk requires
basic measures such as ensuring an adequate fluid intake Reducing urine output is an important sign of impending
and continuing to closely monitor urine output, while AKI; however, checking a catheter for blockage is also
reviewing the patient’s medications, haemodynamic state, important. A bladder scanner may also reveal a full
signs of infection and possible other causes of injury in bladder where no catheter is in place.
order to prevent further deterioration.
594 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Management of the patient monitored using a fluid chart, with the aim of adhering
to the prescribed volume. Nutrition therapy is important
with acute kidney injury for optimising patient outcome but can also contribute to
increased fluid intake. Enteral feeding is preferred for most
Reducing further insults to the critically ill patients and standard enteral feeding formulas
kidneys can contribute about 1.5 L of fluid intake per day in an
After diagnosis, the next management principle is to adult.35 Nutrition is very important in the patient expe-
remove or modify any cause that may exacerbate the riencing ARF where growth and repair is needed with
pathological process associated with AKI. Further inter- damaged kidney cells and protein depletion avoided.36
ventions and investigations are performed in relation to Calorie dense enteral feeding formulas (2 kcal/mL) can be
the findings from the history and presentation. These considered as a strategy to minimise fluid intake associated
may include:13 with enteral feeding (see Chapter 19 for further discussion
on nutrition in critical illness). Fluid balance charting and
• further intravenous fluid resuscitation (despite an a clear understanding of the maximum fluid intake per
oligo-anuric state) and restoration of blood pressure day is vital for managing AKI at this stage, and a maximum
using inotropic/vasoactive drugs intake of 1.5 L per day is a common target in the adult
• physical or diagnostic assessment for renal outflow patient.35 An inability to prevent a positive fluid balance,
obstruction and alleviation if present largely due to meeting nutritional requirements, is often
• avoiding contrast-enhanced radiological investigations the reason CRRT is initiated.37
• ceasing or modifying the dose of any nephrotoxic Electrolyte balance
drugs or agents and treating infection with alternative, Managing serum electrolytes, in particular potassium, is
less toxic antibiotics. essential for patient stability as low or high levels are more
Initial management strategies for the early stages of likely to be associated with life-threatening arrhythmias.38
ARF remain conservative, with careful management However, phosphate, calcium and sodium may also be
of fluid (once adequate circulating volume is assured) abnormal and require strategies to reduce, supplement or
and haemodynamics, encouraging diuresis if present, control the serum level away from toxicity. Hyponatrae-
monitoring blood profiles for changes in urea and elec- mia, for example, may be associated with altered mental
trolytes and limiting or reformulating the administration state, impaired consciousness and even seizures.39
of agents that may contribute to the accumulation of
urea and electrolytes (e.g. enteral or intravenous nutri- Acid–base balance
tional supplements). The use of agents such as mannitol, Control of the acid–base balance is another essential
dopamine and frusemide, while popular in practice, have function of the healthy kidneys and, with failure, metabolic
not been shown to be of any value in improving outcome acidosis will develop due to decreased buffering and
in patients at risk of ARF.13,20 accumulation of many acids not excreted.39 An increased
Despite these efforts, life-threatening biochemistry minute ventilation may be observed in the patient, repre-
may arise in ARF, such as severe acidosis and hyper- senting a physiological attempt to control acidaemia. This
kalaemia (pH of <7.1 and serum potassium >6.5 mmol/L), requires additional energy and caloric consumption and
that requires immediate treatment and is an indication for is another indication that RRT should be implemented
beginning RRT without elevation of serum creatinine using bicarbonate fluids to control the acidaemia.39
and oliguria and fluid overload.33 Pharmacotherapy and altered
Fluid balance pharmacokinetics
As oliguria and anuria are key diagnostic and clinical signs The modification of drug regimens to effect changes to
of renal dysfunction, reducing fluid intake is necessary to excretion and volume of distribution is a further aspect
prevent intravascular overload and tissue oedema until of clinical management during the onset of ARF. Drugs
renal recovery begins or a renal replacement therapy are excreted from the body after hepatic and other organ
is started. Reducing or restricting fluid intake can be a metabolism, which converts them to a water soluble form
challenge in the critically ill as it is not uncommon for such that they appear in the urine.Therefore, modification
these patients to be administered 3 L of fluid in 24 hours.34 of dose (through reduction or frequency of administra-
A balance state for this degree of fluid administration tion) and monitoring for serum levels helps to prevent
suggests a urine output at 125 mL/h without consider- further renal insult while ensuring the desired clinical
ing other insensible losses. Strategies can be considered effect.40
to minimise fluid intake such as preparing drug infusions Aminoglycosides are a key group of antibiot-
without diluent and in a concentrated version of the usual ics requiring adjustment and monitoring in AKI, if not
preparation. Pharmacists may assist with this require- ceasing and substituting for another appropriate but less
ment and offer advice for drug preparation and delivery. nephrotoxic antibiotic.40 Other drugs administered in the
Restriction of oral fluids can be implemented and ICU that warrant attention include narcotics, histamine-2
 CHAPTER 18 SUPPORT OF RENAL FUNCTION 595

receptor antagonists and beta blockers. Pharmacy product

information attached with packaging and/or local FIGURE 18.8 Kolff dialyser.
pharmacy information usually provides helpful sugges-
tions and guidelines for relevant drug use in AKI. If RRT
is started, and is functioning continuously with efficiency,
the clearance and toxicity of drugs is of less concern and
dosing may resume to normal for some drugs with close
monitoring continuing.40
If conservative measures fail, the ongoing manage-
ment of the patient with ARF requires RRT. This
enables control of blood biochemistry, prevents toxin
accumulation, and allows removal of fluids so that
adequate nutrition can be achieved. The criteria and
indications for initiating RRT are listed in Box 18.1.
One indication is sufficient to initiate RRT, while two
or more make RRT urgent. Combined derangements
can create the necessity to commence therapy before
individually-defined limits have been reached. Early
initiation of treatment is widely advocated and may
confer more rapid renal recovery.

BOX 18.1

Proposed criteria for the initiation of renal

replacement therapy in adult critically ill patients14
• Oliguria (urine output <200 mL/12 h)
• Anuria/extreme oliguria (urine output <50 mL/12 h)
• Hyperkalaemia (K+ >6.5 mmol/L)
• Severe acidaemia (pH <7.1)
• Azotaemia (urea >30 mmol/L)
• Clinically significant organ (esp lung) oedema Reproduced from Thomas N. Haemodialysis. In: Thomas N,
• Uraemic encephalopathy ed. Renal nursing. 2nd ed. London: Baillière Tindall; 2002.

• Uraemic pericarditis
• Uraemic neuropathy/myopathy as a large, drum-styled cage. The drum with the blood-
• +
Severe dysnatraemia (Na >160 or <115 mmol/L) filled cellulose tubing was immersed in a bath of weak salt
solution and, as blood passed through, the rotating cellulose
• Hyperthermia
tubing allowed waste exchange to occur by diffusion.
• Drug overdose with dialysable toxin The Kolff rotating drum kidney provided limited
effective waste clearance and prompted design and
development of a new membrane for solute exchange
Approaches to renal that had a greater surface area and required less blood
volume. This led to the development of the hollow-fibre
replacement therapy filter membrane structure in the 1960s, which became the
A brief review of the historical perspectives associated ‘artificial kidney’.42
with the development of modern day dialysis and RRT The combination of an extracorporeal circuit (EC),
provided in the ICU is helpful in understanding key blood pump and filter membrane and the associated
concepts and methods of CRRT, including PD. nursing management are now commonly known as
haemodialysis.With industrial and scientific developments,
History such as plastics moulding and electronics, current dialysis
Dialysis is a term describing RRT and refers to the techniques are safe, effective and a life-sustaining treatment
purification of blood through a membrane by diffusion for the millions of people who suffer acute and chronic
of waste substances.41 Table 18.1 outlines historical kidney failure.43,44
events during the development of dialysis in Europe and Key to the application of these technical and scientific
the USA. The Kolff rotating drum kidney, one of the developments has been the role of nurses, who have made
earliest attempts at RRT (illustrated in Figure 18.8), used a substantial contribution to the safety and efficiency
cellulose tubing rolled around a wooden skeleton built of dialysis.45 Nursing of dialysis patients has developed
596 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 18.1
Historical events in the development of dialysis

TIME PERIOD AND

DEVELOPER DESCRIPTION

1854: Thomas Graham, First used the term ‘dialysis’ to describe the transport of solutes through an ox bladder, which drew
Scottish chemist attention to the concept of a membrane for solute removal from fluid
1920s: George Haas, First human dialysis was carried out, performing six treatments on six patients. Haas failed to make
German physician further progress with the treatment but is recognised as an early pioneer of dialysis
1920–30s Synthetic polymer chemistry allowed development of cellulose acetate, a membrane integral to the
further development of dialysis treatments
1940s: Willem Kolff, Dutch The discovery of heparin, an anticoagulant, enabled further development of dialysis during World
physician War II, the Kolff rotating drum kidney
1940–50s: Kolff and Allis- Further modification of the Kolff dialyser and the development of improved machines
Chalmers, USA
1950s: Fredrik Kiil, Norway Developed the parallel plate dialyser made of a new cellulose, Cuprophane. This required a pump
to push the blood through the membrane and return the blood to the patient
1950–60s Dialysis began to be widely used to treat kidney failure
1960s: Richard Stewart The hollow-fibre membrane dialyser used a membrane design of a cellulose acetate bundle, with
and Dow Chemical, USA 11,000 fibres providing a surface area of 1 m2
1970s Use of the first CAVH circuits for diuretic resistant oedema by Kramer
1980s First continuous therapies using blood pump and intravenous pumps to control fluid removal and
substitution: Australia and New Zealand led the way
1990s New purpose-built machines used; Gambro Prisma, Baxter BM 11 + 14 to provide pump-controlled
therapies with integrated automated fluid balance using scales to measure fluids. Cassette circuits,
automated priming; new membranes
2000 Further purpose-built machines using direct measurement for waste and substitution fluids via
Hygieia–Kimal machine. Introduction of high fluid exchange rates for sepsis treatment. Introduction
of dialysis-based machines in ICU for daily ‘hybrid’ treatments: SLEDD and SLEDDf
2010 Multiple CRRT machines; more advanced graphics interface and smart alarms. Waste disposal
systems. High flux, porous membranes
CAVH = continuous arteriovenous haemofiltration; CRRT = continuous renal replacement therapy; SLEDD = sustained low-efficiency
daily dialysis; SLEDDf = sustained low-efficiency daily diafiltration.

into a specialist field of knowledge and skill, with nurses dialysis fluid into the abdomen, allowing diffusion and
combining their holistic view of patient management with osmosis to occur between the peritoneum and fluid
the specialist needs of patients with renal failure, from the before draining out again in repeated cycles.49 This was
outpatient setting to the ICU, including a collaborative performed by the ICU nurse and prescribed by ICU
approach to further adaptations of dialysis best suited to doctors, but was inadequate in its clearance of waste
the critically ill.46–48 and fluid volume, and was associated with infection,
limitation of respiratory function and exacerbated
Development of renal replacement glucose intolerance.16,49
therapy in critical care In 1977 Peter Kramer, a German ICU doctor,
Improvements in many fields of health care, including developed a new dialytic technique called continuous
resuscitation and treatment for shock, and the growing arteriovenous haemofiltration (CAVH). It was later
number of patients undergoing and surviving extensive renamed slow continuous ultrafiltration (SCUF), as
surgery and trauma, have led to developments and it enabled the removal of plasma water in addition to
challenges in critical care practice. Many patients who dissolved wastes (convective clearance of solutes) at a
would previously have died from an acute illness now flow rate of 200–600 mL/h by passive drainage from the
survive, but develop ARF as a complication. membrane as blood flowed through it.50 This marked
Historically, ARF was treated in the ICU with the use the beginning of continuous RRT in the ICU as an
of PD, which did not require specialist nurses or doctors. intervention prescribed and managed by ICU nurses and
This simple technique removes wastes by infusing a doctors for patients with ARF.
 CHAPTER 18 SUPPORT OF RENAL FUNCTION 597

Refinement of renal replacement TABLE 18.2

therapy Typical fluid constituents for peritoneal dialysis
Although CAVH as developed by Kramer was useful
FR ESEN IUS
in removing excessive body water and some wastes,
BAXTER (FMC, JA PA N,
a dialysis blood pump enabled a much more efficient (TOONGABBIE, FUK UOK A )
technique for therapeutic benefit in the ICU patient NSW, AUSTRALIA) STAY SA F E ®
with ARF. The use of roller blood pumps to generate DIANEAL ® PD-4 BALANC E
pressure and a reliable flow of blood, thus eliminating Volume, mL 2000 2000
the need for arterial puncture and access, was introduced.
Glucose 2.5 % 2.3 %
This approach, termed continuous veno-venous haemo-
filtration (CVVH), could reliably pump blood at a Sodium mmol/L 132 134
constant rate and achieve ultrafiltration volumes of 1000 Calcium mmol/L 1.25 1.25
mL/h.With further modifications to the circuit and filter Magnesium 0.25 0.5
set-up, a diffusive component was added to the therapy mmol/L
by running a dialysate volume through the haemofilter, Lactate mmol/L 40 35
flowing between the membrane fibres and countercurrent
to blood flow. This was termed continuous veno-venous Glucose, g 25 25
haemodiafiltration (CVVHDf).51 Osmolarity, 395 399
mOsm/kg
Principles of peritoneal dialysis
PD relies on the simple physical processes of osmosis and
diffusion to achieve the goal of adequate fluid and toxic A solution component to assist in managing acid–base
metabolite removal and electrolyte balance in the patient balance is also necessary. Originally, acetate was incor-
who can no longer sustain this through deteriorating porated in solutions to counter the acidosis seen in renal
renal function. Unlike extracorporeal approaches for renal failure; more recently lactate has been used. Both of these
replacement, PD uses the abdominal peritoneum as the components are stable in solution and, when exchanged
membrane through which filtration and diffusion occur. at the peritoneal interface, will be metabolised in the
The peritoneum provides simple access to the circulating patient’s liver while contributing to neutralisation
blood and is highly permeable to the range of electrolytes of excessive H+ accumulation. However, critically ill
and metabolites that are the target of therapeutic exchange patients often have impaired liver function that limits the
for any renal replacement approach.52 effectiveness of these agents in controlling excess acidity.
By introducing a solution that has a mix of elec- The use of HCO3− as an acid buffer is preferential but
trolytes and osmotic components formulated to create represents challenges due to its instability in solution and
both a diffusion and osmotic gradient to the peritoneal higher production cost.
cavity, then allowing sufficient dwell time for equilibra-
tion between the solution and peritoneal blood supply to Management of peritoneal dialysis
occur, then draining off the fluid, both solute and fluid The management of PD, apart from the peritoneal cannula
removal can occur. By repeating this simple process of insertion and dose prescription, is largely a nursing
instilling between 1 and 3 L of fluid in a regular cycle responsibility. Running PD for a critically ill patient
of between 30 to 60 minutes (instillation/dwell/drain), with AKI might be considered when resource limitations
fluid balance and metabolic control can be achieved for (equipment, power or fluids) or expertise to use extra-
the patient with AKI.53,54 PD is a gentle but effective form corporeal CRRT is not available. The process of PD can
of dialysis if repeated regularly over days and can bridge be particularly demanding due to the regular cycling of
the gap between failure of the kidneys to adequately fluid required to manage the hypermetabolic state often
perform their function to the point where they then seen in these patients. Major management considerations
recover sufficient function to again control patient fluid include cannula care, fluid formulation and fluid cycling
and metabolite balance with or without medication and in and out. Frequent monitoring of the patient’s blood
dietary manipulation. profile is necessary to determine the impact and identify
Numerous formulations and combinations of untoward effects of the treatment. Common problems
solutions and constituents have been used (Table 18.2). associated with PD include:
Variations in the osmotic component of the solutions
(often a glucose-based element expressed as percentage) • heat loss due to instillation of inadequately warmed
fluids
will increase or decrease the rate of fluid removal along
with the frequency and duration of cycle time. Likewise, • raised intra-abdominal pressure, impinging on
the absence or relative concentration of electrolytes in respiratory and bowel function
the solution will determine the removal or addition of • infection introduced through the cannula at insertion,
substances such as potassium from or into the circulation. or during treatment, or PD fluid contamination.
598 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Cannula care levels is also required when reducing, increasing or ceasing

Soft polyurethane cannulas are preferred in PD as they the glucose load in the dialysate solution for systemic
are more comfortable for the patient, less likely to rebound effects.55
perforate abdominal anatomy and easier to manage.53,54 Potassium may be entirely absent from the solution
The cannula breaches the abdominal wall and floats in in order to allow its removal from the circulation
the peritoneal space (see Figure 18.9) providing an entry as would normally occur in the functioning kidney.
point for infection. While specific research on cannula Once potassium levels normalise it can then be added
care for acute insertion is limited, the same principles used to prevent ongoing loss. The use of an H+ ion buffer
in managing intravascular devices should be applied. Care is also needed; if bicarbonate is used ensure it is added
needs to be taken to ensure the cannula remains straight at the time of administration to retain a useful level in
so flow and effectiveness of the treatment are maintained. solution. The nature of the peritoneum and the crystal-
Repositioning the patient should prompt review of the loid-based infused fluids means significant protein losses
catheter position.55 in the outflow fluid can be anticipated. This may require
A single cannula may be used for both inflow and additional nutritional supplementation and problems
outflow of dialysate solution; a dual-lumen device allows with hypoalbuminaemia.
both inflow and outflow to occur simultaneously as does All of these additions to the solution require careful
placement of two cannulas.54 During cannula insertion concentration calculation to ensure the correct dose is
a catheter may cause trauma or a build-up of fibrin and delivered in a physiologically stable solution. Consulting
connective tissue may occur with time. Instillation of with a pharmacist is recommended if regular additions to
heparin has been suggested to help avoid clotting and dialysate solutions are to occur. Pre-formulation can assist
blockage of the cannula; if used, monitoring of subsequent in ensuring both correct solution and the sterility of the
bleeding within the abdominal cavity is required. solution are maintained.

Fluid selection Circuit design and management

Fluid selection will be based on specific treatment goals PD circuit configurations vary from simple to more
with higher glucose concentrations prescribed to increase complex (see Figure 18.10). Through a closed circuit,
the osmotic gradient and fluid removal over the cycle a machine can be used to deliver 24-hourly cycles of
length. These solutions can be absorbed to the systemic multiple bags. Using a machine to deliver PD minimises
circulation through the peritoneum, so regular monitoring nursing time and maintains a closed circuit, reducing
of patient blood glucose levels is necessary, particularly in infection risk. Of course, using a cycler increases the
the diabetic patient. Careful assessment of blood glucose complexity of the circuit and introduces the need for a
power source, two of the claimed benefits of PD.
Modern PD offers a realistic alternative for uncom-
FIGURE 18.9 PD cannula example.
plicated AKI despite its many limitations. No RRT is
without its problems and PD is possibly underrated as a
treatment alternative. This could be particularly the case
in paediatric patients. In underdeveloped countries it
may be the preferred option of RRT due to its simplicity
of operation and low cost. In disaster areas where high
numbers of victims with injury-induced AKI are likely
it may also offer a treatment that can be instituted on site
and can be a life-saving proposition until more specific
treatment can be accessed.
Principles of extracorporeal CRRT
&DWKHWHU
Both intermittent haemodialysis and CRRT require a
machine to pump blood and fluids;pressure and flow devices
to monitor treatment; a tubing and filter membrane set
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that together create an extracorporeal circuit (EC) (outside
FDYLW\ 3HULWRQHXP the body blood pathway); and a catheter connecting the
patient’s circulation to the circuit (see Figure 18.11). This
catheter enables blood to be drawn from and returned to
the patient (known as ‘access’). Access can be achieved by
three different techniques:
Adapted from National Kidney and Urologic Diseases
Information Clearinghouse website, http://kidney.niddk.nih. • temporary catheters inserted via a skin puncture into
gov/KUDiseases/pubs/peritoneal/index.aspx, with permission. an artery for drawing blood and a vein to return the
blood (AV access)
 CHAPTER 18 SUPPORT OF RENAL FUNCTION 599

FIGURE 18.10 PD circuit example.

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• a surgical joining of an artery and vein (usually in FIGURE 18.11 Renal replacement therapy blood path
the forearm), making a large vessel that is punctured circuit common to all approaches.
with needles to both draw and return the blood
(AV fistula)
• a catheter with two lumens to draw and return blood (&EORRGSDWK
via a large central vein (a dual veno-venous access
catheter).
In the acute renal failure setting and where temporary 0HPEUDQH
treatment is anticipated, the two-lumen catheter is
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kidney support in ARF.The basic blood path or circuit for $FFHVVWRSDWLHQW
these therapies is indicated in Figure 18.11 and is useful to
600 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 18.3
Abbreviations describing modes of renal replacement therapy

TIMING OF THERAPY ROUTE OF ACCESS M E C H A N I S M O F S O L U T E R E M O VA L

I = intermittent A = arterial H (or HF) = haemofiltration – convection

C = continuous V = venous D (or HD) = haemodialysis – dialysis
S = slow AV = arteriovenous HDF = haemodiafiltration – diffusion and convection
VV = veno-venous UF = ultrafiltration – plasma water removal

review to understand each therapy and where the RRT

fluids are then applied to the circuit, differentiating them FIGURE 18.12 Continuous veno-venous
haemofiltration (CVVH) circuit.
as techniques.
The extracorporeal component is a common factor in
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other waste products and the solvent or plasma water are
removed from the blood as it passes through the filter %ORRG
membrane (artificial kidney), and the intermittent versus SXPS
continuous prescription of the therapy. The three physical
mechanisms of fluid and solute management are convection,
diffusion and ultrafiltration. Table 18.3 lists the commonly
used abbreviations to describe the timing of treatment, 3UH ¬ SRVW
blood access for the therapy and mode of solute removal.
Convection
Convection is the process whereby dissolved solutes are )LOWUDWH +HDWHU
removed with plasma water as it is filtered through the
dialysis membrane. The word is derived from the Latin
convehere, meaning ‘to remove or to carry along with’.58 and fresh dialysate is in continuous supply, this process
This process is similar to that occurring in the native performs an effective waste-removal function. Blood and
kidney glomerulus, as plasma water is filtered across dialysate are established in a countercurrent or opposing
the nephron tubule via the Bowman’s capsule. In RRT, flow to each other to maximise the diffusive process,
the plasma water with the dissolved wastes is discarded; mimicking the normal nephron function of the kidneys.61
the deficit is then replaced with manufactured artificial A diffusive clearance technique can be performed with
plasma water in equal or slightly lower amounts to increasing intensity and effect by making the blood and
achieve a desired fluid balance. This blood purification dialysate flow faster, with technical problems associated
process is commonly known as haemofiltration. When with delivering the high fluid and blood flow being the
applied on a continuous basis in the ICU, haemofiltration main limiting factor increasing clearance. The two flows
can adequately replace essential renal functions, and is need to be maintained in relation to each other; for the
particularly effective in managing fluid balance.33,59 Figure diffusive clearance to be efficient the dialysate flow must
18.12 illustrates the circuit and set-up for continuous always equal or exceed the blood flow. A common setting
veno-venous hemofiltration. for an intermittent dialysis treatment would be a blood flow
and dialysate fluid flow of 300 mL/min each. A faster blood
Diffusion flow is not useful unless dialysate flow is also increased, as
Diffusion refers to the physical movement of solutes more waste solutes will not be cleared if the dialysate fluid
across a semipermeable membrane from an area of high and blood are in diffusive equilibrium. The technique of
concentration to that of a relatively low concentration; solute removal using diffusion alone is termed dialysis; when
that is, solutes move across a concentration gradient.60 A used with blood, the process is termed haemodialysis.When
higher concentration gradient results in a greater rate of applied on an intermittent basis, as is normal for patients
diffusive clearance. As blood passes through the dialysis receiving RRT for chronic renal failure, it is called inter-
membrane, dialysate fluid, reflecting normal blood mittent haemodialysis.62 Figure 18.13 illustrates the circuit
chemistry, is exposed to the blood on the opposing side set-up for intermittent haemodialysis.
of the membrane fibre. Diffusive clearance is continuous
as solute exchange occurs with the dialysate fluid and the Ultrafiltration
blood continually moving in and out of the membrane. Ultrafiltration is the process that allows plasma water
As waste-laden blood enters the hollow membrane fibre to leave the blood, achieving body fluid or water loss.61
 CHAPTER 18 SUPPORT OF RENAL FUNCTION 601

FIGURE 18.13 Intermittent haemodialysis circuit. FIGURE 18.14 Continuous veno-venous

RO = reverse osmosis ‘treated water’. haemodiafiltration (CVVHDf) circuit.

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separating plasma water from the blood and/or allowing
the exchange of solutes across the membrane by diffusion.
Dialysis nurses measure a fluid loss by weighing the patient The filter is made of a plastic casing, containing a synthetic
before and after a treatment. This process is primarily polymer inner structure arranged in longitudinal fibres.
used to achieve fluid balance, an important function of A schematic diagram of a haemofilter is shown in
the kidneys. The only difference between this process and Figure 18.15. The fibres are hollow and have pores
the convective clearance of solutes is that this fluid is not along their length with a size of 15,000–30,000 daltons.
replaced, and it is therefore not considered an adequate This allows plasma water to pass through, carrying
solute management method. Ultrafiltration cannot be dissolved wastes out of the blood (most of which have a
undertaken in large amounts without fluid replacement, as molecular weight <20,000 daltons), while larger plasma
it would cause hypovolaemia. It is implemented during a proteins and blood cells (at least 60–70,000 daltons) are
dialysis period by removing small amounts each hour (e.g. retained.58 Plasma water separated from the blood in
250 mL/h for 4 hours) during the intermittent treatment this way is carried away from the filter by a side exit
cycle. port and a pump, where it is measured and directed
There are different therapeutic effects from each form into a collection bottle or bag as waste; this convective
of RRT and different operational prescriptions of blood clearance of solutes is similar to urine produced by
and fluid flow. Combinations of convection and diffusion the normal kidneys. The plasma water loss is replaced
can be used, known as CVVHDf.62 An increase in the in equal volume with a commercially manufactured
diffusive component (i.e. raising the dialysate flow rate in plasma water substitute, either after the ‘filtered’ blood
CVVHDf) will increase the removal of small-molecular- exits the haemofilter (postdilution) or prior to the blood
weight substances such as potassium and assist with entering the haemofilter (predilution), or both at the
hydrogen ion exchange via buffer solution. This can also same time. The plasma water replacement contains no
be achieved via increasing filtration fluid flow (convective metabolic wastes and achieves blood purification as it is
clearance), which will also add an increase in clearance of continuously replaced.63
larger molecules, for example those associated with severe Filter membrane polymers are made of different
infection and systemic inflammation or sepsis. Figure 18.14 materials: AN69 (acrylonitrile/sodium methallyl
illustrates the circuit and set-up for CVVHDf. sulfonate), PAN (polyacrylonitrile) or PA (polyamide)
and polysulfone;63 however, all demonstrate similar
Delivering CRRT artificial kidney effects and are generally chosen
To correctly understand the different variants of RRT, according to the supplier circuit provided or, when
how each achieves waste removal and fluid balance along this is not fixed, by the vendor or doctor preference.46
with knowledge of how to ‘troubleshoot’ the machine The most important characteristics of filters used in
providing RRT, nurses must have a clear understanding of continuous modes of therapy are: 1) a high plasma
the major circuit components and their functions. water clearance rate at low blood flow rates and circuit
pressures; and 2) high permeability to middle-sized
Membranes molecular weight substances (500–15,000 daltons, e.g.
The filter or haemofilter (blood filter) is the primary inflammatory cytokines), which are often encountered
functional component of the RRT system, responsible for in critical illness.
602 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

FIGURE 18.15 Haemofilter (dialysis membrane). Cross-sectional view indicating longitudinal synthetic fibres
conveying blood into and out of the plastic casing outer structure. Plasma water is removed via the side ultrafiltrate
port during CVVH applying convective clearance. In CVVHDf, the blood is exposed to fluid via the membrane fibres
so that diffusive clearance can occur.

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Vascular access a vein but large enough to provide blood flow of at least
As previously noted, in order to establish CRRT it is 200 mL/min for an adult CRRT circuit. Catheters are
necessary to create a blood flow outside the body using the made with different arrangement of the lumens revealing
EC. Blood is most commonly accessed from the venous variation in their cross-section profile (see Figure 18.16B).
circulation of the critical care patient via a catheter placed There is no evidence to suggest which profile is better,
but the larger the internal diameter, the less likely flow
in a central vein (e.g. femoral). Blood is both withdrawn
will be obstructed during patient care with CRRT. After
from the vein and returned to the same vein – that is,
a catheter is threaded into a vein, the blood flow may be
veno-venous (VV) access by means of a double (dual)-
adequate, but later during patient care it may obstruct due
lumen catheter. When the same procedure is carried
to different nursing interventions and patient movement,
out by accessing the blood from the patient’s systemic
which may alter blood flows within the low pressure
circulation via an artery and returning it to a vein, the venous system.65
term arteriovenous (AV) is used.57,64 In this system there Insertion sites may be affected by nursing care
is no mechanical blood pump required, as the patient’s interventions. Placement of the catheter is usually in the
arterial blood pressure provides a flow of blood in the EC. femoral or subclavian vein, and occasionally in the internal
Veno-venous haemofiltration (CVVH) has the advantages jugular vein.64 Anecdotally, the subclavian position is more
of requiring only a single venipuncture, a reliable blood easily managed for dressing and securing, continuous
flow delivered from a blood pump and alternative venous observation and patient comfort, but is more problematic
access sites if site infection or access is difficult.57 While in terms of flow reliability. Intrathoracic pressure changes
it is easy to establish flow within AV-driven circuits and associated with physiotherapy or spontaneous patient
no complex system of blood pumps and pressure sensors coughing and breathing, coupled with the upright position
is necessary, this method is susceptible to flow problems of patients, may hinder blood flow from the subclavian-
associated with low patient arterial blood pressure and sited access catheter.While these issues are not encountered
high venous pressures, a common occurrence in critically with a femoral-placed catheter, flow problems can arise due
ill patients. to side lying and flexion at the groin or hip.65
The dual-lumen catheter used for veno-venous access The flow performance of any vascular-access
has an internal diameter of 1.5–3 mm and the ends of catheter can be affected by the patient’s position in bed,
the catheter are sufficiently separated from each other in spontaneous movement and repositioning activities as part
the patient’s vein to prevent filtered blood from mixing of routine nursing care in the critically ill for pressure-area
with unfiltered blood when used in the recommended prevention. Catheter lumen outlet or inlet obstruction
sequence.64 This ensures that filtered blood does not can be due to contact with the vessel wall, or to the
simply pass back through the artificial kidney, where formation of a sharp bend due to the patient’s movement.
there would be minimal waste clearance compared with These factors contribute to compromising blood flow
‘fresh’ unfiltered blood; this design is illustrated in Figure in the EC,65,66 and have been identified by an ultrasound
18.16(A).The catheter must be small enough to place into Doppler flow probe attached to the circuit tubing.65
 CHAPTER 18 SUPPORT OF RENAL FUNCTION 603

FIGURE 18.16 A Vascular access catheters for CRRT. Dual-lumen, Bard® Niagara™ and Gambro Dolphin Protect™
catheters; B concept diagram of catheter lumen profiles used for dual-lumen CRRT catheters.


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4.

Bard Niagara Vas-cath®

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roller rotates at a rate providing a flow of fresh unfiltered

Practice tip blood to the haemofilter, enabling it to clear metabolic
If CRRT circuits clot or fail, remember, if this is waste products.
associated with failure of the access catheter, restarting The roller pump has a central anticlockwise rotating
a new treatment is also likely to fail unless the catheter shaft driving two roller wheels inside a rigid housing.
is changed or re-sited. The solution is not to increase Blood-filled tubing sits stationary inside the housing and
anticoagulant dose. is compressed by the outer surface of the roller wheels
during 180° (half) of their rotation through the pump
housing. This means that one of the two wheels is almost
Blood pump continuously compressing the tubing, moving blood
In veno-venous modes, a pump component is essential forward out of the roller housing. The compression is not
as part of the patient’s blood volume flows externally absolutely continuous, as there is a short time (<0.5 s)
to the body via the EC. Blood flow is maintained by a when there is no compression to allow the tubing to
‘roller pump’ (see Figure 18.17), which propels the blood refill with fresh blood. The compressed tubing re-expands
along the tubing in a peristaltic fashion (milking along by behind the rotating roller and fills with fresh blood from
compression of the tubing), compressing the blood-filled the access and will be compromised if the catheter is
tubing but having no contact with the blood itself. This obstructed in any way.
604 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

FIGURE 18.17 Roller pump for RRT.

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Venous return line bubble trap

FIGURE 18.18 Schematic of typical venous bubble
chamber trap design.
The purpose of the bubble trap chamber is to prevent
any gas bubbles in the EC from entering the patient’s 6HFRQGDU\,9OLQH
circulation by allowing them to rise to the top of a small, 6\ULQJHWRDGMXVW
3UHVVXUHVHQVLQJOLQH EORRGOHYHO
vertically positioned collection reservoir (see Figure
18.18). Venous pressure is commonly measured via a
tubing connection into the top of the venous chamber,
$LUVSDFHDQGDLU²
and additional intravenous fluids can be administered EORRGLQWHUIDFH
into this chamber via a secondary tube connection. The
level of the blood in the chamber must be below the %ORRGOHYHO
top, to prevent spillage into the pressure monitoring
line. It is advised that the blood level be adjusted to 'LUHFWLRQRI
near full but allow for visual inspection of incoming EORRGIORZ
blood flow and to ensure that any air or gas bubbles
are trapped here.67 As this creates a gas–blood interface
within the venous chamber there is a potential source of
venous chamber clotting and hence circuit failure.46,66,67 %ORRGILOWHU
Addition of replacement fluids into this chamber when
using post-dilution fluid administration can cause a
plasma fluid layer to develop above the blood level
and may reduce clotting by stopping blood foaming
on its surface and eliminates air or gas contact with
the blood.68
Anticoagulation of anti-clotting drugs is to delay clot formation while
There are several different drugs utilised to prevent blood the blood is outside the body, particularly when within
clotting in the EC; heparin, prostacyclin and sodium citrate the densely-packed fibres of the filter. As calcium, blood
have been used separately or in various combinations (see platelet cells and thrombin are vital in clot formation,66
Table 18.4).69–71 As blood comes into contact with the these drugs are targeted to one of these elements. This
plastic tubing and the polymer fibres of the filter, various targeting must not be too pronounced, as the patient may
clotting systems are activated. This is a normal action of begin to bleed when the blood returns from the EC to
blood when exposed to non-biological surfaces. The aim the body.66
 CHAPTER 18 SUPPORT OF RENAL FUNCTION 605

TABLE 18.4
Commonly used anti-clotting agents for CRRT

DRUG BENEFITS PRECAUTIONS

Heparin Inexpensive, wide experience, easily Sensitivity reactions, heparin-induced thrombocytopenia, to be

reversed, easily monitored, short half- effective means increased risk of bleeding systemically
life
Low-molecular- Moderately inexpensive, increasing Difficult to monitor, not easily reversed, longer half-life, dosing
weight heparin experience, less likely to result in varies between types of LMWH
(LMWH) sensitivity reactions
Prostacyclin Very short-acting, has a physiological Expensive, no measure of effectiveness, narrow dose range
role in inhibiting platelet activity, does with associated hypotension, individual patients sensitive to
not exacerbate other drug reactions haemodynamic effects, unstable in solution
Citrate-based Limit anticlotting effect to Substantial metabolic effect if not adequately managed (serum
solutions extracorporeal circuit (EC) – ‘regional ionised calcium must be monitored closely); requires additions
anticoagulation’; results suggest very to EC to administer and reverse and use of specialised
effective in prolonging circuit life replacement/dialysate solutions
Not useful when liver failure present, citrate is converted to
bicarbonate by the liver providing the necessary buffer for renal
replacement therapy (RRT). Acidosis may occur in liver failure
No anti-clotting agent No side effects, no exacerbation of May encounter very short circuit life that consumes remaining
(with saline flushes) unstable haematological status, liver haematological components, risk of fluid overload if saline
failure flushes not part of fluid balance. No evidence saline flushes
have any benefit

Heparin is the most commonly-used agent for the bicarbonate as a necessary buffer.74,75 However, citrate-
prevention of clotting, as it is inexpensive, widely available bound calcium is lost in the waste fluid removed and
and easily reversed by another drug, protamine.69 Heparin requires replacement by a separate calcium infusion
is usually administered into the EC before the blood enters to maintain serum calcium levels to normal, at 1.0–1.3
the filter, although the optimal place to administer any mmol/L.74 With this method, the circuit is anticoagulated,
anticoagulant drug during CRRT is not agreed upon.72,73 but the patient is not (also called a ‘regional’ method of
A bolus is often given prior to circuit connection, either anticoagulation) as the patient blood calcium level is
in the circuit prime or via the venous access catheter. restored to normal, making this approach safer compared
A maintenance dose (5–15 units/kg/h) is then adjusted to heparin use; it can be applied in auto-anticoagulated
against the relevant laboratory tests and a visual inspection patients where premature circuit clotting continues to
for clotting in the EC is undertaken, particularly noting occur.76,77 Due to the complex nature of the citrate-
the venous bubble trap. based anticoagulation approach a number of different
Citrate is another popular anticoagulant for CRRT as protocols have been proposed to aid in management.78
an alternative to heparin. Citrate buffers pH and chelates Not all methods will be applied in the one ICU, and local
calcium, inducing anticoagulation of blood by reducing expertise development of one method and an alternative
serum ionised calcium level. For anticoagulation, the dose is common. Recent reviews provide a good synopsis of
and dose rate of citrate are commonly set to achieve a each method as they are different depending on CVVH
reduction in the CRRT circuit blood ionised calcium or CVVHDF mode.79
level to <0.3 mmol/L.74,75 As ionised calcium is essential Normal clotting time, a laboratory test designed
for the progression of the coagulation cascade to form a to measure the time taken for blood to clot under
stable clot, an anticoagulant effect is achieved when the laboratory conditions, is used as a reference to determine a
calcium is bound or chelated.75 A continuous infusion of suitable therapeutic range of the anti-clotting drug
citrate is administered into the CRRT circuit, as patient during CRRT. Different tests are applicable to different
blood enters the circuit, similar to heparin administration. medications and their site of action in the clotting
A new approach in Australia includes citrate as an additive cascade. When using any anti-clotting agent, a balance is
to commercially prepared CRRT replacement fluids. required between the benefits of increased coagulation
When circuit blood returns to the patient circulation, it suppression and the higher risk of patient systemic
mixes with systemic blood and the calcium concentration bleeding. In each patient this risk may vary, depending on
is restored to normal; free citrate not binding to calcium illness, accompanying liver failure and administration of
is metabolised by the liver to provide carbon dioxide and concurrent anti-clotting agents.
606 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Fluids and fluid balance fluid production from tap-water at the bedside. This
Fluid used during any form of CRRT is a commercially approach can be less expensive, requires no bag changing
manufactured product with an electrolyte composition or reconstituting by nurses,82 but does require the installa-
similar to blood plasma.80 This provides a solution useful tion of a complex and expensive reverse osmosis machine,
as a replacement solution for plasma water removed in the cost of which would be offset if large volumes of fluid
convective mode (CVVH), or as a dialysate solution in were then consumed from this online manufacture. This
diffusive mode or CVVHD(f).These respective applications approach is used in some centres for these reasons, and is
allow for plasma water replacement with ‘clean’ and applied as ICU daily dialysis (EDDf) or extended dialysis
buffered plasma water following toxin laden plasma water modes (SLED) are the therapy of choice.
removal or, during CVVHD(f), for plasma water to be Fluid balance monitoring and adjustment to machine
exposed to the whole blood across the membrane fibres so settings is a key nursing responsibility in managing a
that toxins and molecules will diffusively exchange from patient treated with CRRT.57 This requires an operator of
the blood into the fluid. The additives or recipe for three the machine to enter a rate of fluid removal each hour, or
commonly used commercial fluids are listed in Table 18.5 for a longer set time period, and the machine is intended
together with saline solution and normal blood plasma to achieve this target for the set time. It is important to
chemistry for comparative analysis. The key additives of remember this volume of fluid removed is simply the
note in the commercial fluids are the elevated level of machine-prescribed loss of fluid removed, commonly
bicarbonate and the variable concentration of potassium determined by electronic scales in the machine, and does
(no potassium option also), providing an effective buffer not equate to the overall fluid balance of the patient.83
for the acidaemia and hyperkalaemia associated with AKI. The patient may have substantial fluid inputs and outputs
Throughout the course of a continuous treatment with from other sources such as surgical drains and all amounts
CRRT, hypokalaemia may occur and a higher potassium must be considered to determine the desired fluid balance
added solution may be required to correct and maintain for the day. Therefore, the machine setting to achieve
normal serum levels. First-generation commercial fluids a desired fluid state must be determined in context
used lactic acid as the buffer additive, requiring liver for the entire clinical status of a patient where verbal
metabolism to produce bicarbonate in vivo.80,81 This prepa- communication and written prescribing orders must be
ration is now not used in favour of a bicarbonate added clear to differentiate ‘machine loss – setting’ from patient
fluid, prepared just prior to use using a two-compartment net ‘loss’ or balance per hour.57 Despite simple software
bag (see Figure 18.19) as the two fluids are unstable in and screen interface for setting the desired fluid loss or
long-term storage. The higher cost, problems with recon- removal per hour during treatment, mistakes and errors
stituting bicarbonate solution bags and manual handling occur.83 In some cases, particularly in small children and
of large (5 L) fluid bags has increased interest in ‘online’ babies, this can be fatal.84,85 Most machines now provide

TABLE 18.5
Blood plasma chemistry compared with commonly used commercial CRRT fluids

BAXTER
H A E M O F I LT R AT I O N
SALINE GAMBRO C I T R AT E S O L U T I O N
(BAXTER, HEMOSOL BO (BAXTER,
BLOOD – TOONGABBIE, BAXTER (GAMBRO, TOONGABBIE,
PLASMAa AUSTRALIA) ACCUSOL LUND, SWEDEN) AUSTRALIA)

Sodium (mmol/L) 136–145 150 140 140 152

Chloride (mmol/L) 98–07 150 113.5 109.5 99
Potassium (mmol/L) 3.5–5.1 0 4.0 or 2.0 4.0 or 2.0 5
Bicarbonate (mmol/L) 22–29 0 35 32 0
Calcium 2.15–2.55 0 1.75 1.75 0
Magnesium 0.66–1.07 0 0.5 0.5 0
Citrate 0 0 0 0 90
Lactate 0.5–2.2 0 3.0 0.0
pH (range) 7.35–7.45 4.0–7.0 7.4 7.0–8.5 5–6.5
mOsm/kg 280–300 300 300.3 287 270
(listed or estimated)
a
Adult ranges reproduced with permission from: plasmahttp://www.austinpathology.org.au/test-directory.
 CHAPTER 18 SUPPORT OF RENAL FUNCTION 607

FIGURE 18.19 Two-compartment bicarbonate bag.

Bicarbonate CRRT fluid

Main bag – bicarbonate – B B
Small bag – electrolytes – A

K+ of 0 or K+ of 4
No glucose
A

2 compartments joined on preparation

limits for the amount of accumulative fluid balance error of the patient. Electrolyte disturbances may also occur
(+ve or −ve) before an alarm will sound with a display despite use of balanced replacement solutions. Particular
message to advise the nurse. Such errors can occur due attention should focus on regular assessment of fluid and
to fluid bags remaining clamped, or fluid pathway lines electrolytes, especially potassium, sodium, phosphate and
kinked or clamped. Logically, the machine is removing magnesium levels.
or infusing fluid but the machine scales are not detecting
a weight change. The fluids infused as replacement or Practice tip
removed as waste plus additional fluid for a loss are usually
all recorded on a fluid balance chart at the bedside. This Fluid removal during CRRT is prescribed by doctors and
is presented as traditional inputs and outputs charting, usually to a time frame. The nurse needs to calculate
with the difference between these amounts understood as the rate per hour and must also include a recalculation
the balance; usually a negative in the context of a patient of the treatment if it is off for long periods.
with AKI, anuric and in the ICU setting, is commonly
set for a negative balance overall. Where anticoagulation Patient management
infusions are used in the CRRT circuit, this volume may
be recorded into the CRRT calculations as ‘input’ and Nursing protocols have previously been focused on
contribute to the balance determined. This is all achieved machine priming, patient preparation and use of a CRRT
easily with recent electronic fluid charts included in ICU system as this was the essential training pathway for
clinical information and patient management systems. See nurses learning the operator–machine–patient interface.87
Figure 18.20 as an example of such a spread sheet chart Current CRRT machines are highly automated and have
from a bedside computer. advanced software with instructional on-screen coloured
Irrespective of patient acuity, when CRRT is used, pictures, circuit diagrams and text prompts providing a
individual patient assessment for fluid status must occur at sequential step-by-step approach for priming, patient
least twice a day. Subtle temperature changes in the patient, connection and key alarms. This has often made bedside
surgical drain losses, diarrhoea and variable absorption e-policies and paper documents redundant, with nurses
of feed may all contribute fluid losses not included learning the machine preparation sequence without
in routine fluid maintenance. Similarly, fluid boluses, the need to follow any paper instruction booklet or
transducer flush volumes and drugs administered may on-screen pictures. Nonetheless, the clinical knowledge,
together create a positive fluid balance. If sustained this psychomotor skills and the responsibility for managing
clinical state is reported as a contributor to delayed renal an extracorporeal circuit to efficiently and safely treat a
recovery and increased mortality in the ICU.86 Regular critically ill patient should not be understated. The nurse-
weighing of patients may assist in assessing this situation, to-patient ratio for CRRT is commonly 1:1 worldwide,
in addition to regular physical and clinical assessment acknowledging the attention and focus required despite
608 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

FIGURE 18.20 Screen dump of a bedside e-fluid balance chart.

the advances in machine automation.88 This is a reasonable patient metabolic stability with electrolyte, acid–base and
approach as CRRT in the ICU is very different to the temperature management represent some of the work
use of dialysis for chronic renal failure where a nurse may associated with the nursing care required.57,68 Machine
oversee three or four patients on dialysis under their care and circuit preparation, connection and, when required,
and with different start times (overlapping) for a 3–4-hour stopping and disconnecting a treatment are further skill
treatment in each case. In the ICU these patients are and knowledge sets for ICU nurses. Consideration of
usually in a multi-organ failure state, are intubated and all these factors represents why nurses are particularly
require mechanical ventilation, cardiovascular support, concerned that a new treatment, when started, is stabilised,
enteral feeding, need many intravenous drugs and infusions then functions continuously for as long as possible. This
and have reduced neurological function with or without perspective is an additional consideration to the medical
sedation. This is a picture mandating both technical and aims of treatment ensuring solute, acid–base and fluid
cognitive tasks in addition to comprehensive nursing care, balance are controlled. It is the key interest of both doctors
including full hygiene and all care for the bedridden, and nurses in the ICU that the treatment be ‘continuous’
unconscious patient. as frequent stopping and restarting is a lot of work for
Monitoring correct machine function for reliable flow nurses and may cause instability in the patient.89
of blood, continuous changing of bags as substitution In Table 18.6 a summary of key nursing practice and
fluids empty and waste bags fill, adjustment and constant interventions for bedside use is provided making this
review for stability with anticoagulation agents and the information a suitable reference for nursing knowledge
overall monitoring and response to other parameters of and skills associated with CRRT use in the ICU.
 CHAPTER 18 SUPPORT OF RENAL FUNCTION 609

TABLE 18.6
Trouble-shooting guide: key nursing practice and interventions for CRRT

POTENTIAL PROBLEM KEY NURSING INTERVENTIONS REQUIRED, REFERENCED TO

(NUMBERED LIST) LISTED NUMBER

Patient and 1 Machine alarms and 1 Machine self-test and/or checklist completed
machine/system technical failure on starting 2 Double-check all circuit lines around circuit, particularly for clamps ON or
preparation before treatment OFF as required
use 2 Air entrainment during prime 3 Treatment orders cross-checked with settings
3 Fluid setting errors 4 Double-check fluids used, e.g. any additives required
4 Fluids/electrolytes incorrect 5 Position machine according to access catheter site: at feet for femoral
5 Machine and patient too far line, at bedside for sub-clavian and at bed head for jugular with screen
apart or machine placed out faced to staff desk or charts/computer
of staff view Recommendation:
• Have your own pre-start check routine (paper document list)
Connection 1 Access catheter 1 Prepare access connections with antiseptic, aspirate any instilled drug and
to the system obstruction/failure test easy flush return (venous) lumen and aspirate outflow (arterial) lumen
and initiation of 2 Hypotension on start 2 Connect both circuit lines to access catheter administering priming
therapy volume to patient
(a) Increase vasoactive drugs if necessary to increase MAP
(b) Start blood pump slowly with small increases until blood fills all of the
circuit
Recommendations:
• Use two nurses for connection routine. Start fluid replacement and
removal only after blood circuit is full and at prescribed speed, stay with
patient until stable ~ first 15 min
• Patient in bed, supine position and MAP >70 mmHg, stable
In-use 1 Excessive negative 1 & 2 Maintain access catheter alignment, preventing kinks in access and
troubleshooting pressure >−100 mmHg: circuit lines
alarms and ‘arterial alarm’ 1 & 2 Do not place extra connections or taps between access catheter and
maintenance, fluid 2 High pressure > +100 circuit lines
balance mmHg: ‘venous alarm’ 3 Suggests filter clotting or blood flow too slow for fluids settings
3 High TMP alarm 4 Ensure venous chamber full high with blood, bubbles removed regularly,
4 Air detected alarm prescribe post-dilution fluid into the chamber
5 Hypothermia 5 Heater set to 37°C or greater to compensate for heat loss from
6 Fluid balance errors extracorporeal circuit
7 Electrolyte imbalance 6 Use fluids charting or similar to account for all fluid inputs including
anticoagulant volume. Clarify orders to set machine ‘loss’ in respect
of this. Commonly a net negative. Orders and settings should not be
prescribed to administer fluid – no net positive
7 Potassium additive to CRRT fluid is often required after 24–48 h of
treatment; some patients are hypokalaemic despite acute renal failure.
Phosphate monitoring and correction is important
Recommendations:
• Assess and reset fluid balance settings hourly, particularly in unstable
patients and for inexperienced staff
• Fluid gain or positive fluid balance using CRRT should be considered an
adverse event or complication of use
Monitoring and 1 Premature clotting in 1 Check and monitor effect of anticoagulant therapy according to local
adjustment to circuit and filter policy. With heparin use this could be after first 6 h and then daily
anticoagulation (a) Maintain adequate dose to therapeutic range
(b) Use predilution fluid administration
(c) Use blood flow greater than 150 mL/min
(d) Use large-bore access catheter and take care not to obstruct or kink
catheter
(e) Keep blood pump operating: minimise stops >30 s
Recommendation:
• If frequent failure (clotting <4 h), always check for blood flow obstruction
before more, or alternative anticoagulation; e.g. review to consider
change or replacement of access catheter
610 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 18.6 continued

POTENTIAL PROBLEM KEY NURSING INTERVENTIONS REQUIRED, REFERENCED TO

(NUMBERED LIST) LISTED NUMBER

Access care and 1 Access dislodgement 1 Ensure catheter sutured in place and well secured with dressing; single
dressings 2 Access catheter infection or double (‘sandwich’ technique) biofilm–polyurethane (see Figure 18.22)
3 Access catheter 2 Use asepsis when flushing or connecting to access catheter; monitor
obstruction site for infection and patient for suspected line sepsis. Use catheter site
alcohol patch, e.g. Biopatch™
3 Use heparin to fill catheter dead-space when not in use for >4 h and label
accordingly
Recommendation:
• Use flexible dressing with application to both sides along catheter
allowing movement away off skin surface, preventing obstruction during
patient care/positioning and lifting or tearing off dressing.
Vital sign 1 Arrhythmias, hypotension, 1 Monitor vital signs hourly, consider any links between changes, and
monitoring temperature use of RRT; e.g. low CVP and excessive fluid removal, temperature
fluctuations when CRRT OFF and ON
Recommendation:
• CVP readings should be performed 2–4-h during CRRT; CVP can be used
as a target for daily fluid loss prescription. Weigh the patient if possible.
Do frequent blood gas and electrolytes commonly associated with ICU
care
Assessment of 1 Filter clotting abruptly with 1 If trans-membrane pressure (TMP) or pre-filter pressure (P-IN) >250 mmHg
filter function and inability to return circuit is diagnostic of filter clotting; consider electively returning blood by
patency blood to the patient crystalloid infusion into outflow limb of circuit and ceasing treatment –
2 Inadequate solute removal follow local policy
(a) Observe for venous chamber clot development. If excessive and
venous pressure >150 mmHg, consider electively returning blood –
cease treatment
2 Assess patient’s solute levels: urea and creatinine should be reducing
or stable
Recommendations:
• Predicting circuit or filter clotting can be difficult. TMP and P-IN can
rise quickly after being stable or within normal range. If there is a trend
upwards reflecting diagnosis of clotting, cease treatment electively to
avoid blood flow ‘standstill’ and a failure to restart and blood loss
• Nurses may document these pressures hourly or check the machine
frequently, but they must respond quickly to cease treatment
Cessation of 1 Blockage and/or clotting in 1 Use concentrated heparin (other anticoagulant) to fill dead-space of
treatment and access catheter catheter when not in use >4 h. Use heparin 1000 IU/mL and follow
disconnection 2 Inadvertent blood loss manufacturer’s specifications for volume required
from the 3 Infectious risk 2 Always attempt to cease a circuit before it clots and always return patient
extracorporeal blood if possible
circuit 3 Use asepsis for disconnection procedure
Recommendation:
• Access catheter should not be used for other purposes/infusions when
RRT is not connected
Temporary 1 Maintenance of circuit 1 Flush out any excess blood residue in circuit, keep blood pump
disconnection for before reconnection operational with saline (prime) in circuit
procedures 2 Infection 2 Circuits in use for >24 h before disconnection or not restarted after
3 Inadvertent fluid 6 hours following temporary disconnection, consider discarding
administration 3 After restarting circuit, increase fluid loss to remove fluid used to
re-establish RRT
Recommendation:
• Re-use of circuits in this context is not desirable and with prior planning
should be avoidable. E.g. plan for radiology, surgery etc when circuit off
or restart new circuit around these interventions. If this is done, consider
adding heparin 5000 IU to circuit when temporarily disconnected unless
contraindicated, but flush this out with 200–300 mL prime solution before
reconnection; always use additive label indicating heparin added
CRRT = continuous renal replacement therapy; CVP = central venous pressure; MAP = mean arterial pressure;
TMP = trans-membrane pressure.
 CHAPTER 18 SUPPORT OF RENAL FUNCTION 611

Practice recommendations are also included. This infor- anticoagulation method. See Figure 18.21 as an example of a
mation is general to any CRRT machine, and does not shift checklist.
include a detailed anticoagulation protocol. Antico-
agulation technique for CRRT usually dominates any Continuous renal replacement machines
policy and is viewed more frequently in comparison to There are many machines available for CRRT in the ICU.
the psychomotor skills component for machine prepa- How to identify the machine that a particular ICU should
ration, connection and fluids bags management. Nursing use or purchase is a common question from nurses, and
practice policies can also be supplemented with machine- there is limited literature available to guide this decision;
specific and quick reference ‘one page’ lists for shift check or however, literature providing comparisons of their

FIGURE 18.21 Shift checklist for CRRT at Austin Health, Melbourne, Australia.

Austin Health
Shi check list CRRT as CVVH: Infomed HF 440

Check Raonale
Machine posion relave to paent with Paent movement could cause excess drag
blood lines not too ght - stretched on vascath site and securing tape
Brakes ON Machine must have brakes on to prevent
inadvertent movement and risk of above
Fluids: correct for K + and both bags hanging Fluids should empty at similar rate, minimise
from same point – height, both line clamps mixing, scales and balance alarms more
open likely if the bags hanging at different heights
Flush line connected, correct fluid, clamped Fluid to return paent blood; this may be
as close to blood path as possible. Date this required any me. Clamp close to blood path
bag. prevent blood tracking back up this line and
clong, only to be flushed in with use
Waste bole hanging stable and waste This bole will weigh > 16 Kg on full. Needs
pump hose with end plug ready, coiled on to hang with stability to prevent scales
machine holder. alarms. Hose ready for use with end cap to
prevent drips
Venous – bubble chamber full and inspect Adjust this up slowly, with syringe aached.
for clot Keep full to trap gas / air and allow for the
level to fall during use with gas entry
associated with bicarbonate fluids (CO2)
when heated
Luer syringe (10 ml), 3 way tap and dead end Luer syringe will not fall / slip off during use;
cap(red) in line - for chamber adjustment red cap blocks pathway between venous
blood chamber and UF pathway if 3 way tap
was accidently opened to both chambers.
Screen sengs & Alarms
Blood flow - speed 200 mls/min. standard
UF flow 2000 ml/hr standard CVVH
Manual Pre-diluon % 50:50 for CVVH (Citrate use 70% pre)
‘Weight loss’ – Fluid loss rate ml/hr Check orders – fluid loss target
Next intervenon (hr:min) Time unl fluids bag change or bole empty
Temperature seng Default at 37°, maybe ↑↓ to paent need
Venous +10 ---- + 150 mmHg This pressure always posive, measured on
(influenced by blood flow rate and chamber the return limb of circuit. ~ 50 – 100 mmHg
clong, access funcon – blue lumen)
Arterial -150 ---- -10 mmHg This pressure always negave, measured on
(influenced by blood flow rate and access the ou low limb of circuit. ~ -50 – -100
funcon – red lumen) mmHg
Trans-membrane pressure (TMP) Indicave of clong / clogging in the
(Pin + Pv)/2 - Puf membrane.
Set at 200 mmHg inially. When 250+ mmHg,
usually terminate treatment.
Ancoagulaon and Prescripon orders Check drug dose and orders correct
612 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 18.7
Machine design and build approaches

PRIMING
P R E PA R AT I O N
MACHINE WASTE PRESSURE AND SOFTWARE
TYPE COLLECTION MEMBRANE CIRCUIT MEASUREMENT OPTION(S)

A One 5-L or 10-L AN69, prefitted, not Cartridge In-line pressure Fully automated,
bag, empty when changeable kit-based, transducers software for
full, change bag(s) multipurpose; all management
modes of citrate
anticoagulation
B One 5-L or 2 bags, Different membranes Cartridge In-line pressure Fully automated,
empty when full, possible – kit-based, transducers Intelligence software
change bags polyethersulfone or multipurpose; all for fluid management
others modes

technical characteristics is limited.90,91 Table 18.7 outlines

the major differences in machines or system approaches. FIGURE 18.23 Aquarius CRRT Machine, Nikkiso,
Sydney, Australia.
Two machines adopting common design features from
Table 18.7 are shown in Figures 18.22 (Prismaflex; Hospal,
Lyon, France) and 18.23 (Aquarius, Nikkiso, Sydney,
Australia), each highlighting the major technical differences
in how CRRT machines are presented and used.

FIGURE 18.22 Prismaflex CRRT Machine.

Courtesy Gambro Australia Image courtesy of Nikkiso, Sydney, Australia.

 CHAPTER 18 SUPPORT OF RENAL FUNCTION 613

Teaching and training CRRT methods, updates, orientation for new staff and specialist
training in association with postgraduate certification.
Since introduction of CRRT to the ICU in the 1980s Figure 18.24 provides a list of suggested education topics
and early 90s, medical companies as machine vendors have in sequence for a local teaching and training activity.These
developed and expanded their offerings for teaching and didactic session topics may be scheduled in the sequence
training nurses in the use of CRRT machines and the and over several weeks to become more powerful when
broader aspects of acute kidney injury and patient care. supplemented with simulation activities linked to live
Depending upon the hospital, training and education may patient care and bedside clinical support.46,88 A recent
be conducted for small groups or entire ICU staffing cohorts report suggests that, when simulation is added to didactic
associated with a new machine fleet installation or when CRRT education programs, an improvement in CRRT
CRRT is introduced without any previous experience functional time (filter ‘life’) is observed – a direct benefit
with artificial renal support. More commonly, where to users, lessening cost and better for patients.92
CRRT is imbedded in use for many years, the education Refer to Figure 18.25 for a CRRT demonstration or
focus is with smaller groups teaching new procedures and simulation set-up.

FIGURE 18.24 List of suggested education topics for CRRT.

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DQGDODUPVFLUFXLWDVVHPEO\SULPLQJ SUHS
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FIGURE 18.25 CRRT demonstration or simulation set-up.

Simulang CRRT
• Use a basic resus doll
• Add food dye to a saline bag to
create red fluid
• Insert a vascular access
catheter into the bag and seal
ght with a cable e
• Place the bag into the doll with
access visible e.g. femoral site
• Prepare an unsterile / old circuit
• Demonstrate or simulate
common procedures
• Prismaflex (Hospal Gambro, Lyon,
France) shown here
614 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

The key to successful CRRT education and training with the CRRT-treated patient and ensure safety.47,88
is to develop nurses with clinical experience managing The most useful measure for quality when using CRRT
CRRT regularly in the ICU and encouraging these experts is the progressive ‘life’ of the circuit or filter.57 This data
to teach others around them when they can. This may point may be recorded on bedside charts alongside hourly
require a nurse being allocated to this role formally, such as observations (see Figure 18.26) or electronically into an
a clinical nurse specialist role dedicated to teaching within ICU clinical information system and provides an instant
the ICU, or assigning these experienced nurses close to audit for each circuit used and throughout the patient
those learning CRRT during a shift. Such educators may treatment. This variable is most commonly used to
already be in place for broader aspects of ICU education compare efficacy of different anticoagulation techniques,
and postgraduate trainees but, for any staffing structure but may also be considered a measure of access catheter
with or without dedicated teaching roles, identifying a and blood flow reliability, machine technical function
small number of nurses as CRRT ‘champions’ for training and staff user competence.93 Circuit or filter life (these
and ongoing support when CRRT is in progress is a terms are used interchangeably) is reported widely in the
common and successful approach47,87,88 to provide learning literature and, despite lacking a clear bedside definition,
for others over the 24/7 context in ICU. published data indicate that a median life of 21 hours is
common.94,95 Poor circuit life at 4–6 hours reflects clinical
Quality and measures of success
problems and an interprofessional review before the next
Maintaining quality and nursing expertise for CRRT treatment begins is warranted.
in the ICU will be related to the frequency of use and
the size of the user group. When there are long periods Special considerations
between CRRT use, and/or when the ICU has a large Paediatrics: babies and small children
staff number, ensuring competency may be challenging.
Regular competency checks and staff assessments can be of 3–30-kg body weight
performed88 depending upon resource allocation for this The use of dialysis and haemofiltration in babies and
task but, where CRRT is in frequent use with several small children is a specialty area; however, many aspects
patients treated continuously, such checks may not be of adult CRRT apply, particularly for those patients
done suggesting that continual experience with CRRT >15 kg.96 Key differences, depending on size and
in itself provides the competency process. Shift allocation weight, for this patient group are: 1) a smaller membrane
of the nurse to a patient with AKI and treatment with surface area (size), and smaller circuit tubing to reduce
CRRT care may benefit from predetermined skill sets as priming and circuit volume; 2) a smaller access catheter
a guide to best match the individual nurse’s competency (<7 Fr) depending on body weight and often placed in

FIGURE 18.26 Bedside charts with consecutive filter life hours.

3 circuits = 15 / 24hrs = 62 % ‘On’ or 38% ‘Off’ time

59 hours continuous function – filter life

B
 CHAPTER 18 SUPPORT OF RENAL FUNCTION 615

the femoral vein; 3) blood flow rate 3–5 mL/kg/min; normally negative access pressure when using venous
4) fluids flow (dialysate or substitution) rates – variable access with a CRRT machine. Some machines provide
depending on mode but 2 L/1.73 m2/h is common; a software option to select access pressure +ve, allowing
5) increased prevention of hypothermia as this problem this use with ECMO, others do not and may require some
is exacerbated in babies and small infants.97 Anticoagula- alarm override or restrictive device to create negative
tion is the same as for adults but with reduced drug doses pressure for the outflow from the ECMO into the CRRT
for the size of the infant or child.97 line. The anticoagulation provided for the use of ECMO
is a convenient state for the successful use of the CRRT
Extracorporeal membrane oxygenation and much of this is usually controlled by a perfusionist
Increasingly, extracorporeal membrane oxygenation or a cardiac anaesthetist overseeing the ECMO support.99
(ECMO) is applied for those with refractory hypoxaemia
in association with respiratory failure or used in the Operating theatre
context of right heart failure and combined heart-lung There are some circumstances when CRRT is useful
failure.98 These critically ill patients frequently have AKI in the operating theatre. This is in association with any
and require CRRT.98 It is convenient and often necessary prolonged surgical case where AKI exists in association
to connect the CRRT circuit into the ECMO circuit as with a critical illness and specific surgery such as hepatic
the patient may have other access sites used for multiple transplant. Local factors related to ICU staffing, and the
cannulation. In any case, the high blood flow associated surgical and anaesthetic teams’ working relationship with
with ECMO and the placement of the circuit tubing the ICU, will influence exactly how this is achieved. The
allows for a connection of the CRRT circuit at many literature in this area is sparse; however, retrospective and
places. The only limiting factor is the positive pressure small data sets reflect that CRRT in the operating theatre
in the ECMO circuit, which is not compatible with the is achievable and safe.100,101

Summary
In this chapter a review of the important physiological functions of the kidney is provided and the context of kidney
failure is also defined as an injury, or AKI. Management of patients with AKI is discussed and includes prevention of
further injury, fluid and electrolyte balance and aspects of nutrition and pharmacy before consideration of an artificial
support or RRT. There are now established criteria for stages of AKI indicating when an artificial kidney support
should begin replacing the functions of the kidney. This support is broadly termed dialysis but is provided in the many
variants of RRT, including PD, and as a continuous therapy in the ICU setting, by CRRTs. The history of dialysis
is relevant as nurses have always played an important role in providing this treatment that, when integrated into the
care of the critically ill, requires substantial knowledge and skills. The machine and circuit for CRRT are useful to
understand as this assists preparation, connection to the patient and then troubleshooting during use.The major failing
of CRRT is clotting of the extracorporeal circuit and anticoagulation approaches are the key preventative strategy.
Teaching CRRT and quality review are very important for a successful program in the ICU. Finally, the use of CRRT
in special considerations is briefly discussed and includes use in the operating theatre, with small children and use
with ECMO.

Case study
Ms S is a 46-year-old woman transferred to the ICU from a regional hospital following a paracetamol
overdose associated with an alcohol ‘binge’. Her past history is unremarkable, but she is a heavy drinker of
alcohol, which has increased since her recent divorce.
Current medications include pantoprazole and atorvastatin. Ms S had been suffering with a heavy cold in
the last few days and reported taking 1–2 g of paracetamol every 4–6 hours. However, it appears that she
had ingested approximately 20 g in a short time period suggesting a suicide attempt.
On arrival to ICU she was intubated, ventilated and unconscious, sedated with propofol. Prior to intubation
her GCS was 7. Cardiac and blood pressure monitoring was instituted. A CVC, nasogastric tube and urinary
catheter were inserted. Oliguria was noted on arrival. A brain CT revealed cerebral oedema.
She had elevated AST and ALT. An initial diagnosis of paracetamol overdose with associated acute liver
failure was made.
616 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Her blood profile was as follows (normal values in brackets):

• pH 7.32 (7.35 to 7.45)
• potassium 5.9 mmol/L (3.5 to 5 mmol/L)
• lactate 4.8 mmol/L (0.5 to 1.6 mmol/L)
• INR 5.2 (0.9 to 1.2)
• ammonia 83 micromol/L (20 to 65 micromol/L)
• arterial bicarbonate 14 mmol/L (18 to 23 mmol/L)
• WCC 20.4 ⫻ 104 (3.5 to 9.0 ⫻ 109/L)
• urea 5.9 mmol/L (3 to 7 mmol/L)
• creatinine 165 micromol/L (60 to 90 micromol/L)
• panadol level 220 micromol/L (commonly considered toxic if >100 micromol/L in chronic alcoholics).
She was unconscious and intubated and ventilated with minute volume of 10.8 L/min and FiO2 of 0.6. Her
heart rate was 112 beats per minute with normal sinus rhythm, blood pressure was 95/45 mmHg while
receiving noradrenalin at 18 mcg/min. She was slightly febrile (temperature 37.8°C) with cool peripheries.
Urine output was 20 mL over the past 6 hours. Her body weight is estimated at 80 kg.

TREATMENT
Key primary treatments were to provide some further fluid resuscitation with 1.5 L of 4% albumin solution,
evaluate the CXR and commence antibiotics, followed by the local ICU policy of ‘H’ therapy: hypothermia
(active cooling), hypernatraemia (hypertonic saline infusion commenced) and haemodiafiltration at 4 L/h,
hyperventilation and head of bed elevation. An infusion of the drug N-acetylcystein was started to protect
the liver following paracetamol overdose.
Two hours after ICU admission a femoral vein access catheter was inserted for haemodiafiltration to
manage acute kidney injury and oliguric acute renal failure. The patient’s serum biochemistry (elevated K+,
creatinine and urea) and developing metabolic acidosis (raised ammonia and lactate, pH <7.35) in addition
to the neurotoxicity associated with an elevated ammonia indicated the need to provide RRT. Other benefits
of renal support are to remove some of the toxic metabolites of paracetamol and allow for fluid removal and
a negative fluid balance for cerebral oedema.
Haemodiafiltration provides a combination of convective and diffusive clearance for all solutes and toxins;
however some doctors may also prescribe haemofiltration as CVVH utilising pure convective removal for
these solutes. The dose or intensity of treatment is controlled by the number of litres per hour of fluid
removed in relation to the body weight and this is achieved by the combination of plasma water substitution
fluid and dialysate fluid. In this case a dose of 50 mL/kg/h was prescribed with a body weight of 80 kg
(4 L/h). This is considered ‘high dose’ treatment and is preferred for this acute toxic state until stabilisation.
Fluid loss is achieved with fluid removal and the filtrate volume may exceed 4 L/h.
The patient was not prescribed any anticoagulation as the INR was elevated. If any gastrointestinal bleeding
were to occur, this would aggravate the toxin load into the failing liver, in particular ammonia. Bicarbonate
buffered fluid is preferred where acidosis is present and particularly where liver impairment is present. No
potassium should be added until the serum level has decreased. The treatment would also provide cooling
and the desired reduction in body temperature.
In 24 hours Ms S stabilised and was starting to awaken with limb movements and eye opening, and
started to breathe spontaneously. The dose for noradrenalin was then 4 mcg/min. The ammonia level was
62 mmol/L and other biochemistry normalised. The dose prescription was reduced to 3 L/h and the
circuit continued to function well without anticoagulation. A negative fluid balance was achieved slowly
over this time and the loss setting was then prescribed as ‘patient even’; only inputs were included in
the setting for fluid removal. This was at 100 mL/h over 24 hours to avoid excessive fluid removal and
hypovolaemia.
Ms S continued to improve and after 4 days RRT was ceased. She was producing urine at >60 mL/h and
had normal acid–base balance, biochemistry and low ammonia levels. Ms S was extubated on day 5 after
resolution of a lung infection. Her mild fever had receded (temperature 35.5°C) and the RRT machine fluids
heater was adjusted to maintain a temperature of 36°C. The RRT access catheter was left in place in the
event that RRT was needed again, but her full recovery looked promising.
 CHAPTER 18 SUPPORT OF RENAL FUNCTION 617

CASE STUDY QUESTIONS

1 Consider the RIFLE criteria outlined in this chapter and Ms S’s presentation to the ICU and her
subsequent management with CRRT. Which stage of the criteria was met in the context of RIFLE for
Ms S?
2 Review 10 patients in your ICU who are prescribed CRRT and observe which stage or RIFLE criteria
they satisfy before beginning CRRT. This may be useful and help you better understand AKI, diagnosis
and initiation of CRRT.
3 From the case describing Ms S’s management, a femoral access catheter was placed for CRRT. This is
usually because central line access is in place via the jugular or subclavian site. Review the placement of
access for CRRT in your ICU. Is there a preference for this? Correlate the site used (femoral, jugular vein
or subclavian) with the filter or circuit ‘life’ for the different access sites used. Is there any relationship
reflecting an association between access site and filter life? Your finding may be compared to the
literature; also see key references in the Further reading section.

RESEARCH VIGNETTE

RENAL Replacement Therapy Study Investigators. Bellomo R, Cass A, Cole L, Finfer S, Gallagher M, Lo S et al.
Intensity of continuous renal-replacement therapy in critically ill patients. N Engl J Med 2009;361:1627–38

Abstract
Background: The optimal intensity of continuous renal-replacement therapy remains unclear. We conducted a
multicenter, randomized trial to compare the effect of this therapy, delivered at two different levels of intensity, on
90-day mortality among critically ill patients with acute kidney injury.

Methods: We randomly assigned critically ill adults with acute kidney injury to continuous renal-replacement therapy
in the form of postdilution continuous venovenous hemodiafiltration with an effluent flow of either 40 mL per kilogram
of body weight per hour (higher intensity) or 25 mL per kilogram per hour (lower intensity). The primary outcome
measure was death within 90 days after randomization.

Results: Of the 1508 enrolled patients, 747 were randomly assigned to higher-intensity therapy, and 761 to lower-
intensity therapy with continuous venovenous hemodiafiltration. Data on primary outcomes were available for 1464
patients (97.1%): 721 in the higher-intensity group and 743 in the lower-intensity group. The two study groups had
similar baseline characteristics and received the study treatment for an average of 6.3 and 5.9 days, respectively
(P = 0.35). At 90 days after randomization, 322 deaths had occurred in the higher-intensity group and 332 deaths in
the lower-intensity group, for a mortality of 44.7% in each group (odds ratio, 1.00; 95% confidence interval [CI], 0.81
to 1.23; P = 0.99). At 90 days, 6.8% of survivors in the higher-intensity group (27 of 399), as compared with 4.4% of
survivors in the lower-intensity group (18 of 411), were still receiving renal-replacement therapy (odds ratio, 1.59; 95%
CI, 0.86 to 2.92; P = 0.14). Hypophosphatemia was more common in the higher-intensity group than in the lower-
intensity group (65% vs 54%, P < 0.001).

Conclusions: In critically ill patients with acute kidney injury, treatment with higher-intensity continuous renal-
replacement therapy did not reduce mortality at 90 days. (Clinical Trials gov number, NCT00221013)

Critique
This seminal study was conducted as a prospective, randomised, controlled trial across 35 intensive care units (ICU)
in Australia and New Zealand over a 3-year period in an effort to assess what level of treatment ‘intensity’ might
influence mortality in critically ill patients with severe acute kidney injury. Participants were offered either a higher
dose of treatment, which was an effluent rate of 40 mL/kg/h, with the lower dose intensity at 25 mL/kg/h. The
principal outcome measure was patient survival at 90 days after study entry, with numerous other outcomes including
various death points, lengths of ICU and hospital stay, return of renal function or deterioration of other organ systems.
618 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

The undertaking of this study was driven by clinical equipoise over what the preferred dose of treatment should
be in continuous renal replacement therapy in terms of patient outcome. This question had been prompted by
a number of reports that increasing the dose might be beneficial and outweigh the risks associated with higher
intensity treatments. These risks include hypothermia, electrolyte disturbances, nutrient loss, altered drug levels
and additional cost. The process of treatment dosing for continuous therapies is inherently different to intermittent
treatment for chronic renal failure (CRF) so, while there is some precedent in terms of the benefits of early initiation
and balanced regimens with CRF, the context and approach to therapy demanded a more specific approach for
dosing CRRT.

The RENAL study enrolled 1508 participants who received a standardised CRRT treatment based on post
dilutional continuous veno-venous haemodiafitration. The predetermined sample size was met and patients
were assigned to one of the two treatment intensity groups, although subsequent issues left 1464 participants in
the final study analysis. Both groups were similar in terms of patient characteristics and were seriously ill with
almost three-quarters ventilated and just under half with severe sepsis. In terms of dose delivery, as would be
expected, the higher intensity group had lower creatinine and urea levels as treatment progressed, but used
more circuits.

In terms of the principal outcome of 90-day mortality the same proportion (44.7%) of patients died in both groups.
There were no statistically different outcomes for other mortality measures with the vast majority of those surviving
recovering renal function by day 90. Serious therapy-related events were low in both groups. The only appreciable
difference was hypophosphataemia, which occurred in 65% of high intensity cases versus 54% of low intensity,
as would be expected. The study was conducted using the mode of therapy most commonly used in Australia
and New Zealand, albeit the use of post-dilutional replacement solution differs from many who deliver this in
a predilution approach. Prescribed treatment dose was under-delivered in both groups because of treatment
interruptions and highlighted findings from many studies that ‘continuous’ is not in fact continuous in terms of the
delivery of these treatments.

While no improvement in survival was found by increasing the dose of therapy in this study, this does not translate
to dose not being important. Outcomes were consistent in this study and better than many others reported from
around the world so it is appropriate to conclude a minimum dose, possibly around 25 mL/kg/h, is necessary
to achieve good survival in severe acute kidney injury. It is worth noting that measures focusing on ensuring the
continuity of treatment are important if the prescribed dose is to be achieved. This study tended to consider
clearance of metabolites associated with renal function as a measure of treatment performance, but it is
equally important to emphasise that good fluid balance control is critical when supporting patients with oliguric
renal failure.

Lear ning a c t iv it ie s
1 Review the serum creatinine and the urine output preceding the commencement of CRRT for a patient in your
care. Which of the RIFLE criteria did they meet at this time?
2 Review the medications prescribed for a patient managed with CRRT and check the available information for
clearance with renal failure. Are the prescribed doses modified in this patient?
3 Review the ‘filter life’ in your ICU and compare to the data cited from large multicentre trials associated with
CRRT. How does the experience from your ICU compare?

Online resources
Acute Dialysis Quality Initiative, www.ADQI.org
Continuous renal replacement therapies, www.CRRTonline.com
Pediatric continuous renal replacement therapy, www.pcrrt.com
 CHAPTER 18 SUPPORT OF RENAL FUNCTION 619

Further reading
Dunn W, Shyamala S. Filter lifespan in critically ill adults receiving continuous renal replacement therapy: the effect of patient
and treatment-related variables. Crit Care Resusc 2014;16(3):225–31.
Legrand M, Darmon M, Joannidis M, Payen D. Management of renal replacement therapy in ICU patients: an international
survey. Intensive Care Med 2013;39:101–8.

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37 Fiaccadori E, Cremaschi E, Regolisti G. Semin Dial Nutritional assessment and delivery in renal replacement therapy patients. 2011;24(2):169-75.
38 Bellomo R, Ronco C. Indications and criteria for initiating renal replacement therapy in the intensive care unit. Kidney Int 1998;53:S66, pp. s106–9.
39 Ostermann M, Dickie H, Tovey L, Treacher D. Management of sodium disorders during continuous haemofiltration. Crit Care 2010;14:418.
40 Choi G, Gomersall CD, Tain Q, Joynt GM, Freebairn RC, Lipman J. Principles of antibacterial dosing in continuous real replacement therapy.
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41 Medline Plus. Online Medical Dictionary, <http://www.nim.nih.gov/medlineplus/mplusdictionary.html>; [accessed 12.15].
42 Vienken J, Diamantoglou M, Henne W, Nederlof B. Artificial dialysis membranes: from concept to large scale production. Am J Nephrol 1999;
19:355–62.
43 Cameron JS. Practical haemodialysis began with cellophane and heparin: the crucial role of William Thalhimer (1884–1961). Nephrol Dial
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44 Ronco C, La Greca G. The role of technology in hemodialysis. Contrib Nephrol 2002;137:1–12.
45 Coleman B, Merrill JP. The artificial kidney. Am J Nurs 1952;52(3):327–9.
46 Baldwin I, Elderkin T. Continuous hemofiltration: nursing perspectives in critical care. New Horizons 1995;3(4):738–47.
47 Martin R, Jurschak J. Nursing management of continuous renal replacement therapy. Semin Dial 1996;9(2):192–9.
48 Mehta R, Martin R. Initiating and implementing a continuous renal replacement therapy program. Semin Dial 1996;9(2):80–7.
49 Wild J. Peritoneal dialysis. In: Thomas N, ed. Renal nursing. 2nd ed. London: Baillière Tindall; 2002.
50 Kramer P, Wigger W, Rieger J, Matthaei D, Scheler F. Arteriovenous haemofiltration: a new and simple method for treatment of overhydrated
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51 Ronco C, Brendolan A, Bellomo R. Current technology for continuous renal replacement therapies. In: Ronco C, Bellomo R, eds. Critical care
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52 Teschner M, Heidland A. George Ganter – a pioneer of peritoneal dialysis and his tragic and academic demise at the hands of the Nazi regime.
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53 Burdmann E, Chakravarthi R. Peritoneal dialysis in acute kidney injury: lessons learned and applied. Semin Dial 2011;24:149-56.
54 Lamiere N. Principles of peritoneal dialysis and its application in acute renal failure. In: Ronco C, Bellomo R (eds). Critical care nephrology.
Dordrecht: Kluwer Academic; 1998, pp 1357-71.
55 Goel S, Saran R, Nolph KD. Indications, contraindications and complications of peritoneal dialysis in the critically ill. In: Ronco C, Bellomo R
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56 Baldwin I, Fealy N. Nursing for renal replacement therapies in the intensive care unit: historical, educational, and protocol review. Blood
Purification 2009;27:174–81.
57 Davenport A, Mehta S. The acute dialysis quality initiative – Part VI: access and anticoagulation in CRRT. Adv Renal Replace Ther 2002;9(4):273–81.
58 Ofsthun NJ, Colton CK, Lysaght MJ. Determinants of fluid and solute removal rates during hemofiltration. In: Henderson LW, Quellhorst G,
Baldamus CA, Lysaght MJ, eds. Hemofiltration. Berlin: Springer-Verlag; 1986.
59 Baldwin I and Fealy N. Clinical nursing for the application of renal replacement therapies in the intensive vare unit. Semin Dial 2009;22(2):189–93.
60 Thomas N. Haemodialysis. In: Thomas N, ed. Renal nursing. 2nd ed. London: Baillière Tindall; 2002.
61 Ronco C, Bellomo R. Basic mechanisms and definitions for continuous renal replacement therapies. Int J Artificial Organs 1996;19:95–9.
62 Bellomo R, Ronco C, Mehta R. Technique of continuous renal replacement therapy: nomenclature for continuous renal replacement therapies.
Am J Kidney Dis 1996;28(5 Supp 3):s2–7.
63 Relton S, Greenberg A, Palevsky P. Dialysate and blood flow dependence of diffusive solute clearance during CVVHD. ASAIO J 1992;38(3):M691–6.
64 Kox WJ, Rohr U, Wauer H. Practical aspects of renal replacement therapy. Int J Artificial Organs 1996;19(2):100–5.
65 Baldwin I, Bellomo R, Koch B. A technique for the monitoring of blood flow during continuous hemofiltration. Intens Care Med 2002;28:1361–4.
66 Webb AR, Mythen MG, Jacobsen D, Mackie IJ. Maintaining blood flow in the extracorporeal circuit: haemostasis and anticoagulation. Intens
Care Med 1995;21:84–93.
67 Dirkes S. How to use the new CVVH renal replacement systems. Am J Nurs 1994;94:67–73.
68 Baldwin I. Factors affecting circuit patency and filter life. In: C Ronco, Bellomo R, Kellum J, eds. Contributions to nephrology, Vol 156. Basel:
Karger; 2007, pp 178–84.
69 Gretz N, Quintel M, Ragaller M, Odenwalder W, Bender HJ, Rohmeiss SM. Low-dose heparinization for anticoagulation in intensive care
patients on continuous hemofiltration. Contrib Nephrol 1995;116:130–5.
70 Langeneker SA, Felfernig M, Werba A, Meuller CM, Chiari A, Zinpfer M. Anticoagulation with prostacyclin and heparin during continuous
venovenous hemofiltration. Crit Care Med 1994;22(11):1774–81.
71 Cassina T, Mauri R, Engeler A, Giannini O. Continuous veno-venous haemofiltration with regional citrate anticoagulation: a four year single
center experience. Int J Artificial Organs 2008;31(11):937–43.
 CHAPTER 18 SUPPORT OF RENAL FUNCTION 621

72 Baldwin I, Tan HK, Bridge N, Bellomo R. Possible strategies to prolong circuit life during hemofiltration: three controlled studies. Renal Failure
2002;24(6):839–48.
73 Leslie G, Jacobs I, Clarke G. Proximally delivered high volume heparin does not improve circuit life in continuous venovenous
haemodiafiltration (CVVHD). Intensive Care Med 1996;22:1261–4.
74 Monchi M, Berghmans D, Ledoux D, Canivet JL, Dubois B, Damas P. Citrate vs. heparin for anticoagulation in continuous venovenous
hemofiltration: a prospective randomized study. Intensive Care Med 2004;30(7):260–5.
75 Tolwani A, Campbell R, Schenk M, Allon M, Warnock D. Simplified citrate anticoagulation for continuous renal replacement therapy. Kidney Int
2001;60(1):370–4.
76 Naka T, Egi M, Bellomo R, Cole L, French C, Botha J et al. Commercial low citrate anticoagulation haemofiltration in high risk patients with
frequent filter clotting. Anaesth Intensive Care 2005;33(5):601–8.
77 Mehta R, McDonald B, Aguilar M, Ward D. Regional citrate anticoagulation in continuous arteriovenous hemodialysis in critically ill patients.
Kidney Int 1990;38:976–81.
78 Davies H, Morgan D, Leslie GD. A regional citrate anticoagulation protocol for pre-dilutional CVVHDf: the ‘Alabama concept’. Aust Crit Care
2008;21(3):154–6.
79 Tolwani AJ, Wille K. Anticoagulation for continuous renal replacement therapy. Semin Dial 2009;22(2):141–5.
80 Aucella F, Di Paolo S, Gesualdo L. Dialysate and fluid composition for CRRT. Contrib Nephrol 2007;156:287–96.
81 Davenport A. Replacement and dialysate fluids for patients with acute renal failure treated by continuous veno-venous haemofiltration and/or
haemodiafiltration. Contrib Nephrol 2004;144:317–28.
82 Baldwin I, Bellomo R. Sustained low efficiency dialysis in the ICU. Int J Intensive Care 2002;Winter:177–87.
83 Ronco C, Ricci Z, Bellomo R, Baldwin I, Kellum J. Management of fluid balance in CRRT: a technical approach. Int J Artif Organs
2005;28(8):765-76.
84 Barletta JF, Barletta G-M, Brophy PD, Maxvold NJ, Hackbarth RM, Bunchman TE. Medication errors and patient complications with
continuous renal replacement therapy. Pediatr Nephrol 2006;21(6):842-5.
85 Sutherland SM, Zappitelli M, Alexander SR, Chua AN, Brophy PD, Bunchman TE et al. Fluid overload and mortality in children receiving
continuous renal replacement therapy: the prospective pediatric continuous renal replacement therapy registry. Am J Kidney Dis 2010;55:
316-25.
86 Bouchard J, Soroko SB, Chertow GM, Himmelfarb J, Ikizler TA, Paganini E et al, and the PICARD group. Fluid accumulation, survival and
recovery of kidney function in critically ill patients with acute kidney injury. Kidney Int 2009;76:422-7.
87 Baldwin I. Training management and credentialling for CRRT in critical care. Am J Kidney Dis 1997;30(5):S112–6.
88 Graham P, Lischer E. Nursing issues in renal replacement therapy: organization, manpower assessment, competency evaluation and quality
improvement processes. Semin Dial 2011;24(2):183-7.
89 Fealy N, Baldwin I, Bellomo R. The effect of circuit down time on uraemic control during continuous veno-venous haemofiltration. Crit Care
Resusc 2002;4:266–70.
90 Cruz D, Bobek I, Lentini P, Soni S, Chionh CY, Ronco C. Machines for continuous renal replacement therapy. Semin Dial 2009;22(2):123–32.
91 Ronco C. Machines used for continuous renal replacement therapy. In: Kellum J, Bellomo R, Ronco C, eds. Continuous renal replacement
therapy. New York: Oxford University Press; 2010.
92 Mottes T, Owens T, Niedner M, Juno JS, Thomas P, Heung M. Improving delivery of continuous renal replacement therapy: impact of a
simulation-based educational intervention. Pediatr Crit Care Med 2013;14(8):747-54.
93 Boyle M, Baldwin I. Understanding the continuous renal replacement therapy circuit for acute renal failure support; a quality issue in the
intensive care unit. AACN 2010;21(4):365-75.
94 RENAL Replacement Therapy Investigators. Intensity of renal support in critically ill patients with acute kidney injury. N Engl J Med
2009;361(17):1627-38.
95 VA/NIH Acute Renal Failure Trail Network. Intensity of renal support in critically ill patients with acute kidney injury. N Engl J Med
2008;359(1):7-20.
96 Ronco C, Garzotto F, Ricci Z. CA.R.PE.DI.E.M. (cardio-renal pediatric dialysis emergency machine): evolution of continuous renal replacement
therapies in infants. A personal journey. Pediatr Nephrol 2012;27:1203-11.
97 Askenazi DJ, Goldstein SL, Koralkar R, Fortenberry J, Baum M, Hackbarth R et al. Continuous renal replacement therapy for children ≤10 kg:
a report from the prospective pediatric continuous renal replacement therapy registry. J Pediatric 2013;162(3):587-92.e3.
98 Combesa A, Bacchettab M, Brodieb D, Müllerc T, Pellegrino V. Extracorporeal membrane oxygenation for respiratory failure in adults. Curr
Opin Crit Care 2012;18(1):99–104.
99 Combes A, Brodie D, Bartlett R, Brochard L, Brower R, Conrad S et al. Position paper for the Organization of Extracorporeal Membrane
Oxygenation Programs for Acute Respiratory Failure in Adult Patients. Am J Respir Crit Care Med 2014;190(5):488-96. doi: 10.1164/
rccm.201404-0630CP.
100 Parmar A, Bigam D, Meeberg G, Cave D, Townsend DR, Gibney RT et al. An evaluation of intraoperative renal support during liver
transplantation: a matched cohort study. Blood Purification 2011;32(3):238-48.
101 Douthitt L, Bezinover D, Uemura T, Kadry Z, Shah RA, Ghahramani N et al. Perioperative use of continuous renal replacement therapy for
orthotopic liver transplantation. Transplant Proc 2012;44(5):1314-7.
Chapter 19

Nutrition assessment and

therapeutic management
Andrea Marshall, Teresa Williams

KEY WORDS
Learning objectives
After reading this chapter, you should be able to: anabolism
• describe the changes in metabolism associated with critical illness catabolism
• describe the consequences of malnutrition and how they influence enteral nutrition
recovery from critical illness glycaemic control
• identify appropriate nutrition assessment strategies and critique methods hypermetabolism
of determining nutritional requirements in critical illness total parenteral
• apply theoretical knowledge of nutritional requirements, assessment of nutrition
and potential for malnutrition in critical illness
• rationalise selected nutritional support strategies for specific clinical
conditions
• critically analyse the role of glycaemic control in the context of critical
illness.

Introduction
Critical illness is associated with increased catabolism that occurs at a time when
oral intake may be difficult or impossible. Failure to provide adequate nutrition
during this time will result in an accumulated energy deficit, muscle wasting
and decreased lean body mass, which are associated with adverse outcomes.
During critical illness optimising protein and calorie intake is important because
inadequate nutrition, which results in an overall nutrition deficit, is associated
with increases in morbidity and mortality. Enteral nutrition (EN) is the preferred
method of nutrition therapy for the critically ill although some patients might
require parenteral nutrition (PN) or a combination of EN and PN.
As part of the interdisciplinary team, nurses play an important role in
achieving optimal nutrition and are responsible for monitoring achievement
of nutrition goals and implementing strategies to optimise nutrition intake. In
this chapter an overview of metabolism and the consequences of malnutri-
tion are provided. This is followed by discussion of nutritional assessment and
delivery strategies where an emphasis is placed on nutrition therapy through
the provision of EN.Tailoring nutrition to specific disease states is also included
in this chapter. Lastly, we discuss the importance of glycaemic control in
critical illness.
 CHAPTER 19 NUTRITION ASSESSMENT AND THERAPEUTIC MANAGEMENT 623

Metabolism The breakdown of food to produce energy is carried

out in three phases.The first phase is where protein, carbo-
The body requires energy in order to support normal hydrates and fats are broken down through the process of
body and cellular function. Energy is derived from the digestion into the subunits of amino acids, simple sugars
metabolism of macronutrients including carbohydrate, and fatty acids.The second phase is the further breakdown
protein and fat. Following consumption of food, carbo- of these subunits, within the cytoplasm of the cell. The
hydrates are broken down and stored as glycogen in most important part of the second phase is glycolysis,
the liver and skeletal muscle, and fat, stored in adipose where a molecule of the simple sugar glucose is split and
tissue, is available for long-term energy requirements. two molecules of adenosine triphosphate are produced.
Proteins and amino acids, however, are not stored and In the final phase of catabolism the majority of adenosine
reduced protein intake can result in catabolism of body triphosphate is created within the citric acid cycle and the
protein.1 process of oxidative phosphorylation1 (see Figure 19.1).

FIGURE 19.1 Three phases of catabolism.

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children. 6th ed. Maryland Heights, MI: Mosby Elsevier; 2010, Figure 1-22, p 24, with permission.
624 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Effect of critical illness on metabolism In addition to disease-related malnutrition, critically

ill patients are also at risk of developing iatrogenic or
The stress and injury associated with critical illness triggers
hospital-acquired malnutrition. There are a number of
the hypothalamus, sympathetic nervous system and
contributing factors to the development of hospital-
adrenal medulla to initiate a response that results in hyper-
catabolism.2 An increased release of cytokines including acquired malnutrition related to both the prescription
interleukin-1, interleukin-6 and tumor necrosis factor-α and delivery of nutrition, highlighting the importance
and production of counter-regulatory hormones such as of accurate assessment of nutritional requirements and
catecholamines, cortisol, glucagon and growth hormone strategies to ensure the prescribed nutrition is delivered.
induce catabolism and oppose the anabolic effects of The patient’s clinical presentation can also have an impact
insulin.3 Hypercatabolism occurs with the imbalance on nutritional adequacy with surgical patients receiving
between anabolism and catabolism. To compensate for the less nutrition than medical patients.9
altered metabolic regulation, neuroendocrine stimulation
increases the mobilisation and consumption of nutrients, Practice tip
such as glycogen and protein, from existing body stores. Critically ill patients, particularly the elderly, can
As the metabolic rate rises, nutritional requirements in present to the ICU with existing malnutrition. Obtaining
critical illness are increased, characterised by a rise in information on pre-admission nutrition status can help
resting energy expenditure and oxygen consumption guide nutrition therapy.
which, in some critically ill patients, can be increased by
over 50%.4 Depletion of body energy stores results from
alterations in protein, carbohydrate and fat metabolism. In Consequences of malnutrition
addition to the rise in metabolic demands, patients who When adequate and timely nutrition support is not
are critically ill often experience a concomitant fall in provided, body energy and protein depletion can occur
nutritional intake. The metabolic and nutrition alterations with negative consequences on patient outcome.10
vary with the stress level, severity of illness, type of injury, Critically ill patients require adequate nutrition to limit
organ dysfunction and nutrition status.4 muscle wasting, respiratory and gastrointestinal dysfunc-
tion and alterations in immunity, all of which are
Practice tip associated with malnutrition. Respiratory support is often
Metabolic rate fluctuates throughout an episode of
necessary during critical illness, and decreased respiratory
critical illness and can vary significantly between
muscle function and ventilatory drive may contribute to
patients. Generally, the sicker a patient is the higher
an increase in the number of ventilator days.11 Further-
their metabolic rate.
more, infection rates may be increased in malnourished
critically ill patients. The decrease in lean body mass and
To maintain normal cellular function, body cells require negative nitrogen balance are associated with delayed
adequate amounts of the six basic nutrients: carbohydrates, wound healing and a higher risk of infection.12
fats and proteins to provide energy, and vitamins, minerals These complications are associated with an increased
and water to catalyse metabolic processes. Unlike normal length of stay, cost, morbidity and mortality,13 although
metabolism, which preferentially uses carbohydrates and the extent to which the provision of artificial nutrition
fats for energy, the hypermetabolic state associated with ameliorates these complications is unclear.14 The degree of
critical illness consumes proportionally more fats and critical illness and hypercatabolism varies between patients
proteins than carbohydrates to generate energy.5 As a and is often difficult to determine. For this reason it is
consequence of the gluconeogenesis and the synthesis of necessary to assess, as accurately as possible, the nutritional
acute-phase proteins, there is a decrease in lean body mass requirements of each individual patient.
and negative nitrogen balance.
Practice tip
Malnutrition Malnourished patients are more susceptible to develop-
Malnutrition in critical illness is an important consideration ing infection.
with an estimated 50% of critically ill patients affected.6 In
the critically ill patient malnutrition can be pre-existing
and the result of chronic starvation without inflamma-
Nutritional assessment
tion being present or associated with chronic disease with Not all critically ill patients have the same nutritional
mild-to-moderate degrees of inflammation. Malnutrition needs15,16 with protein and energy requirements influenced
can also occur as the result of recent and acute disease with by the degree and type of critical illness. Nutritional
marked inflammatory response.7 Determining the extent assessment is required to determine the most appropriate
of pre-existing malnutrition in critical care is challenging nutrition therapy for each patient and should incorporate
because of the heterogeneous patient populations and use patient history, clinical diagnosis, physical examination,
of different criteria to characterise malnutrition.8 anthropometric data, laboratory tests, dietary assessment
 CHAPTER 19 NUTRITION ASSESSMENT AND THERAPEUTIC MANAGEMENT 625

and functional outcomes.17,18 The degree of acute or resulting NUTRIC score includes six variables (Table 19.1).
chronic inflammation is an important contributing factor Despite the proposed model being described as ‘adequate’
to the development of malnutrition and can also influence the data did show that patients with a worse NUTRIC
the effectiveness of nutrition therapy.17 score also had poorer clinical outcomes.20 Further work is
Not all critically ill patients are alike and energy expend- needed to refine this or other tools to identify nutrition risk
iture varies from 22 to 34 kcal/kg/day.2 Assessing which in critically ill patients so we can determine which patients
patients might be at greatest nutritional risk is important. are most likely to benefit from nutrition therapy.
Existing nutrition screening tools for hospitalised patients
are often not used in routine clinical practice and have Determining nutritional requirements
not been validated for use in the critically ill.19 Recently, a Determining caloric requirements is largely dependent
novel scoring tool, The NUTritional Risk in the Critically on energy expenditure, influenced by patient activity,
ill (NUTRIC) score20, was developed based on the recent stage of illness, type of injury and previous nutritional
definitions of malnutrition, which incorporate concepts status.4 Resting energy expenditure (REE) is the primary
of inflammation.7 The conceptual basis for the NUTRIC consideration when prescribing energy intake because it
score incorporates variables related to acute and chronic is the largest component of total energy expenditure for
starvation, acute and chronic inflammation, age and severity hospitalised patients.21 Determining REE can be done
of illness. To test this, model data were collected during a through direct measurement using indirect calorimetry or
multicentre observational study of 597 critically ill patients. can be estimated using one of many different predictive
While individual variables (Table 19.1), with the exception equations. While no randomised controlled studies have
of body mass index (BMI), had a statistically significant compared patient outcome according to measured (using
relationship with mortality and ventilator-free days, not all indirect calorimetry) versus predicted energy expenditure,
were included in the final model with oral intake, recent data from two recent observational studies suggest the
weight loss, C-reactive protein and procalcitonin excluded need to monitor changes in energy expenditure and adjust
as they did not improve model fit. Interleukin-6 improved nutrient intake accordingly.22,23 Both approaches are used
model fit but not in a clinically or statistically significant in intensive care units and have advantages and limitations.
way so, where interleukin-6 is not routinely collected, it is
suggested that this too can be dropped from the score. The Practice tip

For severely malnourished patients improving nutrition

TABLE 19.1 support can cause refeeding syndrome to occur. In
Conceptual model and variables included in the this syndrome metabolic disturbances occur that are
NUTritional Risk in the Critically ill (NUTRIC) score20 characterised by electrolyte disorders, particularly
hypophosphataemia.
VA R I A B L E S
PROPOSED R E TA I N E D I N
CONCEPTS VA R I A B L E S FINAL SCORE Indirect calorimetry
Acute Decreased oral intake No Indirect calorimetry is the ‘gold standard’ and most precise
starvation over the last week way of determining energy expenditure in critical illness.21,24
Pre-ICU hospital Yes Despite this, it is infrequently used because of high equip-
admission ment costs and resources constraints.25 Through indirect
Chronic Weight loss over the No
calorimetry energy expenditure is calculated using oxygen
starvation last 6 months
consumption and carbon dioxide production.26 Accuracy of
these measurements can be affected by many factors includ-
BMI <20 No
ing instrument performance,27 ambient temperature21 and
Acute IL-6 Yes volume leaks that might occur through the calorimeter,
inflammation PCT No endotracheal tube or through chest drains.24 Patient-related
CRP No factors also can influence the measurement of REE, such as
physical activity, food consumption and physiological stress
Chronic Comorbid illness Yes
inflammation
such as pain. To obtain the most accurate measurement of
REE it is recommended that these measurements be taken
Severity of Age Yes
under steady-state conditions,28 that is where there is at least
illness APACHE II score Yes a 5-minute period with ≤10% coefficient of variance in the
SOFA score Yes oxygen consumption and carbon dioxide production.29 It is
recognised that metabolic equilibrium is not well defined
APACHE = Acute physiology and chronic health evaluation; and lacks consensus so there is variation in how steady state
BMI = body mass index; CRP = C-reactive protein; IL-6 =
interleukin-6; PCT = procalcitonin; SOFA = sequential organ
is determined and implemented in both clinical practice
failure assessment. and research.29 Comprehensive discussions of practical
aspects of indirect calorimetry are published elsewhere.26,28
626 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Predictive equations to indirect calorimetry in 202 mechanically ventilated

Because indirect calorimetry is not available in many critically ill patients.32 In this study 17 predictive
intensive care units, it is common practice to predict energy equations were evaluated against an accuracy benchmark
expenditure using one of many predictive equations of 10% of the measured energy expenditure. The Penn
(Table 19.2). Many predictive equations are based on State equation was the most accurate (67%) except for
requirements for healthy humans and then are adjusted older obese patients where the accuracy fell to 53%.32
The predictive equations that performed with less than
to account for added stress or injury.30 The accuracy of
50% accuracy were the Harris-Benedict equation (34%)
predictive equations is poor compared to measurement of
and the American College of Chest Physicians equation
REE using indirect calorimetry; however, some predictive
(35%). Accuracy of these equations did not surpass 50%
equations perform better in critical illness than do others.
following adjustment for body weight (American College
Some equations use only static variables (such as height,
of Chest Physicians equation 46%) or activity factor of 1.5
weight, age and sex) to predict resting energy expendi-
(Harris-Benedict equation 46%).32
ture. Others use more dynamic variables (such as body While most predictive equations are likely to under-
temperature, minute ventilation, heart rate) in an attempt estimate measured energy expenditure in the critically
to account for the metabolic variation that occurs in ill wide variations in predicted energy expenditure have
critical illness.31 been reported, which suggest that the use of predictive
Some work has been done to validate the accuracy equations can contribute to both over and under feeding.25
of predictive equations used in critical care. The largest The extent to which these equations accurately predict
of these studies compared predicted energy expenditure energy expenditure is also influenced by factors such as
BMI,32 sex25 and age.33
TABLE 19.2 Although predictive equations may not be as accurate
Predictive equations for estimating energy
as indirect calorimetry in determining energy expendi-
expenditure in critically ill patients ture, they may nevertheless provide some guidance for
nutrition prescription in the absence of this technology.
American 25 × weight
College of Chest
Physicians
If BMI 16–25 kg/m2 use usual body
weight
Nutrition support
If BMI > 25 kg/m2 use ideal body Optimal nutritional support in the critically ill aims to
weight prevent, detect and correct malnutrition, optimise the
If BMI <16 kg/m2 use existing body patient’s metabolic state, reduce morbidity and improve
weight for the first 7×10 days then recovery. Metabolic response to stress is decreased, oxidat-
ideal body weight ive cellular injury restricted and the immune response
Harris-Benedict Men: 66.4730 + (13.7516 × weight) + moderated in patients receiving adequate nutrition.34,35
equation (5.0033 × height) − (6.7550 × age) EN is the preferred method of feeding for patients who
Women: 655.0955 + (9.5634 × weight) are not able to take food and fluids orally. PN alone or
+ (1.8496 × height) − (4.6756 × age) combined with EN may be used for those patients where
Ireton-Jones 1992 1.925 − (10 × age) + (5 × weight) oral intake is not possible.36,37
equation + (281 for males) + (292 if trauma
present) + (851 if burns present) Enteral nutrition
Ireton-Jones 1997 (5 × weight) − (11 × age) + (244 for EN has benefits beyond simply the supply of nutrients
equation males) + (239 if trauma present) + to the body.38 Any amount of nutrition administered
(840 if burns present) + 1,784 to the gut is beneficial. EN increases gastric mucosal
Penn State 1998 (1.1 × value from Harris-Benedict
blood flow, stimulates brush border enzymes, preserves
equation) + (140 × Tmax) + (32 × VE)
epithelial tight cell junctions and provides gut-derived
− 5340 mucosal immunity.35 Major effects of EN are: preservation
of intestinal epithelium,39 mucosal mass and microvilli
Penn State 2003 (0.85 × value from Harris-Benedict
height;40 prevention of bacterial translocation; and a
equation) + (175 × Tmax) + (33 × VE)
positive effect on the gut-associated lymphoid tissue, the
− 6433
source of most mucosal immunity in humans.41 Septic
Swinamer 1990 (945 × body surface area) − (6.4 × complications are decreased when EN is provided.42,43
age) + (108 × temperature) + 24.2 ×
Stimulating and improving gastrointestinal immune
respiratory rate) + (817 × VT) − 4349
function is an important goal of early EN.44
BMI = body mass index.
Early or delayed enteral nutrition?
Adapted from Walker RN, Heuberger RA. Predictive
equations for energy needs for the critically ill. Respir Care Early EN (within 48 hours) is recommended36,45 but the
2009;54(4):509-21, with permission. definition of ‘early’ has not been established and study
results are inconsistent. Meta-analyses have shown early
 CHAPTER 19 NUTRITION ASSESSMENT AND THERAPEUTIC MANAGEMENT 627

EN was associated with decreased mortality.46,47 However, formulae, has anti-inflammatory effects on the gut–brain
the methodological quality of the studies included in the immune axis of the gastrointestinal mucosa.34,66 Outcomes
meta-analyses was questionable and heterogeneity was of gastrointestinal disorders traditionally treated with bowel
high, making interpretation of the results difficult. Other rest are improved with enteral nutrition.34
studies48,49 have also found improved outcomes but evidence Patients can receive enteral nutrition while vasopres-
from large, high-quality, randomised, controlled trials that sors are being administered,34,36 although the evidence for
compare timing of EN in critically ill patients is needed to the effect of vasopressors on gastric tolerance and patient
define the optimal time for commencing EN.50,51 outcomes is weak and inconsistent.67 Splanchnic perfusion
is reduced in critical illness but enteral nutrients improve gut
Hypocaloric intake in the critically ill blood flow enabling the bowel to absorb nutrients during
A significant number of hospitalised patients receiving vasopressor therapy.68,69 The administration of vasopressors
enteral nutrition do not have their nutritional needs met.52 in patients with sepsis and shock, however, is associated with
Hypocaloric feeding in the first few days of critical illness is both improved and diminished perfusion. Mentec et al70
controversial.53 In several observational studies10,13,54,55 the reported gastric intolerance was higher in patients receiving
reduced provision of energy and protein were associated vasopressor therapy while others found patients tolerated
with worse outcomes. However, observational studies enteral nutrition.71,72 Khalid et al68 reported improved
may be confounded by many factors including severity outcomes for patients receiving early rather than late enteral
of illness, where patients who were less sick and tolerated nutrition in patients requiring vasopressors.
enteral nutrition better were more likely to be adequately Patients should not have enteral nutrition withheld if
fed and have better outcomes.34 In a recent randomised they have absent bowel sounds, postoperative ileus34,45 or
controlled trial (the EDEN study), conducted in 1000 after gastrointestinal surgery. The risk of anatomic leaks
patients with acute lung injury who required mechanical and fistulas in patients who have had bowel surgery and
ventilation, trophic feeding was compared with adminis- also receive early enteral nutrition is lower compared to
tration of full enteral feeding for the first 6 days a patient delayed feeding or parenteral nutrition.34 Enteral nutrition
was in the ICU.56 Initial trophic enteral feeding did not following gastrointestinal surgery is associated with a
improve ventilator-free days, 60-day mortality, infectious significantly lower risk of infection and reduced hospital
complications or have an effect on physical and cognitive length of stay.73,74
performance.56,57 The patients enrolled in this study
were reasonably young (mean age 52 years) and were Practice tip
moderately obese (BMI 30).56 Moderate obesity can be
protective during critical illness – the obesity paradox.58 Nurses should regularly assess for barriers to achieving
The findings of the EDEN study may not be generalis- daily nutritional goals and work with the interdisciplinary
able to all critically ill patients, especially those who are team to ensure nutrition intake is optimised.
malnourished or grossly obese. The results of the EDEN
trial are similar to those of Arabi et al,59 who demonstrated Enteral nutrition protocols
similar patient outcomes when permissive underfeeding Enteral nutrition protocols improve the delivery of
was compared to targeted full feeding in a randomised enteral feeds64 and have been shown to improve clinical
controlled trial but outcomes were similar. Despite outcomes.75,76 Protocols vary widely between units and
these results, current evidence-based guidelines do not institutions37,77 mainly because of the lack of robust
recommend the use of trophic feeding because of a lack research in the management of enteral nutrition. In the
of high quality research to support this approach.36 absence of strong research evidence, rituals are embraced
In most cases, hypocaloric feeding is unnecessary and and rarely challenged.78 Furthermore, the implementation
avoidable.60,61 Factors that contribute to unintentional and sustainability of guidelines are influenced by multiple
hypocaloric feeding include staffing shortages, unavailabil- factors such as clinician preference, patient population,
ity of feeds/equipment, low priorities for feeding, fasting clinical contexts and content of guidelines.79,80
for clinical investigations, blockages in feeding tubes and
variations in feed prescriptions.62,63 Delivery issues, such Management of enteral feeding
as elective interruption for investigative procedures or
operations, contributed to hypocaloric feeding with only Routes of enteral feeding
76% of prescribed feeds delivered to critically ill patients.64 Wide-bore nasogastric or orogastric tubes are most
Similar results were observed in mechanically-ventilated commonly used in the critically ill in the early stages of
patients,65 where more than 36% of patients received less enteral nutrition. Should prolonged enteral nutrition be
than 90% of their caloric requirements. anticipated (longer than 1 month), or where patients have
The concept that the bowel should be rested is question- gastric intolerance then gastrostomy, duodenostomy or
able because bowel function is not inhibited by starvation. jejunostomy tubes may be used.81
Starvation actually depresses splanchnic blood flow. Marik34 Postpyloric feeding is useful if patients are not tolerating
likens bowel rest to resting the heart by inducing asystole! gastric feeding82 but has not been shown to be superior
Enteral nutrition, and in particular lipid- and protein-rich to gastric feeding.83,84 A randomised, controlled trial83
628 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

was conducted in 17 multidisciplinary ICUs to test the Assessment of enteral feeding tube
hypothesis that early nasojejunal feeding would improve placement
outcomes for mechanically ventilated adults with mildly
elevated gastric residual volumes who were already receiving The correct placement of enteral feeding tubes is crucial to
enteral nutrition through a nasogastric tube. There was no promote adequate nutrition and avoid adverse events. The
difference in the proportion of targeted energy delivered correct insertion of enteral feeding tubes in the critically
from enteral nutrition or incidence of ventilator-associated ill can be challenging because these patients often have
pneumonia. The study investigators recommended that a reduced cough reflex, altered sensorium and receive
routine placement of nasojejunal tubes in such patients sedative and narcotic medications.87,88 Misplacement of the
should not be performed. Patients may also have a gastric feeding tube into the tracheobronchial tree is an important
tube inserted to aspirate the contents of the stomach. complication of tube insertion.89 Additional complica-
For some critically ill patients, gastric secretions tions such as infusion of tube feedings, pneumothorax,
may increase when small bowel feeding is initiated.85 A pneumonitis, hydropneumothorax, bronchopleural fistula,
double-lumen tube is available, one lumen for gastric empyema and pulmonary haemorrhage have also been
aspiration and decompression and the second for simulta- reported.90 Confirmation of tube placement is routinely
neous jejunal feeding, but these tubes are not widely used done with radiography (Figure 19.2). However, assessment
in the clinical setting.86 of nasogastric tube placement on X-ray does not prevent

FIGURE 19.2 Correct placement of a nasogastric tube.92

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GLDSKUDJP

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IROORZWKHSDWKRID
EURQFKXV

7XEHLVQRWFRLOHG
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EHORZWKHGLDSKUDJP

Reproduced from Patient Safety Authority. Confirming feeding tube placement: old habits die hard. PA PSRA Patient Saf Advis
2006;3(4):23-30, with permission.
 CHAPTER 19 NUTRITION ASSESSMENT AND THERAPEUTIC MANAGEMENT 629

incorrect placement occurring during insertion. Less the aspirate were able to correctly differentiate between
reliable methods of confirming tube placement include gastric and bowel tube placement during continuous
the use of pH, observation of the colour of gastric aspirates feedings in 81% of predictions.
and auscultation and other novel methods such as capno-
graphy.87,91 Practice tip
Assessment of feeding tube placement by auscultation
of air insufflated into the stomach remains a common Radiographic assessment of feeding tube placement is
clinical practice although auscultation should NOT be gold standard. When this is not available feeding tube
used as the sole method to determine placement of the placement should be confirmed using more than one
gastric tube because it is unreliable. Other important method.
points are:
• Nasogastric aspirate from critically ill patients who Feeding regimens
receive continuous feedings may have the appearance Once the enteral feeding tube is successfully placed,
of unchanged formula, regardless of the site of the administration of the feeding solution can begin using
feeding tube; therefore this method should not be a variety of methods, including bolus, intermittent and
used.93 continuous enteral feeding (see Table 19.3). Bolus enteral
• Analysis of the pH of gastric secretions is not feeding is rarely used in ICU. It is less clear whether
reliable. A pH of 0–5 may be used to indicate gastric intermittent or continuous feeding is more beneficial.98
placement of enteral feeding tubes, although this Concerns about increased risk of aspiration with inter-
technique may be problematic for patients receiving mittent enteral feeding has not been substantiated in the
histamine-2-receptor antagonists or proton pump literature; however, the research in this area is limited
inhibitors. If the aspirated fluid has a low pH, it may in both quantity and quality. Because of inconclusive
be assumed that the fluid originated in the stomach evidence regarding feeding regimens, decisions are based
but the pH of fluid from an infected pleural space can on individual patient assessment and the clinician’s clinical
also be acidic;94 therefore pH testing as a sole method judgement.
to determine tube placement is not recommended.
Commencing enteral nutrition
• Capnometry and capnography use end-tidal carbon The appropriate starting rate for enteral nutrition is
dioxide detectors to evaluate enteral tube placement
where respiratory placement is indicated by the controversial and there are no empirical data on which
presence of a capnogram that suggests an increase in to base the decision. Feeding is often started at 30 mL/h,
measured carbon dioxide.95Although not routinely but may range from 10 to 100 mL/h. Increasing the
used in clinical practice there is emerging evidence
that this strategy might be useful in assessing TABLE 19.3
placement of nasogastric tubes in mechanically Methods of feed delivery98
ventilated patients.96 It is important to recognise that
this technique does not help differentiate oesophageal, METHOD DESCRIPTION
gastric or intestinal placement. Bolus • Delivery of a large volume of tube feed
• Measuring the concentrations of pepsin and trypsin into the stomach over a short period of
in feeding tube aspirates can be used as a method time (>100 mL)
of predicting tube placement; however, methods • Associated with complications, such as
to measure pepsin and trypsin at the bedside are aspiration and vomiting
currently unavailable.97 Intermittent • A several-hour infusion a few times a
Ongoing assessment of feeding tube placement day (e.g. 150 mL/h for 3 hours, three
is essential, as feeding tubes may migrate after initial times per day), or delivered over a longer
placement. Marking the feeding tube at the point period (12–16 hours) with an 8–12-hour
rest period
where it exits the nose and measurement of tube length
• Allows gastric acidity and therefore
protruding from the anterior nares will facilitate detection
limits bacterial overgrowth
of migration of the enteral tube. Radio-opaque tubes • Requires a higher hourly rate to meet
have markers to enable accurate measurement and docu- caloric requirements
mentation of tube position. They should be used with the
Continuous • The delivery of small amounts of formula
methods previously described for ongoing assessment.
per hour over a 24-hour period
In the absence of X-ray, several approaches should be
• May make caloric requirements more
used in combination to verify tube position. Metheny achievable
et al93 found measuring: 1) length of tubing extending • Continuous dilution of gastric acid may
from the insertion site, 2) volume of aspirate from the contribute to bacterial overgrowth
feeding tube, 3) appearance of the aspirate and 4) pH of
630 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

rate of enteral feeding is equally variable, but strategies

to progress patients towards meeting their daily caloric Practice tip
requirements should be employed. When a patient has In determining feeding intolerance, a single high gastric
experienced a prolonged period of starvation or total residual volume in the absence of physical examination
parenteral nutrition, the approach to enteral feeding is or radiographic findings should not result in the
somewhat more reserved as the risk of refeeding syndrome cessation of enteral feeding. Persisting with enteral
is increased.99Although not common, this syndrome is feeding has demonstrated benefits.
associated with severe derangement in fluid and electrolyte
levels (particularly hypophosphataemia, hypomagnesaemia
and hypokalaemia), and may result in significant morbidity Practice tip
and mortality.100
When evaluating gastric residual volume in relation
Managing complications of enteral to the rate of enteral feeding, remember to take into
nutrition account the production of gastric secretion, which can
Once enteral nutrition is established, it is important to be as much as 2500 mL/day.
assess for such complications as feeding intolerance that
can result in gastric distension, vomiting, diarrhoea and Development of diarrhoea is another complication
increased gastric residual volume.101 Pulmonary aspiration, for enterally fed patients,111 and is a common reason
hyperglycaemia, hypercarbia, electrolyte imbalances and why enteral feeding is reduced or ceased.112 Diarrhoea
feed contamination are also complications that should be may contribute to fluid and electrolyte disorders, patient
monitored and interventions implemented to minimise (and nursing) distress and a higher cost of patient care.113
their occurrence. Unfortunately, defining diarrhoea is problematic, as it is a
Critically ill patients exhibit elevated gastric residual subjective assessment that relies on nursing interpretation
volume for a variety of reasons including feeding intol- rather than on quantifiable assessment of stool weight.114
erance102 and reduced gastric motility.103 Monitoring Enteral feeding should not be considered a primary cause
tolerance to enteral nutrition through the measurement of diarrhoea. There are many reasons for diarrhoea in
of gastric residual volume has always been viewed as critically ill patients who receive enteral nutrition, often
an important aspect of nursing management, although occurring simultaneously, including:
consensus on what constitutes a high gastric residual and • underlying disease115
any recommendations for interventions remain contro-
versial.104 High gastric residual volumes do not necessarily • medications including antibiotics due to their side3
predict aspiration, and low gastric residual volumes do effects, toxicity and disruption to gut microbiota
not mean that aspiration will not occur. Studies105,106 have • hypoalbuminaemia116
shown no difference in risk for pulmonary aspiration • use of histamine-2-receptor antagonists117
between low and high gastric residual volume groups. It is
assumed that measuring gastric residual volume is accurate
• contamination of enteral feeding solution.118
and useful but gastric residual volume does not correlate Current evidence-based nutrition guidelines suggest
with clinical or radiological abdominal findings.107 that probiotics be considered for critically ill patients.36
In addition to gastrointestinal function there are Human lactoferrin and probiotic derivatives may be helpful
other important factors associated with the accuracy in reducing diarrhoea in tube-fed patients, but more research
of measurement of gastric residual volume such as is needed.119 Probiotic (Saccharomyces boulardii) administra-
tube diameter, tube position, type of gastric access and tion was reported to limit the development of diarrhoea
the patient’s position.34 The amount of gastric residual in a multicentre, randomised, double-blind placebo-con-
volume considered excessive in clinical practice varies. trolled study120 but reports from studies are inconsistent.
The Canadian Clinical Guidelines recommend 250 to No difference was found in the occurrence of diarrhoea in
500 mL as the cut-off because there are insufficient data a double-blind, randomised, controlled trial of 167 adults
to make a recommendation for a specific gastric residual who were mechanically ventilated for more than 48 hours
volume threshold.36 After aspiration of gastric residual and received probiotics or placebo enterally until successful
volume the gastric aspirate is either returned or discarded. weaning from mechanical ventilation.121 Subgroup analysis
The evidence for discarding gastric aspirate is weak,108 of these data demonstrated a decrease in 28-day mortality
and refeeding gastric residual volumes up to a maximum among patients with severe sepsis in the probiotic group;
of 250 mL or discarding gastric residual volumes may however, mortality was higher for those in a non-severe
be acceptable.36 Enteral feeding is interrupted when the septic group who also received probiotics.121
gastric residual volume exceeds a prescribed threshold for Fermentable oligosaccharides, disaccharides, mono-
acceptable gastric residual volume; however, there are no saccharides and polyols, which are common in commercial
data to support this practice. Ceasing feeds in response to enteral nutrition formulas, have been found to reduce
gastric residual volume is questionable,105 particularly as a the likelihood of diarrhoea in patients receiving enteral
balanced enteral diet in itself has a prokinetic effect.109,110 nutrition.122 Randomised controlled trials with human
 CHAPTER 19 NUTRITION ASSESSMENT AND THERAPEUTIC MANAGEMENT 631

patients are needed to evaluate the effect of ferment- randomised controlled trial with 221 patients no difference
able oligosaccharides, disaccharides, monosaccharides was found in outcomes including no increased risk for
and polyols and other probiotics on enteral nutrition- ventilator-associated pneumonia.136 A systematic review of
associated diarrhoea in the critically ill.115,123 research examining the effect of semi-upright position in
ventilated patients including three studies131,136,137 was the
Practice tip basis for developing consensus-based recommendations for
clinical practice.139 The panel recommended the head of
Nurses may be tempted to stop enteral nutrition in the bed of mechanically ventilated patients be elevated 20°
the presence of diarrhoea but there is no evidence to 45°, preferably ≥30°, as long as there were no risks or it
to support withholding enteral feeding in critically did not conflict with other nursing tasks, medical interven-
ill patients. The only exception may be if there are tions or with patients’ wishes. Marik34 suggests that clinical
significant disturbances in fluid and/or electrolyte judgement should be exercised when using semi-upright
balance. positioning in the critically ill because the evidence to
support this practice is not compelling and the balance
Enteral feeding solutions present an excellent medium between benefits and harms is unknown. Nursing patients
for the growth of microorganisms and bacterial contam- semi-recumbent at 45° can be difficult because the patient
ination of enteral feeds is common.124 Infection control often slides down and the position can be uncomfortable
programs are important. Strategies to limit bacterial for the patient. Experimental models also suggest that the
contamination of enteral feeding solutions include: semi-recumbent position may enhance the flow of mucous
• meticulous125preparation of feeding solutions and into the lungs with an increased risk of bacterial colonisa-
equipment tion and pneumonia.140 Until further evidence is available
• commercially prepared formula used in preference to to guide practice decisions, patient positioning should be at
decanted feeds126 the discretion of clinicians.
Prokinetic agents, such as erythromycin and meto-
• use of closed feeding systems37 clopramide, can improve gastric emptying and feeding
• limiting the time feeding solution is kept 127
at room tolerance, and avoid gastro-oesophageal reflux and
temperature once opened and hang times pulmonary aspiration.141 These prokinetic agents do,
• meticulous attention to hand washing and limiting however, have undesirable effects. Use of erythromycin
manipulation of the enteral nutrition bags and is associated with the development of bacterial resistance,
delivery system at the bedside.124 and metoclopramide is associated with numerous systemic
side effects. Erythromycin is more effective than meto-
Prevention of pulmonary aspiration clopramide in treating gastric intolerance among patients
An important complication of enteral feeding is the receiving enteral nutrition. However, combination therapy
development of pulmonary aspiration and nosocomial with erythromycin and metoclopramide is more effective
pneumonia. Determining whether aspiration has than erythromycin alone in improving the delivery of
occurred is difficult, even for experienced clinicians. enteral nutrition.142,143
High gastric residual volumes have been linked to the
potential for pulmonary aspiration, although this has not Assessment of pulmonary aspiration
been shown in research.105 Oropharyngeal secretions Despite preventive strategies, pulmonary aspiration may
can contribute to nosocomial pneumonia and subglottic still occur in some patients, and accurate assessment is
aspiration has improved outcomes.128 Nursing strategies essential. Common methods that can be performed easily
to improve gastric emptying include elevation of the head at the bedside to determine whether a patient has experi-
of the bed 30–45° (unless otherwise contraindicated), enced aspiration of gastric contents and/or enteral feeding
because the likelihood of gastro-oesophageal reflux is formula follow:
likely to be reduced;129,130 however, this recommenda- • The dye method previously was commonly used
tion is based on weak evidence. A small single-centre to assess aspiration of enteral feeds but should not
randomised controlled trial (47 patients)131 demonstrated be standard practice because of safety concerns.
lower frequency of clinically suspected ventilator- The efficacy of this method is questionable as blue
associated pneumonia in 39 intubated patients dye is poorly standardised and has a low sensitivity
randomised to the semirecumbent (45°) group compared in detecting microaspiration.144 There have been
to the supine position. The study was stopped early case reports of blue dye absorption describing
after a very large treatment effect in favour of the 45° discolouration of the skin, urine, serum and organs,145
elevation was shown in an interim analysis. Two earlier and refractory hypotension and severe acidosis,
studies132,133 showed similar results. Based on this weak suggesting poisoning by a mitochondrial toxin.146
evidence, elevating the head of bed to 30–45° position These safety concerns, coupled with minimal benefits,
became standard of care.134,135 have resulted in the recommendation that the practice
More recently, two randomised controlled trials136,137 and of using blue food colouring in enteral feeding
an observational study138 did not support these results. In a solutions be abandoned.145,147
632 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

• Measurement of glucose in tracheobronchial increased free radical formation may be important for
secretions is another method to detect pulmonary patients who are critically ill.34
aspiration.148 As these secretions normally contain Studies report conflicting results on the benefit of
<5 mg/dL glucose, higher amounts of glucose may PN for the nutrition support of critically ill patients. A
indicate the aspiration of glucose-rich enteral feeding meta-analysis of PN versus no nutritional support in
formula. Differences in enteral feeding solutions critically ill patients reported a two-fold increased risk of
affect the sensitivity of this method, with low glucose death in the PN group.154 A retrospective cohort study
solutions being more difficult to detect. Also, patients compared patients with severely injured blunt trauma who
not receiving enteral feeding can have detectable received PN within 7 days after injury with a control group
glucose in aspirates.149 This is further confounded that did not. In these critically ill trauma patients who were
by the presence of blood, which is closely associated able to tolerate at least some EN, early PN administration
with glucose values >20 mg/dL; consequently, contributed to increased infectious morbidity and worse
any blood in the respiratory tract could contribute clinical outcomes.155 A growing trend is to supplement
to a false-positive result. These findings led to the EN with PN in patients who cannot commence early EN
consensus that glucose monitoring in respiratory or until target nutrition goals are achieved.156 Four studies
secretions should also be abandoned.147 examined the effect of supplemental PN and found no
improvement in patient outcomes,42,157–159 and none was
• Measurement of pepsin in tracheobronchial secretions
able to demonstrate a clear benefit to critically ill patients
has been used in an animal study that suggested
when PN was administered.34 The lack of quantity and
that the detection of pepsin, a component of gastric
quality of data on the use of PN in the critically ill means
secretions, may be useful in determining pulmonary that this strategy is not recommended in current evidence-
aspiration.150 Further investigation in acutely ill based nutrition guidelines.36,160,161
patients receiving enteral feeding is necessary. In the patient who is not tolerating adequate EN, the
• Electromagnetic tube placement device data are insufficient and clinicians will have to weigh the
technology enables tracking gastric tube insertion safety and benefits of initiating PN on an individual case-
electromagnetically on a monitoring screen. The stylet by-case basis.36 The American Society for Parenteral and
within the gastric tube transmits an electromagnetic Enteral Nutrition and Society of Critical Care Medicine
signal that is detected over the patient’s epigastric clinical guidelines160 recommend PN be initiated after
region by a receiver. Metheny and Meert151 reviewed 1 week, unless the patient is severely malnourished, and the
reports from 2007 to 2012 of the electromagnetic European Society of Enteral and Parenteral guidelines161
tube placement device technology and concluded recommend consideration of EN supplemented by PN
that there is sufficient room for error with this after 2–3 days in the ICU if enteral nutrition alone is
method and recommend assessment of feeding tube insufficient at that time.
placement through radiographic confirmation. PN solutions contain carbohydrates, lipids, proteins,
electrolytes, vitamins and trace elements. PN, whether
Practice tip supplementary or complete, provides daily allowances
of nutrients and minerals. The components of PN are
Nursing patients with the head of bed elevated is listed in Table 19.4. The addition of vitamins and trace
common in ICU; however, more evidence is needed elements to PN solutions is necessary, particularly as water-
to demonstrate that this practice prevents pulmonary soluble vitamins and trace elements are rapidly depleted
aspiration. (see Table 19.5).162 Standardised PN formulations, although
as effective as custom-made PN in providing caloric
requirements, are less likely to achieve estimated protein
Parenteral nutrition requirements and have been noted to be associated with
EN is the preferred method of nutritional support hyponatraemia.163 Glucose is the primary energy source
because it has physiological advantages, and is associated in PN solutions. Concentrations of 10–70% glucose may
with fewer infectious and metabolic complications. EN be used in PN solutions although the final concentration
as a nutrition therapy is also less expensive than PN and of the solution should be no more than 35%. The high
the use of PN in the context of critical illness remains concentration of PN solutions can cause thrombosis so PN
controversial. PN bypasses the gastrointestinal system is normally infused via a central venous catheter. Catheter
and the crucial role that hormones and nutrients play in insertion, ongoing care and replacement are similar to that
regulating gut function, metabolic pathways and hepatic with any other central venous catheter. A dedicated central
function.34 In addition there are metabolic, immunolog- venous catheter, or lumen of a multilumen catheter, should
ical, endocrine and infective complications from infusing be used for PN.164 Manipulation of the catheter and tubing
solutions of high glucose concentration and fat globules should be avoided to minimise infection of the catheter.
intravenously.152 Grau et al153 found a strong association Peripheral administration can be considered when the final
of PN and the development of liver dysfunction, whereas solution concentration is 10–12%,165 but is not usually used
early EN was protective. PN impairs humoral and cellular in the context of critical illness because high volumes of PN
immunological defences and the association of PN with would be required to meet caloric requirements.166
 CHAPTER 19 NUTRITION ASSESSMENT AND THERAPEUTIC MANAGEMENT 633

TABLE 19.4
Components of PN solutions

COMPONENT R E C O M M E N D AT I O N GRADE*

Carbohydrate The minimal amount of carbohydrate required is about 2 g/kg of glucose per day B
Hyperglycemia (glucose >10 mmol/L) contributes to death in the critically ill patient and B
should also be avoided to prevent infectious complications
Reductions and increases in mortality rates have been reported in ICU patients when blood C
glucose is maintained between 4.5 and 6.1 mmol/L. No unequivocal recommendation on
this is therefore possible at present
There is a higher incidence of severe hypoglycemia in patients treated to the tighter limits A
Lipids Lipids should be an integral part of PN for energy and to ensure essential fatty acid B
provision in long-term ICU patients
Intravenous lipid emulsions (LCT, MCT or mixed emulsions) can be administered safely at a B
rate of 0.7 g/kg up to 1.5 g/kg over 12 to 24 h
The tolerance of mixed LCT/MCT lipid emulsions in standard use is sufficiently documented. C
Several studies have shown specific clinical advantages over soybean LCT alone but require
confirmation by prospective controlled studies
Olive oil-based parenteral nutrition is well tolerated in critically ill patients B
Addition of EPA and DHA to lipid emulsions has demonstrable effects on cell membranes B
and inflammatory processes. Fish oil-enriched lipid emulsions probably decrease length of
stay in critically ill patients
Amino acids When PN is indicated, a balanced amino acid mixture should be infused at approximately B
1.3–1.5 g/kg ideal body weight/day in conjunction with an adequate energy supply
When PN is indicated in ICU patients the amino acid solution should contain 0.2–0.4 g/kg/ A
day of L-glutamine (e.g. 0.3–0.6 g/kg/day alanyl-glutamine dipeptide)
Micronutrients All PN prescriptions should include a daily dose of multivitamins and of trace elements C

*Grade of recommendation – the grade of recommendation is based on the quality of the evidence where A is high, B is moderate,
C is low and D is very low (as quoted in Guyatt GH, Oxman AD, Vist GE, Kunz R, Falck-Ytter Y, Alonso-Coello P et al. GRADE: an
emerging consensus on rating quality of evidence and strength of recommendations. BMJ 2008; 336:924–6).
DHA = docosahexaenoic acid; EPA = eicosapentaenoic acid; LCT = long chain triglycerides; MCT = medium chain triglycerides.
Adapted from Singer P, Berger MM, Van den Berghe G, Biolo G, Calder P, Forbes A et al. ESPEN Guidelines on Parenteral Nutrition:
intensive care. Clin Nutr 2009;28(4):387-400, with permission.

Routine monitoring of the patient’s fluid balance,

TABLE 19.5 glucose, biochemical profile, full blood count, triglycerides,
Trace elements in TPN162 trace elements and vitamins is necessary. The patient is
also assessed for signs of complications associated with the
TRACE ELEMENT ACTION
administration of PN (see Table 19.6).
Zinc Wound healing
Iron Haemoglobin synthesis Transition to oral diet and fluids
Copper Erythrocyte maturation and lipid The patient’s condition, length of stay in ICU and their
metabolism ability to swallow will influence when and how quickly
Manganese Calcium and phosphorus metabolism oral nutrition can commence. Accurate identification of
Cobalt Essential constituent of vitamin B12 swallowing disorders in ICU patients is crucial to determine
Iodine Thyroxine synthesis
the safety and type of oral nutrition. Dysphagia that occurs
in ICU patients following extubation is usually an ICU-
Chromium Glucose utilisation
acquired disorder,167 although it is also possible for patients
to have an undiagnosed swallowing disease. The prevalence
of swallowing disorders in patients with acute respiratory
Practice tip failure who are extubated is unknown. The estimated
prevalence of dysphagia ranges between 3% and 62% for
PN solutions are high in glucose and therefore require
patients recovering from critical illnesses.168 Six potential
vigilance in preventing catheter-related infection.
mechanisms can cause patients in the ICU to develop
634 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 19.6
Short-term metabolic complications associated with total parenteral nutrition

C O M P L I C AT I O N CAUSE D E T E C T I O N A N D T R E AT M E N T

Hyperosmolar coma Occurs acutely if a rapid infusion of hypertonic fluid is Daily blood samples, accurate measurements of
administered. Infusion can cause severe osmotic diuresis, fluid balance, routine blood samples
resulting in electrolyte abnormalities, dehydration and Reduce infusion rate, correct electrolyte
malfunction of the central nervous system imbalances
Electrolyte Disturbances in serum electrolytes, particularly sodium Daily blood samples taken early in treatment to
imbalance potassium, urea and creatinine, may occur early in detect abnormalities
the treatment of TPN. Electrolyte imbalances can be Replacement fluid as required, extra intravenous
caused by the patient’s underlying medical condition; fluids may be required during the stabilisation
requirements vary with individual patients’ needs. Can period
be caused by inadequate or excessive administration of
intravenous fluids
Hyperglycaemia Critically ill patients may be resistant to insulin because Monitor the patient’s blood sugar 4-hourly after
of the secretion of ACTH and adrenaline. This promotes commencement of treatment or as required.
the secretion of glycogen, which inhibits the insulin Monitor daily urinalysis for glucose and ketones
response to hyperglycaemia An insulin infusion may be required to keep blood
sugar levels within prescribed limits
Rebound May occur on discontinuation of TPN because Glucose infusion rate should be gradually
hypoglycaemia hyperinsulinism may occur after prolonged intravenous reduced over the final hour of infusion before
nutrition. A rise in serum insulin occurs with infusion, discontinuing. Some patients may receive a 10%
and thus sudden cessation of infusion can result in glucose solution after cessation of TPN
hypoglycaemia
Hypophosphataemia Glucose infusion results in the continuous release of Monitor phosphate levels daily.
insulin, stimulating anabolism and resulting in rapid influx Hypophosphataemia will usually appear after
of phosphorus into muscle cells. The greatest risk is to 24–48 hours of feeding
malnourished patients with overzealous administration Reduce the carbohydrate load and give
of feeding. Patients who are hyperglycaemic, who phosphate supplementation
require insulin therapy during TPN or who have a history
of alcoholism or chronic weight loss may require extra
phosphate in the early stages of treatment
Lipid clearance Lipids are broken down in the bloodstream with the Blood samples should be taken after the first
aid of lipoprotein lipase found in the epithelium of infusion commences (within 6 hours) to observe
capillaries in many tissues. A syndrome known as fat for lipid in the blood
overload syndrome can occur when infusion of lipid
is administered that is beyond the patient’s clearing
capacity, resulting in lipid deposits in the capillaries
Side effects of lipid Some patients suffer symptoms either during or after an Treat mild symptoms. If tolerated, the TPN
infusion infusion of lipid mix parenteral nutrition. The exact cause solution of non-protein calories can be given in
is unknown. The patient may complain of headache, the form of glucose. However, it is essential that
nausea or vomiting, and generally feels unwell the regimen includes some fat to prevent the
development of fatty acid deficiency
Anaphylactic shock This is a rare complication but may occur as a reaction It may be necessary to administer adrenaline
to the administration of a lipid and/or steroids, and to provide supportive
therapy as required
Glucose intolerance TPN using glucose as the main source of calories is Observe patients for signs of respiratory distress.
associated with a rise in oxygen consumption and Provide non-protein calories in the form of
CO2 production. The workload imposed by the high glucose lipid mix. Slow initial rate of infusion
CO2 production may precipitate respiratory distress
in susceptible patients, particularly those requiring
mechanical ventilation
Liver function Abnormalities with liver function can be associated Monitor liver function tests twice weekly. There are
with TPN. May be attributable to hepatic stenosis with several factors that may contribute to development
moderate hepatomegaly; patients may also develop of abnormal liver function tests. These most often
jaundice. Liver function tests often return to normal after occur after a period of time and appear to be more
cessation of therapy; however, TPN can lead to severe of a problem when there is an excess calorie intake
hepatic dysfunction in neonates or in glucose-based regimens

ACTH = adrenocorticotrophic hormone; TPN = total parenteral nutrition.

 CHAPTER 19 NUTRITION ASSESSMENT AND THERAPEUTIC MANAGEMENT 635

dysfunctional swallowing. Endotracheal and tracheostomy

tubes can cause direct trauma, focal ulceration and inflam- Practice tip
mation.167 Neuromyopathy resulting in muscular weakness Patients who have been intubated for prolonged
can also cause postextubation dysphagia.169 The third periods are at risk for developing dysphagia. Swallow-
mechanism for dysphagia is the development of dysfunc- ing screening and swallowing assessment might be
tional oropharyngeal and laryngeal sensation. Sensation necessary prior to commencing oral intake. Strategies
abnormalities can result from either critical illness poly- should be employed to ensure swallowing assessment
neuropathy or local oedema.170 Swallowing dysfunction is undertaken quickly so nutrition intake is not negatively
in critical illness can be related to impaired sensorium as a impacted.
result of ICU-acquired delirium, underlying critical illness
or the effects of sedating medications.171 Gastro-oesophageal
reflux is disordered swallowing in critically ill patients and Nutrition in specific clinical
some of the pathophysiological processes responsible for
gastro-oesophageal reflux are likely to continue in the conditions
immediate postextubation period.167 Not all critically ill patients are equal. Age, severity of
Swallowing dysfunction can also occur because of illness, BMI and specific clinical presentations can each
dyssynchronous breathing and swallowing in patients with influence nutritional requirements and therefore the
underlying respiratory impairment and tachypnoea. The nutrition approach used.177 Some general approaches to
study of those factors that increase the risk for impaired nutrition therapy may be similar regardless of clinical
swallowing in awake, recently extubated patients without presentation, such as the timing and route of feeding and
strokes or neuromuscular diseases is less advanced. Specific techniques used to monitor nutritional status and tolerance
risk factors for this type of postextubation dysphagia have of nutrition. However, every patient should be individu-
been reported in a few epidemiology studies.168,172,173 Lower ally assessed and nutrition therapy approaches targeted to
preadmission functional status has been independently their specific clinical condition. There are some general
associated with postextubation dysphagia in a cohort of recommendations for specific clinical presentations that
84 elderly patients but there is conflicting evidence on the can serve as a guide for selecting optimal nutrition in
association of age, intubation duration, diabetes mellitus, some patient groups.
renal failure, postoperative pulmonary complications and
tracheostomy as potential risk factors for postextubation Obesity
dysphagia.174 Comparisons of studies are limited by biased As the proportion of the population with obesity increases
patient selection, heterogeneous study populations and so too does the number of obese patients admitted to
differing diagnostic protocols. critical care areas. The key difference for obese patients
The most common diagnostic test to evaluate for is the accumulation of body fat. There can also be an
postextubation dysphagia is a bedside swallow evaluation increase in muscle mass because of the effort of carrying
performed by a speech language pathologist. Although extra body weight.178 However, increased muscle mass
the components of this examination are not standardised is not uniformly present in all obese patients and
and can vary by practitioner,167 patients usually undergo those whose movement is severely restricted, are older
an interview, a structural and functional evaluation of or who have chronic illness may have loss of skeletal
their mouth and their cough response and an assessment muscle mass.179
of swallowing function with different food textures and As most predictive equations of energy expenditure
liquid thicknesses.The bedside swallow evaluation has been are weight-based it is necessary to adjust to ideal body
criticised for poor sensitivity as well as poor inter- and weight so as to avoid overfeeding.180 It is important
intra-rater reliability.175 Despite not being validated against to recognise that, although body weight increases,
gold standard tests, a seven-point scale that incorporates the the energy expenditure does not increase to the same
perceived aspiration risk and subsequent dietary recommen- extent.181 When the BMI is >40 the increase in energy
dations is often used to grade the severity of dysphagia.176 expenditure is only 14%, less than those patients with a
Additional tests may be ordered to assist in the diagnosis BMI <30 or between 30 and 40 where the increase is
of postextubation dysphagia. A videofluoroscopic swallow approximately 25%.
study, often referred to as a modified barium swallow, is Understanding how obesity influences energy expen-
highly sensitive and specific for aspiration.168 The other gold diture can help guide nutrition prescription. Attention
standard instrumental procedure to evaluate for postextu- has been given to hypocaloric feeding for critically ill
bation dysphagia is a fibre optic endoscopic swallow study. obese patients as a strategy to improve outcome.182 This
Patients who are being weaned from nutrition support is based on the premise that nitrogen balance does not
may have oral nutrition slowly introduced. For longer deteriorate during hypocaloric feeding183 and that energy
stay patients, particularly those who have ICU-acquired expenditure is more difficult to accurately determine in
weakness, weaning from enteral or parenteral nutrition obese patients – so overfeeding is more likely. Over-
onto oral nutrition may commence with a trial of oral feeding can also contribute to increased carbon dioxide
feeding by day supplemented by nutrition support at night. production and therefore increase ventilator load, which
636 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

is less efficient in the critically ill obese patient.184 Despite Renal failure
these physiological rationales there is a lack of evidence
Critically ill patients with renal failure have widely variable
to suggest hypocaloric feeding of the critically ill patient
metabolic patterns and nutritional requirements, making
is beneficial.
decisions about patient-specific nutritional requirements
and goals challenging. The optimal nutrition require-
Practice tip
ments for patients with acute kidney injury are unclear and
Effective monitoring of nutrition therapy is essential in assessment of nutritional requirements is complicated not
the critically ill obese patient to avoid complications only by fluctuating fluid balance and body weight194 but
such as hyperglycaemia, dyslipidaemia, hypercapnia, also by the underlying disease and type and intensity of renal
fluid overload and hepatic stenosis. replacement therapy.195 For critically ill patients who require
renal replacement therapy, there can be additional loss of
Protein requirements are another important consid- glucose, amino acids, proteins, trace elements and vitamins
eration for the critically ill obese patient. In critical that are water soluble and have a low molecular weight.196
illness protein requirements are usually increased185 and These losses can be pronounced when highly efficient
most recommendations are for 1.2–1.5 g/kg/day protein renal replacement therapy such as continuous veno-venous
although these recommendations can be as high as 2.0 g haemofiltration or prolonged intermittent strategies such as
protein/kg ideal body weight.45 A recent systematic sustained low-efficiency dialysis are used.197
review of protein provision in critical illness highlights Although each patient requires nutritional assessment
the limited quantity and quality of research in this area and tailored nutritional prescription, it is suggested that a
but suggests that provision of 2.0–2.5 g protein/kg/day calorie intake of 25–30 kcal/kg/day is required for patients
could be optimum.185 For the critically ill obese patient with renal failure.198 Because protein catabolism and a
protein prescription should be based on ideal body sustained negative nitrogen balance are often present in
weight with adjustments for increasing body weight.45 acute kidney injury198 protein supplementation becomes
Whether other specific nutrients, such as arginine, important to prevent lean muscle loss. Optimal intake of
glutamine and leucine, are beneficial for the critically ill proteins and amino acids for the patient with acute kidney
obese patient is unclear.186 injury who may require renal replacement therapy is often
hotly debated. Recommendations range from 1.4 g/kg/
Practice tip day195 up to 2.5 g/kg/day.199 In addition to protein and
calorie replacement, the use of pharmaconutrients with
Obese critically ill patients might have increased gastric anti-inflammatory effects, such as glutamine and omega-3
residual volumes because of increased intra-abdominal fatty acids, might play a role preventing further deterio-
pressure, which inhibits gastric emptying. ration of renal function and assisting with improvement
in renal function following acute kidney injury, although
Sepsis there are insufficient data at present that demonstrate such
an approach improves outcomes in these patients.194
The incidence of sepsis is on the increase worldwide and,
although mortality rates have improved in recent years, Pancreatitis
these can still be high.187,188 Sepsis results in an overwhelm- Severe acute pancreatitis is a disease associated with
ing cytokine-mediated, proinflammatory response to the increased morbidity and mortality.200 Severe acute pancre-
presence of infection and is characterised by widespread atitis causes both local and systemic complications and
inflammation, vasodilation, leukocyte accumulation and results in increased catabolism and hypermetabolism,
increased microvascular permeability.189 although the severity of clinical presentations can vary
Few literature reports specifically address the nutri- widely.
tional needs of patients with sepsis;190 however, multiple Traditionally, patients with pancreatitis have been
randomised trials and large observational studies of fasted and provided nutrition parenterally201 with the
heterogeneous critically ill patients suggest that optimising aim of ‘resting’ the pancreas.34 Early enteral nutrition is
enteral nutrition is beneficial.36 However, the current now encouraged in pancreatitis as significant reductions
recommendations within the Surviving Sepsis Guidelines in morbidity and mortality have been demonstrated.202
suggest mandatory full caloric feeding should be avoided Compared to PN, EN significantly reduces infection,
in favour of low-dose EN during the first 7 days in hospital length of stay, organ failure, need for surgical
ICU.191 There are no contraindications to administering intervention and mortality.203 The beneficial effects of
EN in patients with sepsis and shock; however, it is recom- EN as compared to PN are also observed when enteral
mended that initial resuscitation be accomplished before nutrition is commenced early (within 48 hours).204
EN is commenced.192 A clear approach for how nutrition Despite clear recommendations from evidence-based
support might be provided is lacking because studies using guidelines, adherence to these recommendations can be
different methodologies and different patient populations poor205 and highlights an area where evidence could
have produced conflicting results.193 be further integrated into clinical practice.
 CHAPTER 19 NUTRITION ASSESSMENT AND THERAPEUTIC MANAGEMENT 637

Recommendations for managing nutrition therapy malnutrition.9 Prolonged periods of inadequate oral
for the critically ill patient with pancreatitis are clear and, nutrition are associated with higher mortality and, even
unlike other areas of nutrition therapy, there is consensus for those patients who are well nourished at time of
within recommendations from different professional surgery, should they be unable to eat for more than 7 days,
organisations.206 A summary of the key recommendations nutritional support is indicated.208
is provided in Table 19.7 At present, there are no data to Postoperative patients may, however, continue to
support the use of pharmaconutrition supplements,207 receive little or no nutrition following surgery. Postopera-
except for parenteral glutamine administration.200 tive ileus is often a concern, which means some clinicians
do not provide enteral nutrition. Instead, gastric aspiration
Trauma and surgery is implemented and the patient is given intravenous
Nutritional recommendations for trauma patients are fluids. However, studies of gut motility demonstrate that
generally the same as those for all critically ill patients. small bowel peristalsis returns within hours following a
Like data from more heterogeneous critically ill patients, laparotomy.34 Therefore, interruption of nutritional intake
early enteral nutrition has a demonstrated mortality is not necessary following surgery, even for patients who
benefit.46 Nasogastric feeding is suitable for most trauma have undergone gastrointestinal surgery. A meta-analysis
patients although small bowel feeding might be required of 15 studies that included 1240 patients demonstrated
for those patients who require longer periods of nutrition that early postoperative nutrition was associated with
support.208 significant reductions in complications and there was no
Critically ill surgical patients do require special attention evidence of negative outcomes that commonly concern
because they are at the highest risk of hospital-acquired clinicians, including anastomotic dehiscence.73

TABLE 19.7
Recommendations for nutrition therapy in severe acute pancreatitis206

R E C O M M E N D AT I O N GRADE OF EVIDENCE

Pancreatitis patients are at nutritional risk and should be screened B

For mild-to-moderate disease, analgesics, intravenous fluids and nothing by mouth with a gradual C
advancement to diet within 3–4 days is recommended
Nutrition therapy is generally not needed for mild-to-moderate disease unless complications arise A
Nutrition therapy should be considered in any patient regardless of disease severity if the anticipated B
duration of being nil by mouth is >5–7 days
Nutrition therapy is needed in mild-to-moderate disease when the patient has been nil by mouth for B
5–7 days
Early nutrition therapy is indicated for severe pancreatitis A
Nutrition therapy is useful in the management of patients who develop complications of surgery B
EN is generally preferred over PN, or at least EN should, if feasible, be initiated first A
EN may be used in the presence of pancreatic complications such as fistulas, ascites and pseudocysts C
Continuous EN infusion is preferred over cyclic or bolus administration B
Nasogastric tubes may be used for administration of EN. Postpyloric placement is not always required B
For EN, consider a small peptide-based medium-chain triglyceride oil formula to improve tolerance B
Use PN if nutrition therapy is indicated, when EN is contraindicated or not well tolerated A
Intravenous fat emulsions are generally safe and well tolerated as long as baseline triglycerides are B
below 400 mg/dL (4.4 mmol/L) and there is no previous history of hyperlipidemia
Glucose is the preferred carbohydrate source with metabolic control of glucose as close to normal as C
possible
Consider use of glutamine (0.30 g/kg Ala-Gln dipeptide) C
No specific complications of PN are unique to patients with pancreatitis. Avoid overfeeding C

Grades of evidence:
A: guideline statement meeting the criteria for high grade of evidence with uniform consensus across multiple societal reports
B: guideline statement that meets the criteria for low/intermediate grade of evidence or where there is lack of consensus across
societal reports (at least one societal report is in disagreement)
C: guideline statement meeting the criteria for high grade of evidence, published only in a single societal report (consensus not
applicable in this case).
638 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Enteral feeding may often be withheld in those patients Early and aggressive nutrition therapy, along with
with abdominal compartment syndrome who have a other interventions, is necessary for improvements in
decompressive celiotomy because of the concerns about patient outcome.214 Early EN, that is nutrition provided
bowel dysfunction.34 However, early enteral nutrition within 24 hours of injury, is recommended for the severely
has been shown to be feasible in these situations and is burned patient and can help to modulate the hypermeta-
associated with improved outcomes.209,210 bolic response.215 There are several benefits to early and
Existing malnutrition can be a significant concern for continuous EN including a decreased hypermetabolic
surgical patients because of the association with complica- response; decreased levels of circulating catecholamines,
tion rates, delayed recovery and longer ICU and hospital cortisol and glucagon;216 preservation of gut mucosal blood
stay.208 Preconditioning may be required and is usually best flow and mucosal integrity; and improved gut motility.211
delivered by the enteral route. High protein delivery of 1.5–3.0 g/kg ideal body weight
may be required for burn patients.213 Administering
Burns specific micronutrients may improve immune function
Shortly after injury severe burns are associated with a and positively influence septic morbidity and mortality.217
high degree of hypermetabolism and hypercatabolism.211 Many pharmconutrients have been studied in the context
Burns can also result in destruction of skeletal muscle.212 of nutrition support for the patient with burns218 although
The hypermetabolic and hypercatabolic response to their benefit is yet to be clearly demonstrated.219,220
severe burn injury can result in significant caloric deficits
and weight loss that may lead to immune dysfunction, Glycaemic control in
decreased wound healing, severe infections and death.211
Comprehensive nutritional assessment is important for critical illness
patients with severe burns and helps to inform nutrition Hyperglycaemia and increased insulin resistance are char-
therapy strategies (Table 19.8). Assessing caloric require- acteristics of the body’s stress response and activation of
ments can be challenging and, as for all critically ill the sympathetic and adrenal and hypothalamic–pituitary–
patients, indirect calorimetry is the preferred method adrenal (HPA) axis responses to critical illness.221 Hyper-
of determining resting energy expenditure. When this glycaemia has been considered a beneficial adaptive
equipment is unavailable, predictive equations that response to stress to provide energy substrate to the organs
are specific for patients with burns can be used. Many involved in the ‘fight or flight’ response.222 There is some,
formulas were developed before improvements to burn
management, which reduce the hypermetabolic response,
TABLE 19.9
were implemented and can result in an overestimation of
requirements.213 Of the predictive equations used in burns, Predictive equations for estimating caloric
requirements in patients with burns211
the Toronto Formula is the most complicated and likely
difficult within a busy clinical setting (Table 19.9). AGE, Y NAME FORMULA

0–1 Galveston 2100 kcal/m2 + 1000 kcal/m2 burn

TABLE 19.8 Infant

Comprehensive nutrition assessment in the patient 1–11 Galveston 1800 kcal/m2 + 1300 kcal/m2 burn
with severe burns211 Revised
12–16 Galveston 1500 kcal/m2 + 1500 kcal/m2 burn
H I S T O RY A N D P H Y S I C A L PRE-EXISTING
Adolescent
E X A M I N AT I O N MALNUTRITION
16–59 Curreri 25 kcal/kg body weight +
Malabsorption
formula (40) TBSA
Paralytic ileus
Toronto −4343 + (10.5 × TBSA) + (0.23 ×
Severe shock formula CI) + (0.84 × HBE) + (114 × T) −
Bowel obstruction (4.5 × PBD)
Diffuse peritonitis ≥60 Curreri 20 kcal/kg body weight + 65
Laboratory measurements Serum albumin and formula (TBSA)
prealbumin CI = total calorie intake the previous day; HBE = Harris-
Nitrogen balance Benedict estimates; PBD = number of postburn days to
the day preceding the estimation; T = average of core
Tests for immune function temperatures (°C) the previous day; TBSA = burn size in total
Clinical examination Anthropometric body surface area.
measurements Reproduced from Rodriguez NA, Jeschke MG, Williams
FN, Kamolz LP, Herndon DN. Nutrition in burns: Galveston
Fluid intake and output
contributions. JPEN J Parenter Enteral Nutr 2011;35(6):
Metabolic assessment Indirect calorimetry 704-14, Table 1, with permission.
 CHAPTER 19 NUTRITION ASSESSMENT AND THERAPEUTIC MANAGEMENT 639

although inconsistent, evidence of an association of hyper- of these patients. The Canadian Clinical Guidelines
glycaemia with high mortality and morbidity.223–227 recommend blood glucose values be monitored every
The complexity of the physiological processes associated 1–2 hours until glucose values and insulin infusion rates
with hyperglycaemia in critical illness and the sophisticated are stable, then every 4 hours thereafter.36 The continua-
research required to generate valid information render tion of insulin infusions in patients who have their enteral
clinical decision making related to glycaemic control nutrition decreased or ceased requires more frequent
challenging. Nevertheless, the concept of tight glycaemic blood glucose monitoring because of the risk for hypo-
control is accepted but a ‘gold standard‘ for the range of glycaemia.229 Reports from studies suggest variability
acceptable values for glucose levels is not available. Multiple in glucose levels over time is an important determinant
randomised trials have been conducted in a variety of ICU of mortality238,239 but is not associated with increased
patient groups, health care settings and using different mortality rates in diabetic patients when compared to
study methods.223,228,229 The meta-analyses do not provide non-diabetic patients.238,240
clear resolution of the issue of glycaemic control with The use of intravenous insulin for tight glycaemic
differing results reported by Griesdale et al,230 who found control can contribute to rapidly changing blood glucose
that intensive insulin therapy was beneficial in surgical ICU levels; therefore vigilant monitoring is required. The time
patients, and Friedrich et al,231 who were unable to demon- and frequency of blood glucose measurement that may be
strate a benefit from intensive insulin therapy for surgical required for some patients may impact on the provision
patients. The inconsistent results, even from those studies of patient care, and inability to perform the testing as
that appear to have used similar methods, has continued often as required may contribute to underdetection of
to fuel the debate on tight glycaemic control with some hypoglycaemia. Another potentially important factor that
experts urging caution and others seeing tight glycaemic may contribute to underdetection of hypoglycaemia is
control as a marker of quality practice.232 The discrepan- fatigue in nurses caring for the critically ill. Louie et al241
cies in these studies have been attributed to many factors reported the results of a single-centre study that found
including the variability in target ranges for blood glucose, the increased number of antecedent shifts worked by
methods of blood glucose measurement, difficulty for some bedside nurses was associated with an increased incidence
studies to achieve separation of the treatment and control of hypoglycaemia.
groups, compliance with the therapy and employment of The validity of blood glucose measurement is also
different nutritional strategies.233 an important consideration. Formal laboratory testing is
Insulin protocols for blood glucose levels often have an considered ‘gold standard’ for blood glucose measurement
upper target blood glucose level of 10.0 mmol/L (180 mg/ but point-of-care testing of blood glucose is common in
dL) or less based on the NICE-SUGAR study protocol,223 the critical care setting. Blood glucose may be sampled
although different targets of insulin therapy are reported from arterial, venous and capillary blood. The use of
where the glucose is ≤6.1 mmol/L or ≤8.3 mmol/L.230 capillary blood in testing blood glucose may be problem-
Several consensus statements for glycaemic control of atic, particularly in those patients for whom hypoperfusion
hospitalised patients have been published234–237 that do is an issue.191 It is recommended that point-of-care testing
include a lower threshold other than hypoglycaemia and using capillary blood be interpreted with caution because
recommend avoidance of hyperglycaemia, hypoglycae- the measurements may not accurately estimate arterial
mia and wide swings in glucose levels. Data from several blood or plasma glucose values.36
studies indicate that the risk of hypoglycaemia is increased It is clear that hyperglycaemia should be avoided.
with intensive insulin therapy and that there is no overall However, the inconsistencies in published studies mean
mortality benefit conferred when this therapy is used in that an agreed specified target for blood glucose in the
critically ill patients.230 critically ill patient population is difficult to achieve.233 The
Insulin infusions are used to control high blood glucose optimal target blood glucose level is unknown and may
levels and nurses have an integral role in the management differ depending on the patient’s clinical presentation.191

Summary
Critically ill patients are at increased risk of malnutrition because of increased metabolic requirements coupled with
challenges in delivering prescribed nutrition. Critical care nurses play a pivotal role in ensuring nutritional adequacy
and are well positioned to coordinate interdisciplinary collaboration to optimise nutrition therapy. Optimising
nutrition in critical illness is assisted by accurate assessment of nutritional requirements and prescribing nutrition that
closely matches the patient’s individual needs. Delivery of prescribed nutrition is the role of the nurse and attention
should be given to minimising interruptions to nutrition therapy. During recovery from critical illness and when the
patient resumes oral intake, nutritional risk can be increased because of factors that impact on the patient’s ability to
eat. Assessment of the ability to safely resume oral intake might be necessary for those patients at risk of dysphagia.
Attention to nutritional requirement should commence on admission to the ICU and extend beyond both ICU and
hospital discharge.
640 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Case study
Peter was admitted to ICU following clinical deterioration on the ward. He was originally admitted with
acute abdominal pain, suspected to be caused by pancreatitis. He was morbidly obese and had a medical
history of hypertension. Peter lived independently before admission to hospital.
On arrival to ICU the patient was tachycardic, tachypnoeic and hypotensive. He was intubated and
mechanically ventilated and required moderate doses of noradrenaline and vasopressin to correct
hypotension. He had acute kidney injury with a creatinine of 177 micromol/L and metabolic acidosis
requiring continuous renal replacement therapy. His bilirubin was elevated at 24 micromol/L on admission.
On arrival to ICU a nasogastric tube was inserted and Peter was commenced on enteral feeding at
10 mL/h of a concentrated enteral feeding solution of 2 kcal/mL. EN was supplemented with standard
total PN at 40 mL/h for the first 24 hours Peter was in ICU. On day 2 of ICU admission enteral feeding
was increased to 37 mL/h and the PN was ceased. Peter tolerated EN well and had minimal aspirates
from the nasogastric tube.
The patient continued to be dialysed for the next 16 days and had a tracheostomy tube inserted on day
7 for a slow respiratory wean from mechanical ventilation. Peter was decannulated 2 days prior to being
transferred to the ward.

DISCUSSION
Critically ill patients often have increased nutritional requirements either as a result of pre-existing malnutrition
or because of decreased nutritional intake that is insufficient to meet the increased energy expenditure that
is typical in critical illness. There are a number of key issues relating to nutritional status and the provision
of nutrition that are central to this case study. These include pre-existing obesity, hypotension and shock
requiring vasopressors, presence of pancreatitis and renal failure.
Obesity: It can be challenging to accurately determine nutritional requirements for critically ill patients
and this is particularly the case in the context of obesity. While obese patients do accumulate increased
body fat they can also have an increased amount of muscle mass because of the need to carry extra
body weight. Most ICUs do not have the benefit of a metabolic cart to measure energy expenditure so
predictive equations are often used to determine caloric requirements. Most of these equations are weight
based; therefore, adjustment needs to be made so ideal body weight is used in the equation, otherwise
overfeeding might result. Some clinicians believe that hypocaloric feeding is optimal in obese critically
ill patients because overfeeding can result in increased carbon dioxide production and ventilator load – a
challenging situation for the obese patient. There is, however, a lack of evidence to support this approach in
obese critically ill patients. In this case study Peter was fed at goal rate, based on his ideal body weight. It
is possible that the estimation of Peter’s energy expenditure could have led to either over- or underfeeding.
Indirect calorimetry, where available, could assist with more accurate measures of energy expenditure and
caloric requirements.
Hypotension: Hypotension and the use of vasopressors can reduce splanchnic perfusion and is sometimes
perceived as a contraindication to EN. Enteral nutrients have been shown to increase gut blood flow, which
allows the bowel to absorb nutrients during vasopressor therapy. There is insufficient evidence to suggest
whether EN should continue or be withheld when vasopressors are being administered with the results from
a limited number of studies being inconsistent. Individual patient assessment is required to guide clinical
practice in this area. In this case study EN was commenced despite vasopressor therapy and the patient
did not exhibit any signs of gastric intolerance.
Pancreatitis: It has been commonly thought that patients with pancreatitis should not ingest food or fluid
orally. In such cases, nutrition is often provided parenterally with the aim of allowing the gut to rest. Current
research now suggests that EN should be provided, even in the context of acute severe pancreatitis,
and can contribute to significant reductions in morbidity and mortality. In this case study the patient
was commenced on EN on ICU admission but at a low rate (even for a concentrated EN solution), which
was unlikely to address metabolic requirements so EN was supplemented with PN. Within 24 hours of
admission the patient was able to receive EN alone, which raises a question as to whether PN could have
been avoided initially.
Renal failure: Optimal nutrition requirements in renal failure are unclear and assessment of nutritional
requirements is complicated by shifting fluid balance and body weight. In this case study actual body
 CHAPTER 19 NUTRITION ASSESSMENT AND THERAPEUTIC MANAGEMENT 641

weight should not be used as a factor in determining nutrition intake so fluctuations in fluid balance are
unlikely to confound decisions. It is important, however, to consider the potential loss of glucose, amino
acids, proteins, trace elements and vitamins that can occur in the setting of renal replacement therapy. An
additional consideration is the provision of adequate amounts of protein because of protein catabolism
and sustained negative nitrogen balance that occurs in renal failure. The recommendations for protein for
patients with renal failure do vary considerably from 1.4 g/kg/day up to 2.5 g/kg/day.

CASE STUDY QUESTIONS

1 On admission, what information might you request from the family to help you to assess whether Peter
was nutritionally at risk prior to admission?
2 In the case study the patient presented with pancreatitis and was also morbidly obese. Discuss how
these two factors might influence tolerance of enteral nutrition.
3 During the course of recovery from critical illness Peter had a tracheostomy but was eventually
decannulated. Discuss the implication of this treatment on nutritional intake and recovery after ICU
discharge.

RESEARCH VIGNETTE

Needham D, Dinglas VD, Morris PE, Jackson JC, Hough CL, Mendez-Tellez PA et al, for the HIH NHLBI ARDS
Network. Physical and cognitive performance of patients with acute lung injury 1 year after initial trophic versus full
enteral feeding: EDEN Trial Follow-up. Am J Respir Crit Care Med 2013;188(5):567–76

Rationale: We hypothesized that providing patients with acute lung injury two different protein/calorie nutritional
strategies in the intensive care unit may affect longer-term physical and cognitive performance.

Objectives: To assess physical and cognitive performance 6 and 12 months after acute lung injury, and to evaluate
the effect of trophic versus full enteral feeding, provided for the first 6 days of mechanical ventilation, on 6-minute-
walk distance, cognitive impairment, and secondary outcomes.

Methods: A prospective, longitudinal ancillary study of the ARDS Network EDEN trial evaluating 174 consecutive
survivors from 5 of 12 centers. Blinded assessments of patients’ arm anthropometrics, strength, pulmonary function,
6-minute-walk distance, and cognitive status (executive function, language, memory, verbal reasoning/concept
formation, and attention) were performed.

Measurements and main results: At 6 and 12 months, respectively, the mean (SD) percent predicted for 6-minute-
walk distance was 64% (22%) and 66% (25%) (P = 0.011 for difference between assessments), and 36% and
25% of survivors had cognitive impairment (P = 0.001). Patients performed below predicted values for secondary
physical tests with small improvement from 6 to 12 months. There was no significant effect of initial trophic versus full
feeding for the first 6 days after randomization on survivors’ percent predicted for 6-minute-walk distance, cognitive
impairment status, and all secondary outcomes.

Conclusions: EDEN trial survivors performed below predicted values for physical and cognitive performance at
6 and 12 months, with some improvement over time. Initial trophic versus full enteral feeding for the first 6 days after
randomization did not affect physical and cognitive performance.

Critique
The EDEN follow-up study did not show any difference in physical and cognitive performance of patients with acute
lung injury at 1 year. Sample size was small and consequently there may have been insufficient patients to demonstrate
a statistical difference. Nevertheless, the results of this study are consistent with the patient-reported outcomes from
525 patients with acute lung injury from 11 of 12 EDEN study centres evaluated via telephone survey.242 They are also
consistent with the findings of other follow-up studies of survivors of acute lung injury.243–245 The multicentre study
was conducted in the USA. Engaging multiple centres enables a larger sample size and improves interpretation of the
results but generalisability may be threatened if conducted in different health care settings to your clinical practice.
642 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

The study used a comprehensive battery of physical and cognitive tests and demonstrated impairments across
multiple aspects of physical and cognitive performance. The impairments may have existed prior to the episode of
critical illness but Needham et al57 argue that the patient group was relatively young and 93% were living independently
without assistance before admission.
The longitudinal study design was an appropriate method to follow up patients over time but loss to follow-up can
be problematic.246 In this follow-up study half of the patients from 12 EDEN study hospitals were included; 20%
died before hospital discharge, 6% died after discharge but before follow-up and 24% who met exclusion criteria
were excluded.57 The study used several strategies to minimise loss to follow-up, including conducting research visits
at patients’ homes or healthcare facilities for those who were unable to attend the research clinic.247,248 In addition,
the validated cognitive performance tests were completed by telephone if a personal visit was not feasible.249 To
promote consistency in data collection, research personnel underwent in-person training and annual in-person quality
assurance reviews for conducting the physical and cognitive performance tests in this study. In addition, staff also
conducted validated and reliable daily assessments of sedation and delirium status at study sites that did not routinely
assess for delirium. Post-hoc analyses and their inherent bias were avoided by deciding subgroup analyses a priori.
Long-term sequelae to critical illness are common. This study did not find a difference in outcomes between those
who received initial trophic enteral nutrition to those receiving full enteral nutrition. The patients in this study had acute
lung injury, were relatively young and well-nourished and it is unknown if the results of this study (and the EDEN study)
can be extrapolated to older and less well-nourished patients. The investigators acknowledge that caution should
be taken in interpreting the results of the study before considering changes in clinical practice because there are no
other randomised controlled trials examining the effects of this feeding strategy on outcomes, and our understanding
of anabolism and catabolism during critical illness and its effect on long-term functional outcomes is limited.250,251
Further research is needed.

Lear ning a c t iv it ie s
1 Review your patients’ notes and calculate what their total daily caloric intake was for the previous day. Once you
have obtained this figure, compare this to the prescribed intake. If patients have not received their total daily
caloric intake, consider what factors may have contributed to this and how these might be overcome in future.
2 What strategies can be used to minimise the risk of aspiration pneumonia in enterally fed, critically ill patients?
3 Should critically ill patients who have had gastrointestinal surgery not receive enteral nutrition postoperatively?
4 Tight glycaemic control can increase the incidence and severity of hypoglycaemia. Consider what factors might
contribute to wide fluctuations in blood glucose levels.

Online resources
American Society for Parenteral and Enteral Nutrition, www.nutritioncare.org
Australasian Society for Parenteral and Enteral Nutrition, www.auspen.org.au
Critical Care Nutrition, www.criticalcarenutrition.com
The European Society for Clinical Nutrition and Metabolism, www.espen.org

Further reading
Canada T, Crill C, Guenter P, eds. A.S.P.E.N. Parenteral nutrition handbook. Maryland: The American Society for Parenteral
and Enteral Nutrition; 2009.
Farber P, Siervo M. Nutrition in critical care. Cambridge: Cambridge University Press; 2014.
Merritt R, ed. The A.S.P.E.N. Nutrition support practice manual. 2nd ed. Maryland: The American Society for Parenteral and
Enteral Nutrition; 2005.
Singer P. Nutrition in intensive care medicine: Beyond physiology. In: Koletzko B. World review of nutrition and dietetics,
Vol 105. Basel: Karger; 2013.
 CHAPTER 19 NUTRITION ASSESSMENT AND THERAPEUTIC MANAGEMENT 643

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125 Patchell CJ, Anderton A, Holden C, MacDonald A, George RH, Booth IW. Reducing bacterial contamination of enteral feeds. Arch Dis Child
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129 Metheny NA, Frantz RA. Head-of-bed elevation in critically ill patients: a review. Crit Care Nurse 2013;33(3):53-66; quiz 7.
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195 Druml W. The renal failure patient. In: Singer P, ed. Nutrition in intensive care medicine: Beyond physiology. Basel, Switzerland: Karger; 2013,
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196 Wiesen P, Van Overmeire L, Delanaye P, Dubois B, Preiser JC. Nutrition disorders during acute renal failure and renal replacement therapy.
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211 Rodriguez NA, Jeschke MG, Williams FN, Kamolz LP, Herndon DN. Nutrition in burns: Galveston contributions. JPEN J Parenter Enteral Nutr
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212 Garcia de Lorenzo y Mateos A, Ortiz Leyba C, Sanchez SM, Metabolism, Nutrition Working Group of the Spanish Society of Intensive Care M,
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213 NSW Statewide Burn Injury Service. Clinical practice guidelines: nutrition burn patient management. 2nd ed. Chatswood, NSW: Agency for
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 Chapter 20

Gastrointestinal, metabolic
and liver alterations
Andrea Marshall, Christopher Gordon

KEY WORDS Learning objectives

diabetic After reading this chapter, you should be able to:
ketoacidosis • describe the changes in gastrointestinal physiology and metabolism
extracorporeal liver associated with critical illness
support • identify patients at risk for the development of stress ulcers and
hepatic rationalise therapeutic interventions for their prevention
encephalopathy • identify patients at risk for the development of intra-abdominal
hepatorenal hypertension and abdominal compartment syndrome and suggest
syndrome management strategies to decrease intra-abdominal pressure
hyperosmolar • describe the physiological changes that occur during diabetic
hyperglycaemic ketoacidosis and rationalise assessment and treatment strategies
state • discuss the effects of critical illness on hepatic function and evaluate the
intra-abdominal consequences of liver dysfunction
hypertension • describe the treatment of liver failure, including liver support therapies and
liver failure transplantation.
liver transplantation
stress-related
mucosal disease
Introduction
During episodes of critical illness, patients often experience disturbance in their
metabolic and/or endocrine function. In the previous chapter, the changes to
metabolism that occur during critical illness and the role of the gastrointestinal
system in nutrition were outlined.The gastrointestinal system is also involved in
many other important functions including immunity and protection.
Effective gastrointestinal function requires an adequate blood supply to
ensure oxygen and nutrients are available at the cellular level. However, in
critical illness splanchnic circulation may be compromised without overt signs
being evident. This alteration in regional blood flow and tissue oxygen delivery
can compromise normal metabolic and endocrine function.
In this chapter the effect of gastrointestinal physiology on critical illness
is discussed. Gastrointestinal dysfunction, including the development of
stress-related mucosal diseases and development of increased intra-abdominal
pressure, is discussed. A major component of this chapter is dedicated to the
assessment and management of liver dysfunction, including liver transplanta-
tion. An overview of the assessment and management of diabetic ketoacidosis
is also provided.
652 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Gastrointestinal physiology alterations to glucose absorption.7,8 Changes can also

occur with gastric acid production, which is commonly
As described in Chapter 19, digestion and absorption of thought to increase in critical illness. There is some
nutrients such as carbohydrates, amino acids, minerals evidence to suggest that many critically ill patients do
and water are key functions of the gastrointestinal system. not hypersecrete gastric acid9 with increased gastric
Another important role of the gastrointestinal tract is pH being observed in some critically ill patients, even
immunity. Part of this immunity is the established barrier in the absence of pharmacological inhibition of gastric
between the gastrointestinal tract and the blood supply. acid secretion.10 The ability of the small intestine to
There are a number of different mechanisms by which absorb nutrients can be impaired during critical illness,11
the gastrointestinal system prevents the movement of although most critically ill patients appear to be able to
substances (other than nutrients, water and electrolytes) tolerate enteral nutrition, making the clinical signifi-
into the systemic circulation and these are outlined in cance of impaired absorption unclear.
Table 20.1. In the setting of critical illness, gastrointesti- Some alterations to normal gastrointestinal physiology
nal hypoperfusion may be present, resulting in decreased in critical illness relate to hypoperfusion and decreased
oxygen and nutrient delivery at the cellular level, and oxygenation in this area and have high metabolic
this in turn can lead to decreased effectiveness of these demands.12 Historically, gastrointestinal dysfunction in
protective functions. critical illness was described in relation to symptoms, such
Alterations to normal gastrointestinal as gastrointestinal bleeding, mechanical obstruction and
pancreatitis13 resulting from ischaemia.14 However, the
physiology in critical illness presence of covert ischaemia has resulted in a heightened
During critical illness, there are a number of alter- interest in the prevention and early detection of gastro-
ations that can occur to gastrointestinal physiology. The intestinal ischaemia in the critically ill, in an attempt to
digestion and absorption of nutrients may be altered, as minimise ischaemia-related dysfunction.

TABLE 20.1
Protective mechanisms of the gastrointestinal system and impacts of critical illness

MECHANISM ACTION

Motility Propels bacteria through the GI tract. In critical illness, motility may be altered because of enteric nerve
impairment and altered smooth muscle function, inflammation (mediated by cytokines and nitric oxide),
gut injury, hypoperfusion, medications (opioids, dopamine), electrolyte disturbances, hyperglycaemia,
sepsis and increased intracranial pressure1
Hydrochloric acid Reduces gastric acidity and destroys bacteria. Parietal cells in the stomach produce hydrochloric acid
secretion and keep the intragastric environment relatively acidic (pH approx 4.0). An acidic pH has bactericidal
and bacteriostatic properties,2 thus limiting overgrowth in the stomach
Bicarbonate Bicarbonate ions bind with hydrogen ions to form water and carbon dioxide, preventing the hydrogen
ions (acid) from damaging the duodenal wall6
Bile salts Bile salts provide protection against bacteria by breaking down the liposaccharide portion of endotoxins,
thereby detoxifying gram-negative bacteria in the gastrointestinal tract. The deconjugation of bile salts
into secondary bile acids inhibits the proliferation of pathogens and may destroy their cell walls3
Mucin production Prevents the adhesion of bacteria to the wall of the GI tract. Mucous cells secrete large quantities of very
thick, alkaline mucus (approximately 1 mm thick in the stomach). Glycoproteins present in the mucus
prevent bacteria from adhering to and colonising the mucosal wall4
Epithelial cell Limits bacterial adhesion. The mucosal lining of the entire gastrointestinal tract is composed of epithelial
shedding cells that create a physical barrier to bacterial invasion. These cells are replaced approximately every
3–5 days,4 limiting bacterial colonisation
Zona occludens (tight The junctions between epithelial cells provide a barrier to microorganisms. Intermediate junctions
junctions surrounding (zonula adherens) function primarily in cell–cell adhesion, while the tight junctions (zonula occludens)
each cell in the limit the movement of bacteria and toxins across the gut wall5
epithelial sheet)
Gut-associated Protection against bacterial invasion is provided by gut-associated lymphoid tissue, capable of cell-
lymphoid tissue mediated and humoral-mediated immune responses4
Kupffer cells Kupffer cells in the liver and spleen provide a back-up defence against pathogens that cross the barrier
of the gastrointestinal wall and enter the systemic circulation
 CHAPTER 20 GASTROINTESTINAL, METABOLIC AND LIVER ALTERATIONS 653

Gastrointestinal mucosal hypoperfusion bilirubin levels in septic patients, to an acute elevation

The gastrointestinal system is particularly susceptible to following haemodynamic shock. Ischaemic hepatic
alterations in regional blood flow and oxygen delivery injury influences morbidity and mortality but remains
because it has a higher critical oxygen delivery than underdiagnosed, probably because the clinical signs
the rest of the body. Splanchnic vasoconstriction is also become apparent long after hypoperfusion has occurred.
proportionally greater than in other vascular beds and the Physiological changes contributing to ischaemic hepatitis
countercurrent oxygen exchange between vessels within include changes to the portal and arterial blood supply
as well as hepatic microcirculation. The degree to which
the villi further contributes to decreased regional oxygen
the liver is damaged is directly related to the severity and
delivery.4
duration of hypoperfusion, and both anoxic and reper-
During shock states, decreased blood flow due to
fusion injury can damage hepatocytes and the vascular
vasoconstriction occurs in this region first. It is the last
endothelium.18
place where blood flow is restored following successful
resuscitation.15 In shock states, the gastrointestinal system
attempts to maintain adequate cellular oxygenation by Stress-related mucosal damage
increasing the amount of oxygen extracted from the blood. The reported incidence of stress-related mucosal damage
This increase in oxygen extraction may prevent serious is variable19 and complicated by definitions of end points,
compromise of tissue oxygenation even in the presence of difficulty in measuring the end points and the hetero-
reduced oxygen delivery.16 geneity of patient populations.20 It is estimated that
between 74% and 100% of critically ill patients have
Practice tip evidence of stress-related mucosal erosion and subep-
ithelial haemorrhage on endoscopy at their first day of
Remember, assessment of arterial blood pressure, admission to the intensive care unit (ICU).20 With occult
heart rate and urine output provides information about bleeding (drop in haemoglobin level or positive stool
the haemodynamic and oxygenation status of the whole occult blood test) as an end point, it is estimated that
body. A reduction in regional perfusion and oxygenation 15–50% of critically ill patients would be reported to have
may occur despite conventional clinical assessment stress-related mucosal damage.21 Reported incidence is
findings being normal. reduced to 25% or less when haematemesis or nasogastric
lavage positive for bright red blood is used as an end point
During periods of ischaemia and hypoxia, oxygen to describe clinically overt bleeding.19,22 The incidence of
free radicals are generated as byproducts of anaerobic clinically significant bleeding, that is bleeding associated
metabolism. With successful resuscitation of the gastro- with hypotension, tachycardia and a drop in haemoglobin
intestinal tract, blood flow and oxygen delivery are restored level necessitating transfusion, is estimated to be 3–4%.23
but the oxygen free radicals are liberated, contributing to Over time the incidence of stress-related mucosal damage
the microvascular and mucosal changes characteristic of has continued to decrease and this is largely attributed to
ischaemia and reperfusion of the gut mucosa.17 overall advances and improvements in the management of
critically ill patients, particularly optimal resuscitation and
Consequences of gastrointestinal targeted nutritional therapy.24
hypoperfusion Factors influencing the development of stress-related
The consequences of gastrointestinal hypoperfusion are mucosal damage include splanchnic hypoperfusion, which
significant, and include disruption of the physical barrier may influence mucosal ischaemia and reperfusion injury.25
to pathogens; disruption of chemical control of bacterial The mucus–bicarbonate gel layer26 and decreased prosta-
overgrowth; decreased peristalsis; and reduced immuno- glandin levels, which impair mucus replenishment, and
logical activities of gastrointestinal-associated lymphoid increased nitric oxide synthase contribute to reperfusion
tissue. In health, all of these mechanisms work efficiently injury and cell death.27 The protective mechanisms and
to contain bacteria within the gastrointestinal tract. factors that promote injury are detailed in Table 20.2.
During critical illness, however, reduced oxygenation
contributes to decreased cellular function and failure
Risk factors for stress-related
of the protective mechanisms described in Table 20.1. mucosal damage
Consequently, bacterial proliferation and translocation A number of risk factors are associated with the develop-
from the gastrointestinal tract to the systemic circulation ment of stress-related mucosal damage, including respiratory
may occur.17 Changes in gastrointestinal perfusion also failure requiring at least 48 hours of mechanical ventila-
have the capacity to affect hepatic perfusion, oxygen- tion and coagulopathy,38 acute hepatic failure, hypotension,
ation and function. In approximately 50% of critically ill chronic renal failure, prolonged nasogastric tube placement,
patients, ischaemic hepatitis or ‘shock liver’ occurs, which alcohol abuse, sepsis and an increased serum concentration
is evidenced by jaundice, elevation of liver function tests of anti-Helicobacter pylori immunoglobulin A.39
or overt hepatic dysfunction.18 Ischaemic hepatitis can Although the reported prevalence of overt gastrointes-
vary from a mild elevation of serum aminotransferase and tinal bleeding is reported to be between 0.6% and 4%,40,41
654 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 20.2
Factors contributing to stress-related mucosal disease206

FA C T O R S MECHANISM ACTION

Protective Mucosal prostaglandins Protect the mucosa by stimulating blood flow, mucus and bicarbonate production28
mechanisms Stimulate epithelial cell growth and repair
Mucosal bicarbonate Forms a physical barrier to acid and pepsin, preventing injury to the epithelium29
barrier
Epithelial restitution and Epithelial cells rapidly regenerate but the process is highly metabolic and may be
regeneration impaired by physiological stress29
Mucosal blood flow Mucosal blood flow helps remove acid from the mucosa, supplies bicarbonate and
oxygen to the mucosal epithelial cells30
Cell membrane and tight Tight junctions between mucosal epithelial cells prevent the back diffusion of
junctions hydrogen ions31
Factors Acid Acid is a key issue in the pathogenesis of stress-related mucosal injury but not all
promoting critically ill patients hypersecrete acid.31 However, small amounts of acid may still
injury cause injury and the prevention of acid secretion has led to a reduction in injury32
Pepsin May cause direct injury to the mucosa33
Facilitates the lysis of clots22
Mucosal hypoperfusion Reduced mucosal blood flow results in reduced oxygen and nutrient delivery, making
epithelial cells susceptible to injury31
Contributes to mucosal acid–base imbalances
Results in the formation of free radicals
Reperfusion injury Nitric oxide, which causes vasodilation and hyperaemia, is released during
hypoperfusion and results in an increase in cell-damaging cytokines
Intramucosal acid–base The mucus layer protects the epithelium and traps bicarbonate ions that neutralise
balance acid, thus a decrease in bicarbonate secretion results in intramucosal acidosis and
local injury29
Systemic acidosis Results in increased intramucosal acidity30
Free oxygen radicals Generated as a result of tissue hypoxia, free oxygen radicals cause oxidative injury to
the mucosa34
Bile salts Bile salts reflux from the duodenum into the stomach and may have a role in stress-
related damage although the exact mechanism is uncertain35
Helicobacter pylori Conflicting results about the role of H. pylori as a cause of stress-induced mucosal
disease in the critically ill36,37
Reproduced with permission from Marshall AP. The gut in critical illness. In: Carlson K, ed. AACN Advanced critical care nursing.
Philadelphia: Elsevier; 2009, Table 29-3.

when this occurs mortality rates approximate 50%.42 It is common for the majority of critically ill patients
Consequently, there is a strong imperative to implement to receive some form of stress-ulcer prophylaxis during
stress-ulcer prophylaxis, particularly in those patients who their episode of critical illness, likely because of recom-
are considered at risk. mendations from influential groups such as the Surviving
Sepsis Campaign.46 With the risk for clinical substantial
Preventing stress-related mucosal bleeding being low, it is important to consider whether
damage stress-ulcer prophylaxis is always warranted, especially
Prophylaxis for stress-related mucosal damage is often considering the pharmacological therapy is not risk-free
part of the care of the critically ill, although evidence and is associated with economic consequences.47,48 There
demonstrating an added benefit when this therapy is are a variety of pharmacological strategies that can be
applied to those patients who are not identified as at risk used to prevent stress ulcers from developing and, most
for developing stress-related mucosal damage is limited commonly, histamine-2-receptor antagonists (H2RAs)
in both quantity and quality.43,44 A positive impact on and proton pump inhibitors (PPIs) are used as first-line
mortality and intensive care length of stay associated with therapy20 although sucralfate can be used if neither of
stress ulcer prophylaxis is also yet to be established.45 these agents is suitable.49
 CHAPTER 20 GASTROINTESTINAL, METABOLIC AND LIVER ALTERATIONS 655

Histamine-2-receptor antagonists Sucralfate

H2RAs inhibit the production of gastric acid by binding Sucralfate provides protection against stress-related mucosal
to the histamine-2 receptor on the basement membrane of disease through a number of mechanisms. Sucralfate
the parietal cell.20 However, gastric acid secretion may also provides a protective barrier on the surface gastric
occur through stimulation of the acetylcholine or gastrin epithelium, stimulates mucus and bicarbonate secretion,
receptors present in parietal cells;50 therefore, complete stimulates epithelial renewal, improves mucosal blood flow
blocking of gastric acid production does not occur when and enhances prostaglandin release.21 Given orally or via
H2RAs are used. Further limitations of H2RAs are that a nasogastric tube, sucralfate is well tolerated but appears
tachyphylaxis can occur quickly20 and tolerance may to be less effective than H2RAs in decreasing clinically
develop within 72 hours of administration.51,52 Neverthe- significant bleeding.20 Earlier reports comparing sucralfate
less, this pharmacological strategy to prevent stress-related with ranitidine showed a decrease in the development of
mucosal disease remains commonplace in critical care.53 pneumonia in those patients receiving sucralfate; however,
The decrease in gastric acidity as a result of H2RA use may these findings were not supported in a subsequent level I
be beneficial from the perspective of preventing stress- randomised controlled trial.32
related mucosal disease, but changes in gastric pH could
lead to bacterial overgrowth in the stomach, micro-
Enteral nutrition
aspiration and, consequently, an increase in the incidence It is postulated that enteral nutrition has a role in stress-
of nosocomial pneumonia,54 although there is some ulcer prophylaxis because its administration can buffer
research that does not support this notion.55 gastric acid and increase intragastric pH,20 improves
gastric mucosal blood flow60 and promotes the release of
Proton pump inhibitors protective substances such as prostaglandins and mucus.61
PPIs have a greater ability to maintain an increased intra- In critically ill patients, enteral nutrition administration
gastric pH than H2RAs. These drugs work by irreversibly is more effective at increasing intragastric pH than either
binding to the proton pump, effectively blocking all H2RAs or PPIs.62 In a recent systematic review, stress-ulcer
three receptors responsible for gastric acid secretion by prophylaxis with H2RAs reduced the risk of gastrointes-
the parietal cell.56,57 PPIs are also able to limit vagally- tinal bleeding (odds ratio 0.47; 95% confidence interval,
mediated gastric acid secretion.58 0.29–0.76) but this was only observed in a subgroup of
PPIs are more effective than H2RAs in reducing patients who did not receive enteral nutrition63 suggesting
clinically important bleeding and do not appear to increase that, for patients receiving enteral nutrition, stress-ulcer
the risk of nosocomial pneumonia.41 Clinical evaluation prophylaxis may not be warranted. The lack of well-
of the efficacy of PPIs is, however, somewhat limited; few designed prospective studies examining the role of enteral
studies have specifically studied the prophylactic use of PPIs nutrition in stress-ulcer prophylaxis prevents the use of
for stress-related mucosal damage and many have method- this therapy as a sole therapeutic agent for this purpose.
ological limitations.55 PPIs are similar to H2RAs in their
ability to raise the gastric pH above 4, a level considered Intra-abdominal hypertension
adequate to prevent stress ulceration, and the use of PPIs is and abdominal compartment
not associated with the development of tolerance, such that
is seen with the use of H2RAs.20 PPIs are also more likely to syndrome
maintain the pH at greater than 6, which may be necessary Intra-abdominal hypertension (IAH) and abdominal
to maintain clotting in those patients at risk of re-bleeding compartment syndrome have received increased attention
from peptic ulcer.57 However, the administration of PPIs is in recent years and clinical research in this area is on the
associated with an increased risk of developing Clostridium increase. IAH occurs in nearly half of all intensive care
difficile-associated diarrhoea.59 patients and is associated with significant morbidity and
PPIs that may be administered intravenously include mortality. The development of IAH is not isolated to
omeprazole, esomeprazole and pantoprazole. Omeprazole surgical patients or those with abdominal injury, and is
has the highest potential for drug interactions and an important consideration for medical patients without
interferes with the metabolism of some drugs commonly abdominal conditions.
used in intensive care, including cyclosporine, diazepam,
phenytoin and warfarin.27 Pantoprazole has the lowest Aetiology
potential for drug interactions.58 IAH and abdominal compartment syndrome can and
do occur in a variety of patient populations.64 Factors
Practice tip associated with IAH include body mass index, fluid
Stress-ulcer prophylaxis is still commonly used in
resuscitation, multiple transfusions, total sepsis-related
critical illness. Histamine-2-receptor antagonists,
organ failure score and respiratory, renal and coagulation
such as ranitidine, are effective at reducing clinically
sepsis-related organ failure sub-scores. However, only
blood transfusion and the rate of fluid resuscitation are
important bleeding but patients can develop resistance
significantly correlated with IAH.65 There are a number
to these drugs within 72 hours of commencement.
of different risk factors for the development of IAH with
656 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

large volume crystalloid resuscitation, respiratory status it is a sustained increase in abdominal pressure or the devel-
and hypotension being factors that were associated with opment of IAH that affects regional blood flow and impairs
IAH and abdominal compartment syndrome.66 Risk tissue perfusion, contributing to the development of multiple
factors that are more specific to critically ill patients organ failure.69 The pathophysiological consequences occur
include obesity, sepsis, abdominal surgery and ileus. as a direct result of increased pressure within the abdominal
Abdominal compartment syndrome is potentially fatal. cavity, resulting in vascular compression, direct compres-
Consequently, it is imperative that all clinicians be aware sion of the organs and elevation of the diaphragm,70 which
of the underlying physiological changes, assessment and can falsely elevate intracardiac pressures. A summary of the
management in at-risk patients. physiological changes associated with abdominal compart-
ment syndrome is provided in Table 20-3.
Practice tip
Normal intra-abdominal pressure
The critically ill obese patient is at higher risk of In the spontaneously breathing patient, IAP is normally
developing intra-abdominal hypertension and abdom- either atmospheric or subatmospheric. Mechanical
inal compartment syndrome and may benefit from ventilation, however, causes the IAP to increase near
intra-abdominal pressure monitoring. end-inspiration. After abdominal surgery, IAP may be
increased slightly. The patient’s clinical context must be
Pathophysiology considered when evaluating IAP. The most recent grading
Increased intra-abdominal pressure (IAP) results from an system for IAP is provided in Table 20.4.79
increase in pressure within the confined anatomic space Because IAP is variable between patients, it has been
of the abdominal cavity.64 When IAP rises in this closed suggested that abdominal perfusion pressure be calculated
anatomic space, blood flow may be reduced and tissue by subtracting IAP from mean arterial pressure. It appears
viability threatened.67 that the calculation of abdominal perfusion pressure may
This increase in pressure may result from causes such as be a more clinically useful resuscitation end point and is
intraperitoneal bleeding, peritonitis, ascites or distention of statistically superior in predicting survival from IAH and
the gas-filled bowel. Clinical data show that increases in IAP abdominal compartment syndrome than either mean
result in physiological changes in vital organ function.68 arterial pressure or IAP;80 however, further well-designed
Early detection of increases in IAP can be challenging, and research is needed in this area.

TABLE 20.3
Physiological changes associated with abdominal compartment syndrome

SYSTEM PHYSIOLOGICAL EFFECTS

Respiratory Cephalad deviation of diaphragm leads to decreased lung and chest wall compliance71
Peak inspiratory pressures increase64
Functional residual volume and lung capacity are reduced, resulting in ventilation/perfusion mismatching
Hypoxia and hypercarbia may result, necessitating mechanical ventilation
Pulmonary vascular resistance increases72
Cardiovascular Inferior vena cava and portal vein compression results in decreased venous return
Decreased left ventricular compliance68
Artificially increased right atrial pressure, pulmonary artery occlusion pressure73
Decreased cardiac index74
Elevated systemic vascular resistance from arteriolar vasoconstriction and increased intra-abdominal
pressure (IAP)72
Renal Oliguria (IAP 15–20 mmHg)75
Anuria (IAP >30 mmHg)
May be a consequence of decreased cardiac output, compression of renal vessels, increased renal vascular
resistance or redistribution of blood flow to renal medulla71
Gastrointestinal Decreased splanchnic perfusion and tissue hypoxia
Increased GI mucosal acidosis76
Reduced hepatic blood flow64
Abnormalities in normal gut mucosal barrier function that may permit bacterial translocation72
Decreased abdominal wall blood flow68
Increased pressure on oesophageal varices may result in bleeding77
Neurological Increased intracranial pressure because of impaired venous return78

Reproduced with permission from Marshall AP. The gut in critical illness. In: Carlson K, ed. AACN Advanced critical care nursing.
Philadelphia: Elsevier; 2009, Table 29-4.
 CHAPTER 20 GASTROINTESTINAL, METABOLIC AND LIVER ALTERATIONS 657

TABLE 20.4 TABLE 20.5

Intra-abdominal Hypertension Grading System79 Key principles for measuring intra-abdominal
pressure (IAP)
GRADE BLADDER PRESSURE (MMHG)
R E C O M M E N D AT I O N
I 12–15
Measurement • IAP should be measured in mmHg
II 16–20
techniques • Measurement should be recorded at
III 21–25 end-expiration
IV >25 • The transducer should be zeroed at
the mid-axillary line at the level of the
Adapted from Kirkpatrick AW, Roberts DJ, De Waele J,
iliac crest90
Jaeschke R, Malbrain ML, De Keulenaer B et al. Intra-
• Determine measurement 60 seconds
abdominal hypertension and the abdominal compartment
syndrome: updated consensus definitions and clinical after instillation of saline to allow
practice guidelines from the World Society of the Abdominal bladder detrusor muscle to relax91
Compartment Syndrome. Intensive Care Med 2013;39(7): Instillation • A maximum of 25 mL sterile saline
1190–206, with permission. volume should be used as the instillation
volume in adults
• In children the volume instilled
Measurement of intra-abdominal should be 3 mL/kg92

pressure Patient • IAP should be measured in supine

position position, where possible90
Clinical assessment of the abdomen is not a sensitive • IAP is significantly increased when
or accurate technique for detecting increased IAP.81 the head of bed is elevated more
Measurement of pressure within the bladder has been than 20°
validated as closely approximating IAP82 and is the • If head-of-bed elevation is required,
recommended standard approach for the measure- consider the reverse Trendelenberg
ment of intra-abdominal pressure.79 This technique can, position during IAP measurement
however, be influenced by the measurement technique. to minimise compression of the
For example, air bubbles in the system and changes in abdomen by the chest
transducer positions may influence pressure measure-
ment, with wide variations in IAP being noted.83 There
is also little consistency in the amount of fluid used
to prime the bladder; this may result in overestimates in most intensive care units. The procedures for IAP
of IAP.84,85 measurement techniques may differ; however, the key
There are a variety of techniques for measuring IAP principles for performing measurements are outlined in
described in the literature86,87 and the direct peritoneal Table 20.5.
catheter measurement is the most ideal but not the
most practical. IAP measurements should be performed Management of intra-abdominal
when patients exhibit one or more of the risk factors hypertension and abdominal
and the trans-bladder technique is the measurement
technique recommended by the World Society of the compartment syndrome
Abdominal Compartment Syndrome.79 The reliabil- Surveillance for IAH and abdominal compartment
ity of other methods, such as intragastric measurement, syndrome requires close observation of the patient to
is not well demonstrated in clinical practice.88 identify potential risk factors and relevant changes to
Continuous measurement of IAP is becoming more physiological parameters. For those patients who are
common.89 at risk, close monitoring of IAP is required and pre-
emptive measures are instituted. For example, a decision
Practice tip may be made to delay closure of the abdomen or to
use an alternative means of abdominal content coverage.
The trans-bladder technique is the most common
For the nonsurgical patient, optimal resuscitation may
method used for measuring intra-abdominal pressure.
be important in preventing IAH; over-resuscitation
Attention should be given to consistent and accurate
measurement to track trends.
needs to be avoided. The approach to managing the
patient with IAH or abdominal compartment syndrome
IAP measurement should be accurate and reproduc- is dependent on their clinical presentation. The World
ible. There are a number of commercial devices now Society of the Abdominal Compartment Syndrome
available to aid the measurement of IAP; however, these has developed evidence-based management algorithms
are not required and a measurement system can easily that are useful in guiding clinical management (see
be created from existing equipment normally available Figures 20.1 and 20.2).
658 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

FIGURE 20.1 Intra-abdominal hypertension and abdominal compartment syndrome management algorithm.79

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 CHAPTER 20 GASTROINTESTINAL, METABOLIC AND LIVER ALTERATIONS 659

FIGURE 20.2 Intra-abdominal hypertension and abdominal compartment syndrome medical management algorithm.79

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from the World Society of the Abdominal Compartment Syndrome. Intensive Care Med 2013;39(7):1190–206, Figure 2.
660 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

The critically ill patient with TABLE 20.6

diabetes Comparison of presentation and electrolyte deficits in
DKA and HHS105
Diabetes is a major cause of morbidity and mortality
worldwide.93 The prevalence of diabetes internationally is P R E S E N TAT I O N DKA HHS

rising and follows a global trend.94 Reasons for this include Prodromal illness Days Weeks
an increase in the rates of obesity, physical inactivity, Coma ++ +++
the ageing population, better detection of diabetes and Blood glucose ++ +++
longer survival of affected individuals.95 The prevalence Ketone +++ 0 or +
of diagnosed diabetes continues to increase worldwide, Acidaemia +++ 0 or +
in adults as well as youth.96 In 2013, a reported 382 Anion gap ++ 0 or +
million people worldwide had diabetes and this number Osmolality ++ +++
is projected to increase to 592 million by the year 2035.97 TYPICAL DEFICITS
Worryingly, reports of undiagnosed diabetes are on the
Total water (litres) 6 9
increase with type 2 diabetes remaining undetected for
Water (mL/kg) 100 100–200
many years, particularly in developing countries.98
Na+ (mmol/kg) 7–10 5–13
Aetiology of diabetes Cl− (mmol/kg) 3–5 5–15
Diabetes mellitus is a disorder of metabolism that is charac- K+ (mmol/kg) 3–5 4–6
terised by glucose intolerance. Diabetes is not a single disease PO4 (mmol/kg) 5–7 3–7
per se, but a group of heterogeneous disorders where the Mg2+ (mmol/kg) 0.5–1.0 0.5–1.0
aetiology of glucose disturbance is multifactorial. Ongoing Ca2+ (mmol/kg) 0.5–1.0 0.5–1.0
effect of poor glycaemic control can ultimately contribute Adapted with permission from Keays RT. Diabetic
to the development of end-organ damage. In the long term, emergencies. In: Bersten AD, Soni N, eds. Oh’s intensive care
diabetes is associated with increased morbidity and mortality manual. 6th ed. Philadelphia: Elsevier; 2009, pp 613–20.
but acute complications of diabetes, such as diabetic ketoaci-
dosis and hyperosmolar hyperglycaemic state, may necessitate
patient management in the intensive care unit. Pathophysiology
The metabolic profile seen in DKA is similar to that seen
Acute complications of diabetes in the fasting state, with substrate utilisation shifting from
Diabetic ketoacidosis (DKA) and hyperosmolar hyper- glucose to fat in insulin-sensitive tissues (fat, liver, muscles).
glycaemic state (HHS) are two extremes of what can The brain is insulin-insensitive, and requires a continuous
occur when a deficiency in insulin is present.99 DKA supply of glucose to support metabolism even in a fasting
is a metabolic derangement resulting from a relative or state or DKA.106
absolute insulin deficiency, characterised by hypergly- Inadequate production (or administration) of insulin
caemia (>11.1 mmol/L), metabolic acidosis (pH <7.3) to meet metabolic need (or a rise in metabolic demand
and ketosis (raised blood ketone bodies or ketonuria).100 It resulting from the stress of infection, trauma or surgery,
is usually precipitated, in insulin- and non-insulin-depen- for instance) is associated with a rise in the secretion
dent diabetics, by infection or the omission (or inadequate of the counter-regulatory hormones glucagon, the
dosing) of insulin.101 It may also be the cause of the first catecholamines and cortisol.107 The effects of the counter-
presentation in new-onset diabetes. Additionally, DKA regulatory hormones are presented in Box 20.1.
is increasingly being identified in patients with type 2
diabetes.102 BOX 20.1
HHS is seen more often in older patients with type 2
diabetes, and is characterised by hyperglycaemia and Effects of counter-regulatory hormones in DKA108,109
the pathological consequences of extreme dehydration. • Catecholamines:
Unlike DKA, where there is insufficient insulin, in HHS Promote lipolysis, resulting in the production
insulin excretion is maintained, so lipolysis and ketoacido- of FFA and glycerol; FFA and glycerol used as
sis do not feature. Although DKA and HHS are considered precursors for gluconeogenesis
separate entities, DKA and HHS may coexist in about a • Glucagon:
third of cases, especially among older patients.103 Stimulates gluconeogenesis
While these are often considered two distinct states, • Cortisol:
Promotes lipolysis
they can present simultaneously.104 DKA usually occurs
Promotes protein breakdown and release of
much more quickly with the onset of HHS being more
amino acids
insidious. Both complications are characterised by polyuria,
Promotes hepatic gluconeogenesis
polydipsia and weight loss. Patients with DKA can also
present with nausea and vomiting.105 A comparison of DKA = diabetic ketoacidosis; FFA = free fatty acids.
DKA with HHS is provided in Table 20.6.
 CHAPTER 20 GASTROINTESTINAL, METABOLIC AND LIVER ALTERATIONS 661

Hyperglycaemia results from increased gluconeo- has been variable, there is evidence to suggest that a stan-
genesis (glucose production from precursors other dardised approach can have a positive impact on patient
than carbohydrates, e.g. amino acids), the conversion outcome.113,114
of glycogen stores to glucose (glycogenolysis) and Management of HHS is similar to that for DKA, and
the reduced uptake of glucose resulting from insulin includes: respiratory support; fluid replacement; insulin
deficiency.107 Free fatty acids and glycerol are produced treatment to turn off ketogenesis and the accompany-
by the breakdown of triglycerides that results from ing metabolic derangement; electrolyte replacement;
increased catecholamine secretion.107 Metabolism of correction of acidosis (in DKA); monitoring for and
free fatty acids results in accumulation of ketone bodies prevention of complications of hypoglycaemia, hypo-
or ketoacids (acetone, beta-hydroxybutyrate, acetoace- kalaemia, hyperglycaemia and fluid volume overload; and
tate).107 These compensatory mechanisms are ultimately patient teaching and support.100,115,116 Assessment of blood
responsible for the pathophysiological effects seen in glucose levels is essential.
DKA (see Table 20.7). The pathophysiology of DKA is Effectiveness of treatment is usually assessed by
illustrated in Figure 20.3. resolution of the acidosis and the control of hyperglycae-
mia. Regular testing of arterial blood gases, blood sugar and
Management of diabetic ketoacidosis electrolytes (especially potassium) is vital until the blood
and hyperosmolar hyperglycaemic state sugar has stabilised and the ketosis and acidosis resolves.105
Management of DKA involves rehydration and electro- Considering that fewer patients are now admitted to ICU
lyte replacement, insulin administration, correction of with DKA and HHS, understanding the management of
acidosis and treatment of the precipitating factor.106,112 these patients is vital and protocols have been developed
Although historically the approach to managing DKA to guide practice.115,116

FIGURE 20.3 Pathophysiology of diabetic ketoacidosis.106,108

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TABLE 20.7
Pathological effects of diabetic ketoacidosis (DKA)

MECHANISM ACTION

Cellular dehydration • Hyperglycaemia increases the extracellular fluid osmolality and results in water movement from the cell
and intravascular • Osmotic diuresis results from obligatory excretion of glucose in the urine
volume depletion • Osmotic diuresis results in reduction of total body water and severe dehydration
Metabolic acidosis • Ketoacids are fully dissociated at physiological pH (strong acids). Because of the complete dissociation,
acetoacetate and beta-hydroxybutyrate are strong ions (anions)108
• The metabolic acidosis is explained by extracellular (and intracellular) buffering of the dissociated H+,
resulting in a decrease in bicarbonate. Alternatively, the acidosis can be explained by accumulation
of strong anions (acetoacetate and beta-hydroxybutyrate) with resulting reduction of the strong ion
difference, causing an increased H+ dissociation from plasma water and thus a metabolic acidosis110,111
• The presence of ketone bodies widens the anion gap, strong ion gap and base excess gap. These
‘gaps’ can be used to assess the degree of ketonaemia. As ketosis resolves, acidosis caused by high
chloride relative to sodium levels is often seen and probably results from administration of normal
saline in the initial resuscitation, especially in the setting of decreased renal function where the ability to
excrete chloride is reduced
Electrolyte • The osmotic diuresis results in potassium, phosphate and magnesium loss
imbalances • Total body potassium losses are particularly significant, as potassium shifts from the intracellular to
the extracellular space in concert with the osmotically driven water shift. Acidosis and lack of insulin
exacerbates the potassium shift. The final pathway for potassium loss is via the urine108

Blood ketones (beta-hydroxybutyrate) can now reference to ketones in addition to usual blood sugar
easily be measured using blood from a finger prick with monitoring.117An outline of the treatment of DKA and
a bedside handheld monitor. It has been suggested that HHS is presented in Table 20.8.
blood ketone monitoring allows for insulin titration with

TABLE 20.8
Treatment of DKA and HHS105,106

ISSUE T R E AT M E N T C O N S I D E R AT I O N S

Dehydration and • Intravenous fluid is initially given to restore intravascular volume. Isotonic fluid such as normal saline or
sodium loss a colloid solution may be used. Solutions containing sodium are used in order to replace sodium lost as
a result of the osmotic diuresis
• Assessment of volume status is undertaken using basic clinical assessment, such as heart rate, blood
pressure, urine output (allowing for the possibility of continuing osmotically-driven diuresis) or invasive
haemodynamic monitoring
• Hypotonic solutions are added after the initial fluid resuscitation to correct the total body water deficit
• Adequate resuscitation and rehydration reduces the effect of the counter-regulatory hormones
Insulin therapy • A soluble insulin is usually administered via continuous infusion to allow rapid titration of dose
• Blood glucose levels and blood chemistry should be regularly monitored
• Care is taken to prevent too rapid a change in blood sugar level, as this will cause a rapid reduction in
the extracellular fluid osmolarity. This rapid reduction would result in fluid shift from the extracellular
space to the intracellular space, which may result in cerebral oedema
• There is a risk of hypoglycaemia resulting from insulin therapy. Sympathetic activation accompanies
a low blood glucose level and results in sweating, tremor, tachycardia and anxiety. Reduced blood
glucose levels also cause global central nervous system depression and result in decreased level of
consciousness and possibly fitting. Severe hypoglycaemia with a blood glucose level <2 mmol/L is a
medical emergency and is treated with administration of 50 mL 50% glucose
Electrolytes • Intravenous potassium replacement will be required
• Plasma potassium levels will fall rapidly as a result of commencement of insulin therapy and, to a lesser
extent, with rehydration. Insulin causes the lowering of plasma potassium by mediating the re-entry of
potassium into the intracellular compartment
• Phosphate and magnesium replacement may be required
 CHAPTER 20 GASTROINTESTINAL, METABOLIC AND LIVER ALTERATIONS 663

Liver dysfunction a result of cellular stress and the triggering of apoptotic

pathways, leading to programmed cell death. Major factors
The liver is responsible for a vast array of metabolic functions. for the triggering of the apoptotic pathway are hypoxia
It performs the vital functions of controlling metabolic causing ischaemia and reperfusion; reactive oxygen
pathways, participating in digestion, immunological metabolites resulting from alcohol or drug ingestion;
protection, detoxifying chemicals and clearing toxins and accumulation of bile acids resulting from cholestasis; and
drugs. This means that alterations to normal liver function inflammatory cytokines such as tumour necrosis factor
can have broad-ranging consequences, from changes alpha (TNF-α).119 The apoptotic pathway results in the
in metabolic processes (such as glucose homeostasis), deconstruction of the cellular structure from the inside
failure to produce clotting factors (with resultant severe out, while necrosis results in cell rupture and release of
haemorrhage) to other organ effects such as brain, lung cellular contents. Although these processes may overlap, it
and kidney impairment and injury. Accordingly, liver is thought that the apoptotic pathway is a way of preventing
dysfunction can impact substantially on the nursing care the inflammatory response that is triggered with cell
needs of the critically ill patient. necrosis. The activation of the inflammatory response
Related anatomy and physiology results in secondary liver cell injury and contributes to the
multiple organ dysfunction seen in liver failure. 119,120
The liver is the largest internal organ, weighing The degree and time course of liver cell damage from
approximately 1200 to 1600 g in the adult. It receives viral hepatitis depends on the immune response. Immune
approximately 25% of total cardiac output through a recognition and destruction of infected cells may result
dual vascular supply consisting of the hepatic artery and in either clearance of the virus or ongoing inflammation,
portal vein. Approximately 75% of all hepatic blood flow
cell death and fibrosis if the virus is not cleared. This
arises from the portal vein with the remaining 25% from
process may progress over 20–40 years to cirrhosis and
the hepatic artery. Anatomically, the liver consists of four
hepatocellular carcinoma.121 Chronic excessive alcohol
lobes: the major left and right lobes and the minor caudate
intake may also result in a slower chronic course of liver
and quadrate lobes. The right lobe is considerably larger
injury that eventually results in cirrhosis, liver failure or
than the left. Functionally, the liver is divided into eight
segments each with their own inflow and outflow blood hepatocellular carcinoma.122
supply and biliary drainage. Hepatic lobules, or liver acinus, Liver cells may also be injured by the toxic effects of
are small units consisting of a single or double layer of drugs or their metabolites, as in paracetamol overdose, or
hepatocytes arranged in plates interspersed with capillaries by therapeutic doses of drugs such as non-steroidal anti-
(sinusoids) that receive inflowing blood from the portal inflammatory drugs, phenytoin or antimalarial agents.
and hepatic pathways. To protect the systemic circulation Other poisoning from the ingestion of mushrooms (e.g.
from the toxins absorbed from the intestines, the sinusoids Amanita phalloides) and from the use of recreational drugs
are lined with macrophages known as Kupffer cells. The such as ecstasy and amphetamines may result in liver cell
hepatic vein then drains effluent blood from the liver into death and liver failure.123–125 Diseases of the biliary system
the general circulation. such as primary biliary cirrhosis and primary sclerosing
The liver is responsible for the synthesis and drainage cholangitis also result in liver dysfunction and failure.126,127
system for bile (used in the breakdown and absorption The liver has a remarkable regenerative capacity. After
of lipids from the intestine). Biliary salts are formed from injury and necrosis, liver cells rapidly regenerate around
multiple enzymatic reactions in the hepatocytes. Bile areas of surviving cells to restore the lost tissue while
drains from the hepatocytes into bile ducts and then into maintaining homeostasis during hepatic regeneration.128,129
the common hepatic duct, before passing into the gall However, with chronic injury, fibrosis or scarring occurs,
bladder via the common bile duct.118 resulting in the loss of the functional architecture and
The arrangement of the circulation to the liver with cell mass and ultimately in cirrhosis. Cirrhosis results
its rich vascular architecture enables it to perform the vital in destruction of the normal liver vasculature, increased
functions of carbohydrate, fat and protein metabolism; resistance to blood flow and back pressure into the portal
production of bile to aid in digestion; production, circulation. Dilation of the venous system leading into the
conjugation and elimination of bilirubin; immunological liver results in the formation of varices.130
and inflammatory responses; glycogen storage; and Liver cell injury may occur to such a degree that a
detoxification of toxins and drugs. As the kidneys are critical amount of hepatic necrosis results in the failure of
responsible for clearance of water-soluble toxins from the liver to maintain metabolic, synthetic and clearance
the body, the liver clears protein (largely albumin)-bound functions leading to death. Liver cell injury may also occur
toxins and excretes them into the gastrointestinal tract more slowly, giving rise to chronic liver injury.131
for elimination, or reabsorption in water-soluble form for
subsequent renal excretion.118 Epidemiology of viral hepatitis
Worldwide, the incidence of hepatitis B and C is
Mechanisms of liver cell injury estimated to be 390 million. 121,132–135 This has led to a high
Liver cell injury and death can occur either as a direct mortality rate from hepatitis accounting for approximately
result of injury to the cell, resulting in cell necrosis, or as 1.3 million deaths worldwide annually.136,137 In Australia
664 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

and New Zealand, chronic hepatitis B and hepatitis C residual function to maintain homeostasis, and liver
viral infections are the major cause of hepatic dysfunction transplantation is the only viable treatment. However,
that may lead to cirrhosis and hepatocellular carcinoma. in AoCLF, the function of the residual liver cell mass
While the prevalence of hepatitis B in Australia and may be adequate to maintain hepatic homeostasis if the
New Zealand is generally low, newly diagnosed infection precipitating event can be treated.
rates are predominantly related to people with a recent Liver dysfunction is also a common consequence
history of injecting drug use.138 In Australia in 2013, of critical illness, and may be caused by inadequate
approximately 230,000 people were living with chronic perfusion leading to ischaemic injury or as a result of
hepatitis C infection, with 58,000 in the moderate-to- the inflammatory response in sepsis. Given the number
severe liver disease category.138 It should be noted, however, of drugs that critically ill patients receive, the possibility of
that approximately 25% of people with hepatitis C virus liver injury as a result of drug reactions and toxicity should
exposure have cleared the virus and are not chronically always be considered.
infected. Also, many patients can be cured of hepatitis C
virus due to newer therapies; however, lack of access to Consequences of liver failure
antiviral therapy may limit the number of people who can The consequences of liver failure manifest as a syndrome
be successfully treated and reducing newer infections is a of hepatic encephalopathy (HE), hepatorenal syndrome
major focus of health organisations.139 (HRS), oesophageal and gastric varices, ascites, respiratory
Liver dysfunction/failure compromise, haemodynamic instability, susceptibility to
infection, coagulopathy and metabolic derangement.140
Liver dysfunction can be acute or chronic. Chronic
liver disease is usually associated with cirrhosis and can Hepatic encephalopathy
develop from viral (hepatitis B and C), drug (alcohol), Hepatic encephalopathy is a reversible neuropsychiatric
metabolic (Wilson’s disease) or autoimmune (primary complication due to metabolic dysfunction associated
biliary cirrhosis) conditions. Acute liver failure (ALF) with liver disease.144 The cerebral effects of liver failure may
is an uncommon condition associated with rapid liver manifest as an altered sleep–wake cycle, mild confusion/
dysfunction leading to jaundice, hepatic encephalopathy disorientation, asterixis and coma. Patients with AoCLF
and coagulopathy.140 Terminology for acute liver failure is may develop a mild degree of cerebral oedema, while a
not standardised and several terms have been proposed, differential feature of ALF is the risk of death from cerebral
including acute hepatic failure and fulminant hepatic
oedema and raised intracranial pressure.145
failure. Historically, fulminant hepatic failure was used to
The exact mechanisms responsible for the develop-
refer to the rapid onset of liver failure accompanied by
ment of hepatic encephalopathy are unknown, although
hepatic encephalopathy within 8 weeks of diagnosis in
raised ammonia levels resulting from the failure of the liver
the absence of pre-existing liver disease.141 Unfortunately,
this was problematic because determining the onset urea cycle are thought to be central to the pathogenesis.
of jaundice and encephalopathy is often difficult and The raised ammonia levels disrupt the blood–brain barrier,
coagulation results, such as INR, are more reliable which leads to the development of cerebral oedema.
indicators of liver failure. It has also been proposed that Ammonia levels also seem to be related to the disruption
‘hyperacute’, ‘acute’ and ‘subacute’ liver failure should of neurotransmission, resulting in decreased cerebral
be used instead,142 with hyperacute referring to the function.145,146 In addition, reactive oxidative species
development of encephalopathy within 7 days of the causing oxidative stress and inflammatory cytokine release
onset of jaundice, acute related to 8–28 days from jaundice have been suggested; however, the exact pathophysiology
to encephalopathy and subacute liver failure when is yet to be fully elucidated.147
encephalopathy occurs within 5–12 weeks of the onset Hepatic encephalopathy is usually classified using the
of jaundice.142 It has further been proposed that acute West Haven criteria,148 a four-stage scale, according to
and subacute hepatic failure should be used;143 however, the severity of clinical signs and symptoms (Table 20.9).
universal acceptance of these terms has not occurred with Although used in clinical practice, the West Haven criteria
clinical use of all of the above terms. have poor sensitivity and no inherent metric component.
Acute liver failure without pre-existing liver disease For instance, in patients with grades III–IV encephalopathy,
can result from drug reactions, toxins or viral infection, the Glasgow Coma Scale (GCS) is probably a more
or from the effect on inflammatory mediators released in sensitive tool for neurological assessment.145 Accordingly,
response to tissue injury. Liver failure can also occur as an other grading criteria have been proposed but are yet to
acute decompensation of chronic liver disease, described as be validated in large clinical trials.149,150
acute-on-chronic liver failure (AoCLF), or as an end-stage
decompensation in chronic liver failure. AoCLF can be Hepatorenal syndrome
precipitated by bacterial or viral infection, bleeding or Hepatorenal syndrome (HRS) is the development of
intoxication, and results in the same clinical syndrome as renal failure in patients with severe liver disease (acute or
seen in ALF.140 chronic), in the absence of any other identifiable cause
End-stage decompensation of chronic liver failure of renal dysfunction. HRS that develops rapidly in the
represents irreversible deterioration with inadequate setting of ALF or AoCLF is classified as type 1 HRS, while
 CHAPTER 20 GASTROINTESTINAL, METABOLIC AND LIVER ALTERATIONS 665

TABLE 20.9 Practice tip

West Haven grading of hepatic encephalopathy148
Coagulation state and the risk of trauma to varices
GRADE CHARACTERISTICS should be carefully considered before insertion of
nasogastric or orogastric tubes, or suctioning of the
I Trivial lack of awareness
Euphoria or anxiety
upper airway. Trauma may result in epistaxis with
Shortened attention span significant bleeding or variceal bleeding.
Impaired performance of simple tests, e.g. addition
II Lethargy or apathy
Ascites
Subtle personality changes Ascites is usually present in patients with chronic liver disease.
Inappropriate behaviour In the ICU setting it becomes an issue when abdominal
III Somnolence to semi-stupor, but unresponsive to
pressures rise, resulting in reduced cardiac output due to
verbal stimuli decreased venous return and renal impairment. Pressure
Confusion on the diaphragm causes loss of lung volume, resulting in
Gross disorientation increased work of breathing and compromised oxygenation.
IV Coma: unresponsive to verbal or painful stimuli Respiratory compromise
Patients with liver failure may have poor oxygen exchange,
type 2 HRS is slowly progressing and is usually associated fluctuating GCS that requires intubation for airway protec-
with diuretic-resistant ascites.151 tion and hepatopulmonary syndrome. Hepatopulmonary
The pathophysiological features of HRS appear to syndrome is found in 15–20% of patients with cirrhosis.156
be caused by an inflammatory response from the injured It is defined as pulmonary microvascular dilation resulting
liver, resulting in upregulation of nitric oxide production in impaired oxygenation, and it is generally assumed that
that results in splanchnic vasodilation.152,153 Splanchnic vascular production of vasodilators, specifically nitric oxide,
vasodilation results in redistribution of circulating blood underlies the vasodilation in hepatopulmonary syndrome.
volume and a lowered mean arterial pressure. The It has also been hypothesised that the mechanisms that
reduction in perfusion pressure results in an enhanced trigger hepatopulmonary syndrome are the same as those
sympathetic nervous system response and local renal that result in the hyperdynamic circulation (low systemic
autoregulatory responses. The net result of these effects vascular resistance and high cardiac output) seen in liver
is a reduction in renal blood flow and increased activity failure.156 Other factors, such as pleural effusions or severe
of the renin–angiotensin–aldosterone system, resulting ascites, may impinge on ventilation.
in sodium (aldosterone) and water retention (arginine Haemodynamic instability, susceptibility
vasopressin; see Chapter 18).
to infection, coagulopathy and
Practice tip metabolic derangement
A hyperdynamic, low vascular resistance picture, similar
Avoid using lactate- or citrate-buffered substitution/ to that associated with sepsis, is seen in liver dysfunction.
dialysis fluid for renal replacement therapy in patients This probably results from the production of vasodilator
with liver dysfunction, as they will be unable to substances (nitric oxide) from the inflammatory response of
metabolise the lactate or citrate and will develop an the injured liver cells.157 Sepsis may also be a complication
increasing metabolic acidosis. of liver dysfunction because of the failure of the liver to
produce acute-phase proteins and the impaired function
Varices and variceal bleeding of Kupffer cells.158
The development of varices and variceal bleeding arises Hepatocyte damage leads to a decreased production of
from portal hypertension. This manifests when blood the majority of clotting factors and, therefore, haemostasis.
flowing from an area of high pressure (i.e. the cirrhotic Hence, the risk of bleeding is elevated.159 Disordered
liver) to areas of lower pressure (i.e. the collateral metabolic function and failure of synthetic function can
circulation, involving veins of the oesophagus, spleen, manifest as unstable blood glucose levels.
intestines and stomach) causes the tiny, thin-walled vessels
to become engorged and dilated, forming varices that are Practice tip
vulnerable to gastric secretions, resulting in rupture and Patients in ALF or AoCLF are at risk of hypoglycaemia,
haemorrhage.154 Variceal haemorrhage is a major cause of and blood glucose levels should be measured routinely.
acute decompensation and a reason for admission to the
ICU. It is an acute clinical event characterised by severe
gastrointestinal haemorrhage presenting as haematemesis, Patient management
with or without melaena, and haemodynamic instability Early signs of the patient presenting with ALF are
(tachycardia and hypotension).155 malaise, loss of appetite, fatigue, nausea, jaundice, bruising,
666 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

bleeding, inflamed/enlarged liver, possibly epigastric and Neurological considerations

right-upper-quadrant pain, deranged liver function tests, Cerebral oedema is present in 80% of patients with grade IV
fluctuating GCS due to cerebral oedema and high or low encephalopathy and is the leading cause of death due to
blood glucose levels.140 Fluctuating blood glucose levels brain herniation.160 Patients with cerebral oedema and raised
may require close monitoring, at least every 4 hours; intracranial pressure due to ALF are managed primarily as
patients may require insulin infusion or 10–50% dextrose patients with acute head injury (see Chapter 17).
infusion to maintain normoglycaemia. If acute liver failure
is suspected, admission to an ICU is recommended to Assessment of liver function
monitor for further deterioration, and provide supportive Patients presenting with ALF require a careful history to
management and airway protection. The patient establish the cause of liver injury. The well-known signs of
presenting with AoCLF will have similar symptoms but chronic liver disease (e.g. palmar erythema, spider naevi and
will present with other unique characteristics. Cirrhosis ascites) may not be present. Biochemical and haematological
and portal hypertension will often lead to oesophageal and tests determine whether liver cell injury is occurring,
gastric varices, ascites, hepatorenal and hepatopulmonary with liver synthesis and clearance functions assessed by
syndrome, malnutrition, bone disease, sepsis, palmar albumin level and prothrombin time, and bilirubin level,
erythema, spider naevi and feminisation in males.122 If liver respectively.161 These measures have been incorporated
failure is suspected, investigating ingestion of hepatotoxic into a scoring system to determine liver dysfunction and
substances, such as paracetamol, steroids and ethanol, prognostic information for liver transplantation suitability
oral or intravenous recreational drug use and any recent (model for end-stage liver disease [MELD], see later in this
travel that might have exposed the patient to viral chapter under Liver transplantation).162 Liver function test
infections is required. values and indications are listed in Table 20.10.

TABLE 20.10
Liver function tests163

BLOOD TEST N O R M A L VA L U E DESCRIPTION

Alanine ALT: <35 U/L • ALT and AST are enzymes that indicate liver cell damage; they are produced within
aminotransferase AST: <40 U/L the liver cells (hepatocytes) and leak out into the general circulation when the liver
(ALT) and cells are damaged
aspartate • ALT is a more specific indication of liver inflammation
aminotransferase • In acute liver injury, ALT and AST may be elevated to the high 100s, even 1000s, of U/L
(AST) • In chronic liver damage, such as hepatitis or cirrhosis, there may be mild-to-
moderate elevation (100–300 U/L)
• ALT and AST are commonly used to measure the course of chronic hepatitis and the
response to treatments
Alkaline ALP: 25–100 U/L • These are enzymes that indicate obstruction to the biliary system
phosphatase GGT: males <50 • They are produced in the liver, or within the larger bile channels outside the liver
(ALP) and U/L; • GGT is used as the supplementary test to be sure that a rise in ALP is indeed
gamma-glutamyl- females <30 U/L coming from the liver or biliary tree
transpeptidase • A rise in GGT but normal ALP may indicate liver enzyme changes induced by alcohol
(GGT) or medications, causing no injury to the liver
• ALP and GGT are commonly used to measure bile flow obstructions due to
disorders such as gallstones, a tumour blocking the common bile duct, biliary tree
damage, alcoholic liver disease or drug-induced hepatitis
Bilirubin < 20 micromol/L Results from the breakdown of red blood cells. Thus bilirubin is protein-bound and
circulates in the blood in an unconjugated form. The liver processes bilirubin to a water-
soluble conjugated form that is excreted in the urine and faeces.
• Liver injury or cholestasis results in an elevated bilirubin level
• Raised unconjugated bilirubin without an accompanying rise in conjugated bilirubin
is consistent with red blood cell destruction (haemolysis)
• Raised bilirubin levels result in jaundice
• In cases of chronic liver disease, bilirubin levels usually remain normal until
significant damage occurs and cirrhosis develops
• In cases of acute liver failure (ALF), bilirubin levels will rise rapidly and result in
marked jaundice; the degree of rise is indicative of the severity of illness
Albumin 32–45 g/L • Albumin is a major protein formed by the liver; it provides a gauge of liver synthetic
function (i.e. albumin levels are lowered in liver disease)
 CHAPTER 20 GASTROINTESTINAL, METABOLIC AND LIVER ALTERATIONS 667

Treatment and the Linton tube. The Sengstaken-Blakemore is a

ALF or AoCLF therapy often involves the support and four-lumen tube with oesophageal and gastric balloons,
treatment of the consequences of liver failure, such as and oesophageal and gastric aspiration ports. The benefit
sepsis, encephalopathy, renal failure and coagulopathy (see of this tube is that direct pressure can be applied to
Table 20.11).Treatments are usually directed to supportive gastric and oesophageal varices by balloon inflation and
therapy, depending on the severity of manifestation; traction.166 The Linton tube has one lumen for inflation of
however, liver transplantation is used according to the pear-shaped gastric balloon and two additional lumens
selection criteria in acute liver failure and several different for oesophageal and gastric aspiration.
liver support systems have been trialled without long-term Prior to insertion (oral or nasal), balloons are lubricated,
survival benefits.164 checked for leakage and the distance to the cardio-
oesophageal junction is estimated (nose to ear, then to
Oesophageal balloon tamponade and xiphisternum). Once inserted, the gastric balloon is inflated
transjugular intrahepatic portosystemic with 50 mL air and pulled back until resistance is felt.
stent/shunt Position (lying compressed against the cardio-oesophageal
There are two types of balloon tamponade devices junction) is confirmed by X-ray. Then, the gastric balloon
available on the market: the Sengstaken-Blakemore tube is inflated according to the manufacturer’s instructions and

TABLE 20.11
Treatment of liver failure complications

CONDITION T R E AT M E N T

Hepatic • Treatment revolves around general supportive therapy until liver function recovers or liver transplant is
encephalopathy undertaken145,146
• Cerebral oedema and raised intracranial pressure are treated as for an acute head injury (see Chapter 17)
• Reduce production and absorption of ammonia by preventing/controlling upper gastrointestinal bleeding
and gastrointestinal administration of non-absorbable disaccharides such as lactulose or lactitol to
remove protein derived from dietary intake or bleeding165
Hepatorenal • Liver transplant is the primary treatment for type 1 HRS in patients with cirrhosis
syndrome (HRS) • If transplant is contraindicated or delayed, vasoconstrictors (e.g. terlipressin) may be effective in
constricting the dilated splanchnic arterial bed, thus improving renal perfusion pressure and renal
function. Vasoconstrictors may be given in association with intravenous albumin in order to increase
intravascular volume152,153
Variceal bleeding A successful outcome, as in all cases of gastrointestinal haemorrhage, hinges on prompt resuscitation,
haemodynamic support and correction of haemostatic dysfunction, preferably in the intensive care setting.
• The patient is intubated for airway protection
• Adequate intravenous access in inserted, preferably large, wide-bore cannulas for rapid fluid resuscitation
• Haemodynamic instability is corrected with volume expanders initially and then blood products
• The source of bleeding is identified by endoscope, and varices are banded/ligated (latex bands placed
around the varices to ‘strangle’ the vessel), or sclerotherapy or diathermy (heat used to cauterise
bleeding vessel) is used
• Terlipressin and octreotide infusions may be used to reduce portal circulation pressure
• If bleeding is uncontrollable, a balloon tamponade device is inserted
Ascites Salt and water restrictions along with diuretic therapy are methods that have been used to control ascites in
the preliminary phases of end-stage liver failure; however, in the intensive care setting these measures are
impractical and usually unsuccessful.
• Paracentesis is very effective at reducing ascites and is a simple procedure to remove fluid and an aid in
diagnosis
• Correction of coagulopathy or thrombocytopenia should be considered when the INR is greater than 2.5
or the platelet count is markedly reduced
• Paracentesis may aid in determining the cause of ascites (ascites-serum albumin gradient, ascitic
cytology, microscopy and culture for acid-fast bacilli, chylous ascites) and in establishing or excluding
primary or secondary peritonitis in patients with ascites (ascitic white cell and neutrophil count, culture)
• Litres of ascites are normally removed, and the volume is replaced with IV concentrated albumin to
prevent fluid shifts and hypotension
• Mean arterial pressures, central venous pressures, heart rate and urine output are carefully monitored
during the procedure
668 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

traction is applied using a weight (500 or 1000 mL IV fluid Liver transplantation

bag) attached to rope; traction is applied via a pulley and IV
pole at the foot of the bed. Nursing care of patients involves: Liver transplantation is the definitive treatment for
patients suffering acute and chronic end-stage liver failure
• sedation for comfort when other supportive critical care therapies have been
• head of the bed raised at least 30° to facilitate gastric exhausted.161,174 Over the past 20 years, survival after liver
emptying and prevent aspiration
transplantation has improved, which has been related
• ensuring that gastric/oesophageal ports are on to better pre-transplant and postoperative therapies
free drainage, with regular monitoring of type and and increases in intraoperative surgical refinement and
amount of drainage management.175 This has also reduced time in critical care
• ensuring that correct traction is maintained, with and reduced overall hospital length of stay. Survival rates
regular checking of tube migration and checking of all patients who have undergone liver transplantation
position at nares/lips at regular intervals (4/24 hours).166 exceed 80% at 1 and 5 years,176,177 with children having
Tamponade is generally maintained for 24–48 hours, superior survival rates to adults.176 Acute liver failure
then traction is removed and the balloon deflated to assess patients accounted for 7% in the USA and 8% in Europe
for further bleeding. If the patient is stabilised, endoscopy of all liver transplantations with lower survival rates (68%
can be performed. If bleeding persists, the balloon(s) is/are at 5 years) compared to all liver transplants.175
reinflated and traction reapplied.166
Once the patient has been stabilised, a transjugular
Indications for transplantation
intrahepatic portosystemic stent/shunt, also known as Indications for liver transplantation are patients with severe
TIPS, may be considered to control variceal haemorrhage. liver disease in whom alternative treatments have been
TIPS is a metal expandable stent inserted to decompress exhausted. Categories consist of acute liver failure, end-stage
the portal venous system.167 liver disease, metabolic liver disease and primary liver
cancer.178 Timing and patient selection is of critical impor-
Extracorporeal liver support tance, as this has contributed to the success of transplantation.
The aim of extracorporeal liver support therapy is to allow Re-transplantation for any disorder is considered only in
time for liver recovery or to provide support until a liver patients with acceptable predicted survival.179
transplant is possible. 149,168,169 There are two main types
of extracorporeal liver support therapy, namely artificial Contraindications for transplantation
and bioartificial devices. The artificial devices are cell-free Patients with extrahepatic malignancy and uncontrolled
systems that use a combination of dialysis, mainly using systemic infection where high-dose immunosuppressive
albumin, and plasma exchange.170 These systems aim to therapy is contraindicated are not suitable for transplan-
reduce toxins and have been shown to reduce bilirubin tation. In addition, patients with alcoholic liver disease
and improve hepatic encephalopathy.171–173 In contrast, with social instability and patients with inadequate or
bioartificial extracorporeal liver support devices are absent social support are relative contraindications due
biological systems utilising either porcine hepatocytes or to increased risk of non-adherence to immunosuppressive
a human hepatoblastoma cell line to sustain temporary therapy.180
hepatic function; however the construction and use of
these devices is complex and has been limited to specialist
Recipient selection
centres. There are continuing challenges with extracting Recipient selection for liver transplantation is of critical
viable hepatic cells and incorporation into the bioreactors importance as it affects mortality, especially when deter-
with which the extracorporeal circuits interface, thereby mining patients with ALF. There are a variety of prognostic
limiting their use.168,170 indicators and selection scoring systems, including the
Despite much research, the clinical use of extracorporeal Kings College, Clichy, Child-Turcotte-Pugh and model
liver support therapies has been difficult due to a lack of for end-stage liver disease (MELD) classification systems.161
clinical guidelines about when to institute and which types While there are different systems, most incorporate the
of patients should be selected, and technical considerations, severity of hepatic encephalopathy and coagulation status.
such as flow rate and duration of therapy, have yet to be In Australia and New Zealand, the MELD and paediatric
elucidated. 149,169,171 In many cases, the definitive treatment end-stage liver disease (PELD) scoring systems are used
for severe ALF is liver transplantation when irreversible for liver transplantation eligibility.180,181 The MELD score
liver injury has occurred;161 however, extracorporeal liver is a mathematical model that includes bilirubin, creatinine
support systems may provide sufficient liver support until and the international normalised ratio (INR), which was
transplantation is available.169 To date, evidence suggests originally devised to predict survival after TIPS.182 The
that there may be a reduction in mortality in ALF using MELD/PELD score is an excellent predictor of mortality,
extracorporeal liver support, yet the number and size of especially in ALF (Figure 20.4).162,181
the randomised controlled trials limits clinical efficacy.172 Once the need for transplantation is established, the
In patients presenting with AoCLF, there has been little decision to allocate a donor liver to a patient is based on
evidence to warrant the use of these liver support systems.169 donor and recipient blood group; donor size and size of
 CHAPTER 20 GASTROINTESTINAL, METABOLIC AND LIVER ALTERATIONS 669

FIGURE 20.4 The model for end-stage liver disease (MELD/PELD) calculation.162,181

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recipient; suitability of donor liver for splitting; severity This technique involves removal of the left lobe from the
of disease; matching of functional status of donor with live donor, usually the recipient’s parent, which is then
severity of liver disease; and hepatitis B and C status of transplanted into the child. It is a relatively straightforward
donor and recipient. Extensive testing and consultation is procedure, with little risk to the donor.187,188
part of the liver transplant process. Clinical consultation
occurs with hepatologists, clinical nurse consultants, social Postoperative management
workers, dietitians, psychiatrists, psychologists and drug Initial management and nursing care
and alcohol professionals if required. The initial postoperative care of liver transplant patients on
Surgical techniques return to critical care involves stabilisation, management of
positive pressure ventilation, continuous haemodynamic
Orthotopic liver transplantation monitoring and physical assessment, as with all critically
Orthotopic liver transplantation is the replacement of ill surgical patients. It is common for patients to be
the diseased liver. It was pioneered in the 1960s and has hypertensive post-surgery, displaying systolic blood
been improved considerably due to technical aspects of pressure above 160 mmHg with a mean arterial pressure
the surgery itself and enhanced haemodynamic stability of 110 mmHg. Aggressive treatment is required due to
during the procedure.183 the risk of stroke, which is compounded by low platelet
Two main techniques are used for orthotopic liver counts and abnormal clotting. Once pain is controlled
transplantation: portal bypass or the piggyback technique. and excluded as a cause of hypertension, clonidine or
Portal bypass occurs where an internal temporary hydralazine is considered. Oliguria is commonly related to
portocaval shunt or external veno-venous bypass is intraoperative fluid losses and fluid shifts.
used.184 In the piggyback technique, the recipient’s inferior Once initial stabilisation is achieved, treatment is
vena cava (IVC) is left and the donor IVC is piggybacked governed by clinical progress. Typically, the critical care
onto the recipient’s IVC.The advantages of this technique stay for a routine postoperative liver transplantation does
include haemodynamic stability during the anhepatic not exceed 24–48 hours; as long as physiological systems
phase, reduced operating times and reduced use of blood are maintained, discharge to the ward can be anticipated.
products, enabling a shorter length of hospital stay.185 An abdominal CT scan may be considered at 7–10 days
postoperatively or when clinically indicated.
Split-liver transplantation The initial postoperative care is similar for all liver
The disparity between the increasing number of people transplant patients. However, progress, stability and
on transplant waiting lists and the shortage of donor livers discharge from critical care can be affected by the patient’s
available has led to several innovative strategies. Split-liver preoperative condition and severity of liver failure. The
transplantation occurs when the donated organ is divided unique pathophysiology inherent in the liver failure
for two recipients, with the larger right segment to an adult patient will predispose to varying effects on coagulopathy,
and the smaller left lobe to a child.186 The complication cardiopulmonary, neurological, haemodynamic and meta-
rate is higher in split-liver than whole-liver transplants due bolic functions.140,161,189
to biliary leaks and anastomosis strictures. This technique
has significantly reduced the number of children waiting Blood loss and coagulopathy
for liver transplantation, although little impact has been The major risk during and post-surgery is massive blood loss,
made on adult waiting lists.186 due to a combination of factors. The surgical process itself
involves anastomosis of major arteries and veins, predisposing
Adult living donor liver transplantation the patient to bleeding and hypovolaemia during surgery
Living donor liver transplantation is an established option and anastomotic leaks post-surgery.190 Patients are likely
for paediatric patients with end-stage liver disease.187 to be coagulopathic from hepatic synthetic dysfunction,
670 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

leading to failure of synthetic clotting factors.191 Correction can supplement caloric needs (see Chapter 19). If caloric
of coagulopathy with blood products such as fresh frozen intake is inadequate, consultation with a dietitian will assist
plasma, platelets, cryoprecipitate and factor VIIa may control with enteral supplementation. Total parenteral nutrition is
minor postoperative bleeding, but if bleeding continues rarely required.196
an exploratory laparotomy may be required. Conversely,
Renal
it is not desirable to overcorrect coagulopathy, due to the
potential for vascular complications such as hepatic artery Renal dysfunction is a significant post-transplantation
thrombosis. Careful monitoring is required to identify and problem.197 Risk factors include pre-existing renal disease
manage hypotension, tachycardia, excessive blood loss from or hepatorenal syndrome, intraoperative hypotension,
drains, falling haemoglobin, abdominal swelling and oozing extensive transfusion of blood products, nephrotoxic
from insertion sites. Thrombocytopenia is a common drugs such as cyclosporin and tacrolimus, sepsis and graft
postoperative problem, with platelet counts often falling dysfunction.189 Hepatorenal syndrome is reversible post-
in the first week post-transplant. If platelet counts are low, transplantation. Patients who are receiving renal support
a platelet transfusion may be necessary, especially prior to such as continuous renal replacement therapy usually
removal of drains, lines, cannulae and sheaths. require continuation of renal support postoperatively for a
period of time until recovery of kidney function is evident
Cardiovascular (see Chapter 18).
Haemodynamic instability in the early postoperative Graft dysfunction and rejection
period may be due to hypovolaemia or haemorrhage.
Treatment includes fluid boluses to increase preload and Acute graft rejection was the most challenging obstacle
the initiation of inotropes may be necessary. The patient in the early years of transplantation but, with the devel-
may present with a hyperdynamic profile including a high opment of current immunosuppressive therapy, acute
cardiac output, low systemic vascular resistance and low rejection can be avoided, resulting in improved success
mean arterial pressure,192 although this usually reverses rates of transplantation.198 Immunosuppressive therapy has
1 week after transplantation. improved with the use of newer drugs and patients are
most commonly placed on a combination of tacrolimus
Neurological or cyclosporine and steroids.199,200
The most frequent neurological complications relate to Allograft dysfunction occurs within 48 hours of
patients with pre-existing hepatic encephalopathy. In ALF transplantation, and is characterised by varying degrees
patients, cerebral oedema with raised intracranial pressure of coma, renal failure, worsening coagulopathy, poor bile
is common and, after liver transplantation, cerebral oedema production and marked elevation in the liver enzymes
may take up to 48 hours to subside.Therefore, continuation (AST, ALT) and worsening acidosis. The cause of allograft
of preoperative measures to reduce intracranial pressure dysfunction is not always known; possible causes are injury
is necessary. These include elevating the head of the bed to the liver, either before or during the donor operation
30°; ensuring head, neck and body alignment; maintaining procedure, ischaemic-reperfusion injury or graft stenosis.
endotracheal tapes so they are not constrictive to allow Acute rejection is generally evident in the second week
venous return and prevent cerebral congestion; reducing post-transplant, and is generally suspected with an
neurological stimuli; and timing activities to prevent spikes elevation in liver enzymes, a decline in bile quality (only if
in intracranial pressure (see Chapter 17).192,193 a T tube is present), occasional fever and tachycardia.
Primary graft non-function is defined as failure of
Respiratory the graft to function in the first postoperative week. It
Pre-existing pulmonary complications associated with is manifested by failure to regain consciousness, sustained
liver disease can affect postoperative recovery and need to elevated transaminases, increasing coagulopathy, acidosis
be considered when weaning ventilation and maintaining and poor bile production. Causes include massive
adequate oxygenation. Patients post-transplant often haemorrhagic necrosis, ischaemia-reperfusion injury and
experience bi-basal collapse and consolidation, and are hepatic artery thrombosis.
prone to infection, similar to other critical care patients
who undergo complex surgical procedures that are Management of late complications
extended.194 Incentive spirometry, chest physiotherapy, Readmission to critical care after liver transplantation
early mobilisation and adequate pain relief are recom- is not uncommon. Factors include cardiopulmonary
mended, with early extubation the most effective in dysfunction from infection or fluid overload, respiratory
reducing pulmonary complications.194,195 failure from collapse and consolidation, tachypnoea,
recipient age, preoperative liver function, bilirubin, the
Gastrointestinal amount of blood products administered intraoperatively,
Patients with end-stage liver disease often have graft dysfunction, severe sepsis and postoperative surgical
malnutrition and bone disease, which may influence complications such as bleeding and biliary anastomotic
postoperative management. Fluid overload and ascites can leaks.201 Outcomes are affected by intraoperative and
quite often mask signs of malnutrition. Early nutrition is postoperative complications, renal failure, advanced liver
imperative in the postoperative period, and enteral feeding disease and malnutrition.202
 CHAPTER 20 GASTROINTESTINAL, METABOLIC AND LIVER ALTERATIONS 671

Summary
The gastrointestinal system can become significantly compromised during critical illness. Alterations in the gastrointes-
tinal system can also cause critical illness. The gastrointestinal system involves not just the gastrointestinal tract but also
organs that support digestion including the pancreas and liver. Disruptions to the gastrointestinal system and normal
gastrointestinal physiology can be altered during critical illness because of redistribution of blood flow away from the gut
and other abdominal organs. Specifically, the gastrointestinal system can become hypoperfused and normal physiological
processes responsible for digestion, absorption, immunity and protection become compromised.
Critically ill patients can be at risk of developing stress-related mucosal disease although incidence of clinically
important bleeding remains relatively low. Nevertheless, it remains common practice to provide stress-ulcer prophylaxis
to critically ill patients, particularly for those patients considered at high risk. During critical illness patients may also
be at risk for the development of IAH, with approximately half of all ICU patients having increased IAP. Recognising
potential risk factors for the development of IAH is essential so that monitoring can be commenced and treatment
initiated where necessary.
Critical illness can also result from the inability of the body to effectively use glucose in energy production.
An increasing number of people worldwide have diabetes and when illness occurs this can precipitate significant
alterations in blood glucose and result in the development of DKA or HHS. Because of the ensuing physiological
derangements these patients often need to be admitted to a critical care area for close monitoring and treatment until
they are stabilised.
Liver dysfunction causing hepatocellular injury and death can occur due to direct injury or cellular stress. This can
be mediated via several avenues, such as metabolic disturbances, ischaemia, inflammatory processes or reactive oxygen
metabolites from drug and alcohol ingestion. Acute failure can be acute or preceded by a chronic dysfunction. In
Australia and New Zealand, high rates of hepatitis B and C predispose individuals to chronic liver dysfunction that can
lead to acute hepatic decompensation. While acute liver failure is uncommon, patients who present are often critically
ill. In addition, liver failure causes major disturbances in other body systems often resulting in coagulopathy, cerebral
oedema (hepatic encephalopathy), sepsis, renal failure and metabolic derangement. Therapy is usually directed at
multi-organ support as extracorporeal liver support therapies have not sufficiently developed to sustain liver function
during the acute phase.
Liver transplantation remains the definitive treatment option for acute and chronic liver failure patients when
supportive multi-organ therapy is not sustainable. Pre-existing hepatic dysfunction and liver transplantation surgery can
lead to a high risk of haemorrhage and coagulopathy postoperatively. Careful haematological management is required to
control postoperative bleeding. Clinicians must ensure that patients receive appropriate haemodynamic management for
hyperdynamic states and that measures to avoid rises in intracranial pressure are implemented.

Case study
A 56-year-old woman was admitted to the ICU after presenting to the emergency department with
icterus and confusion and a history of alcoholism. She was emaciated and dehydrated with renal failure,
hyponatraemia, hypokalaemia, tachycardia and tachypnoea. In the emergency department she received
thiamine 300 mg, flucloxacillin 2 g, gentamicin 320 mg, ceftriaxone 1 g, acyclovir 400 mg and vitamin K 1 mg.
She also received 2 L of normal saline for fluid resuscitation.
On arrival in ICU she became very agitated. She was intubated and sedated and had a central line and
arterial line placed and nasogastric tube inserted, through which enteral nutrition was commenced at
20 mL/h. A diagnosis of acute hepatitis was made and an abdominal ultrasound revealed hepatomegaly.
She remained mechanically ventilated for 3 days and was then successfully weaned to spontaneous
ventilation and extubated. Laboratory tests in ICU revealed disseminated intravascular coagulation
(DIC) with an increased INR of 2.2, which decreased to 1.5 by day 4. Following extubation oral intake
was poor and to avoid dehydration a central line remained in place in the event parenteral nutrition
was required.
The day after extubation the patient deteriorated and showed signs of hepatic encephalopathy. She was
highly agitated and confused. She was unable to swallow and had a poor cough. Korsacoff’s encephalopathy
was diagnosed. She developed left side pneumonitis as a result of aspiration. In consultation with the family
treatment limitations were initiated and palliative management was commenced. The patient’s condition
continued to worsen – resulting in death within 24 hours.
672 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

DISCUSSION
Alcoholism results in about 2.5 million deaths worldwide each year and, although it is associated with
many diseases, mortality is usually associated with alcoholic liver disease. The development of alcoholic
liver disease is dose dependent with the risk of developing the disease increased for both men and women
who consume more than 30 g of alcohol per day (a standard drink contains approximately 14 g of alcohol).
Women are, however, at increased risk of developing alcoholic liver disease because of differences in the
way that they metabolise ethanol.203
The spectrum of alcoholic liver disease includes alcoholic fatty liver, alcoholic hepatitis and alcoholic
cirrhosis. Alcoholic steatosis is characterised by microvesicular and macrovesicular fat accumulation in the
hepatocytes and is often reversible with abstinence. Patients might have elevated liver enzymes and the
INR and albumin levels tend to be normal. Alcoholic hepatitis is an inflammatory process with neutrophil
infiltration. Clinical findings are similar to what was observed in this case study and include jaundice,
pyrexia, unintentional weight loss, malnutrition and a tender, enlarged liver. Liver enzymes are usually
moderately elevated. Ascites and encephalopathy might be present.
Alcoholic cirrhosis is less common and present in about 15% of patients with alcoholic liver disease.
Patients present with the stigmata of chronic liver disease including gynaecomastia, palmar erythema,
spider angiomata, testicular atrophy, parotid gland enlargement and signs of portal hypertension, including
caput medusa. There are multiple complications as a result of alcoholic cirrhosis. Patients can exhibit
low albumin, increased bilirubin, thrombocytopenia and alterations in coagulation including prolonged
prothrombin time and increased INR, as demonstrated in this case study.
Malnutrition is common in alcoholic liver disease and can negatively influence outcomes for critically ill
patients (see Chapter 19). This patient was emaciated on admission suggesting prolonged malnutrition.
While early nutrition support is important, when long periods of malnutrition have been present it is
important to commence enteral nutrition slowly to avoid refeeding syndrome. Refeeding syndrome is
associated with severe derangement in fluid and electrolyte levels that may result in significant morbidity
and mortality. During commencement of enteral nutrition this patient should have been monitored closely
for signs for hypophosphataemia, hypomagnesaemia and hypokalaemia. In this case study, the patient
had feeds commenced on admission to ICU but only at 20 mL/h, which would not have met her nutritional
requirements. Addition of parenteral nutrition to support nutrition therapy can be implemented alongside
enteral nutrition to help match nutrition intake with requirements.
During the ICU admission the patient had DIC. The main feature of DIC is intravascular clotting in the
microcirculation, which can contribute to the development of multiple organ failure. Platelets and
coagulation factors were also depleted and these cannot be quickly replaced by the liver and bone marrow.
Consequently, this microvascular formation of clots occurs alongside the inability to form clots where
needed, resulting in bleeding.
As the patient’s condition continued to deteriorate a decision was made with the family to limit
treatment.

CASE STUDY QUESTIONS

1 What management might you expect for this patient specific to the diagnosis of DIC?
2 Following extubation all critically ill patients are at risk for decreased nutritional intake. What strategies
might be useful in ensuring adequate nutrition in this case study?
3 Describe the nursing management of a patient with hepatic encephalopathy.
 CHAPTER 20 GASTROINTESTINAL, METABOLIC AND LIVER ALTERATIONS 673

RESEARCH VIGNETTE

Hunt L, Frost SA, Hillman K, Newton PJ, Davidson PM. Management of intra-abdominal hypertension and
abdominal compartment syndrome: a review. J Trauma Manag Outcomes 2014;8(1):2

Patients in the intensive care unit (ICU) are at risk of developing of intra-abdominal hypertension (IAH) and abdominal
compartment syndrome (ACS).
Aim: This review seeks to define IAH and ACS, identify the aetiology and presentation of IAH and ACS, identify IAP
measurement techniques, identify current management and discuss the implications of IAH and ACS for nursing
practice. A search of the electronic databases was supervised by a health librarian. The electronic databases
Cumulative Index of Nursing and Allied Health Literature (CINAHL), Medline, EMBASE and the World Wide Web were
searched from 1996 to January 2011 using MeSH and key words that included but were not limited to: abdominal
compartment syndrome, intra-abdominal hypertension, intra-abdominal pressure in adult populations. Articles that
met the search criteria were reviewed by three authors using a critical appraisal tool. Data derived from the retrieved
material are discussed under the following themes: 1) aetiology of intra-abdominal hypertension; 2) strategies for
measuring intra-abdominal pressure; 3) the manifestation of abdominal compartment syndrome; and 4) the importance
of nursing assessment, observation and interventions. Intra-abdominal pressure (IAP) and abdominal compartment
syndrome (ACS) have the potential to alter organ perfusion and compromise organ function.

Critique
This integrative review provides a summary of the literature on IAH and abdominal compartment syndrome, including
measurement techniques, and goes beyond other reviews79,204 by providing a discussion of the implications for
nursing practice. The methodology provides a description of the databases searched and keywords used in the
search. The search terms used, however, aren’t described in a way that would permit replication of the search as
the way in which search terms have been combined and the databases to which they are applied are not clear. The
omission of medical subject headings (MeSH) could have resulted in some relevant papers being omitted from the
search results. The search is strengthened by the inclusion of hand searching relevant reference lists for additional
publications, although no further publications were identified through this method.
In total 514 articles were retrieved, although it is not clear from the flow diagram which databases yielded the most
results. According to the flow diagram 374 papers were excluded. It is not clear how many of these papers were
duplicates. The reasons for exclusion of papers are provided but confusing. Specifically, they refer to papers being
excluded because they were ‘not culture related’ , were ‘ICU practice culture’ or ‘other discipline practice culture’;
this is confusing and it is difficult to see how these exclusion criteria related to the stated aim of the paper.
Although the authors indicate that papers meeting the aim of the review were included the inclusion/exclusion criteria
were not clearly articulated so the decision path is not clear. Whether all manuscript types were included or only those
based on primary research is not stated although review of the reference list suggests that opinion pieces and/or
discussion papers might have been included. Figure 1 in the article provides an overview of the flowchart for the study
selection process and indicates that a total of 53 papers were included in the review. The data from papers included
in this review are summarised according to key areas including: diagnosis of IAH; aetiology of IAH; IAP measurement;
definition of abdominal compartment syndrome; indications for IAP monitoring; and implications for nursing practice.
As a summary paper, this integrative review provides a broad overview of IAH and abdominal compartment
syndrome and includes important aspects of nursing practice. Aspects of nursing practice that are highlighted in
this paper include vigilance in monitoring IAH or abdominal compartment syndrome, assessing organ function, pain
management, vital signs, lower extremity perfusion and assessment of wound drainage.
Although not a systematic review, this paper would have been strengthened methodologically by following the
Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) recommendations.205 Specifically,
articulating the selection criteria for the papers and addressing limitations of the research included in this review would
be helpful, particularly as there seems to be a mix of research articles and opinion pieces. Despite the limitations of
this publication, this integrative review provides a useful summary of the literature and incorporates clear messages
for nursing practice that can be readily implemented in the intensive care unit. Directions for future research are also
included and highlight opportunities for nursing and interdisciplinary research.
674 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Lear ning a c t iv it ie s
1 On your next clinical shift, identify what stress-ulcer prophylaxis your patient is receiving (if any) and whether
they have risk factors for the development of stress-related mucosal disease.
2 When you are next in the clinical area, consider the clinical presentations of the patients in the ICU and identify
which patients might most benefit from intra-abdominal pressure monitoring.
3 Compare and contrast the physiological changes that occur in DKA and HHS. How do these differences
influence the management strategy for restoring normoglycaemia?
4 Liver transplantation can be considered in patients with alcoholic liver disease. What would make liver
transplantation in this group most successful?

Online resources
Australian Diabetes Council, www.australiandiabetescouncil.com
European Association for the Study of the Liver, www.easl.eu
National Diabetes Education Program, http://ndep.nih.gov
Online MELD Calculator, http://optn.transplant.hrsa.gov/resources/professionalResources.asp?index=8
The Australia and New Zealand Liver Transplant Registry, www.anzltr.org
The Transplantation Society of Australia and New Zealand, www.tsanz.com.au
World Society of the Abdominal Compartment Syndrome, www.wsacs.org

Further reading
Holt RIG, Cockram C, Flyvbjerg A, Goldstein BJ. Textbook of diabetes. 4th ed. Hoboken: Wiley Blackwell; 2010.
Lee WE, Williams R. Acute liver failure. Cambridge: Cambridge University Press; 2011.

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156 Fallon MB. Mechanisms of pulmonary vascular complications of liver disease: hepatopulmonary syndrome. J Clin Gastroenterol 2005;39
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171 Leckie P, Davies N, Jalan R. Albumin regeneration for extracorporeal liver support using prometheus: a step in the right direction.
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173 Kortgen A, Rauchfuss F, Gotz M, Settmacher U, Bauer M, Sponholz C. Albumin dialysis in liver failure: comparison of molecular adsorbent
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174 Liou IW, Larson AM. Role of liver transplantation in acute liver failure. Semin Liver Dis 2008;28(2):201-9.
175 O’Grady J. Liver transplantation for acute liver failure. Best Pract Res Clin Gastroenterol 2012;26(1):27-33.
176 Lynch SV, Balderson GA. ANZLT Registry Report 2012. Brisbane, QLD, Australia: ANZLT; 2012.
177 Thuluvath PJ, Guidinger MK, Fung JJ, Johnson LB, Rayhill SC, Pelletier SJ. Liver transplantation in the United States, 1999–2008.
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178 O’Leary JG, Lepe R, Davis GL. Indications for liver transplantation. Gastroenterology 2008;134(6):1764-76.
179 Yoo PS, Umman V, Rodriguez-Davalos MI, Emre SH. Retransplantation of the liver: review of current literature for decision making and
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180 Transplantation Society of Australia and New Zealand. Organ transplantation from deceased donors: Consensus statement on eligibility
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181 Trotter JF, Osgood MJ. MELD scores of liver transplant recipients according to size of waiting list: impact of organ allocation and patient
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182 Llado L, Figueras J. Techniques of orthotopic liver transplantation. HPB (Oxford) 2004;6(2):69-75.
183 Agopian VG, Petrowsky H, Kaldas FM, Zarrinpar A, Farmer DG, Yersiz H et al. The evolution of liver transplantation during 3 decades: analysis
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188 Russo MW, Brown RS, Jr. Adult living donor liver transplantation. Am J Transplant 2004;4(4):458-65.
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 Chapter 21

Pathophysiology and
management of shock
Margherita Murgo, Ruth Kleinpell

KEY WORDS Learning objectives

anaphylactic shock After reading this chapter, you should be able to:
cardiogenic shock • describe the clinical manifestations of shock
distributive shock • distinguish between the various shock states
hypovolaemic shock • describe general principles of shock management
neurogenic shock • discuss end points of resuscitation
obstructive shock
• identify appropriate monitoring for a patient with shock
sepsis
• review and evaluate care for a patient with a specific shock type.
septic shock
severe sepsis
systemic
inflammatory Introduction
response It is a bad symptom when the head, hands, and feet are cold, while the belly and sides are
syndrome hot, but it is a very good symptom when the whole body is equally hot.
The Book of Prognostics by Hippocrates, 400 BC1
Shock is an altered physiological state that affects the functioning of every cell
and organ system in the body. It is a complex syndrome reflecting changing blood
flow to body tissues with accompanying cellular dysfunction and eventual organ
failure. Shock presents as a result of impaired nutrient delivery to the tissue:
• when compensatory mechanisms can no longer respond to decreases in
tissue perfusion2
• when nutrient uptake is impaired at the cellular level.
While the cause of shock may be multifactorial, treatment focuses on
optimising tissue perfusion and oxygen delivery. Shock is often classified
according to the primary underlying mechanism: a disruption of intravascular
blood volume, impaired vasomotor tone or altered cardiac contractility.3 The
shock syndrome is one of the most pervasive manifestations of critical illness
present in intensive care patients.
Early detection and management of shock to reverse pathological processes
improves patient outcomes.4 Although the traditional hallmark of shock is hypo-
tension – where the systolic blood pressure is <90 mmHg – this can be a late or
misleading sign and is considered a medical emergency.5 It is therefore critical
that other signs and symptoms are identified early by frequent observations to
682 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

detect a patient’s deteriorating state and respond before Pathophysiology

irreversible shock ensues.6 No single vital sign is adequate
in determining the level or extent of shock4 nor is there a Shock is classified by aetiology: hypovolaemic, cardio-
specific laboratory test that diagnoses the shock syndrome. genic, distributive2,7,8 and obstructive (Figure 21.1).9 Each
In this chapter an overview of the pathophysiology of type has a specific mechanism of action that leads to
shock, the commonly described categories and associated altered tissue perfusion and oxygen and nutrient uptake
pathologies, along with appropriate monitoring and inter- at the cellular level (see Table 21.1). In practice, it is
ventions for managing a patient in shock are provided. common for different shock types to be existent in the

FIGURE 21.1 Types of shock.

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Adapted from Vincent J-L, De Backer D. Circulatory shock. New Engl J Med 2013;369:1726–34, with permission.
 CHAPTER 21 PATHOPHYSIOLOGY AND MANAGEMENT OF SHOCK 683

(fluid retention), redirection of blood flow to vital organs,

TABLE 21.1 hyperglycaemia, immunomodulation and procoagulation.
Shock types This universal response to impending shock is particu-
larly effective in compensating for loss of circulating
SHOCK TYPE MAIN CHARACTERISTIC
blood volume, but may be counterproductive when pump
Hypovolaemic A reduction in circulating blood volume failure occurs or is ‘uncoupled’ in distributive shock states.
through haemorrhage or dehydration or As adaptive responses fail, cardiac output becomes
plasma fluid loss
insufficient to provide adequate organ perfusion despite
Cardiogenic Pump failure (impaired cardiac increasing tissue oxygen consumption (see Chapters 9 and
contractility) usually as a result of 10). When oxygen is ‘supply dependent’, oxygen delivery
myocardial infarction is decreased and, to compensate, increased extraction
Obstructive Characterised by blockage of circulation occurs to enable continued tissue oxygen consumption.
to the tissues by impedance of outflow However, when oxygen delivery falls below a critical
or filling in the heart (e.g. due to cardiac threshold, and extraction demand rises above the available
tamponade or pulmonary emboli) blood oxygen levels, this compensation mechanism fails
Distributive A maldistribution of circulation from and oxygen debt results.4,11
sepsis, anaphylaxis or neurogenic injury Hypoperfusion may also exist despite a relatively
normal cardiac output, and may not be immediately
Adapted from Manji RA, Wood KE, Kumar A. The history and
clinically evident.4 This results in maldistribution of blood
evolution of circulatory shock. Crit Care Clin 2009;25:1–29,
with permission. flow to some tissues while other areas receive more blood
flow than needed2,5,10,11 and is often referred to as distrib-
utive shock. This response is typical of the shock types
same presentation, for example a patient with septic shock that affect vasomotor tone, for example septic, neurogenic
might also be hypovolaemic and/or have myocardial and anaphylactic shock. Maldistribution may leave some
dysfunction. organ systems ischaemic for long periods leading to
Shock occurs when there is an inability of the body persistent organ dysfunction and failure.4 There is also
to meet metabolic demands of the tissues; hypoperfusion evidence supporting the presence of cytopathic hypoxia
(decreased blood flow to the tissues) results in cellular as a result of excessive production of cellular proinflam-
dysfunction, as there is homeostatic imbalance between matory mediators such as nitric oxide and tumour
nutrient supply and demand, and adaptive responses can no necrosis factor-alpha. Adenosine triphosphate (ATP) stores
longer accommodate circulatory changes.2,10 These adaptive become depleted due to this impaired mitochondrial
responses are moderated via numerous ‘sensors’ throughout oxygen utilisation11–13 interfering with electron transport
the thorax and large vessels in particular, which detect and metabolism. Nitric oxide is associated with vascular
subtle changes in pressure (baroreceptors) or biochemical relaxation and is a major contributor to alterations in
changes (chemoreceptors).These receptors feed back to the microvasculature and capillary leak in sepsis.14
hypothalamus, which regulates, through the pituitary gland Organ systems have varying responses in shock and are
and adrenal cortex, the release of a number of hormones not measured directly. Often surrogate markers of global
including antidiuretic hormone and adrenocorticotrophic hypoperfusion are used to indicate the severity of shock.
hormone to target organs such as the kidney. The adrenal Lactate and acid–base disturbances, such as an increase in
cortex mediates the mineral and glucocorticoid response strong ion gap, have been suggested as early markers of
to counter the developing effects of shock.This concurrent mitochondrial dysfunction and cellular hypoperfusion.6,9,15
direct feedback stimulates the sympathetic nervous system These ‘surrogate’ biochemical markers of hypoper-
to act on blood vessel tone, particularly the arterioles, and fusion (pH, serum lactate and standard base excess) assess
organs such as the adrenal gland and kidney to respond via acidaemia and provide some insight into the degree of
the release of endogenous catecholamines (adrenaline and shock.16 Lactate, a strong anion with basal production
noradrenaline), mineral and glucocorticoids (aldosterone, of approximately 1300 mmol/day,17 is a product of
cortisol) and the renin–angiotensin–aldosterone system. metabolism. Increased levels are present in tissue hypoxia,
Activation of the renin–angiotensin–aldosterone system hypermetabolism, decreased lactate clearance, inhibition
results in synthesis of angiotensin II, a powerful vasocon- of pyruvate dehydrogenase and activation of inflamma-
strictor that further potentiates the reduction in peripheral tory cells, all characteristics of developing shock (Table
blood vessel capacity. 21.2). Increased lactate production is a warning sign of
Collectively, these responses form a sympatho– impending organ failure, as it is indicative of anaerobic
endocrine–adrenal axis that moderates the systemic metabolism. Blood lactate levels have been directly linked
response to shock. The axis maintains circulation to the to deteriorating patient outcomes in shock.16,18
vital organ system and combines with the inflamma- Serum concentrations greater than 5 mmol/L in the
tory response to limit local and systemic tissue damage setting of metabolic acidosis are indicative of high mortality.17
and ultimately confer a survival advantage. Combined As the shock state deteriorates and the body fails
responses include profound vasoconstriction, oligoanuria to compensate, organ systems begin to fail. This is
684 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 21.2 Patient assessment

Hyperlactataemia due to tissue hypoxia Critically ill patients often exhibit signs of tissue hypoxia as
a result of cardiovascular disturbances.21 Table 21.3 provides
MECHANISMS SERUM LEVELS CAUSES an overview of the physiological changes in shock. Therapy
Increased Lactate >5 mmol/L Hypoxaemia is targeted to maintain oxygen delivery to vital organs to
glycolysis and pH <7.35 Anaemia prevent ischaemia and cell death.21,22 Ideally, organ systems
Decreased (normal lactate Hypoperfusion and tissues should be monitored individually;21 however
clearance <2 mmol/L) Shock global measures, such as perfusion pressure, cardiac output and
Sepsis oxygen delivery, are commonly used as surrogates to assist in
treatment decision making.23 Patient assessment and haemo-
Adapted from Phypers B, Pierce JT. Lactate physiology in dynamic monitoring, including calculation of cardiac output,
health and disease. Continuing Education in Anaesthesia,
are used to differentiate shock states and assess progress in
Crit Care Pain 2006;6:128–32, with permission.
relation to treatment.22,24,25 Cardiac output is seen by many
clinicians as an important assessment of shock patients as it
complicated by a systemic inflammatory response is a major determinant of oxygen delivery.21,22 Critically ill
(SIRS), which can be a direct cause of the shock state patients are frequently assessed clinically, although cardiac
or develop as a consequence of protracted shock. SIRS output estimations from physical examination alone are
results in ‘capillary leak’ or increased microvascular generally unreliable and patient status may change quickly.26
permeability that leads to interstitial oedema due to Therefore, invasive techniques are most commonly used in
alterations to the vascular endothelium. Many immune critical care to measure cardiac output (see also Chapter 9).
mediators including circulating cytokines, oxygen free Non-invasive assessment
radicals and activated neutrophils alter the structure of Perfusion status is determined clinically using gross organ
the endothelial cells, creating space to allow larger intra- function such as mental status, urine output and peripheral
vascular molecules to cross into the extravascular space,19 warmth and colour.4,9 Basic physical assessment of cardiovas-
with proteins and water moving from the intravascular cular, central nervous system and renal function is essential
space into the interstitium.20 This response mechanism when assessing a patient at risk of shock. Subtle changes in
improves the supply of nutrient-rich fluid to the site of mentation, urine output, heart rate and capillary refill are all
injury; however, systemically, fluid shifts lead to hypo- signs of physiological compensation in response to altered
volaemia, impaired organ function and development of tissue perfusion associated with shock. Regular tracking of
acute organ injury such as acute kidney injury.20 This these vital signs and trend monitoring through careful docu-
developing organ injury is the precedent to organ failure mentation can alert clinicians to impending deterioration
(see Chapter 22). in the shock state. Level of consciousness may deteriorate;
The next sections of this chapter describe the general an early sign may be anxiety, and progress to restlessness,
assessment and management of shock, different classifi- agitation or coma. Other assessment findings include
cations of shock and specific management principles to cool, clammy skin, postural hypotension, tachycardia and
avoid or limit tissue injury and the eventual progression decreased urine output.8,9 The reliability of these measures
to organ failure. is questionable, particularly where multiple assessments by

TABLE 21.3
Physiological changes in shock

PHYSIOLOGICAL CHANGE
SYSTEMIC P U L M O N A RY P U L M O N A RY
CARDIAC VA S C U L A R C A P I L L A RY C A P I L L A RY VA S C U L A R
S H O C K C L A S S I F I C AT I O N OUTPUT R E S I S TA N C E C I R C U L AT I O N PRESSURE R E S I S TA N C E

Hypovolaemic ↓ ↑ ↓ ↓ ↑
Cardiogenic ↓ ↑ ↓ ↑ ↑
Distributive:
• septic ↑ ↓ ↓ ↓ ↑
• anaphylactic ↓ ↓ ↓ ↓ ↓
• neurogenic ↓/NC ↓ ↓ ↓ ↑
Obstructive ↓ ↓ ↓ ↑ ↑

↑ = increase; ↓ = decrease; NC = no change.

Adapted from Weil M. Personal commentary on the diagnosis and treatment of circulatory shock states. Curr Opin Crit Care 2004;
10:246–9, with permission.
 CHAPTER 21 PATHOPHYSIOLOGY AND MANAGEMENT OF SHOCK 685

different clinicians are performed. In the intensive care extraction rises, the residual oxygen content of blood
unit (ICU) continuous electrocardiograph monitoring and returning to the lungs will fall; in effect, this is a surrogate
invasive monitoring techniques are employed to assist in indicator of failure to meet body tissue oxygen demand.
the objective assessment of changes in cardiovascular state. This technology was used in the landmark study by Rivers
Although estimation of cardiac output based on physical and colleagues34 to monitor early deterioration of septic
assessment findings is unreliable, physical examination using shock patients presenting to the emergency department
an estimation of vascular resistance has shown reasonable in need of resuscitation and was part of a goal-directed
accuracy.28 Clinical assessment may determine cardiac approach to managing patients. This single-centre study
output using the rearranged equation where the systemic was the subject of much interest for its claimed improve-
vascular resistance equals the mean arterial pressure minus ment in patient outcome, with this goal-directed approach
the central venous pressure/cardiac output.28 A reliable being assessed in a number of major multicentre studies to
and accurate non-invasive clinical assessment technique verify findings within an international context and varying
of estimating cardiac output would be clinically useful,24 approaches to critical care delivery.35 The recent publication
allowing assessment of patients without invasive monitoring, of the ProCESS36 and ARISE37 trials has further impacted
or used to verify accuracy of invasive devices. While a this approach and will be discussed later in the chapter.
number of non-invasive cardiac output measuring devices
are available, further research and refinement is required Management principles
before widespread application in critical care.29 New tech- Managing a patient in shock focuses on treating the
nologies hold promise in aiding clinician assessment of underlying cause, and restoration and optimisation of
haemodynamic status using non-invasive methods. Clinical perfusion and oxygen delivery; this includes relevant
ultrasound is being used with increasing frequency with activities using the acronym VIP.27 It is also suggested
assessment of inferior vena cava (IVC) collapsibility during that giving critically ill patients a daily ‘FASTHUG’, to
respiration to assess volume status. A meta-analysis of studies ensure daily assessment and interventions in priority areas,
comparing IVC diameter in hypotensive versus normoten- improves the quality of care for patients in ICU38 (see
sive individuals demonstrated a trend towards a decreased Practice tips below). Specific management of patients with
IVC size in the hypotensive group compared to the control different types of shock is discussed separately below.
group. However, measures such as cardiac output or stroke
volume variation were not consistently examined to assess Practice tip
for clinical changes based on increased IVC diameter.
Additional research is warranted to evaluate the clinical ‘VIP’ acronym
application of clinical ultrasound using IVC.30 • Ventilation, including airway, added oxygen and
ventilation
Invasive assessment
• Infusion of appropriate volume expanders
Continuous assessment of heart rate and blood pressure
by an intra-arterial catheter also enables circulatory access • Improved heart Pumping with drug therapy such as
for frequent blood sampling to assess serum lactate levels, antiarrhythmics, inotropes, diuretics and vasodilators
electrolytes and blood gas estimation, including pH and Adapted from Weil M. Personal commentary on the diagnosis
lactate levels. and treatment of circulatory shock states. Curr Opin Crit Care
The indicator dilution method using a thermal (thermo- 2004;10:246–9, with permission.
dilution) signal (cold or hot) is the customary clinical
standard for measuring cardiac output in ICU.22 This has
been achieved by placement of a pulmonary artery catheter, Practice tip
or a central line, in conjunction with a thermistor-tipped
arterial cannula (transpulmonary aortic thermodilution). ‘FASTHUG’ mnemonic
Other invasive techniques measure cardiac output contin- Feeding (prevent malnutrition, promote adequate
uously using pulse contour or arterial pressure analysis and caloric intake)
ultrasound Doppler methods using an oesophageal probe. Analgesia (reduce pain, improve physical and psycho-
All methods have degrees of invasiveness, can be time-
logical wellbeing)
consuming to yield measurements of acceptable accuracy,31
may be expensive and are not without risk of complica- Sedation (titrate to the 3Cs – calm, cooperative,
tions.24,32 The pulmonary artery catheter is a controversial comfortable)
assessment tool22,25,32 due to the risk associated with the Thromboembolic prophylaxis (prevent DVT)
invasive device versus benefits for the measurement of Head of bed elevated (up to 45° to reduce reflux and VAP)
cardiac output.33 This has led to decreased use and increased
interest in less or non-invasive measures of cardiac output. Ulcer prophylaxis (to prevent stress ulceration)
A further invasive assessment approach is the continuous Glycaemic control (to maintain normal blood glucose levels)
estimation of mixed venous oxygen saturation using a
Adapted from Vincent J-L. Give your patient a fast hug (at least)
light-emitting sensor in a pulmonary artery catheter. As once a day. Crit Care Med 2005;33:1225–9, with permission.
tissue oxygen delivery fails to meet demand and oxygen
686 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Hypovolaemic shock inserted and lost circulating volume is replaced by colloids,

isotonic crystalloids or blood products to achieve haemo-
Hypovolaemia is a common primary cause of shock and dynamic end points, such as a mean arterial pressure
also a factor in other shock states. Insufficient circulat- >65 mmHg. Body heat can be lost rapidly due to blood
ing blood volume is the underlying mechanism, leading loss, the rapid infusion of room temperature fluids and
to decreased cardiac output and altered perfusion.39,40 exposure in the pre-hospital setting or during repeated
Death related to haemorrhage is most likely in the first physical examination. It is therefore important to institute
few hours after injury.40 The most obvious cause is direct measures to maintain patient temperature >35°C to avoid
injury to vessels leading to haemorrhage, but there are coagulopathies and loss of thermoregulation.42 The aim is
more insidious causes such as dehydration from prolonged to ameliorate the lethal triad of anaemia, coagulopathy and
vomiting or diarrhoea, sepsis and burns.41 Hypovolaemic hypothermia, which can lead to worsening hemorrhage
shock is classified as mild, moderate or severe, depending and eventual death (see Figure 21.2).40–42
on the amount of volume loss (see Table 21.4). As the Critical care nurses must be efficient and practised at
shock state worsens, associated compensatory mechanisms initial patient assessment to establish the degree of compen-
will be more pronounced,8 and hypovolaemic shock may sation occurring in a hypovolaemic patient. Figure 21.2
deteriorate to multiple organ dysfunction syndrome if highlights clinical manifestations of haemorrhage. Careful
poor oxygen delivery is prolonged39 (see Chapter 22). consideration of a patient’s clinical picture will establish a
Clinical manifestations hierarchy and priority of needs. Many hospitals have some
Symptoms of haemorrhage may not be present until more level of track and trigger response that escalates care to
than 15–30% of blood volume is lost, and will deterio- appropriate levels such as medical emergency teams or
rate as the shock state worsens.8,41 Estimating blood or rapid response teams. However, nurses are in a position to
plasma loss is difficult and dilutional effects of resuscitation institute first-line management, such as establishing intra-
fluids may be evident when assessing haemoglobin and venous access, if this is a core skill. There are also many
hematocrit.41 As the body compensates for the reduced
circulating volume, widespread vasoconstriction occurs FIGURE 21.2 Physiological derangements during
in most body systems apart from the heart and central haemorrhage/massive transfusion
nervous system; systemic vascular resistance rises markedly
in an attempt to retain a viable circulatory system; this
accounts for many of the signs and symptoms associated
with circulatory compensation. However, as tissues Hypothermia
Temp <35°C
are starved of oxygen and nutrients over a prolonged
ischaemic time, local mediators are released as part of the Acidosis Coagulopathy
INR >1.5
inflammatory responses, leading to organ microvasculature pH <7.2
PT >18 secs
SBE >-6
vasodilation, and capillaries re-open to maintain oxygen Lactate >4 mmol/L APTT >45 secs
Fibrinogen <1.0 g/L
delivery and reduce hypoxia.41 This is a hallmark of lonised Ca <1.1 mmol/L
Platelets <50
developing multiple organ dysfunction syndrome.
Physiological
Patient management derangements
Clinical management of hypovolaemia focuses on with massive
transfusion
minimising fluid loss and restoration of circulating blood
volume41 once the airway and breathing are secure. More
than one large-bore intravenous cannulae are usually

TABLE 21.4
Signs and symptoms of hypovolaemic shock

PA R A M E T E R MILD (15–30% LOSS) M O D E R AT E ( 3 0 – 4 0 % L O S S ) SEVERE (>40% LOSS)

Blood pressure No change Lowered Hypotensive

Pulse (beats/min) ≥100 ≥120 ≥140
Respirations (breaths/min) >20 >30 >40
Neurological Normal to slightly anxious Mildly anxious to confused Confused, lethargic
Urine output (mL/h) >30 20–30 5–15, negligible
Capillary refill Normal Reduced, >4 s Reduced, >4 s

Adapted from Kelley D. Hypovolemic shock: an overview. Crit Care Nurs Q 2005;28:2–19, with permission.
 CHAPTER 21 PATHOPHYSIOLOGY AND MANAGEMENT OF SHOCK 687

protocols and guidelines available to guide initial fluid of the appropriate fluid for surgical management and
resuscitation where a patient has indications of inadequate ‘permissive hypotension’ (deliberate limiting or minimising
circulating blood volume. Although such guidelines resuscitation until after adequate surgical control of haem-
might vary slightly, they aim to restore circulating blood orrhage)40,42 will be assessed by the multidisciplinary team.
volume through the administration of fluid boluses. Up This restrictive fluid regimen is a process linked to damage
to 20 mL/kg of colloid or 30–40 mL/kg crystalloid may control surgery.47 The goal of this management strategy is
be recommended. Critical bleeding and massive transfu- to maintain the systolic blood pressure end point using
sion protocols (see Figure 21.3) should also be available to blood products in an effort to limit coagulopathy47 and
guide patient management. BloodSafe Australia (https:// stopping the haemorrhage through direct pressure,
www.bloodsafelearning.org.au) has lessons available on tamponade devices and other techniques.46
this issue. Debate surrounds early surgical intervention prior to
aggressive fluid resuscitation.40 The premise is that allowing
Fluid resuscitation a lower perfusion pressure prior to achieving haemostasis
Fluid resuscitation is a first-line treatment for hypovolae- with controlled or no fluid infusion results in less blood loss,
mic shock; providing fluid volume increases preload and as the compensatory mechanisms described earlier in this
therefore cardiac output and organ perfusion. A related chapter are not as profound.40 Use of medications such as
principle is that the fluid infused should reflect fluid loss. factor IVa and erythropoietin also remains controversial in
For example, in burns, plasma replacement might be the setting of critical haemorrhage.42 Guidelines for ‘massive
warranted or, in massive haemorrhage, fresh blood may be transfusion’ released by the Australian National Blood
indicated. It has been suggested that fluid therapy should Authority do not recommend use of factor IVa beyond
be managed in the same way as prescribing medication licensed indications, although there may be an indication
after consideration of the risks and benefits of a selected when conventional therapy has failed to secure haemosta-
fluid.44 Giving a fluid challenge is not always appropri- sis following massive blood loss and transfusion of blood
ate; the determining factors will be assessment of volume products.43 The current debate also includes dosage and
responsiveness, and whether the infusion will not be thromboembolic complications associated with its use.42
deleterious, causing overload, fluid shifts and perpetuating
inflammatory responses.4 The fluid type, volume, rate and Crystalloids versus colloids
targeted end points should be documented;41 and often The scientific rationale for using colloids over crystal-
this is structured as a bolus dose in volume/kg to achieve loids is to preserve plasma oncotic pressure so as to retain
a measured haemodynamic variable. See Table 21.5 for a intravascular fluid and minimise oedema. Colloids may
list of some of the frequently used resuscitation fluids and also attenuate the inflammatory response.15 This scientific
their compositions. When massive transfusion is required, rationale has not been supported by the research. The
attention should be given to product selection and this recently published CRISTAL study has not improved
should be guided by an evidence-based protocol. understanding around which fluid is most suitable in
hypovaolaemic shock as no treatment benefit between
Practice tip crystalloids and colloids was identified.48 This unblinded
multicentre randomised controlled trial was conducted
Fluid bolus in high risk groups over a decade and enrolled nearly 3000 patients. The
• Care should be taken when administering fluid primary outcome was 28-day mortality.48 The colloid
bolus to all patients with particular attention to high versus crystalloid fluid resuscitation debate will continue
risk groups such as the elderly. as other large trials have also been unable to demonstrate
• Assess regularly for signs of fluid overload and
outcome benefits except in some subsets of patients.49–51
If moderate-to-severe hypovolaemia is suspected, blood
pulmonary oedema including: shortness of breath,
is often used to improve oxygen-carrying capacity. Further
orthopnoea, bibasal auscultation of fine end-
dilution of blood by volume expanders increases hypoxia,
inspiratory crackles, oedema, increased central
otherwise known as isovolaemic anaemia, and red cells
venous pressure. Escalate signs of distress
are usually required. Use of isotonic saline as a volume
immediately for medical review.
expander is common, although resuscitation with large
volumes of saline solutions can be associated with hyper-
Minimum volume resuscitation chloraemic acidosis40 and haemodilution.46 Blood and
The use of high ratios of blood products and low fluid blood components are usually considered necessary where
volume during damage control resuscitation confers patients exhibit signs of moderate-to-severe haemorrhage.
a survival benefit.45 Much of the knowledge around There is no perfect resuscitation fluid, and selection is
major trauma and haemorrhage has come from military guided by patient condition and the type of fluid lost.
research and management of ‘field trauma’.46 Maintain-
ing a systolic blood pressure of approximately 90 mmHg Blood and blood products
may be beneficial as clotting factors are not diluted and There are a number of factors to consider when admin-
remaining blood volume retains its viscosity.47 Selection istering large amounts of blood products. Massive
 688
TABLE 21.5
Resuscitation fluids

SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

COLLOIDS C RY S TA L L O I D S
4% SUCCI-
NYLATED 3.5% COM-
MODIFIED UREA- POUNDED BALANCED
FLUID LINKED 0.9% SODIUM S A LT
H Y D R O X Y E T H Y L S TA R C H GELATIN G E L AT I N SALINE L A C TAT E SOLUTION
HUMAN 4% 10% 6% 6% 6%
VA R I A B L E PLASMA ALBUMIN (200/0.5) (450/0.7) (130/0.4) (130/0.42)

Hartmann’s
Normal or Ringer’s
Trade name Albumex Hemohes Hextend Voluven Volulyte Venofundin Tetraspan Gelofusine Haemaccel saline lactate PlasmaLyte
Colloid Human Potato Maize Maize Maize Potato Potato Bovine Bovine
source donor starch starch starch starch starch starch gelatin gelatin
Osmolarily 291 250 308 304 308 286 308 296 274 301 308 280.6 294
(mOsm/L
Sodium 135-145 148 154 143 154 137 154 140 154 145 154 131 140
(mmol/L)
Potassium 4.5-5.0 3.0 4.0 4.0 5.1 5.4 5.0
(mmol/L)
Calcium 2.2-2.6 5.0 2.5 6.25 2.0
(mmol/L)
Magnesium 0.8-1.0 0.9 1.5 1.0 3.0
(mmol/L)
Chloride 94-111 128 154 124 154 110 154 118 120 145 154 111 98
(mmol/L)
Acetate 34 24 27
(mmol/L)
Lactate 1-2 28 29
(mmol/L)
Malate 5
(mmol/L)
Gluconate 23
(mmol/L)
Bicarbonate 23-27
(mmol/L)
Octanoate 6.4
(mmol/L)

Note: to convert the values for potassium to milligrams per decilitre, divide by 0.2558. To convert the values for calcium to milligrams per decilitre, divide by 0.250. To convert the
values for magnesium to milligrams per decilitre, divide by 0.4114.
Adapted from Myburgh JA, Mythen MG. Resuscitation fluids. New Engl J Med 2013;369:1243–51, with permission.
 CHAPTER 21 PATHOPHYSIOLOGY AND MANAGEMENT OF SHOCK 689

transfusion is defined as replacement of a patient’s total

blood volume in less than 24 hours. This equates to Practice tip
approximately 10 units of packed red blood cells,46,52,53 Blood product usage
although there are inconsistent descriptions in the
Keep up to date and download abbreviated recom-
literature.53 A number of complications following massive
mendations and tools for use at the bedside from the
transfusion can be evident such as transfusion reactions,
National Blood Authority (Australia) website as they are
coagulopathies, hypothermia and sepsis.8 Massive trans-
completed (see Online resources). Always refer back
fusion is also associated with high mortality.53
to your local policies and guidelines before patient
Patients receiving massive blood transfusions require
intervention.
careful monitoring for signs of metabolic derangements,
hypothermia, citrate toxicity, hyperkalaemia and coag-
ulopathies because clotting factors are often depleted. The Australian National Blood Authority Critical
Bleeding/Massive Transfusion guideline makes clear
Dilution and clotting factor consumption cause micro-
recommendations about blood product use during haem-
vascular bleeding, often manifesting as oozing from
orrhage. See Figure 21.3 for the Massive Transfusion
multiple sites even after surgical correction.52,53 Massive
Protocol template.
transfusion of stored blood with high oxygen affinity
The use of tranexamic acid, an antifibrinolytic agent,
adversely affects oxygen delivery to the tissues. It is
is on the increase for patients in need of massive trans-
therefore preferable to transfuse blood cells that are
fusion.54 Mortality was reduced in a large randomised
less than 1 week old; 2,3-diphosphoglycerate levels rise
controlled trial of more than 20,000 trauma patients in
rapidly after transfusion, and normal oxygen affinity
those patients that received tranexamic acid.55 The survival
is usually restored within a few hours of transfusion.52
benefit in this study was greatest when treatment occurred
Current research is underway by the Australian and
in the first hour. This effect was all but lost if adminis-
New Zealand Intensive Care Society Clinical Trials
tered more than 3 hours after injury. Even though a large
Group to determine if fresher blood decreases 90-day sample, these results have given rise to significant debate
mortality (TRANSFUSE ClinicalTrials.gov identifier: about including the use of tranexamic acid in guidelines
NCT01638416 – see Online resources). due to insufficient evidence.56
Each unit of blood contains approximately 3 g of
citrate, which binds to ionised calcium. A healthy adult
liver metabolises 3 g of citrate every 5 minutes. If blood Cardiogenic shock
is transfused rapidly or liver function is impaired, citrate Cardiogenic shock manifests as circulatory failure from
toxicity and hypocalcaemia may develop. The patient cardiac dysfunction,57 and is reflected in a low cardiac output
should therefore be monitored for signs of tetany, (cardiac index <2.1 L/min/m2), hypotension (systolic
hypotension and electrocardiographic evidence of hypo- blood pressure <90 mmHg), severe pulmonary congestion
calcaemia.52 As stored blood ages, plasma potassium and high central vascular filling pressures (pulmonary
levels rise (possibly to over 30 mmol/L). Hypokalae- artery occlusion pressure >18 mmHg).58 Additional
mia may be more common as red cells begin active parameters obtained through invasive monitoring include
metabolism and intracellular uptake of potassium restarts intrathoracic blood volume index >850 mL/m2, global
with transfusion.52 end-diastolic volume >700 mL/m2 and extravascular
Acid–base disturbances may also be evident due to the lung volume index >10 mL/kg.59,60 Cardiogenic shock
stored blood lactic acid levels and the citric acid. Citrate is commonly associated with acute myocardial infarction
is metabolised to bicarbonate, and metabolic alkalosis and manifests when 40% or more of the left ventricle is
may result from massive blood transfusion. As hypo- ischaemic. It is also related to mechanical disorders such as
thermia causes reduced citrate and lactic acid metabolism, acute cardiac valvular dysfunction or septal defects, deteri-
an increase in the affinity of haemoglobin to oxygen, orating cardiomyopathies or congestive cardiac failure,61
platelet dysfunction and an increased tendency for cardiac and trauma. Cardiogenic shock can also occur as a result
dysrhythmias,52 the patient and the blood transfused of obstruction or inhibition of left ventricular ejection,
should be warmed to avoid complications. also referred to as obstructive shock, such as occurs in
Leucocyte depletion occurs during donation in many pulmonary embolus, dissecting aneurysm or cardiac
countries. This decreases upregulation of the inflam- tamponade27,61 (see Chapter 10). Myocardial depression
matory immune response associated with transfusion. from non-cardiac causes such as sepsis, acidosis, myocardial
Internationally, there are a number of organisations that depressant factor, hypocalcaemia or drug impact62 may be
produce guidelines for blood transfusion. The Council so severe as to present as cardiogenic shock.
of Europe has published a high level guide on the prepa- Incidence has been estimated at 3% of patients
ration of and quality assurance on the use of blood presenting with acute myocardial infarction. Mortality
components. The Australian National Blood Authority remains high (50–80%)63 given death from acute
has published four comprehensive and easy-to-use myocardial infarction overall is 7%.This increased mortality
clinical practice guidelines (see Practice tip). occurs despite treatment advances such as emergency
690 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

FIGURE 21.3 Massive transfusion protocol.

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Adapted from http://www.blood.gov.au/system/files/documents/pbm-module1-mtp-template_0.ppt, with permission.

revascularisation.64,65 Wider distribution of interventional Because of similar clinical presentation, obstructive

cardiac revascularisation services has likely improved shock is at times described as cardiogenic shock. Obstruc-
outcome for patients who present early in the course of tive shock is not as common as other types of shock9 and
their acute disease. Current timing recommendations for is associated with a low cardiac output due to extra cardiac
treating myocardial infarction with ST elevation with processes inhibiting circulatory flow. The two main types
primary percutaneous coronary intervention include a are associated with impedance to cardiac filling from causes
door-to-balloon time of 90 minutes or less to improve such as tension pneumothorax and cardiac tamponade and
outcomes.66 factors that increase afterload such as aortic dissection or
Clinical signs include poor peripheral perfusion, massive pulmonary embolus.67 Examples of conditions
tachycardia and other signs of organ dysfunction such that can lead to obstructive shock are provided in
as confusion, agitation, oliguria, cool extremities and Table 21.6. Obstructive shock may be temporarily treated
dyspnoea, many of which are present in hypovolaemic by maintaining preload with fluid resuscitation until
shock.57 Compensatory mechanisms are conflicting, as definitive intervention to remove the obstruction to
cardiac workload is increased on an already-failing heart forward blood flow.
yet cardiac muscle oxygen delivery may be compro- Managing patients with heart failure as a result of cardio-
mised. A careful but rapid assessment of the clinical genic shock can be challenging and is often undertaken
history is helpful in differentiating the precipitant cause simultaneously with preparation for definitive treatment.
of this shock. Maintaining perfusion is difficult, as compensatory
 CHAPTER 21 PATHOPHYSIOLOGY AND MANAGEMENT OF SHOCK 691

TABLE 21.6
Obstructive shock types

TYPE DESCRIPTION SIGNS AETIOLOGY TYPICAL MANAGEMENT

Cardiac Acute circulatory Anxiety, hypotension, Pericardial injury, aortic Pericardial drainage
tamponade failure secondary to chest pain, tachypnoea, dissection, trauma, post
compression of the heart pulsus paradoxus, cardiac surgery and
chambers by a pericardial tachycardia, high CVP rarely infective causes
effusion Symptoms include
right sided diastolic
collapse
Tension Progressive build-up Deviated trachea away Penetrating chest injury, Needle thoracostomy
pneumothorax of air within the pleural from the affected side, blunt trauma, hospital as soon as possible
space by allowing air hyperexpansion on the procedures such as (large cannula inserted
in but not out; pressure side of the pneumothorax insertion or removal of to the 2nd intercostal
in the pleural space with little air movement central lines, lung biopsy space at the mid-
pushes the mediastinum and distended neck veins clavicular line); however
to the opposite side, this procedure is not
obstructing venous return without complications
to the heart and it has been
suggested that the
diagnosis should be
confirmed on X-ray prior
to the procedure, and
a pleural drain will be
required after
Pulmonary Thrombotic occlusion of Increases right-sided Shortness of breath, Thrombolysis or surgical
embolism a pulmonary artery afterload, enlarges RV chest pain, haemoptysis embolectomy
and deviates septum to
left, thus decreasing left
ventricular volume and
compliance

CVP = central venous pressure; RV = right ventricle.

Adapted from Bodson L, Bouferrache K, Vieillard-Baron A. Cardiac tamponade. Curr Opin Crit Care 2011;17:416–24, with permission.

mechanisms usually cause further harm to the heart.

BOX 21.1
While judicious administration of fluid is considered in
terms of optimising remaining cardiac function, admin- Clinical features of cardiogenic shock:
istration of pharmacological agents that reduce cardiac
• low cardiac output and hypotension
workload and improve function is paramount: dobutamine
for inotropic and afterload-reducing effects via vaso- • poor peripheral perfusion – pale, cool, clammy
dilation and morphine to reduce pain, improve coronary peripheries
perfusion and reduce oxygen demand. Treatment of the • oliguria
underlying cause is critical and may include surgery to • altered mentation, restlessness and anxiety
repair obstruction to flow or percutaneous resolution of • tachycardia and arrhythmias
a coronary artery blockage. See Chapter 10 for a more • pulmonary congestion with widespread inspiratory
detailed discussion of the management of acute myocardial crackles and hypoxaemia (perhaps with frank
infarction and heart failure. pulmonary oedema)
Clinical manifestations • dyspnoea and tachypnoea
The clinical features of cardiogenic shock are reflective of • respiratory alkalosis (hyperventilation) or acidosis
congestive cardiac failure, although with greater severity58,59 (respiratory fatigue)
(see Box 21.1). Other symptoms consistent with the cause • lactic acidosis
of the cardiogenic shock may also be present, including • distended neck veins, elevated jugular venous
chest pain and ST-segment changes, murmurs, features of pressure.
pericardial tamponade and arrhythmias.
692 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

In the absence of invasive monitoring, the profile requirements. Systemic oxygen delivery falls in proportion
of hypotension, peripheral hypoperfusion and severe to a declining cardiac output, and is further exacerbated
pulmonary and venous congestion is evident although as hypoxaemia develops with pulmonary oedema. Initially,
this ‘classic’ profile is not universal. On initial examination, oxygen consumption may be sustained by an increase in
approximately 30% of patients with shock of left ventric- tissue oxygen extraction ratio.72 A quarter of delivered
ular aetiology will have no pulmonary congestion and an oxygen is extracted by tissues but, as delivery falls, tissues
estimated 9% will have no hypoperfusion.69 extract proportionally more oxygen to meet metabolic
Based on the underlying pathology of an acute left needs. Oxygen consumption can therefore be sustained
ventricular myocardial infarction, the structural or contrac- until the severity of oxygen delivery deficit exceeds
tile abnormality impairs systolic performance resulting the ability to increase extraction. Maximal extraction
in incomplete left ventricular emptying.58 This results in is approximately 50%, and consumption falters when
subsequent progressive congestion of first the left atrium, oxygen delivery falls to around 500–600 mL/min (cardiac
then the pulmonary circulation, right ventricle, right index <2.2 L/min/m2).72,73 While use of a pulmonary
atrium and finally the venous circulation.58,70,71 When artery catheter is a well-described measure of severity in
invasive haemodynamic monitoring is available, changes cardiogenic shock (as with hypovolaemic shock), evidence
that may be observed include decreased cardiac output of improved patient outcome is unclear.25,33
and increased systemic resistance and myocardial oxygen Once oxygen consumption falls, subsequent anaerobic
demand (see Figure 21.4). metabolism leads to lactic acidosis.21,58 Progressive tissue
A patient with cardiogenic shock is also assessed and ischaemia and injury ensues, along with worsening
monitored for their oxygen delivery and tissue oxygen metabolic acidosis unless oxygen delivery can be restored.

FIGURE 21.4 Sequence of haemodynamic changes in cardiogenic shock.

Systolic dysfunction
stroke volume, ejection fraction

Blood pressure Cardiac output

Sympathoadrenal activation
(compensation)

Systemic
Heart rate Inotropy
vascular resistance

Myocardial oxygen demands

(± ischaemia)

Congestion
left ventricular end-diastolic volume and pressure
left atrial pressue
global end-diastolic volume index
pulmonary capillary wedge pressure
pulmonary artery pressure
extravascular lung water index
intrathoracic blood volume index
right ventricular systolic/diastolic pressure
right atrial pressure
 CHAPTER 21 PATHOPHYSIOLOGY AND MANAGEMENT OF SHOCK 693

Myocardial contractile performance continues to deteri- Optimising oxygen supply and demand
orate when myocardial ischaemia develops or when As cardiogenic shock is associated with an imbalance of
existing ischaemia or infarction extends, leading to a oxygen supply and demand throughout the body, measures
vicious cycle of ischaemia and dysfunction.72 to optimise this balance by increasing oxygen supply and
Compensatory responses effective in hypovolaemic decreasing demand are essential (see Box 21.2).
shock are initially advantageous, but may ultimately be
counterproductive when cardiogenic shock is due to
myocardial infarction: BOX 21.2

• Tachycardia offsets low stroke volume but increases Managing oxygen supply and demand
myocardial oxygen consumption and decreases Strategies to increase oxygen supply include:
diastolic duration, reducing coronary perfusion time.
• positioning the patient upright to promote optimum
• Vasoconstriction limits the severity of hypotension ventilation by reducing venous return and lessening
but increases resistance to left ventricular emptying pulmonary oedema; this strategy may contribute to
and may contribute to worsening of the cardiac hypotension
output, in particular when cardiogenic shock is due
• administering oxygen, continuous positive airway
to contractile dysfunction.
pressure and bi-level positive airway pressure
• An increase in cardiac workload to overcome the support as required.75
rise in systemic afterload increases myocardial oxygen
Strategies to reduce oxygen demand include:
demand, which cannot be met due to coronary artery
occlusion. • limiting physical activity

• Developing pulmonary congestion is no longer • implementing measures to reduce patient anxiety,

contained within the pulmonary capillary and moves including communication, explanation and
into the alveolar capillary space, creating pulmonary analgesic and sedative medications. Avoid those
oedema, further impeding oxygen delivery to the medications that are cardio-depressive.
circulation.
Patient management Preload management
Treatment of cardiogenic shock includes haemodynamic Preload reduction relieves pulmonary congestion, reduces
management, respiratory and cardiovascular support, myocardial workload and improves contractility, which
biochemical stabilisation and reversal or correction of the is in part impaired by overstretched ventricles. Careful
underlying cause. This complex presentation requires a assessment of patient fluid status is necessary prior
coordinated approach to the multiple aspects of care of to either the administration of small aliquots of fluid to
a patient with cardiogenic shock. enhance deteriorating myocardial function or enhanced
A rapid response to impending deterioration associated diuresis to reduce circulating blood volume. Any fluid
with cardiogenic shock includes repeated assessment offloading is balanced against the risk of excessive blood
and measures to optimise oxygen supply and demand. volume depletion and depression of cardiac output
Frequent, thorough assessment of the patient’s status is and blood pressure. Desired end points of therapy may
essential, and should focus on: include a reduction in right atrial, pulmonary artery and
1 identification of patients at risk of clinical pulmonary artery occlusion pressures, or improvements in
deterioration
2 assessment of the severity of shock and identification Practice tip
of organ or system dysfunction
3 assessment of the impact of treatment Measures to reduce preload include:

4 identification of complications of treatment. • sitting a patient up with their legs either hanging
over the side of the bed or in a dependent position
Assessment follows a systematic approach and is
conducted as often as indicated by the patient’s condition, • IV diuretics such as frusemide1 usually administered
centring on the cardiovascular system as well as related as an intermittent bolus or if necessary as a
systems that cardiac function influences, including respira- continuous infusion
tory, renal, neurological and integumentary systems. • venodilation (glyceryl trinitrate infusions at
Typical treatment regimens require preload reduction, 10–200 mcg/min titrated to blood pressure)3
augmentation of contractility with intravenous inotropes • ultrafiltration (may be considered to rapidly reduce
and afterload manipulation. These aspects are undertaken circulating volume)
concurrently due to the potential severity of cardiogenic • respiratory support with continuous positive airway
shock. Endotracheal intubation with mechanical ventilation pressure (indicated for pulmonary relief, with the
is implemented if necessary, but the need for mechanical additional benefit of reducing venous return).
ventilation is associated with an increase in mortality.74
694 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

intrathoracic blood volume, global end-diastolic volume Currently available inotropes are not uniform in their
and extravascular lung water, depending on available beneficial effect on cardiac output and blood pressure
monitoring equipment. because of additional vasoactive actions (either vaso-
Additional measures to reduce pulmonary hyper- dilation or constriction) (see Table 21.7). Selection of
tension may be employed. Morphine is useful to lessen an inotropic agent is therefore partly based on inotropic
anxiety and oxygen demands during cardiogenic shock, potency as well as the desired effect on vascular resistance:
and may offer additional benefits by reducing pulmonary
artery pressure and pulmonary oedema.76 Other treatment • vasodilation in addition to inotropy (inodilator effect)
favours cardiac output, but may compromise blood
options include correction of hypercapnoea, if present,
and nitric oxide by inhalation. pressure76
• vasoconstriction in addition to inotropy
Inotropic therapy (inoconstrictor effect) improves blood pressure,
Intravenous positive inotropes promote myocardial but may at times compromise left ventricular
contractility to improve cardiac output and blood pressure. emptying and cardiac output.

TABLE 21.7
Vasoactive agents

PHYSIOLOGICAL NURSING
DRUG ACTIONS DOSE RANGE EFFECTS C O N S I D E R AT I O N S
dobutamine Synthetic adrenergic 100–200 mcg/min Inotropy CVC administration
agonist Vasodilation Arrhythmia risk
β1-agonist ↑↑ Cardiac output Excess dilation may cause
β2-agonist ↑Blood pressure hypotension
↑Heart rate
dopamine Dopaminergic ‘Inotropic’ dose: Mainly inotropic CVC administration
β1-agonist 5–10 mcg/kg/min ↑Blood pressure Tachycardia
α-agonist (at higher doses) ‘High’ dose: ↑Cardiac output Arrhythmia risk
10–20 mcg/kg/min Vasoconstriction Risk peripheral vascular
dominates compromise
↑↑Blood pressure
levosimendan Calcium sensitiser Loading: 6–12 mcg/kg Inotropy Tachycardia
over 10 min Vasodilation Arrhythmia risk
Infusion: 0.05–0.2 mcg/kg/ ↑↑Cardiac output Risk hypokalaemia
min (max 24–48 hours use) Risk Q-T prolongation
Excess dilation may cause
hypotension
Half-life: 5 days
adrenaline Sympathomimetic 1–20 mcg/min or higher Potent inotrope and Tachycardia common
α-agonist constrictor Arrhythmia risk
β1-agonist ↑Cardiac output Risk peripheral vascular
β2-agonist ↑↑Blood pressure compromise
↑↑Heart rate Myocardial work
milrinone Phosphodiesterase Loading: 50–75 mcg/kg Inotropy Vasodilation may be
inhibitor Infusion: 0.375–0.75 mcg/ Potent vasodilator marked
kg/min ↑↑Cardiac output Observe for hypotension
↓Blood pressure
noradrenaline Sympathomimetic 1–20 mcg/min or higher Potent inotrope and Reflex bradycardias
α-agonist constrictor Arrhythmia risk
β1-agonist ↑↑Blood pressure Risk peripheral vascular
Little effect on β2-receptors ↑Coronary artery blood flow compromise
vasopressin Vascular (V-1) receptors 0.1–0.4 mcg/min Inotropy Check liver function
Renal (V-2) receptors ↑SVR
↑Vasoconstriction

CVC = central venous catheter; SVR = systemic vascular resistance; ↑ = increase; ↓ = decrease.
Adapted from: Lampard JG, Lang E. Vasopressors for hypotensive shock. Ann Emerg Med 2013;61:351–2 Magder SA. The highs
and lows of blood pressure: toward meaningful clinical targets in patients with shock. Crit Care Med 2014;42:1241–51.
 CHAPTER 21 PATHOPHYSIOLOGY AND MANAGEMENT OF SHOCK 695

All inotropes present a paradox in the treatment of Afterload control

cardiogenic shock, as they have the potential to increase Specific management of afterload, independent of
heart rate and myocardial oxygen demands, and increase the contractility, is sometimes necessary, although caution
frequency of arrhythmias. Monitoring is used to identify is needed as the maintenance of blood pressure often
heart rate, rhythm and the development of ST-segment or provides little scope for further afterload reduction. Arte-
T-wave changes. The best regimen for cardiogenic shock riodilators such as sodium nitroprusside reduce afterload
has not been established. There is controversy about using and increase cardiac output, although with limitations due
drug combinations with opposing effects; however, there is to hypotension.85 The introduction of oral angiotensin-
evidence that using dilators and pressors together is superior converting enzyme inhibitors is recommended as soon
to the use of inopressors alone.80 The vasodilation seen with as possible after stabilisation of the patient with infarct-
inodilator agents may reduce both preload and afterload, related cardiogenic shock.86,87
leading to more effective myocardial pumping and an
increased cardiac output. The effect on blood pressure is Adjunctive therapies
variable, as the opposing actions of increased contractility A range of adjunctive therapies is available for refractory
and vasodilation are not uniform in potency, and occur with shock, when first-line treatments are ineffective, and
differing effects between patients. By reducing afterload, left can include insertion of an intra-aortic balloon pump
ventricular emptying is favoured with a reduction in cardiac (IABP), extracorporeal membrane oxygenation (ECMO),
contractility, reducing myocardial oxygen demand.81–83 In initiation of mechanical ventilation and correction of
a large study of more than 900 patients with cardiogenic metabolic disturbances. These strategies are discussed
shock requiring a vasopressor agent to maintain perfusion, below in relation to cardiogenic shock.
short-term mortality was improved when a dilator was part
of the medication regimen.80 Intra-aortic balloon pumping
Inoconstrictors constrict the vasculature, resulting Low cardiac output, pulmonary congestion, reduced
in increased preload and afterload while also increasing mean arterial pressure and myocardial ischaemia from
myocardial contractility.77 These increases, particularly cardiogenic shock may all be improved by the introduc-
in afterload, generally result in a raised blood pressure, tion of IABP therapy (see Chapter 12). Balloon inflation
but the impact on cardiac output is less predictable. An during diastole raises mean arterial pressure and promotes
increase in cardiac output is often seen with these agents, coronary and systemic blood flow, while balloon deflation
but the increase in afterload may become limiting to left in advance of systole reduces afterload. This afterload
ventricular emptying when there is significant contrac- reduction improves cardiac output and reduces left ventric-
tile impairment. Inoconstrictors are therefore generally ular systolic pressure, lessening the oxygen demands of the
selected when the afterload and resultant blood pressure are ischaemic ventricle by reducing the necessary contractile
more severely compromised than the cardiac output.Vaso- force of the left ventricle. In a large trial database, IABP
constriction also further increases myocardial work and did not impart a survival benefit at 12 months in an open
myocardial oxygen demand, and may worsen ischaemia.80 label trial comparing outcomes from patients with early
Dobutamine has traditionally been the inodilator of revascularisation and optimal medical management.88
choice,84 although accumulating evidence for levosi-
mendan, a calcium-sensitising agent, suggests improved Extracorporeal membrane oxygenation
outcomes.81,83 The slow onset of action time of levosi- ECMO is an accepted treatment of cardiac failure when
mendan (hours) makes it a less suitable drug for acute persistent shock is evident despite adequate fluid resusci-
resuscitation; other inotropes are therefore currently used tation and administration of vasopressors and inotropes.
initially and, if required, levosimendan is introduced later. ECMO is defined as the temporary use of a modified
The long half-life (>5 days) of levosimendan confers a cardiopulmonary bypass circuit for support of patients with
lasting impact on contractility after cessation of the infusion. potentially reversible cardiac and/or respiratory failure.89
Milrinone is also an effective inodilator,77 but excessive ECMO provides a mechanism for gas exchange as well as
vasodilation may contribute to significant hypotension; in cardiac support thereby allowing for recovery from existing
practice, a concurrent vasoconstrictor (e.g. noradrenaline) disease. This therapy is complex and should be provided in
may be administered. Close management of intravascular centres where adequate facilities and human resources are
fluid volume is critical when using these agents. available to ensure optimal implementation.90
Dopamine and adrenaline are the major agents in Management of the patient receiving ECMO is
the inoconstrictor class, and are more effective at raising complex. Often, more than one nurse is required to
blood pressure than inodilators. Both agents also increase provide support in the first 24 hours. Large bore catheters
cardiac output, but when there is significant impairment are used to ensure adequate extracorporeal circulation.
of contractility the increase in afterload may cause cardiac Apart from the infective risk, disconnection poses a risk
output to suffer. Importantly, inoconstrictors increase of rapid exsanguination. While ECMO provides cardiac
myocardial work and oxygen demands, raise heart rate support and gas exchange it is vital to continue to promote
and increase the risk of tachyarrhythmias; these impacts recovery by maintaining cardiac function and reducing
are stronger with adrenaline than for dopamine. the risk of complications.
696 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Respiratory support • hypokalaemia or hypomagnesaemia due to aggressive

Varying degrees of pulmonary oedema accompany cardio- diuretic use
genic shock, causing hypoxaemia due to intrapulmonary • hyperkalaemia due to severe acidosis, especially in the
shunt, decreased compliance and increased work of presence of renal failure
breathing. Hyperventilation with respiratory alkalosis may • hyperglycaemia due to the stress response to acute illness,
initially compensate for hypoxaemia and lactic acidosis, and in response to sympathomimetic administration
but fatigue during this increased work of breathing may
cause patient progression to hypoventilation and respira-
• decline in bicarbonate levels due to pH buffering,
although replacement therapy is not routinely
tory acidosis. Oxygen is administered for hypoxaemia, but undertaken unless the arterial pH is life-threatening
the response may be limited as the primary gas exchange
defect is an intrapulmonary shunt. Non-invasive venti- • urea and creatinine to detect the onset of acute renal
latory approaches may be sufficient, but intubation and failure due to renal hypoperfusion.
mechanical ventilation may be required in the acute Renal replacement therapies may be used for fluid
phase of treatment. Continuous positive airway pressure and electrolyte control when renal function suffers or as
at conventional levels of 5–15 cmH2O is well established a strategy for unloading fluid from the circulation (see
as a support for the spontaneously breathing patient with Chapter 18).
pulmonary oedema.91 This respiratory support strategy
improves hypoxaemia, decreases work of breathing, Sepsis and septic shock
reduces left ventricular afterload and provides additional
benefit by impeding venous return, an effect that may Severe sepsis and septic shock is a leading cause of
lessen pulmonary congestion. These benefits are weighed admission to ICU and has an associated high mortality.
against the potential for hypotension. The terms ‘severe sepsis’ and ‘septic shock’ were defined
If hypoventilation and dyspnoea continue despite the and then refined during international consensus
use of continuous positive airway pressure, non-invasive meetings that also described the systemic inflammatory
bi-level positive airway pressure may be considered. response syndrome.95 The incidence of severe sepsis in
Additional pressure support is applied during inspiration, the European Union has been estimated at 90.4 cases
above existing baseline pressure, improving inspiratory per 100,000 population and the estimated annual rate
efficiency, with increased tidal volume and reduced work worldwide is 1.8 million cases.96 Accuracy of this figure
of breathing.92,93 Endotracheal intubation and ventilation is likely hampered by the ongoing worldwide issues with
should be undertaken when neither strategy results in recognition. The incidence of severe sepsis in Australia
improvement, or when the patient continues to deterio- and New Zealand was 11.8% of ICU admissions, with
rate or tire. Many clinicians prefer to intubate and ventilate median ICU and hospital stays of 6 days and 18 days,
early, even in the absence of a specific respiratory need, to respectively, and corresponding mortality rates of 32% at
decrease the cardiovascular demands of the greater venti- 28 days and an in-hospital mortality of 40%.97 Recent
latory effort. However, this approach is controversial as Australian data show mortality remaining relatively high
mechanical ventilation is associated with poorer patient but in decline.35,98 In fact, between 2000 and 2012 a retro-
outcomes93 and disturbs cardiovascular balance as it exerts spective observation study showed a mortality decrease of
changes to intrathoracic pressures, particularly at inspira- 16.1% over the time period.99 The consequence of early
tory initiation. reports of such high mortality focused attention on sepsis
Ventilation strategies largely reflect those for other and its associated sequelae in the critical care literature,
compliance disorders such as adult respiratory distress and led to a worldwide campaign in 2002 to reduce the
syndrome and are described in more detail in Chapter mortality from sepsis.
15. Initially, full mechanical ventilation with little or no The Surviving Sepsis Campaign
contribution from the patient is appropriate to correct
The Surviving Sepsis Campaign is an international
arterial blood gases and lessen the cardiovascular demands
collaborative formed after the Barcelona Declaration
of the ventilatory burden. Subsequent reduction of venti-
in 2002 to reduce the mortality of sepsis by 25% over
latory support, as the patient’s respiratory ability improves,
a 5-year period. The aims included increasing awareness
follows conventional processes.
and developing treatment guidelines for severe sepsis and
Biochemical normalisation shock, including a comprehensive list of graded recom-
mendations (now in its third version).100–102 Worldwide
Frequent biochemistry measurement is necessary to detect
Sepsis Day occurs on September 13 each year to continue
and monitor the following aspects of care:
the push for improving outcomes. Although the first
• arterial blood gases to identify the adequacy of version of the sepsis guidelines was supported by many
ventilation and oxygenation and the presence countries, the second and much expanded version was
of metabolic acidosis not endorsed in Australia,98 as many of the recommenda-
• lactic acid measurement to assess the level of shock tions were based on research involving non-ICU and/or
and changes in patient response to treatment non-sepsis patients.
 CHAPTER 21 PATHOPHYSIOLOGY AND MANAGEMENT OF SHOCK 697

The most recent update of the ‘Surviving Sepsis to severe hypoglycaemia.109 A meta-analysis of 26 ICU-
Campaign Guidelines’ was published in 2013 and outlines related ‘tight glycaemic control’ studies suggested that
evidence-based recommendations for the management the practice could increase risk to ICU patients.110 The
of severe sepsis and septic shock. Various recommenda- more pragmatic approach of maintaining blood glucose
tions were combined to form ‘care bundles’, which are levels close to normal without inducing hypoglycaemia
interventions or care elements implemented together to and other metabolic imbalances is therefore appropri-
achieve better outcomes.103 Bundles have been introduced ate.107 The Surviving Sepsis guideline was modified in
to change processes of care and as quality or benchmarking 2009 to maintain currency.The 2012 version recommends
measures (see Chapter 3). Further research and evaluation a protocolised approach to instituting insulin to manage
is needed as mortality benefits of ‘care bundles’ may be hyperglycaemia when two consecutive measurements are
a result of increased clinician awareness rather than the greater than 10 mmol/L with blood glucose measured
impact of treatment changes.104 In a recent meta-analysis every 1–2 hours until stable and then 4-hourly, preferably
of the 6- and 24-hour sepsis bundles, the better treatment using arterial sampling to target an upper blood glucose
effect was seen with the 6-hour bundle.105 Current bundles ≤180 mg/dL (10 mmol/L).101
can be found on the Surviving Sepsis website and include
the 3- and 6-hour bundle. The current suggested sepsis Clinical manifestations
bundles appear in Box 21.3. Septic shock results when infectious agents or infection-
Some bundles were developed then refuted, so it is induced mediators in the bloodstream produce haemody-
important for critical care nurses to continuously update namic compromise. Primarily a form of distributive shock,
knowledge as further evidence becomes available. An it is characterised by ineffective tissue oxygen delivery and
example of a refuted bundle relates to tight glycaemic extraction associated with inappropriate peripheral vaso-
control. The recommendation in the Surviving Sepsis dilation, despite preserved or increased cardiac output.70
guidelines supported tight glycaemic control in earlier Hypovolaemia is also associated with septic shock due
versions.107,108 The NICE-SUGAR study subsequently to the characteristic increased vasodilation. This presents
concluded that measures to maintain blood glucose level a clinical picture of a warm, pink and apparently well-
of ≤10 mmol/L increased mortality, particularly in relation perfused patient in early stages of septic shock with an
elevated cardiac output, in contrast to that seen in hypo-
BOX 21.3 volaemic or cardiogenic shock patients.
Unchecked, cellular dysfunction in the presence of a
Types of sepsis bundles failing compensatory process leads to cellular membrane
Resuscitation bundle (now called the 3-hour bundle): damage, loss of ion gradients, leakage of lysosomal
1 Measure lactate. enzymes, proteolysis due to activation of cellular proteases
and reductions in cellular energy stores that may result
2 Culture prior to administration of antimicrobials.
in cell death. Once enough cells from vital organs have
3 Administer empirical (broad spectrum) reached this stage, shock becomes irreversible and death
antimicrobials as soon as possible. can occur despite eradication of the underlying septic
4 Volume-load as appropriate. (Administer 30 mL/kg focus. About half of patients who succumb to septic shock
crystalloid for hypotension or lactate ≥4 mmol/L.) die of failure of multiple organs.70
Sepsis management bundle (now called the 6-hour The effect of sepsis and septic shock on the cardio-
bundle): vascular system is profound; the haemodynamic hallmark
is generalised arterial vasodilation with an associated
1 Use vasopressors for persisting hypotension or
decrease in systemic vascular resistance. Arterial vaso-
apply vasopressors (for hypotension that does not
dilation is mediated in part by cytokines that upregulate
respond to initial fluid resuscitation) to maintain a
the expression of inducible nitric oxide synthase in the
mean arterial pressure ≥65 mmHg.
vasculature. Vascular response to the vasodilatory effect of
2 In the event of persistent arterial hypotension nitric oxide and the activation of ATP-sensitive potassium
despite volume resuscitation (septic shock) or initial channels combine to cause closure of the voltage-gated
lactate ≥4 mmol/L (36 mg/dL): calcium channels in the cell membrane. As the vasocon-
a maintain adequate central venous pressure strictor effect of noradrenaline and angiotensin II depends
b maintain adequate central venous oxygen on open calcium channels, lack of response to these pressor
saturation hormones that are central to compensatory mechanisms
c re-measure lactate if initial lactate was elevated.
in shock can occur with the inevitable failure of delivery
of oxygen to the functional mitochondria, resulting in
lactic acidosis in patients with sepsis.111 With high circu-
Adapted from Barochia A, Cui X, Vitberg D, Suffredini AF,
O’Grady NP, Banks SM et al. Bundled care for septic shock:
lating levels of endogenous vasoactive hormones during
an analysis of clinical trials. Crit Care Med 2010;38:668–78, sepsis, downregulation of their receptors occurs.
with permission. Severe sepsis and septic shock includes four different
phenotypes, when using lactate level and blood pressure112
698 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

as clinical indicators: severe sepsis without hyperlactat- of early goal-directed therapy (EGDT) protocols34,117–119
aemia (where hyperlactataemia is defined as lactate >4 and is an often-documented end point of resuscitation,
mmol/L) and normotension (systolic blood pressure at EGDT has been widely discussed and criticised in the
least 90 mmHg); vasoplegic shock, persistent hypotension literature. Australian data indicate that the incidence of
without hyperlactataemia; dysoxia with hypotension and patients meeting the criteria and mortality is lower than
hyperlactataemia; and cryptic shock, defined as a hyper- the treatment group in the original EGDT trial.35 EGDT
lactataemia and normotension.112 There are increasing was the focus of the ProCESS trial,36 the ARISE trial in
numbers of studies comparing these profiles. Cryptic Australia and New Zealand37 and the ProMISe trial.120
shock and overt shock (vasoplegic and dysoxic profile), The ProCESS trial showed no significant outcome
defined as hypotension (systolic blood pressure lower difference between three resuscitation groups including
than 90mmHg), had a similar mortality in one study.113 two protocol-based approaches, EGDT and standard
This research is still evolving and the results from studies resuscitation, and the third group of ‘usual care’.36 Of note,
are equivocal; for example, another study was only able mortality rates were 18+% in all three groups, including
to demonstrate cryptic shock and vasoplegic shock had the control group. ARISE results showed no significant
similar outcomes.114 The learning from these studies is the difference in all-cause mortality at 90 days between EGDT
importance of vigilance in checking the haemodynamic and usual care. At the time of randomisation (median
profile of a patient and the biochemical results to ensure 2.8 hours), over 2.5 litres of fluid had been given to
deterioration is not overlooked. patients and time to antibiotics after arrival in emergency
department was <70 minutes. Similarly, mortality rates were
Early identification and diagnosis 18.6% in the EGDT and 18.8% in the usual care group.
Where a patient is able to respond cogently during history The EGDT group in the ARISE trial received more
and physical assessment, timelines of the infective process fluid in the first 6 hours and was more likely to receive
should be documented. Sites considered as infective vasopressors, red cell transfusions and dobutamine.37 Study
sources include decubitus ulcers, invasive lines, drains, critiques have identified the potential role that sepsis iden-
wounds, sinuses, ears, teeth, throat, chest, blood, lungs, tification and treatment in patients prior to randomisation
back, abdomen, perianal, genital/urinary tract, bones and may have played, along with notable lower mortality
joints. More invasive sampling may include bronchioalve- rates in both study groups. However, there is a plan to
olar lavage, cerebral spinal fluid, pleural fluid, abdominal pool the data from the three trials to perform a meta-
collections or biopsy of other sites as clinically appropri- analysis. It seems likely, given the results to date, the
ate. X-rays, computerised tomography scans and surgical Surviving Sepsis guidelines recommendations related to
consultation will also be a priority. EGDT may need to be reconsidered. Additionally, the role
of non-invasive evaluation using ultrasound assessment of
Patient management volume status and fluid infusion responsiveness and echo-
As with other forms of shock, initial management includes cardiography evaluation of cardiac contractility will need
not only acting to correct physiological deterioration by further consideration based on additional clinical trial data.
initiating fluid management and frequent observation and The current statement available on the Surviving Sepsis
assessment, but also addressing the underlying cause of website regarding EGDT indicates that the evidence is
sepsis through source (of infection) control. Goal-directed under review and that the guidelines will be updated
therapy includes prevention of tissue hypoxia, typically pending this review process.
through rigorous fluid resuscitation with either crystal- The ProMISe trial conducted in the UK was a
loids or colloids to achieve specific haemodynamic end pragmatic randomised controlled trial of 1260 patients
points, such as a central venous pressure of 8–12 mmHg, who received either EGDT or usual care. Despite patients
mean arterial pressure of >65 mmHg, and urine output in the EGDT group receiving more intravenous fluids,
>0.5 mL/kg/h. Vasopressor and inotropic therapy may vasoactive drugs and red-cell transfusions there was no
then be added to maintain adequate perfusion pressure; difference between the two groups in terms of 90-day
noradrenaline is the vasopressor of choice because of vaso- mortality.120
constrictor effects.115 Minimum continuous monitoring includes electro-
cardiogram, blood pressure, pulse oximetry and other
Initial resuscitation measures to assess preload and volume responsiveness,
The 2012 sepsis guidelines recommend a protocolised along with regular assessment of lactate, oxygenation and
approach for resuscitation for sepsis-induced shock, markers of inflammation and coagulation.
defined as tissue hypoperfusion where hypotension persists
after initial fluid challenge or where there is a blood lactate Source control and antimicrobial therapy
concentration ≥4 mmol/L. Measuring surrogate markers Identifying and removing the source of infection and
of preload as an indicator of volume status is a contentious treating the infection with appropriate antimicrobial
issue, as central venous pressure as a measure of preload therapy are the mainstays of therapy for a patient with
is not a good marker of volume responsiveness.31,116 sepsis. Research indicates that in the ICU setting the most
While central venous pressure was used in sepsis trials prevalent site of primary infection is pulmonary, followed
 CHAPTER 21 PATHOPHYSIOLOGY AND MANAGEMENT OF SHOCK 699

by abdominal, together accounting for approximately 70% odds ratio for death for albumin versus saline was 0.71.128
of cases.97,121,122 There have been a number of landmark studies published
To provide patients with appropriate antimicro- since SAFE but the fluid of choice remains controver-
bial treatment for targeting the infecting organism, sial. CHEST129 compared 0.9% sodium chloride with 6%
obtaining appropriate samples prior to instigating anti- hydroxyethyl starch and showed that fluid resuscitation of
microbial therapy is the clinical standard, although any all-comers requiring fluid resuscitation had no significant
prescribed treatment should not be delayed as time to outcome difference at 90 days but higher levels of renal
antibiotic administration is important in severe sepsis.123 injury. Nearly 29% of patients in the study were septic.130
The Surviving Sepsis guidelines recommend that, to Hydroxyethyl starch is not recommended for patients
optimise identification of causative organisms, at least with sepsis. This study, along with the retraction of many
two blood cultures should be obtained before antimi- research papers related to prior research,131 led to changes
crobial therapy with at least one drawn percutaneously globally in the recommendations for use of hydroxyethyl
and one drawn through each vascular access device.101 starch. More recently, the ProCESS trial showed no signif-
In a large retrospective study, every additional hour to icant outcome difference between three resuscitation
effective antimicrobial initiation in the first 6 hours after groups including two protocol-based approaches, EGDT
onset of hypotension was associated with >7% decrease and standard resuscitation, and the third group of ‘usual
in survival.123,124 Optimising dosage to achieve a thera- care’.36 A 2013 Cochrane review of eligible randomised
peutic concentration is also important. Current practice trials in critically ill patients supports the use of crystalloids
depends on the mechanism of action of the antibiotic. for resuscitation given the lack of clear outcome benefit of
For example glycopeptides are often continuously infused other fluids.132
to maintain a serum concentration above the minimum The Surviving Sepsis Campaign response to ProCESS
inhibitory concentration and therefore kill microbes more and ARISE maintains its 2012 guideline. The guidelines
effectively. More recently there has been evidence that do not advocate a preferred resuscitation fluid but support
beta-lactams should also be infused.125 Beta-lactams are fluid challenge in volume responsive patients.101 Crystal-
time dependent and the concentration needs to be 4 times loids are recommended as the initial fluid choice (up to
above the minimum inhibitory concentration in order to 30 mL/kg). Albumin is suggested when patients require a
have efficacy.126 Aminoglycosides have an effect through substantial fluid resuscitation.101
rapid administration to reach target concentrations and Irrespective of fluid selection, the disruption of the
have a ‘post-antibiotic effect’. vascular bed in early septic shock through widespread vaso-
Recently, a paradigm shift has been suggested in relation dilatation results in increased capillary permeability and
to antimicrobial therapy: to get it right the first time with rapidly developing interstitial oedema. Large amounts of
high doses, while limiting the duration of therapy and the fluid can be administered without seemingly improving
potential to increase resistance.127 Regardless, empirical oxygen delivery while adding to developing generalised
therapy should be de-escalated as soon as microbiology oedema that further impairs cellular delivery of oxygen and
results support directed therapy. nutrients. Fluid resuscitation alone is therefore of limited
value in septic shock and other measures must be considered.
Haemodynamic support and adjunctive
therapy Inotropes and vasopressors
A range of drug therapies aimed at supporting and amelio- A goal of maintaining mean arterial pressure greater
rating the signs and symptoms of septic shock is available than 65 mmHg is common, with inotropes and vaso-
and, while inotropes in particular provide an important pressors commenced when fluid resuscitation is
adjunct in managing the acute shock phase, other drug considered adequate. Administration of these drugs
therapies remain controversial. requires continuous blood pressure monitoring and
enables effective titration to meet the treatment goal. The
Fluid therapy in sepsis Surviving Sepsis guidelines recommend noradrenaline for
Fluid resuscitation with crystalloid or colloid has long been its specific alpha-receptor effects as the first choice vaso-
controversial in the critical care literature. The landmark pressor, with use of adrenaline (added or substituted) when
Saline versus Albumin Fluid Evaluation (SAFE) study49 an additional agent is needed, with the use of vasopressin
demonstrated that, in the adult intensive care patient 0.03 units/min added to or substituted for noradrenaline.
population, albumin can be considered safe, without Dobutamine (2.5–10 mcg/kg) may be added to
demonstrating any clear advantage over sodium chloride support patients with myocardial dysfunction to increase
0.9%. In the study, 6997 patients were randomised to receive myocardial contractility and oxygen delivery to the
either saline (n = 3500) or albumin (n = 3497). No signif- tissues.101 Refractory hypotension, resistant to vasopres-
icant differences were noted between the two treatment sors, has been linked to downregulation of receptors.
groups for 28-day all-cause mortality, days in intensive care, Vasopressin (0.4–0.6 units/h) has been shown to reduce
days in hospital, days on mechanical ventilation and days the requirements of other vasopressor agents.133
of renal replacement therapy.49 In a pre-defined subgroup Administration of vasopressin in vasodilatory shock
analysis of severe sepsis patients in this study, the adjusted may help maintain blood pressure despite the relative
700 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

ineffectiveness of other vasopressor hormones.111 Specifi- support for the first time.Adequate nutritional support with
cally, arginine vasopressin (AVP) may inactivate the KATP oral or enteral feeding to offset high caloric and protein
channels and thereby lessen vascular resistance to noradren- demands is preferred to fasting or parenteral glucose admin-
aline and angiotensin II. It also decreases the synthesis of istration. Chapter 19 provides further discussion of the
nitric oxide (as a result of a decrease in the expression of nutrition support relevant to patients with sepsis. Equally
nitric oxide synthase) as well as cyclic guanosine mono- important to patient-specific measures is institution of
phosphate signalling by nitric oxide.111 The sites of major diligent infection control practices in ICU.136
arterial vasodilation in sepsis – the splanchnic circulation, As the patient with severe sepsis and shock has a high
the muscles and the skin – are vascular beds that contain mortality rate, addressing goals of care is an additional area
abundant arginine vasopressin (AVP) receptors. In sepsis, of focus recommended in the guidelines. The guidelines
vasopressin stores are quickly depleted. Administration of outline that the prognosis for achieving goals of care
exogenous arginine vasopressin (0.04–0.06 units/min) can and the level of certainty for the prognosis be discussed
raise blood pressure by 25–50 mmHg by returning plasma with patients and families; that treatment plans should
concentrations of antidiuretic hormones to their earlier incorporate palliative care principles and, as appropri-
high levels.111 ate, end-of-life care planning; and that goals of care be
Steroids addressed as early as feasible but no later than within
72 hours of ICU admission.101 As critical care nursing
The use of steroid therapy in severe sepsis remains contro- promotes patient- and family-centred care, addressing
versial. At times, steroid replacement therapy may be used the needs of families and providing ongoing information
when patients display resistance to increasing doses of and support are essential. A modified Delphi study using
adrenergic agonists, as might occur in adrenal insufficiency. a group of international nurses used the Surviving Sepsis
Some research indicates that patients with septic shock guidelines as the basis of making 63 consensus recom-
who are unable to increase cortisol levels in response to
mendations for sepsis care.137 Recommendations relate
a challenge may benefit from administration of low-dose
to prevention and management, particularly in relation to
corticosteroids134 (see Chapter 22). The Surviving Sepsis
recognition and management of deterioration. Paediatric
guidelines recommend not using intravenous hydrocorti-
recommendations are also included (see Further reading).
sone to treat adult septic shock patients if adequate fluid
resuscitation and vasopressor therapy are able to restore Symptom management of fever is prevalent in hospitals.
haemodynamic stability. Where this is not achievable, Treatment with medicines that have an antipyretic effect
the use of intravenous hydrocortisone alone at a dose of has been considered a standard of care without the support
200 mg per day is recommended.101 of good evidence. Fever is an adaptive response to infection
and is beneficial in activating various immune responses.
Supportive therapy A study in progress is the HEAT trial,138 which aims to
The Surviving Sepsis guidelines outline several areas of explore if permissive hyperthermia through avoidance
supportive therapy including blood product administra- of paracetamol in known or suspected infection in ICU
tion, renal replacement therapy, stress ulcer prophylaxis, improves survival to 28 days. In the absence of good
deep vein thrombosis prophylaxis and nutritional support. evidence around the benefit of reducing temperature
Red blood cell transfusion is recommended when the in sepsis and the potential harm from inhibiting normal
haemoglobin concentration decreases to <7.0 g/dL to immune responses, the pragmatic approach of supporting
target a haemoglobin concentration of 7.0 to 9.0 g/dL in patient comfort seems reasonable when considering
adults. In patients with severe sepsis, platelets are recom- measures to normalise temperature.
mended to be administered prophylactically when counts
are ≤10,000/mm3 in the absence of apparent bleeding, as Anaphylaxis
well as when counts are ≤20,000/mm3 if the patient has a
significant risk of bleeding.101 Anaphylaxis is the most severe, potentially life-threatening
The Surviving Sepsis guidelines recommend continuous form of an allergic or hypersensitivity reaction,139–143 and
renal replacement therapies or intermittent haemodialysis is mostly immunoglobulin E mediated.144 Food-induced
to facilitate the management of fluid balance in haemo- anaphylaxis has been defined by the National Institute
dynamically unstable septic patients. The guidelines also of Allergy and Infectious Diseases (NIAID) as a serious
recommend that patients with severe sepsis receive daily allergic reaction that is rapid in onset, typically mediated
pharmacoprophylaxis against venous thromboembolism by immunoglobulin E, involving systemic mediator release
and that a combination of pharmacological therapy and from sensitive mast cells and basophils.145 Food-induced
intermittent pneumatic compression devices be used.101 anaphylaxis is being increasingly studied due to increasing
Translocation of gut bacteria due to splanchnic hypoper- prevalence because of both genetic and unspecified environ-
fusion and increased permeability is a factor in secondary mental factors.146 Food anaphylaxis has the same mechanism
septic insults and stress ulceration.135 Stress ulcer prophylaxis and clinical manifestations as other allergens with sensitised
using an H2 blocker or proton pump inhibitor is therefore mast cells and basophils. Exercise-induced anaphylaxis,
recommended for patients who have bleeding risk factors100 where a reaction depends on the temporal association of
(see Chapter 20). The new guidelines address nutritional allergen ingestion and exercise, has also been described.145
 CHAPTER 21 PATHOPHYSIOLOGY AND MANAGEMENT OF SHOCK 701

Allergies are common; however, anaphylaxis appears Clinical manifestations

rare.141 Although data are sporadic in the literature,
The allergic response is via a host mast-cell reaction
0.01–0.02% of the general population is affected.144
Anaphylaxis appears more common in Western countries mediated by immunoglobulin E,139 and antibody produced
with a rising incidence,145,147,148 but this may be related in response to the allergen that is attached to basophils
to better reporting mechanisms. The prevalence of allergy (mast cells). Once sensitised to an allergen, subsequent
with anaphylaxis has been documented to be as high as 7% exposure may lead to an anaphylactic reaction in affected
in an Australian study of children, with insect stings, oral individuals. One suggested mechanism is that subsequent
medications or food the most often cited causes. However, exposure leads to mast-cell–allergen complexes and the
in this study, less than 1% of the population actually release of histamine.152 Reactions to an allergen cannot
suffered an anaphylactic reaction manifesting with gener- be predicted, however, and subsequent exposure may lead
alised multisystem allergic reaction, including evidence of to either an amplified or lesser response.140 There may be
airway involvement, rashes, gastrointestinal and cardiovas- an initial reaction, which subsides with treatment over
cular dysfunction.149 The published American prevalence about 24 hours, but there has been described a second or
is based on large population surveys and estimates that rebound reaction up to 8–10 hours after initial exposure
anaphylaxis affects 1.6% of the population.150 There have to an allergen.139
been more than 100 food allergens identified but there Exposure to an allergen causes release of histamine
are a few responsible for most reactions and this differs and other mediators, with subsequent vasodilation
based on geographical location147,148 and cannot always be and increased microvascular permeability – a distribu-
explained by genetic factors.146 The International Collabo- tive form of shock. Histamine peaks at 5–10 minutes
ration in Asthma, Allergy and Immunology are developing and is metabolised rapidly, returning to baseline within
consensus guidelines to support management.147 60 minutes. Other mediators have a sustained effect.144 This
Three criteria have been established in order to makes histamine a poor clinical biomarker for anaphy-
rapidly diagnose anaphylaxis as set out in Box 21.4.145 There laxis. The antigen–antibody reaction may directly damage
are currently no recommended biomarkers to support vascular walls, while release of vasoactive mediators such
clinical diagnosis although histamine and tryptase are as histamine, serotonin, bradykinins and prostaglandins
sometimes used.151 triggers a systemic response, resulting in vasodilation

BOX 21.4

Diagnostic criteria for anaphylaxis

1 Acute onset of an illness (over minutes to several b Respiratory compromise (for example,
hours) involving skin, mucosal tissue or both (for dyspnoea, wheeze/bronchospasm, stridor,
example, generalised hives, pruritus or flushing, reduced peak expiratory flow rate, hypoxaemia)
swollen lips/tongue/uvula), c Reduced BP or associated symptoms of end-
plus either organ dysfunction (for example, hypotonia,
a Respiratory compromise (for example, syncope, incontinence)
dyspnoea, wheeze/bronchospasm, stridor, d Persistent GI symptoms (for example, crampy
reduced peak expiratory flow rate, abdominal pain, vomiting)
hypoxaemia) or
b Reduced blood pressure (BP) or associated 3 Age-related decrease in systolic blood pressure
symptoms of end-organ dysfunction (for or a greater than 30% decrease from baseline
example, hypotonia [circulatory collapse], after exposure to a known allergen for that patient
syncope, incontinence) (minutes to several hours):
or a 1 month to 1 year: systolic blood pressure of
2 Two or more of the following that occur rapidly after less than 70 mmHg
exposure to a likely allergen for that patient (minutes b 1–10 years old: systolic blood pressure of less
to several hours): than (70 mmHg plus twice the age)
a Involvement of the skin/mucosal tissue (for c 11 years to adult: systolic blood pressure of less
example, generalised hives, itch/flush, swollen than 90 mmHg or greater than 30% decrease
lips/tongue/uvula) from baseline

Adapted with permission from Sampson HA, Munoz-Furlong A, Campbell RL, Adkinson NF Jr, Bock SA, Branum A et al. Second
symposium on the definition and management of anaphylaxis: summary report – Second National Institute of Allergy and Infectious
Disease/Food Allergy and Anaphylaxis Network Symposium. [Reprint in Ann Emerg Med. 2006 Apr;47(4):373-80; PMID: 16546624].
J Allergy Clin Immunol 2006;117:391-7.
702 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

and increased capillary permeability, with widespread

loss of fluid into the interstitial space and hypovolaemia. TABLE 21.8
Blood pressure and cardiac output/index may fall with Symptoms of allergic reactions
a compensatory rise in heart rate. Severe bronchospasm
ORGAN I M M E D I AT E D E L AY E D
may also occur from mediator-induced bronchial oedema SYSTEM SYMPTOMS SYMPTOMS
and pulmonary smooth muscle contraction.7 Abdominal
Cutaneous Erythema Erythema
pain is thought to be due to the inflammation of Peyer’s Pruritus Flushing
patches, which are clusters of lymphatic tissue containing Urticaria Pruritus
B lymphocytes, located in the mucosa and submucosa of Morbilliform eruption Morbilliform eruption
the small intestine.152 Angioedema Angio-oedema
A list of signs and symptoms for anaphylaxis appears Eczematous rash
in Table 21.8. It is thought that anaphylaxis is sometimes Ocular Pruritus Pruritus
misdiagnosed because up to 20% of presentations do not Conjunctival erythema Conjunctival erythema
have obvious cutaneous signs.145 Anaphylaxis should be Tearing Tearing
considered when there are two or more organ systems Periorbital oedema Periorbital oedema
involved.150 There is a high mortality in patients with Upper Nasal congestion
asthma and those on beta-blocker or ACE inhibitor medi- respiratory Pruritus
cations;140,153 these medications may limit the effectiveness Rhinorrhoea
of adrenaline therapy. Age and pre-existing lung disease Sneezing
are the most important factors in relation to severity; older Laryngeal oedema
people and those with asthma or airways disease have a Hoarseness
Dry staccato cough
higher risk of a life-threatening reaction.152
Lower Cough Cough, dyspnoea,
Patient management respiratory Chest tightness wheezing
Dyspnoea
Initial management Wheezing
Diagnosis of an anaphylactic reaction requires an appro- Intercostal retractions
priate assessment and history, including acute onset, Accessory muscle use
history of allergic reaction and initial measures instituted GI (oral) Angio-oedema of the
to support airway, breathing and circulation. Removal lips, tongue or palate
of the causative agent, if possible, and treatment within Oral pruritus
30 minutes of exposure to an allergen result in improved Tongue swelling
outcomes. GI (lower) Nausea Nausea
The Australian and New Zealand Anaesthetic Allergy Colicky abdominal Abdominal pain
Group have produced a consensus guideline (see Online pain Reflux
resources) and devised a number of useful resources to Reflux Vomiting
Vomiting Diarrhoea
support management of anaphylaxis during anaesthesia.154
Diarrhoea Haematochezia
These guidelines are broadly applicable in critical care Irritability and food
units. See Practice tip below for a list of suggested anaphy- refusal with weight
laxis emergency equipment. loss (young children)
Cardiovascular Tachycardia
Practice tip (occasionally
bradycardia in
Anaphylaxis emergency box
anaphylaxis)
• Adrenaline 1:1000 (consider adrenaline Hypotension
autoinjector availability in rural locations for Dizziness
initial administration by nursing staff) Fainting
• 1-mL syringes; 21 gauge needles Loss of consciousness
Miscellaneous Uterine contractions
• Oxygen
Sense of ‘impending
• Airway equipment, including nebuliser and suction doom’
• Defibrillator
Adapted from Sampson HA, Munoz-Furlong A, Campbell
• Manual blood pressure cuff RL, Adkinson NF Jr, Bock SA, Branum A et al. Second
• Intravenous access equipment (including large bore symposium on the definition and management of anaphylaxis:
cannulae) summary report – Second National Institute of Allergy and
Infectious Disease/Food Allergy and Anaphylaxis Network
• Pressure sleeve (aids rapid infusion of fluid under
Symposium. [Reprint in Ann Emerg Med. 2006 Apr;47(4):373-
pressure) 80; PMID: 16546624]. J Allergy Clin Immunol 2006;117:391–7,
• At least 3 litres of normal saline with permission.
 CHAPTER 21 PATHOPHYSIOLOGY AND MANAGEMENT OF SHOCK 703

Measures to assess and support airway, breathing and reaction, the colloid should cease as it may be respons-
circulation are important, considering the rapid impact of ible.154 A maximum of 50 mL/kg in the first 30 minutes is
circulating mediators and potential decline in respiratory and suggested for persistent hypotension.154,155
cardiovascular function. Securing the airway and providing
high oxygen concentration is vital as most anaphylactic- Airway management
related deaths are due to asphyxiation.144 Adrenaline is Early elective intubation is recommended for patients with
recommended as first-line drug treatment140,144,152 and in a airway oedema, stridor or any oropharyngeal swelling.
recent systematic review the evidence suggested prompt use Patients with airway swelling and/or angio-oedema
of adrenaline to reduce the risk of death.143 Administration are at high risk for rapid deterioration and respiratory
is usually via intramuscular injection (to the vastus lateralis compromise.154 Late presentation to hospital or delayed
muscle or mid-outer thigh) as it leads to a more rapid intubation when airway swelling is present may mean that
increase in plasma concentration than subcutaneous admin- intubation and other emergency airway procedures may
istration.143 The first dose is often given using the patient’s be extremely difficult. Multiple attempts at intubation
own injecting device (e.g. Epipen or Anapen) for common increase laryngeal oedema or cause trauma to the airway.
food and venom allergies as they are more likely to occur Early recognition of the potentially difficult airway allows
out of hospital. Subsequent doses are usually required once planning for alternative airway management by experts in
a patient is in hospital. The Australasian Society of Clinical difficult airways.
Immunology and Allergy Incorporated suggest intramuscu-
lar adrenaline in the doses suggested in Table 21.9.155 Adjunctive support
Intravenous doses of adrenaline depend on the Adjunctive drugs include H1- and H2-antagonists, anti-
severity and condition of the patient. If the patient is histamines, corticosteroids and other beta-2-agonists for
unresponsive and life support algorithms are in play, airway symptoms. The H2-antagonists are competitive
the dose of adrenaline is 1 mg as per the International antagonists of histamine at the parietal cell histamine-2
Liaison Committee on Resuscitation Guidelines and the receptor. A systematic review assessed the evidence related
algorithms for cardiopulmonary resuscitation are followed to efficacy of H2-antihistamines. The review did not find
for subsequent dosing. The dose of adrenaline admin- any studies based on the inclusion criteria and made no
istered in anaphylaxis for patients that have not been specific treatment recommendation.142 However, it seems
managed with Advanced Life Support algorithms is more at this stage that it is likely to be beneficial to block
controversial. When a continuous infusion is required both H1 and H2 receptors when urticaria is present.143
for ongoing symptom management it is suggested an H1-antihistamines are also helpful to reduce pruritus.143
adrenaline infusion be prepared and administered at a It is important to note the use of antihistamines is not
dose of 0.1 mcg/kg/min with titration to maintain the recommended for anaphylaxis crisis management.155
desired blood pressure. The same monitoring as for any Corticosteroids (1 mg/kg up to 200 mg)155 may be
patient on an adrenaline infusion should be used including beneficial for persistent bronchospasm, asthma and severe
continuous blood pressure.154,155 cutaneous reactions but not in acute management,154,155 and
Aggressive fluid resuscitation (20 mL/kg) is also usually their use remains unproven.155 Glucagon and noradrena-
required154,155 as the intravascular blood volume may quickly line may be required for patients on beta-blockers who
be depleted by up to 70%. The type of fluid used in resus- may have resistant severe hypotension and bradycardia.156
citation can vary and, if a colloid is being administered to Glucagon exerts positive inotropic and chronotropic
the patient and there is no known other trigger for the effects, independently of catecholamines, while atropine

TABLE 21.9
Adrenaline doses

VOLUME OF ADRENALINE
AGE (YEARS) WEIGHT (KG) 1:1000 ADRENALINE AUTOINJECTORS

<1 5–10 0.05–0.1 mL

1–2 10 0.1 mL
2–3 15 0.15 mL 10–20 kg (~1–5 years): 0.15 mg (green-labelled) device
4–6 20 0.2 mL
7–10 30 0.3 mL
10–12 40 0.4 mL >20 kg (~>5 years): 0.3 mg (yellow-labelled) device
>12 and adults >50 0.5 mL

Adapted with permission from Australasian Society of Clinical Immunology and Allergy Inc. Acute management of anaphylaxis
guidelines, <http://www.allergy.org.au/health-professionals/papers/acute-management-of-anaphylaxis-guidelines>; 2013.
704 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

may reverse bradycardia. Vasopressin and other vasopres- volume and subsequent cardiac output/index. The usual
sors such as metaraminol are suggested where shock is response to reduction in cardiac output (a raised heart rate)
refractory to adrenaline.144 Given that a second reaction does not occur due to the parasympathetic nervous system
(biphasic) may occur after the initial allergic response, and blockage of sympathetic compensatory responses, and
monitoring should continue for up to 48 hours.144 the patient may be bradycardic and hypotensive,160 with
their skin warm and dry.
Preventative care In spinal shock there may be an initial rise in blood
There is no current cure for anaphylaxis.147 Individuals pressure due to release of catecholamines, followed by
with known allergies are taught avoidance of allergens as hypotension,160 which usually resolves within 24 hours.161
a first line, and then to have a management plan for inad- Flaccid areflexic paralysis,161 including that of the bladder
vertent exposure including the use of emergency kits with and bowel, is observed and sustained priapism may also
adrenaline for intramuscular injection (Epipen).141,147,152,157 develop. Symptoms may last hours to days, until the reflex
Antihistamines are also used in food allergy to manage arcs below the level of injury begin to regain function.
non-severe reactions and immune-modulating phar- This is a result of damage to the spinal cord, and obvious
macological agents are a probable future direction for manifestations include pale, cold skin above the site
management.145 Desensitisation therapy may also reduce of injury, and warm, pink skin below the site of injury.
severity of symptoms and therefore improve quality of life. Anhidrosis (absence of sweating) may be present. Heart
rate may be slow, requiring intervention.
Neurogenic/spinal shock Secondary injury may occur from impaired vasomotor
Neurogenic shock is a form of distributive shock caused tone, ischaemia, thrombosis, increased permeabil-
by loss of vasomotor (sympathetic) tone from disruption ity, inflammatory and cellular dysfunction. Spinal cord
to or inhibition of neural output. Characteristics include oedema occurs 3–6 days after injury and may lead to a
a systolic blood pressure <90–100 mmHg and a heart rate shocked state.161
<80 beats per minute without other obvious causes.158 Patient management
Note that the heart rate is within otherwise accepted
The extent of injury, whether complete (no sensory or
normal limits. Most often it is described as a triad of
motor function) or incomplete (some sensory or motor
hypotension, bradycardia and hypothermia. However, the
function), determines clinical medical management.
precise mechanisms are unknown.159 The primary cause is
Priority focuses on airway, breathing and circulation. The
a spinal cord injury above T6, secondary to disruption of
most risky time is the first 7–10 days after injury.162
sympathetic outflow from T1–L2 and to unopposed vagal
Haemodynamic support is required and is usually
tone, leading to decreased vascular resistance and associated
provided in an escalating manner with fluid first followed
vascular dilation.160 It may also develop after anaesthesia,
by pharmacological agents to maintain targets. Mean
particularly spinal, cerebral medullary ischaemia or when
arterial pressure augmentation may be required but is the
there is spinal cord complete or partial injury above the
subject of ongoing debate.162
mid-thoracic region (thoracic outflow tract).
Spinal shock is a subclass of neurogenic shock, with Initial stabilisation and neck
a transient physiological (rather than anatomical) reflex
immobilisation
depression of cord function below the level of injury
and associated loss of sensorimotor functions. Incidence After neck and torso stabilisation, the patient with
has been reported at 14% of patients presenting to the confirmed or suspected spinal cord injury is placed in a
emergency department within 2 hours of injury and position that supports spinal precautions (neutral neck
predominantly affects patients with cervical damage.158 positioning with immobilisation) with spinal boards
Spinal shock can also occur with a spinal cord laceration or removed within 20 minutes if possible. Immobilisation
contusion, and is associated with varying degrees of motor may be achieved with sandbags either side of the head, the
and sensory deficit (see also Chapters 17 and 23). Trauma use of collars and log rolling.161 Caution for spinal insta-
is frequently the reason for primary injury,158 with traffic bility remains despite medical imaging clearance, due to
accidents, assault, falls at work and sport the most common the potential for spinal ligament damage. The patient is
causes and a 4:1 ratio of males to females.161 Simultane- positioned supine, with their legs in alignment with the
ous injuries may also be responsible for haemodynamic torso.
compromise,158 and neurogenic shock with hypotension Elevation of the head may cause pooling of blood in
may have multiple aetiologies.159 Haemorrhagic shock in the lower limbs, exacerbating hypotension,163 and makes
combination with neurogenic shock has a poor outcome. the patient sensitive to sudden position changes. It is
important to note that while this is a standard practice it
Clinical manifestations also may cause additional unintended issues for the patient
Inhibited sympathetic outflow results in dominance of such as discomfort, occipital pressure areas and impaired
the parasympathetic nervous system, with a reduction in respiratory function. These precautions also inhibit airway
systemic vascular resistance and lowered blood pressure. interventions and increase risk of aspiration and raised
Preload to the right heart is reduced, which lowers stroke intracranial pressure.161
 CHAPTER 21 PATHOPHYSIOLOGY AND MANAGEMENT OF SHOCK 705

Fluid therapy
TABLE 21.10
Loss of sympathetic outflow requires close cardiac and
Respiratory muscle innervation by cord level
haemodynamic monitoring for bradycardia and hypoten-
sion. Symptomatic bradycardia is treated and may require C O R D L E V E L I N N E R VAT I O N A C C E S S O RY M U S C L E
cardiac pacing if unresponsive to atropine. Therapies C3–C5 (mostly C4) Diaphragm
include fluid resuscitation with the addition of inotropes, C6 Serratus anterior
if necessary, to improve vasomotor function.This increases Latissimus dorsi
preload and maintains a mean arterial pressure >80–85 Pectoralis
mmHg160,162 to restore spinal cord perfusion and to T1–11 Intercostals
prevent secondary neuronal hypoperfusion.164 This higher T6–L1 Abdominals
(supranormal) mean arterial pressure may be targeted
to improve recovery and prevent secondary injuries.164
Volume expansion with colloids and crystalloids or blood Adjunctive support
products will vary depending on patient situation; however, Hypothermia may be present, resulting from dilated
subgroup analysis in the SAFE trial indicated that colloids peripheral blood vessels allowing radiant loss of heat. A
and hypotonic solutions may not be the best options.49 patient is monitored for core temperature changes, and
external warming devices may be required.
Respiratory support Paralytic ileus is a concern in the acute phase of injuries
Respiratory insufficiency is common162 and, as such, above T5, where disruption of integrative innervation
respiratory function is closely monitored to prevent or pathways leads to unmodulated colonic functioning165
minimise atelectasis, pneumonia164 and secretion retention. and peristaltic hypomotility. Ileus may lead to respiratory
The level of injury is indicative of the potential for respi- compromise and should be managed. The patient should
ratory muscle weakness (see Table 21.10). The diaphragm remain ‘nil by mouth’ and treatment includes gastric
is innervated by the phrenic nerve (originating at C3– decompression, adequate intravenous hydration and elec-
C5); any injury above C3 leads to complete respiratory trolyte balance. Drug therapy with prokinetics, probiotics,
muscle paralysis and patients will require ventilatory aperients and intravenous neostigmine or lignocaine has
support.164 Incomplete injuries between C3 and C5 may been reported to be useful.
also require ventilation initially but subsequently recover Pressure care is attended every second hour and, where
some respiratory function. Intubation is complicated by Jordan frames are used, slats should be removed between
any spinal cord injury as airway interventions cause some use. The patient is susceptible to deep venous thrombosis
level of spinal movement and respiratory failure is an inde- particularly high risk when spinal cord injury is involved,
pendent predictor of mortality in spinal cord injury.161 so sequential calf compression devices and other prophy-
Coughing, and therefore secretion clearance, is reliant on laxis such as anticoagulants are initiated early with
‘expiratory muscles’ and, for patients with injuries that D-dimers monitored regularly.
interfere with abdominal and intercostal muscle function,
careful monitoring of the work of breathing and secretion Resuscitation end points
clearance should be initiated. There will be varying End points of resuscitation in shock states are similar but
levels of decreased respiratory function with substantially will differ depending on the cause. Table 21.11 outlines
reduced lung volumes. some of the discussed targets.

TABLE 21.11
Resuscitation endpoints

PA R A M E T E R TA R G E T S / R E C O M M E N D AT I O N S PRECAUTIONS

Blood pressure Target diastolic blood pressure ≥65 mmHg This target may be higher depending on pre-morbid
Target systolic blood pressure >90 mmHg as soon as state and specific organ requirements such as closed
possible head injury
Urine output Target ≥0.5 mL/hour
Serum lactate There is evidence that serum lactate is a clear marker For patients presenting to emergency with a suspicion
levels for outcome in patients17,166 of sepsis it should be measured and assessed in the
There have been suggestions that any patient with first hour
a lactate >4 should be managed in a critical care
environment
Improving lactate levels to ‘normal’ is associated with
improved survival
706 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

TABLE 21.11 continued

PA R A M E T E R TA R G E T S / R E C O M M E N D AT I O N S PRECAUTIONS

Arterial base In combination with lactate base deficit in shock is A high base deficit (≥4) is indicative of abnormal
deficit related to oxygen transport imbalance at the cellular oxygen utilisation and patients have a higher mortality
level and it is a good marker with lactate level for
adequacy of resuscitation167
Oxygen Monitoring of oxygen saturation is readily available A P/F ratio <250 in the presence of high supplemental
monitoring and required when any shock state is suspected oxygen should be regarded as indicative of serious
It is important to assess oxygen requirements even respiratory dysfunction
in the setting of acceptable oxygen saturation as Any patient requiring maximum oxygen support
increasing requirement is indicative of deterioration should be investigated
P/F ratio (partial pressure of oxygen-to-fraction of
inspired oxygen ratio) may be used as a guide to
assess the level of dysfunction given that the normal
result is approximately 500 (100/0.21)
Oxygenation should also be assessed through arterial
blood gas sampling and utilisation assumptions may
be made by comparing with a venous sample
Mixed venous Normal mixed venous oxygen saturation levels are A reduced mixed venous saturation indicates
oxygen between 60% and 80% increasing extraction and worsening shock state
saturation It may be used to guide resuscitation but is an High levels may be seen that may be indicative of
invasive method of monitoring cellular dysfunction in relation to oxygen extraction
Haemoglobin should be measured in conjunction
with this variable
End-tidal carbon End-tidal carbon dioxide monitors usually provide End-tidal carbon dioxide monitoring is unreliable in
dioxide both numeric and graphic waveform displays of the the setting of increased ventilation perfusion (V/Q)
concentration using non-invasive measurement of mismatch with worsening arterial carbon dioxide
exhaled carbon dioxide168 retention and increased peripheral carbon dioxide
End-tidal carbon dioxide is an estimate of the production20
patient’s alveolar ventilation status
‘Stat cap’ devices are standard on resuscitation
trolleys for supporting confirmation of endotracheal
tube placement by quickly establishing if carbon
dioxide is exhaled
Preload Preload should be maximised without Where preload is leading to congestion and cardiac
overstretching failure, pharmacotherapy and ventilator support may
Usually this is achieved using fluid bolus in shock be required
states (refer to the relevant sections)
Right ventricular Provides a clinical estimate of right ventricular
end-diastolic preload and has a normal adult parameter of
volume index 60–100 mL/m2
Observing for changes with fluid challenge may
support resuscitation by providing information about
volume responsiveness169
Afterload Afterload reduction strategies are employed in During shock states, resistance is increased through
many shocked states to improve cardiac output constriction and oxygen and energy are required for
as increased afterload increases the work of the function
myocardium
Afterload is affected by vascular resistance
Calculations for systemic vascular resistance (SVR)
are used to measure afterload
Contractility Contractility is not easily measured clinically but
the improvement would be observed usually
by increased cardiac output or other surrogate
measures with the addition of inotropes
P/F ratio = PaO2/FiO2
 CHAPTER 21 PATHOPHYSIOLOGY AND MANAGEMENT OF SHOCK 707

Summary
Shock is a generic term describing a syndrome and pervasive set of potentially life-threatening symptoms. The patho-
physiological changes associated with shock feature a complex interaction of generic compensatory mechanisms that
attempt to sustain perfusion and particularly oxygen delivery to the vital organ systems of the body. These protective
responses are particularly strong in supporting cerebral perfusion and combine responses from the sympathetic nervous,
endocrine and adrenal/renal systems. As shock develops cellular dysfunction occurs in response to the release of a large
collection of systemic and local inflammatory mediators, which inevitably overwhelm cell function and lead to diffuse
organ injury if shock continues unabated. The classification system described here differentiates shock into categories
including hypovolaemic, cardiogenic and distributive; classification is dependent on aetiology. Distributive shock states
result in impaired oxygen and nutrient delivery to the tissues as a result of failure of the vascular system (the blood distri-
bution system).While there may be additional factors (e.g. infection) beyond simple failure to provide sufficient perfusion
to the capillary bed due to widespread vascular dilation, the common factor for all underlying causes of distributive shock
is widespread failure of the vasculature. The most common categories of distributive shock are associated with systemic
inflammatory response syndrome, anaphylaxis and neurogenic shock.
Clear assessment is required to distinguish the type of shock aids in appropriate treatment decisions, targeting the
cause and managing associated symptoms. Critical care nurses are in a position to provide clear assessment and first-line
emergency management of the various shock states. Collaborative integrated care is important to provide the patient
with the best possible outcome.

Case study
An independent 70-year-old man, Matthew, presented to the emergency department at 1630 hours with
abdominal cramping, nausea and vomiting for the past day. Matthew had a history of end-stage renal
failure, type 2 diabetes and hypertension. Previous hospital admission noted he was positive for MRSA.
He attends the dialysis unit three times a week and is dialysed through a tunnelled catheter that had
been in situ for 3 months with no complications. His initial observations in the emergency department
included a blood pressure of 143/75 mmHg, heart rate of 93 beats per minute, temperature of 37.5°C
and respiratory rate of 18 breaths per minute, with an oxygen saturation of 95%. Routine blood tests
were ordered and 1000 mL of intravenous 0.9% sodium chloride was given as a ‘bolus’, with a second
litre commenced and prescribed to be administered over the next 8 hours. Intravenous metaclopramide
10 mg was administered and blood cultures were taken after Matthew had been in the department for
approximately 4 hours.
The next set of observations included a temperature of 38.5°C. Matthew was also noted to be drowsy with
a GCS of 14. He was then transferred to the medical assessment unit pending admission to the renal ward.
Blood cultures were taken prior to him being transferred for ongoing care.
The next morning Matthew was reviewed on the ward round and he continued to be drowsy with some
abdominal pain. His observations included an increased temperature of 38.2°C, blood pressure of 160/80
mmHg and oxygen saturation of 94% on room air. His ongoing diagnosis was gastroenteritis although other
types of infection were considered given his long-term medical issues. A stool culture was ordered and
intravenous metronidazole and vancomycin prescribed. A note was made in the patient’s medical record
to administer the antibiotics after his dialysis treatment and following checking of blood culture results. An
abdominal computerised tomography scan was ordered, which delayed dialysis. Just after Matthew left for
the dialysis unit, the hospital microbiology department contacted the ward to report a preliminary positive
blood culture for gram-positive cocci – this was not communicated to the staff in the dialysis unit. About
3 hours later, a medical officer was called to review him in the dialysis unit as he was looking unwell and,
during dialysis, had rigors increasing abdominal discomfort with the following observations: temperature
38.6°C, heart rate 90 beats per minute, blood pressure 140/90 mmHg, respiratory rate 20 breaths per
minute. The medical officer took additional blood cultures, ordered a stat dose of vancomycin after
reviewing current blood pathology, noting the positive culture and increased white cell count of 24 × 109/L.
When dialysis was concluded Matthew returned to the renal unit. There was no handover provided. An
hour after his return to the ward his observations included a temp of 39.2°C, respiratory rate of 22 breaths
per minute, SpO2 88% on room air and HR of 115 beats per minute with a decreased level of consciousness.
These observations automatically triggered an immediate clinical emergency response call.
708 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Matthew was assessed by the medical emergency team and transferred to ICU for ongoing care. He
required intubation and ventilation to support respiratory function and noradrenaline to support blood
pressure and continuous renal replacement therapy commenced. Matthew was persistently febrile over the
next few days even with vancomycin in a therapeutic range. Matthew also had a fluctuating GCS and repeat
CT scans indicated changes consistent with multiple cerebral infarcts.
Matthews’s poor prognosis was considered by the medical team and discussed with his family. There was
a decision made not to escalate interventions and to ensure Matthew’s comfort by instituting palliative
measures. Matthew died 12 days after admission.
This case study is a good example of care provided with confirmation bias towards gastroenteritis that
probably led to less importance placed on providing antibiotic therapy. The delay to treatment may have
been implicated in Matthew’s decline and, given his pre-admission status, every effort should have been
made to prevent this. Hospital processes and transfers between services are risky times where handover
may be limited or incomplete. It is important in these cases to consider the checking procedures to ensure
all interventions have been performed.

CASE STUDY QUESTIONS

1 Identify what the possible sources of infection are for Matthew.
2 What early clinical indications are there that Matthew is seriously unwell?
3 What opportunities existed during Matthew’s time in the emergency department to optimise his ‘sepsis
path’?

RESEARCH VIGNETTE

Corfield AR, Lees F, Zealley I, Houston G, Dickie S, Ward K et al, on behalf of the Scottish Trauma Audit Group
Sepsis Steering Group, 2013. Utility of a single early warning score in patients with sepsis in the emergency
department, Emerg Med J 2014;31(6):482–7. doi:10.1136/emermed-2012-202186

Abstract
Background: An important element in improving the care of patients with sepsis is early identification and
early intervention. Early warning score (EWS) systems allow earlier identification of physiological deterioration.
A standardised national EWS (NEWS) has been proposed for use across the National Health Service in the UK.170

Aim: To determine whether a single NEWS on emergency department (ED) arrival is a predictor of outcome, either
in-hospital death within 30 days or intensive care unit (ICU) admission within 2 days, in patients with sepsis.

Methods: Data were collected over a 3-month period as part of a national audit in 20 EDs in Scotland. All adult
patients who were admitted for at least 2 days or who died within 2 days were screened for sepsis criteria. Patients
with systemic inflammatory response syndrome criteria were included. An EWS was calculated based on initial
physiological observations made in the ED using the NEWS.

Results: Complete data were available for 2003 patients. Each rise in NEWS category was associated with an
increased risk of mortality when compared to the lowest category (5–6: OR 1.95, 95% CI 1.21 to 3.14), (7–8: OR 2.26,
95% CI 1.42 to 3.61), (9–20: OR 5.64, 95% CI 3.70 to 8.60). This was also the case for the combined outcome (ICU
and/or mortality).

Conclusions: An increased NEWS on arrival at ED is associated with higher odds of adverse outcome among patients
with sepsis. The use of NEWS could facilitate patient pathways to ensure triage to a high acuity area of the ED and
senior clinician involvement at an early stage.

Critique
Vital signs falling outside of ‘normal ranges’ are associated with adverse events for patients. There are many reports
that demonstrate systematic hospital challenges for inpatients who develop shock. Identified issues include failure
 CHAPTER 21 PATHOPHYSIOLOGY AND MANAGEMENT OF SHOCK 709

to recognise or respond to deteriorating patients, inadequate or delayed treatment, unstable patient transfers and a
lack of clinical supervision at the point of care. This has led to the implementation of track and trigger systems and
development of various standards and performance indicators aimed at improving patient care.

This recently published multicenter prospective study in 20 Scottish emergency departments assessed a ‘track
and trigger’ system for identifying sepsis patients at risk using the NHS Early Warning Score (NEWS). End points for
the study included ICU admission within 2 days of attendance and 30-day in-hospital mortality.

Case note review was performed on more than 27,000 patients to determine if sepsis criteria were present. The
sample was reduced to approximately 2000 with exclusion criteria applied. The NEWS is based on medical
emergency team research and assigns a score to physiological derangements for six physiological parameters and
the use of supplemental oxygen. The maximum score is 20 with higher scores indicating worsening patient state. The
parameters appear in Table 21.12.

TABLE 21.12
NHS early warning score (NEWS)

N H S E A R LY W A R N I N G S C O R E
3 2 1 0 1 2 3

Respiration rate ≤8 9–11 12–20 21–24 ≥25

Oxygen saturation ≤91 92–93 94–95 ≥96
Supplemental oxygen Yes No
Temperature ≤35° 35.1–36° 36.1–38° 38.1–39° ≥39.1°
Systolic blood pressure ≤90 91–100 101–110 111–219 ≥220
Pulse ≤40 41–50 51–90 91–110 111–130 ≥131
Conscious level A V, P, U

A = alert; V = voice; P = pain; U = unresponsive.

Adapted from Corfield AR, Lees F, Zealley I, Houston G, Dickie S, Ward K et al. Utility of a single early warning score in
patients with sepsis in the emergency department. Emerg Med J 2014;31(6):482–7, with permission.

It is not surprising that patients admitted to ICU had a higher median NEWS score – it was more surprising that the
ICU group was significantly younger. Increased age was associated with 30-day mortality. A score of ≥7 put patients
at increased risk of ICU admission or death. There were a number of limitations acknowledged. At least 5% of the
potential sample was excluded because of missing physiological observations so that scoring was incomplete. Poor
compliance with scoring is not unusual and has been reported in other ED studies that have adopted scoring of
physiological parameters.171 This is an acknowledged problem for all track and trigger systems as more than one
observation is required to complete the assessment.

Patients who were discharged within 2 days were also not included although the authors note that they may have
had less incidence of significant illness. Patients that may have required ICU after 2 days were also excluded and this
would potentially include patients where early deterioration may have been missed. Patients were also not followed
up after discharge so outcomes are not known beyond the hospital stay.

The study continues to support the value of close, frequent clinical observation and the linking of signs and symptoms
within the patient’s overall physiological condition that provides the astute clinician with numerous indicators of the
health or otherwise of the cardiovascular system and the impending shock syndrome. This study was a retrospective
case note audit and, as such, it is not representative of the outcomes that may have been evident if the system was
implemented within the jurisdiction and scoring was routine.

The criteria for scoring are based on reasonable data and are similar to other track and trigger observations. These
scoring systems are of benefit in the setting of access to appropriate scoring tools such as standard observation charts
with embedded scoring. They have the additional and often-cited benefit of supporting less-experienced clinicians
710 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

in seeking help to interpret the patient’s clinical state and gaining support to avoid deterioration such that late signs
become an all-too-obvious message of imminent patient mortality. This is only the case when scoring is related to
standards for escalation and the escalation response such as medical emergency teams or outreach services.

The scoring of NEWS is easy to apply and has been supported in the UK as a mechanism for early warning of
deterioration but without supporting implementation strategies. A standard bedside observation chart could be used
across jurisdictions and highlight appropriate calling criteria and escalation procedures. This has been demonstrated
in the ‘Between the Flags’ program in New South Wales, Australia.172 Standardisation in this way supports
organisations to provide equitable service to patients. This jurisdiction-wide program includes a colour-coded chart,
escalation procedure and in-depth online training modules. This program enables clinicians to respond appropriately
and communicate effectively when patients deteriorate. Regardless of the method, these are important initiatives to
combat avoidable in-hospital complications and deaths.

Lear ning a c t iv it ie s
1 What are the implications for dosing patients receiving renal replacement therapies?
2 What assessments are important to obtain appropriate information for a patient presenting with signs of
hypoperfusion?
3 What are key monitoring strategies to assess end-organ perfusion?
4 What are the common management strategies for all shock types?

Online resources
American Heart Association, www.heart.org/HEARTORG
Australian and New Zealand Anaesthetic Allergy Group, www.anzaag.com/Default.aspx
Australian and New Zealand Anaesthetic Allergy Group Anaphylaxis Management Guidelines, www.anzaag.com/Docs/PDF/
Management%20Guidelines/Mx%20Guidelines%20Intro%20v1.1Jun13.pdf
Australian Commission on Safety and Quality in Healthcare, www.safetyandquality.gov.au/internet/safety/publishing.nsf/
Content/home
Clinical Excellence Commission: Between the flags, www.cec.health.nsw.gov.au/programs/between-the-flags
National Blood Authority Australia, www.nba.gov.au
Patient Blood Management guidelines App: for iPad, www.blood.gov.au/pbm-ipad
Sepsis, www.ihi.org/Topics/Sepsis/Pages/default.aspx
Spinal cord injury network, https://spinalnetwork.org.au/
Surviving Sepsis, www.survivingsepsis.org/
TRANSFUSE, http://clinicaltrials.gov/show/NCT01638416 and http://clinicaltrials.gov/show/NCT00975793
World Allergy Organization, www.worldallergy.org/index.php

Further reading
Aitken LM, Williams G, Harvey M, Blot S, Kleinpell R, Labeau S et al. Nursing considerations to complement the Surviving
Sepsis Campaign guidelines. Crit Care Med 2011;39(7):1800–18.
Australian Commission on Safety and Quality in Healthcare. Recognising and responding to clinical deterioration:
background paper, <http://www.safetyandquality.gov.au/internet/safety/publishing.nsf/Content/AB9325A491E10CF1CA25
7483000C9AC4/$File/BackgroundPaper-2009.pdf>; June 2008.
Dellinger RP, Levy MM, Rhodes A, Annane D, Gerlach H, Opal SM et al. International guidelines for management of severe
sepsis and septic shock, <http://www.survivingsepsis.org/Pages/default.aspx>; 2012.
Manji RA, Wood KE, Kumar A. The history and evolution of circulatory shock. Crit Care Clin 2009;25(1):1–29.
 CHAPTER 21 PATHOPHYSIOLOGY AND MANAGEMENT OF SHOCK 711

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e76ef78eabcusersshyerdocumentselsoguidelinesforadultcardiacfailure1.3.pdf>; 2013.
90 Extracorporeal Life Support Organisation. ELSO guidelines for ECMO centres, <https://www.elso.org/Portals/0/IGD/Archive/FileManager/
faf3f6a3c7cusersshyerdocumentselsoguidelinesecmocentersv1.8.pdf>; 2014.
91 Murray S. Bi-level positive airway pressure (BiPAP) and acute cardiogenic pulmonary oedema (ACPO) in the emergency department. Aust Crit
Care 2002;15:51–63.
92 Agarwal R, Aggarwal AN, Gupta D, Jindal SK. Non-invasive ventilation in acute cardiogenic pulmonary oedema. Postgrad Med J 2005;81:
637–43.
93 Park M, Sangean M, Volpe Mde S, Feltrim M, Nozawa F, Leite PF et al. Randomized, prospective trial of oxygen, continuous positive airway
pressure, and bilevel positive airway pressure by face mask in acute cardiogenic pulmonary edema. Crit Care Med 2004;32:2546–8.
94 Tallman T, Peacock W, Emerman C, Lopatin M, Blicker JZ, Weber J et al. Noninvasive ventilation outcomes in 2,430 acute decompensated
heart failure patients: an ADHERE Registry Analysis. Acad Emerg Med 2008;15:355-62.
95 Bone RC, Balk RA, Cerra FB, Dellinger RP, Fein AM, Knaus WA et al. Definitions for sepsis and organ failure and guidelines for the use of
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Medicine. Chest 1992;101:1644–55.
96 Daniels R. Surviving the first hours in sepsis: getting the basics right (an intensivist’s perspective). J Antimicrob Chemother 2011;66:ii11-ii23.
97 Finfer S, Bellomo R, Lipman J, French C, Dobb G, Myburgh J. Adult-population incidence of severe sepsis in Australian and New Zealand
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98 Hicks P, Cooper DJ, Webb S, et al. The Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic
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99 Kaukonen K, Bailey M, Suzuki S, Pilcher D, Bellomo R. Mortality related to severe sepsis and septic shock among critically ill patients in
Australia and New Zealand, 2000–2012. JAMA 2014;311:1308-16.
100 Dellinger RP, Levy MM, Carlet JM, Bion J, Parker MM, Jaeschke R et al. Surviving Sepsis Campaign: international guidelines for management
of severe sepsis and septic shock: 2008. Crit Care Med 2008;36:296-327.
714 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

101 Dellinger RP, Levy MM, Rhodes A, Annane D, Gerlach H, Opal SM et al. Surviving Sepsis Campaign: international guidelines for management
of severe sepsis and septic shock: 2012. Crit Care Med 2012;41:580-637.
102 Dellinger R, Carlet J, Masur H, Gerlach H, Calandra T, Cohen J et al. Surviving Sepsis Campaign guidelines for management of severe sepsis
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103 Organizations JCoAoH. Raising the bar with bundles treating patients with an all-or-nothing standard. Jt Comm Pers Patient Saf 2006;6:5-6.
104 Finfer S. The Surviving Sepsis Campaign: robust evaluation and high-quality primary research is still needed. Intens Care Med 2010;
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105 Chamberlain DJ, Willis EM, Bersten AB. The severe sepsis bundles as processes of care: a meta-analysis. Aust Crit Care 2011;24:229-43.
106 Barochia A, Cui X, Vitberg D, Suffredini AF, O’Grady NP, Banks SM et al. Bundled care for septic shock: an analysis of clinical trials. Crit Care
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107 Van den Berghe G, Schetz M, Vlasselaers D, Hermans G, Wilmer A, Bouillon R et al. Clinical review: intensive insulin therapy in critically ill
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108 van den Berghe G, Wouters P, Weekers F, Verwaest C. Bruyninckx F, Schetz M et al. Intensive insulin therapy in the critically ill patients.
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109 NICE-SUGAR Study Investigators, Finfer S, Chittock D, Su SY, Blair D, Foster D, Dhingra V et al. Intensive versus conventional glucose control
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110 Griesdale DE, de Souza RJ, van Dam RM, Heyland DK, Cook DJ, Malhotra A et al. Intensive insulin therapy and mortality among critically ill
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111 Schrier R, Wang W. Acute renal failure and sepsis. New Engl J Med 2004;351:159–69.
112 Ranzani OT, Monteiro MB, Ferreira EM, Santos SR, Machado FR, Noritomi DT. Reclassifying the spectrum of septic patients using lactate:
severe sepsis, cryptic shock, vasoplegic shock and dysoxic shock. Revista Brasileira de Terapia Intensiva 2013;25:270-8.
113 Puskarich MA, Trzeciak S, Shapiro NI, Heffner AC, Kline JA, Jones AE. Outcomes of patients undergoing early sepsis resuscitation for cryptic
shock compared with overt shock. Resuscitation 2011;82:1289-93.
114 Ranzani O, Monteiro M, Ferreira E, Santos SR, Machado FR, Noritomi DT et al. Stratifying septic patients using lactate: severe sepsis and
cryptic, vasoplegic and dysoxic shock profile. Crit Care 2013;17:P37.
115 Bauer M. Multiple organ failure: update on pathophysiology and treatment strategies. In: Euroanesthesia: European Society of
Anaesthesiology, 2005. Vienna, Austria; 2005, pp 203–6.
116 Marik PE, Varon J. Early goal-directed therapy: on terminal life support? Am J Emerg Med 2010;28:243-5.
117 Puskarich MA, Marchick MR, Kline JA, Steuerwald MT, Jones AE. One year mortality of patients treated with an emergency department based
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118 Focht A, Jones AE, Lowe TJ. Early goal-directed therapy: improving mortality and morbidity of sepsis in the emergency department. Jt Comm
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119 Rivers EP, Coba V, Whitmill M. Early goal-directed therapy in severe sepsis and septic shock: a contemporary review of the literature. Curr
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120 Mouncey PR, Osborn TM, Power GS, Harrison DA, Sadique MZ, Grieve RD et al for the ProMISe Trial Investigators. Trial of early,
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121 Padkin A, Goldfrad C, Brady AR, Young D, Black N, Rowan K. Epidemiology of severe sepsis occurring in the first 24 hrs in intensive care
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122 Brun-Buisson C, Meshaka P, Pinton P, Vallet B, Episepsis Study Group. EPISEPSIS: a reappraisal of the epidemiology and outcome of severe
sepsis in French intensive care units. Intensive Care Med 2004;30:580-8.
123 Kumar A. Optimizing antimicrobial therapy in sepsis and septic shock. Crit Care Clin 2009;25:733-51.
124 Kumar A, Roberts D, Wood KE, Light B, Parrillo Je, Sharma S et al. Duration of hypotension before initiation of effective antimicrobial therapy
is the critical determinant of survival in human septic shock. Crit Care Med 2006;34:1589-96.
125 Taccone FS, Laterre P-F, Dugernier T, Spapen H, Delattre I, Wittebole X et al. Insufficient beta-lactam concentrations in the early phase of
severe sepsis and septic shock. Crit Care 2010:R126.
126 Dulhunty JM, Roberts JA, Davis JS, Webb SA, Bellomo R, Gomersall C et al. A protocol for a multicentre randomised controlled trial of
continuous beta-lactam infusion compared with intermittent beta-lactam dosing in critically ill patients with severe sepsis: the BLING II study.
Crit Care Resusc 2013;15:179-85.
127 Lipman J, Boots R. A new paradigm for treating infections: “go hard and go home”. Crit Care Resusc 2009;11:276-81.
128 Finfer S, McEvoy S, Bellomo R, McArthur C, Myburgh J, Norton R. Impact of albumin compared to saline on organ function and mortality of
patients with severe sepsis. Intensive Care Med 2011;37:86-96.
129 Myburgh JA, Finfer S, Bellomo R, Billot L, Cass A, Gattas D et al. Hydroxyethyl starch or saline for fluid resuscitation in intensive care. N Engl
J Med 2012;367:1901-11.
130 Bagshaw SM, Chawla LS. Hydroxyethyl starch for fluid resuscitation in critically ill patients. Can J Anaesth 2013;60:709-13.
131 Myburgh J. CHEST and the impact of fraud in fluid resuscitation research. Crit Care Resusc 2011;13:69-70.
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132 Perel P, Roberts I, Ker K. Colloids versus crystalloids for fluid resuscitation in critically ill patients. Cochrane Database Syst Rev 2013;2:CD000567.
133 Obritsch MD, Bestul DJ, Jung R, Fish DN, MacLaren R. The role of vasopressin in vasodilatory septic shock. Pharmacotherapy 2004;24:1050-63.
134 Lipiner-Friedman D, Sprung CL, Laterre PF, Weiss Y, Goodman SV, Vogeser M et al. Adrenal function in sepsis: the retrospective Corticus
cohort study. Crit Care Med 2007;35:1012-8.
135 Magnotti L, Deitch E. Burns, bacterial translocation, gut barrier function, and failure. J Burn Care Rehab 2005;26:383-91.
136 Maragakis L. Recognition and prevention of multidrug-resistant Gram-negative bacteria in the intensive care unit. Crit Care Med
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137 Aitken LM, Williams G, Harvey M, Blot S, Kleinpell R, Labeau S et al. Nursing considerations to complement the Surviving Sepsis Campaign
guidelines. Crit Care Med 2011;39:1800-18.
138 Young PJ, Weatherall M, Saxena MK, Bellomo R, Freebairn RC, Hammond NE et al. Statistical analysis plan for the HEAT trial: a multicentre
randomised placebo-controlled trial of intravenous paracetamol in intensive care unit patients with fever and infection. Crit Care Resusc
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139 Ellis A, Day J. Diagnosis and management of anaphylaxis. CMAJ 2003;169:307–11.
140 McLean-Tooke A, Bethune C, Fay A, Spickett G. Adrenaline in the treatment of anaphylaxis: what is the evidence? Br Med J 2003;327:1332–5.
141 Gold M. EpiPen epidemic or good clinical practice? J Paediatr Child Health 2003;39:376–7.
142 Nurmatov UB, Rhatigan E, Simons FER, Sheikh A. H2-antihistamines for the treatment of anaphylaxis with and without shock: a systematic
review. Ann Allergy Asthma Immunol 2014;112:126-31.
143 Dhami S, Panesar SS, Roberts G, Muraro A, Worm M, Bilo MB et al. Management of anaphylaxis: a systematic review. Allergy 2014;69:168-75.
144 Kanji S, Chant C. Allergic and hypersensitivity reactions in the intensive care unit. Crit Care Med 2010;38:S162-8.
145 Sampson HA, Munoz-Furlong A, Campbell RL, Adkinson NF Jr, Bock SA, Branum A et al. Second symposium on the definition and
management of anaphylaxis: summary report – Second National Institute of Allergy and Infectious Disease/Food Allergy and Anaphylaxis
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146 Berin MC, Sampson HA. Mucosal immunology of food allergy. Curr Biol 2013;23:R389-400.
147 Burks AW, Tang M, Sicherer S, Muraro A, Eigenmann PA, Ebisawa M et al. ICON: Food allergy. J Allergy Clin Immunol 2012;129:906-20.
148 Sicherer SH, Sampson HA. Food allergy. J Allergy Clin Immunol 2010;125:S116-25.
149 Boros C, Kay D, Gold M. Parent reported allergy and anaphylaxis in 4173 South Australian children. J Paediatr Child Health 2000;36:36–40.
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158 Guly HR, Bouamra O, Lecky FE, Trauma Audit and Research Network. The incidence of neurogenic shock in patients with isolated spinal cord
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159 Summers RL, Baker SD, Sterling SA, Porter JM, Jones AE. Characterization of the spectrum of hemodynamic profiles in trauma patients with
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160 Dawodu S. Spinal cord injury: definition, epidemiology, pathophysiology. Medscape 2005.
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severe sepsis and septic shock. Crit Care Med 2004;32:1637-42.
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167 Kincaid EH, Miller PR, Meredith JW, Rahman N, Chang MC. Elevated arterial base deficit in trauma patients: a marker of impaired oxygen
utilization. J Am Coll Surg 1998;187:384-92.
168 St John RE. End-tidal carbon dioxide monitoring. Crit Care Nurs 2003;23:83-8.
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positive end-expiratory pressure. Crit Care Med 1998;26:1801-6.
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 Chapter 22

Multiple organ
dysfunction syndrome
Melanie Greenwood, Alison Juers

KEY WORDS Learning objectives

apoptosis After reading this chapter, you should be able to:
cytokines/mediators • define the common terminology related to multiple organ dysfunction
syndrome
inflammation
multiple organ • describe the related pathophysiology of multiple organ dysfunction
syndrome
dysfunction
syndrome • identify the clinical manifestations of multiple organ dysfunction syndrome
multiple organ • identify patients at risk of developing multiple organ dysfunction, including
failure predictors of mortality
procoagulation • initiate appropriate monitoring, care planning and evaluation strategies
sepsis for the patient with multiple organ dysfunction in relation to the current
evidence base
• discuss treatment strategies that promote homeostasis in the patient with
multiple organ dysfunction syndrome.

Introduction
The term multiple organ dysfunction syndrome (MODS) was established by an
expert consensus conference in 1992 to describe a continuum of physiological
derangements and subsequent dynamic alterations in organ function that may
occur during a critical illness.1,2 Previous terminologies in the literature were
confusing. For example, multiple organ failure was a term commonly used, but
somewhat misleading as normal physiological function can, in most cases, be
restored in survivors of a critical illness who have temporary organ dysfunc-
tion.3,4 Although the syndrome affects many organs, it also affects physiological
systems such as the haematological, immune and endocrine systems. MODS
therefore more accurately describes altered organ function in a critically ill
patient who requires medical and nursing interventions to achieve homeostasis.4
MODS is associated with widespread endothelial and parenchymal cell
injury because of hypoxic hypoxia, direct cytotoxicity, apoptosis, immuno-
suppression and coagulopathy.4 Four clinical stages describe a patient with
developing MODS:5
1 increasing volume requirements and mild respiratory alkalosis, accompanied
by oliguria, hyperglycaemia and increased insulin requirements
718 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

2 tachypnoea, hypocapnia and hypoxaemia, organ dysfunction are discussed, expanding on dialogue in
with moderate liver dysfunction and possible previous chapters, particularly Chapter 20. Assessment of
haematological abnormalities the severity of MODS and nursing considerations in the
3 developing shock with azotaemia, acid–base treatment of the MODS patient are presented.
disturbances and significant coagulation abnormalities
4 vasopressor dependence with oliguria or anuria, Pathophysiology
ischaemic colitis and lactic acidosis. The syndrome of multiple organ dysfunction is most
Cellular damage in various organs in patients who closely related to an outcome of sepsis, which is described
develop MODS begins with the onset of local injury that in Chapter 21. MODS is a state characterised by aberrant
is then compounded by activation of the innate immune cellular responses involving multiple organ systems and
system. This includes a combination of pattern recogni- sequential processes. The pathogenesis of MODS is
tion, receptor activation and release of mediators at the complex, simultaneously involving every cell type, neuro-
microcellular level, leading to episodes of hypotension hormonal axis and organ system.7
or hypoxaemia and secondary infections.4,5 The primary In brief, hypoxic hypoxia results from altered metabolic
therapeutic goal for nursing and medical staff is prompt, regulation of tissue oxygen delivery, which contributes
definitive control of the source of infection or pro- to further organ dysfunction. Microcirculatory injury as
inflammation6 and early recognition of pre-existing a result of lytic enzymes, and vasoactive substances (nitric
factors that may lead to subsequent organ damage away oxide, endothelial growth factor), is compounded by the
from the initial site of injury. This pre-emptive therapy inability of erythrocytes to navigate the septic micro-
is instituted to maintain adequate tissue perfusion and circulation. Mitochondrial electron transport is affected by
prevent the onset of MODS. Recognition and response to endotoxins in sepsis, nitric oxide and tumour necrosis factor
early signs of clinical deterioration are therefore important alpha (TNF-α), leading to disordered energy metabolism
to minimise further organ dysfunction. (see Figure 22.1). This causes cytopathic or histotoxic
In this chapter the pathophysiology of inflammatory anoxia.8 This context of impaired oxygen utilisation where
and infective conditions that may lead to multiple organ oxygen delivery is normal7,8 results from diminished
dysfunction is described. System responses and specific mitochondrial production of cellular energy – adenosine

FIGURE 22.1 Pathophysiology of cellular dysfunction.

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cellular dysfunction. Melbourne: Cambridge Press; 2004, with permission.
 CHAPTER 22 MULTIPLE ORGAN DYSFUNCTION SYNDROME 719

triphosphate (ATP) – despite normal or even supranormal bidirectional neural networks.14 The endothelium acts as a
intracellular oxygen levels.9 Cellular hypoxia increases free communication interface between cells, organs and systems
radicals further compounding oxidative stress, which results and is involved in orchestration of systemic responses,
in calcium entering the endoplasmic reticulum and mito- including haemodynamic regulation, inflammation and
chondria leading to cell death.10 Cytopathic hypoxia appears coagulation; oxygen and nutrient delivery; oxidative stress;
resistant to resuscitation measures, and may ultimately and sensing of psychological stress and neuroendocrine
worsen already-existing organ dysfunction. During sepsis or alterations.7 In critical illness, endothelia release molecules
ischaemia, mitochondria respond by facilitating cell death that trigger the immune and neuroendocrine systems to
rather than the restoration of homeostasis.7 produce a generalised inflammatory response.7 The combi-
Apoptosis is normal physiological programmed cell death nation of the pathophysiological processes involved with
and is the main mechanism to eliminate dysfunctional cells.11 the development of MODS, compensatory mechanisms
Apoptosis involves chromatin condensation, membrane and the effect on target organs and systems is now discussed.
blebbing, cell shrinkage and subsequent breakdown of
cellular components into apoptotic bodies. This normally Systemic response
orderly process is deranged in critical illness, leading to
tissue or organ bed injury and MODS. Pro-inflammatory After an overwhelming incident such as trauma, sepsis
cytokines released in sepsis may delay apoptosis in activated or non-infectious inflammation, a complex range of
macrophages and neutrophils, but in other tissues, such as interrelated reactions occurs that result in a cascade of
gut endothelium, accelerated apoptosis occurs.8 responses. The complex host-response generated involves
In contrast, necrosis is a form of cell death character- the inflammatory immune systems, hormonal activation
ised by cellular swelling and loss of membrane integrity as and metabolic derangements, resulting in multiple organ
a result of hypoxia or trauma. Necrosis has been termed system involvement.15,16 These host-responses are initially
‘cellular energy crisis’,11 and is unregulated resulting in adaptive to maintain nutrient perfusion to the tissues;
loss of membrane sodium/potassium/ATP-ase pumps. however, eventually organ systems become dysfunc-
This loss leads to cell swelling, rupture and spillage of tional and fail, and the body is no longer able to maintain
intracellular contents into surrounding regions creating homeostasis17 (see Figure 22.2).
collateral damage.11 Necrosis therefore can involve signif- Initially, pro-inflammatory mediators are released
icant amounts of tissue and organ bed damage. Apoptosis locally to fight foreign antigens and promote wound
differs from necrosis in that it does not seem to involve healing. Anti-inflammatory mediators are also released to
the recruitment of inflammatory cells or mediators to downregulate the initial response to the insult.18 If the local
complete its task. Activation of an enzyme cascade system- defence system is overwhelmed, inflammatory mediators
atically cleaves proteins and degrades the cell’s nuclear appear in the systemic circulation and recruit additional
deoxyribonucleic acid (DNA) with the end result being leucocytes to the area of damage. A whole-body stress
death of the cell. This requires energy from mitochondria response ensues, further compounding the situation. If the
and, if not available, necrosis of the cell occurs. Apoptosis pro-inflammatory mediators and the anti-inflammatory
and necrosis are processes important to understand in response are imbalanced, the patient may develop systemic
relation to future MODS research. inflammatory response syndrome (SIRS) and subsequent
Increased concentrations of cell-free plasma DNA immunological dissonance18 of organ dysfunction.2,17,19
are present in various clinical conditions such as stroke, Regardless of the trigger event, lymphocytes (T cells,
myocardial infarction and trauma, a likely result of accel- B cells, natural killer cells) and macrophages are activated
erated cell death. Maximum plasma DNA concentrations by cytokines (cellular signaling agents) to commence the
correlated significantly with Acute Physiology and Chronic inflammatory or anti-inflammatory response. A number of
Health Evaluation (APACHE) II scores and maximum interleukins (IL) have been identified as key cytokines in
Sequential Organ Failure Assessment (SOFA) scores pro-inflammatory (e.g. IL-1, IL-6; and similar to TNF-α
(described later in this chapter), with cell-free plasma DNA actions) or anti-inflammatory (e.g. IL-10, IL-6, IL-4)
concentrations higher in hospital non-survivors than in responses. The inflammatory response results in clinical
survivors. Using regression analysis, maximum plasma DNA signs of hypoperfusion, culminating in shock.
was an independent predictor of hospital mortality.12 Intracellular transcription factors, in particular nuclear
Other cellular organelles may also exhibit pathological factor kappa B (NF-κB), are important in innate and
reactions in MODS. In ischaemia/reperfusion, endoplas- adaptive immunity,20,21 as they regulate the transcription
mic reticulum loses its ability to process proteins, which of genes involved in the inflammatory and acute stress
induces the expression of heat shock proteins,7 affecting response, leading to expression of TNF-α, interleukins and
transcription of proteins necessary for organ-specific tissue factor.21,22 NF-κB therefore plays an important role
functions. For example, liver cell metabolism, renal cell in response pathways in critical states including hypoxia,
function or cardiac cell contractility may be affected.7 This ischaemia, haemorrhage, sepsis, shock and MODS.21,23,24
has led to the concept of a mode of hibernation10,13 of cells The inflammatory cascade activates a number of
at the expense of survival of the whole organism.7 prostaglandins and leucotrienes that also have pro- and
Cellular communication is also altered in MODS. anti-inflammatory effects. Thromboxane A2 plays a role
Cells normally communicate through highly interactive in the acute phase, in part due to stimulation of platelet
720 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

FIGURE 22.2 Tissue factor pathway.

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699-709.

aggregation, leading to microvascular thrombosis and tissue space where they play the main role in successive phases
injury;17 it may also play a role in pulmonary broncho- of the inflammatory response.The endothelium thus plays
constriction and myocardial depression. a bidirectional mediating role between blood flow and the
The specific pathophysiological concepts of inflamma- interstitial space where inflammation mainly takes place.28
tion, oedema and infection are discussed below. Macrophages, neutrophils and monocytes are responsible
for phagocytosis and the production of toxic free radicals
Inflammation to kill invading pathogens.27 The complement system, a
Inflammation is part of innate immunity, a generic collection of 30 proteins circulating in the blood, is also
response to injury, and is normally an excellent mechanism activated, with plasma and membrane proteins acting as
to localise injury and promote healing.25,26 The basis of adjuncts to inflammatory and immune processes.27 When
this immune response is recognition of and an immediate activated by inflammation and microbial invasion, these
response to an invading pathogen without necessarily processes facilitate lysis (cellular destruction) and phago-
having previous exposure to that pathogen.27 Neutrophils, cytosis (ingestion) of foreign material.26,29
macrophages, natural killer cells, dendrites, coagulation Dysfunction of organ systems often persists after the
and complement are the principal active components of initial inflammatory response diminishes; this is largely
the innate host response.26 unexplained, although dysoxia (abnormal tissue oxygen
The classic signs of inflammation are: metabolism and utilisation) has been implicated.25,30 Hypoxia
• pain induces release of IL-6, the main cytokine that initiates the
• oedema acute phase response. After reperfusion of ischaemic tissues,
tissue and neutrophil activation forms reactive oxygen
• erythema and heat (from vasodilation) species (e.g. hydrogen peroxide) as a byproduct. These
• leucocyte accumulation and capillary leak.25,26 strong oxidants damage other molecules and cell structures
Nitric oxide and prostaglandins (e.g. prostacyclin) are that they come into contact with,13,26 resulting in water and
the primary mediators of vasodilation and inflammation at sodium infiltrate and cellular oedema.
the injury site.26 Injured endothelium produces molecules
that attract leucocytes and facilitate movement to the tissues. Oedema
White blood cells accumulate by margination (adhesion to Oedema occurs as a consequence of alterations to tissue
endothelium during the early stages of inflammation) and endothelium, with increased microvascular permeabil-
neutrophils accumulate at the injury site, where rolling ity or ‘capillary leak’. As noted earlier, many mediators,
and adherence to binding molecules on the endothelium including circulating cytokines, oxygen free radicals
occurs with eventual movement across the endothelium and activated neutrophils, alter the structure of endo-
into the tissues.26 Different blood components therefore thelial cells, enabling larger molecules such as proteins
escape the intravascular space and occupy the interstitial and water to cross into the extravascular space.26,31
 CHAPTER 22 MULTIPLE ORGAN DYSFUNCTION SYNDROME 721

This response mechanism improves supply of nutri- plasminogen–tissue plasminogen activator–plasmin pathway
ent-rich fluid to the site of injury but, if this becomes (involving antithrombin, activated protein C [APC] and
systemic, fluid shifts can lead to hypovolaemia or tissue factor pathway inhibitor). APC:38
third-spacing (interstitial oedema) or affect other organs • reduces inflammation by decreasing TNF and NF-κB
(e.g. acute lung injury, acute kidney injury).26 production
Infection and immune responses • reduces thrombin production when activated via
thrombin–thrombomodulin complexes (anticoagulant
Infection exists when there is one of the following: action)
positive culture, serology,32 presence of polymorpho-
nuclear leucocytes in a normally sterile body fluid except • inhibits thrombin-activatable fibrinolysis inhibitor
blood or clinical focus of infection such as perforated and plasminogen activator inhibitor-1 (profibrinolytic
viscus or pneumonia.33 action).34,35
The immune response to infection has both non- APC is consumed in severe sepsis, and thrombo-
specific and specific actions, with inflammation and modulin is unable to activate protein C,34,35,38 promoting a
coagulation responses intricately linked in sepsis patho- proinflammatory, prothrombotic state.35
physiology.26,27,34,35 Tissue injury and the production of
inflammatory mediators lead to: Endocrine response
• coagulation via the expression of tissue factor and Physiological changes are triggered as a normal response to a
factor VIIa complex (tissue factor pathway)31,34–36 stressor. In a critically ill patient, however, chronic activation
of the stress response, including the hypothalamic–pituitary–
• coagulation amplification via factors Xa and Va, adrenal (HPA) axis and the sympathetic–adrenal–medullary
leading to massive thrombin formation and fibrin clots
axis, results in ongoing production of glucocorticoid
(common coagulation pathway).31,34
hormones and catecholamines.20 This response interferes
Note that blood cell injury or platelet contact with endo- with the regulation of cytokine-producing immune cells,
thelial collagen initiates the contact activation pathway.34 leading to immune dysfunction. Other compensatory
mechanisms are instigated in an attempt to maintain supply
Procoagulation and perfusion to organs.18
Tissue factor is a procoagulant glycoprotein-signal- These homeostatic mechanisms are activated through
ing receptor,37 expressed when tissue is damaged or positive or negative feedback systems to counteract
cytokines are released from macrophages or the endo- stress. When stress is extreme or prolonged, these normal
thelium (see Figure 22.3). Prothrombin is formed, homeostatic mechanisms may be insufficient and a patient
leading to thrombin and fibrin generation from activated may respond through a sequence of physiological changes
platelets. Resulting clots are stabilised by factor XIII and called the stress response. The stress response occurs in
thrombin-activatable fibrinolysis inhibitor.34,37 Fibrinoly- three stages: the alarm reaction, the resistance reaction and
sis is a homeostatic process that dissolves clots via the exhaustion (see Figure 22.4).39

FIGURE 22.3 Progression of SIRS–sepsis–shock–MODS.

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SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

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Adapted from McCance KL, Heuther SE, Brashers VL, Rote NS. Pathophysiology: The biological basis for disease in adults and children.
6th ed. Mosby Elsevier: St Louis; 2010, with permission.
 CHAPTER 22 MULTIPLE ORGAN DYSFUNCTION SYNDROME 723

The alarm reaction (flight-or-fight response)39 is initiated shunted to the vital organs (brain, heart, lungs), and away
when stress is detected, increasing the amount of glucose from less vital areas such as the gastrointestinal system,
and oxygen available to the brain, skeletal muscle and heart. skin and reproductive organs.40 Important hormonal
Two-thirds of total blood volume is also redistributed to regulators of blood flow are also activated from decreased
support central circulation.39 A rise in glucose production blood flow to the kidneys, including adrenocorticotrophic
and the breakdown of glycogen in skeletal muscle increases hormone and the renin–angiotensin–aldosterone system
circulating glucose levels, providing an immediate energy (see Chapter 18). Adrenal medullary hormones, adrenaline
source.The long-lasting second stage is a resistance reaction, and noradrenaline, vasopressin (antidiuretic hormone)
involving hypothalamic, pituitary and adrenal hormone and atrial natriuretic peptide also regulate blood flow to
release.39 Response exhaustion occurs when these physio- maintain adequate circulation and tissue oxygenation.15,39,40
logical changes can no longer maintain homeostasis. Arterial pressure is a major determinant of tissue
perfusion as it forces blood through the regional vascula-
Compensatory mechanisms ture.23 Hypotension (systolic blood pressure <90 mmHg
Internal equilibrium (homeostasis) is maintained by the or mean arterial pressure [MAP] <70 mmHg) results from
nervous and endocrine systems, and these work sym- either low systemic vascular resistance or a low cardiac
biotically with other compensatory mechanisms, such output.23 Glomerular filtration falls, leading to reduced
as endothelial cells, to maintain cellular perfusion. The urine output; low cerebral blood flow results in an altered
nervous system responds rapidly to maintain homeostasis level of consciousness; and other manifestations reflect
by sending impulses to organs to activate neurohormonal low-flow states in other organ systems.To maintain oxygen
responses (see Chapters 16 and 21).Autonomic dysfunction supply, respirations and heart rate increase to meet organ
reflects ‘uncoupling’ of neurally mediated organ interac- oxygenation demands.41 Heart rate variability is suggested
tions in MODS14 characterised by heart rate, baroreflex as a strong predictor of mortality in MODS.15 Organ
and chemoreflex variability. Endothelins (ET-1, ET-2, dysfunction ensues if balance is not sufficiently restabilised
ET-3) are potent vasoconstrictors produced by endothe- (see Table 22.1).
lial cells that regulate arterial pressure.23 The endocrine
system works in a slow and sustained manner by secreting
hormones, which travel via the blood to end-organs.
Organ dysfunction
An initial acute-adaptive response is activated when Organ dysfunction is a common clinical presentation in
an insult or stress occurs. For example, the body senses ICU. Patients with dysfunction in the respiratory, cardio-
a disruption of blood flow through baroreceptor and vascular, hepatic or metabolic systems are 50% more likely
chemoreceptor reflex actions: baroreceptors located in the to require ICU treatment and have a higher mortality
carotid sinus detect changes in arterial pressure;16 chemo- than patients not requiring intensive care.42 Timely iden-
receptors co-located with the baroreceptors detect oxygen, tification of organ dysfunction is therefore critical, as early
carbon dioxide and hydrogen ion concentration. When intervention reduces damage and improves recovery in
alterations are sensed, the cardiovascular centre in the brain organ systems. As each organ fails, the average risk of death
adjusts autonomic outflow accordingly.39 In a patient with rises by 11–23%.43 The organ system that most commonly
decreased tissue perfusion, there is increased peripheral fails is the pulmonary system, followed by the cardiovascu-
vasoconstriction, contractility and heart rate. Blood flow is lar, renal and haematological systems.44 Organ and system

TABLE 22.1
Acute organ dysfunction49,110

ORGAN SYSTEM C L I N I C A L PA R A M E T E R S

Cardiovascular Patient requires vasopressor support for systolic BP <90 mmHg or MAP <70 mmHg for 1 hour despite
fluid bolus
Respiratory Patient requires mechanical ventilation: PF ratio <250, PEEP >7.5 cmH2O
Renal Low urine output <0.5 mL/kg/h; raised creatinine >50% from baseline or requiring acute dialysis
Haematological Low platelet count (<1,000,000/mm3) or APTT/PTT >upper limit of normal
Metabolic Low pH with increased lactate (pH <7.3 and plasma lactate >upper limit of normal)
Hepatic Liver enzymes >2 ⫻ upper limit of normal
Central nervous Altered level of consciousness/reduced Glasgow Coma Scale score
Gastrointestinal Translocation of bacteria, possible elevated pancreatic enzymes and cholecystitis

APTT = activated partial thromboplastin time; BP = blood pressure; MAP = mean arterial pressure; PEEP = peak end-expiratory
pressure; PF = PaO2/FiO2 = partial pressure of arterial oxygen/fraction of inspired oxygen; PTT = partial thromboplastin time.
724 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

dysfunctions are a result of hypoperfusion, inflammation, markers of coagulation and DIC also present.47 Treatment
cellular dysfunction and oedema. Dysfunctions of the is supportive and aimed at removing the triggering
cardiovascular (Chapters 10 and 12), respiratory (Chapters insults. Clinical biomarkers include a simultaneous rise in
14 and 15), renal (Chapter 18) and hepatic and gastrointes- prothrombin time, activated partial thromboplastin time
tinal systems (Chapter 20) have been previously addressed. (aPTT) and thrombocytopenia.35 A patient may exhibit
The next sections address the haematological, endocrine bleeding from puncture sites (e.g. invasive vascular access),
and metabolic systems. Neurological dysfunction is also mucous membranes including bowel or upper gastrointes-
common in the patient with MODS and complements tinal tract. Bruising or other subcutaneous petechiae may
previous discussions in Chapter 17. be evident. The skin should be protected from trauma.
Primary therapy is directed at the cause of the
Haematological dysfunction insult, with SIRS, ischaemia, uraemia, hepatotoxins and
SIRS and disseminated intravascular coagulation (DIC) sources of infection, injury or necrosis managed concur-
have pivotal and synergistic roles in the development of rently. Aggressive resuscitation includes crystalloid
MODS.42 The coagulopathy present in MODS results or colloid administration and replacement of blood
from deficiencies of coagulation system proteins such as components and clotting factors using packed cells,
protein C, antithrombin III and tissue factor inhibitors.8 platelets, cryoprecipitate and fresh frozen plasma. End
Inflammatory mediators initiate direct injury to the points for haemoglobin, platelets and coagulation levels
vascular endothelium, releasing tissue factor, triggering have not been agreed upon and replacement is therefore
the tissue factor pathway (extrinsic coagulation cascade) individualised.48
and accelerating thrombin production.8 Coagulation The role of heparin or fractionated heparin is contro-
factors are activated as a result of endothelial damage with versial in the presence of sepsis, particularly in those with
binding of factor XII to the subendothelial surface and overt thromboembolism or extensive fibrin deposition,
activation of factors VIII, X, XI, XII, calcium and phos- such as in purpura fulminans or ischaemia in the extremi-
pholipid.8 The final pathway is production of thrombin, ties.49 Administration of APC in its role as inhibitor of the
which converts soluble fibrinogen to fibrin. Fibrin and coagulation cascade is controversial. A Cochrane review of
aggregated platelets form intravascular clots. four studies involving 4911 participants (4434 adults and
Inflammatory cytokines also initiate coagulation 477 paediatric patients) identified no reduction in risk of
through activation of tissue factor, a principal activator of death (28-day mortality) in adult participants with severe
coagulation. Endotoxins increase the activity of inhibitors sepsis, but was associated with a higher risk of bleeding.
of clot breakdown (fibrinolysis). Levels of protein C and Effectiveness was not associated with the degree of severity
endogenous activated protein C are decreased in sepsis; of sepsis52 and, therefore, APC is no longer commercially
this inhibits coagulation cofactors Va and VIIa and acts as available.
an antithrombotic in the microvasculature.8
Microvascular thrombosis that leads to MODS results Endocrine dysfunctions
from two major syndromes: thrombotic microangiopathy Numerous endocrine derangements are noted in critically
and DIC. Thrombotic microangiopathy is characterised ill patients, including abnormalities in thyroid, adreno-
by formation of microvascular platelet aggregates and cortical, pancreas, growth and sex hormones. A high
occasionally fibrin formation. Typically, there is history of thyrotropin level is a significant independent predictor of
injury to the microvascular endothelium (e.g. thrombotic non-survival in critically ill patients,51 while subclinical
thrombocytopenic purpura, haemolytic uraemic syndrome, hypothyroidism has significant negative effects on cardiac
haemolytic anaemia, elevated liver enzymes and low platelet function and haemodynamic instability.51,52
syndromes of pregnancy or antiphospholipid antibody
syndrome).42 Thrombotic microangiopathy usually presents Adrenal insufficiency
with normal coagulation profiles such as prothrombin Adrenal insufficiency is present in approximately 30% of
times and partial thromboplastin time.45 patients with sepsis or septic shock,44,53,54,55 and is associated
DIC results from widespread activation of tissue with chronic adrenal insufficiency and recent physiolog-
factor-dependent coagulation, insufficient control of ical stress, or in new-onset adrenal insufficiency.51 This
coagulation and plasminogen-mediated attenuation of adrenal insufficiency can be caused by sepsis, surgery,
fibrinolysis.45 This leads to formation of fibrin clots, bleeding and head trauma. Adrenal insufficiency as a
consumption of platelets and coagulation proteins, cause of shock should be considered in any patient with
occlusion of the microvasculature and resultant reductions hypotension with no signs of infection, cardiovascular
in cellular tissue oxygen delivery.45 DIC is most commonly disease or hypovolaemia. Incidence ranges from 0–95%,56
a result of trauma or sepsis and is an exaggerated response partly because there is no standard definition for adrenal
to normal coagulation aimed at limiting infection and insufficiency.
exsanguination and promoting wound healing.45 Eosinophilia (>3% of total white blood cell count) is
Thrombocytopenia (a platelet count of <80,000/mm3 reported as a marker of adrenal insufficiency. Methods to
or a decrease of ≥50% over the preceding 3 days) signifies diagnose acute adrenal insufficiency include: 1) a single
haematological failure,46 with leucocytopenia/cytosis, random cortisol level check, or a change in cortisol
 CHAPTER 22 MULTIPLE ORGAN DYSFUNCTION SYNDROME 725

level after endogenous adrenocorticotrophic hormone Multiorgan dysfunction

(ACTH) is administered; or 2) a short corticotrophin
stimulation test with administration of high-dose ACTH. MODS contributes to significant morbidity and use
A change in cortisol level (≤9 mcg/dL) is considered of intensive care resources worldwide. Patients with
relative adrenal insufficiency. It is, however, argued that MODS have an increased ICU length of stay when
patients with severe sepsis may have appropriate cortisol compared to high-risk patients without multiple organ
levels, but not the reserve function to respond to the involvement63,63 and very high 5-year mortality.64 The
stimulation test.34 epidemiology of MODS varies with North American and
Australian studies in post-injury organ failure indicating
Hypocalcaemia a reduction in incidence,62,63 versus increasing incidence
Hypocalcaemia is common in patients with SIRS58 reported in a recent German study.65 These contrasting
and affects myocardial contractility and neuromuscular findings are in part due to different inclusion/exclusion
functions. The link between neuromuscular changes such criteria and MODS scoring systems used. Internationally,
as polyneuropathy or polymyopathy and critical illness a reduction or stabilisation of MODS-related mortality is
has not been established beyond early investigations into reported;62,63,65 however, data from the developing world
corticosteroid use, neuromuscular blocking medication are scant. Mortality 15 years ago was estimated at 40–60%,
administration and prolonged mechanical ventilation.58 rising with subsequent organ dysfunction.43,66,67 More
recent data in post-injury MODS indicate mortality
Neurological dysfunction rates between 11% and 27%.62,63,68 This overall decrease
Evidence has highlighted that multiple organ dysfunc- in mortality is occurring despite increasing patient
tion can result from severe traumatic brain injury or acuity and may reflect improvements in the delivery of
subarachnoid haemorrhage (see Chapter 17). Cardiovas- critical care.6
cular and respiratory dysfunction contribute to mortality
in approximately two-thirds of all deaths following severe Scoring systems
traumatic brain injury.59 In non-traumatic subarachnoid Organ dysfunction can be a consequence of a primary
haemorrhage the incidence and importance of life- insult or a secondary insult due to circulating mediators
threatening conditions from non-neurological physiology (e.g. the patient with acute lung injury from pneumonia
has been identified, including lethal arrhythmias, that also has renal dysfunction or failure as a consequence).
myocardial ischaemia and dysfunction and neurogenic This is sometimes quantified by scoring systems, tradi-
pulmonary oedema.59 The cause of cardiovascular and tionally used for predicting mortality but increasingly
respiratory organ dysfunction following these acute, being explored as clinical management tools.69–71,72 These
severe neurological events is associated with dysfunction systems are continually being tested and modified, to assess
of the sympathetic nervous system. Beta-blockers may organ dysfunction severity and prognosis in an effort to
modulate the sympathetic storm resulting from severe identify patients who will benefit most from timely
neurological injury.59 clinical intervention.71 Scoring systems such as APACHE,
Critically ill patients may develop a syndrome of simplified acute physiology score and mortality probabil-
neuromuscular dysfunction characterised by generalised ity models account for information relating to a 24-hour
muscle weakness and an inability to wean successfully cycle of patient data (commonly in the first 24 hours of
from mechanical ventilation. ICU-acquired weakness, admission), but do not account for the dynamic nature
including critical illness neuromyopathy syndromes, has of many of the factors that affect clinical outcomes, thus
been associated with risk factors including hypergyl- potentially limiting their use for early MODS diagnosis
caemia, SIRS, sepsis, MODS, renal replacement therapy, and intervention.
glucocorticoids, neuromuscular blocking agents and cate- Specific instruments designed to assess organ dysfunc-
cholamine administration.60 The risk of ICU-acquired tion or failure include the sepsis-related/SOFA score, the
weakness is nearly 50% in patients with sepsis, MODS more trauma-specific Denver multiple-organ failure score,
or protracted ventilation,58 with short-term survival the multiple organ dysfunction score and the logistic
uncertain. Glycaemic control may be a potential strategy organ dysfunction system.63,70,72–75 Traditionally, SOFA
for decreasing ICU-acquired weakness.60 uses the worst values for six commonly measured clinical
Survivors of sepsis-induced multiple organ dysfunc- parameters within a 24-hour period: PaO2/FiO2 (PF
tion may also suffer long-term cognitive impairment, ratio), an index that may be used to characterise acute
including alterations in memory, attention, concentration respiratory distress syndrome;75 platelet count; bilirubin
and/or global loss of cognitive function.61 The partic- level; blood pressure; Glasgow Coma Scale score; and
ipation of the brain during sepsis is poorly understood; urine output or creatinine concentration. As the number
septic encephalopathy is the more common neurological of dysfunctional organ systems increases, there is a rise in
dysfunction, accounting for up to 70% of brain dysfunc- mortality as measured by SOFA scores (see Table 22.2).
tions.61 In Chapter 4 the physical, psychological and Many variations of SOFA-based models have emerged
cognitive sequelae for survivors of a critical illness during in the literature, such as single SOFA scores calculated at
their recovery are described. admission or at a set time after admission, sequential SOFA
726 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

scores (mean SOFA score), dynamic SOFA scores and 1 (PAI-1), which is a key element in the inhibition of fibri-
scores of separate SOFA components.69,70 SOFA scores at nolysis and is active during acute inflammation84 (the gene
admission are comparable with severity of illness models most studied is found at the 4G/5G insertion/deletion
such as APACHE or the simplified acute physiology score loci), and have found that different aspects bind as either
for predicting mortality.70 SOFA scoring has the advantage a repressor (5G) or activator (4G) protein. For example,
of ease of use, as the clinical and laboratory data required the 4G allele (position on the gene) of the 4G/5G gene
are routinely available. As such, the use of dynamic SOFA sequence variation has been associated with increased
scoring as a means of monitoring patient response to susceptibility to community-acquired pneumonia and
treatments is being explored.69,71 Other scoring systems increased mortality in cases of severe pneumonia. It has
that allow pre-hospital identification of trauma patients also been reported to affect the risk of developing severe
predisposed to MODS are also being developed.72 Overall, outcomes and higher mortality in meningococcal sepsis
there is no one universally accepted gold standard scoring and trauma.84 Among critically ill patients with severe
system with different systems used in MODS research.76,77 sepsis due to pneumonia, carriers of the PAI-1 4G/5G
genotypes have higher risk for MODS and septic shock.84
Other factors In future, identification of genetic factors may assist
Biomarkers such as lactate, base deficit and platelet count selection of appropriate therapy for the patient at risk.
are also being studied as indicators of occult hypoper- Experimental BRCA1 gene therapy research is showing
fusion and severity of organ dysfunction.78–81 Blood lactate early promising results on key cellular processes involved
levels are routinely collected in the early stage of ICU in stimulating DNA repair and cellular defense.84
admission, supporting early resuscitation as a management
strategy to prevent organ dysfunction. Serial lactate scores
may therefore be appropriate to guide optimal oxygen
Patient management
delivery in early resuscitation, with hyperlactataemia a sign Improvement in patient survival with MODS is thought
of impending organ dysfunction. With the production of to be due to improved identification of patients pre-
point-of-care lactate analysers, pre-hospital lactate levels disposed to MODS, improved shock and critical care
may also identify patients predisposed to MODS and management, awareness of secondary insults and a better
influence care delivery.82 Prospective, well-controlled understanding of the risk factors associated with MODS.
studies are, however, needed to confirm the role of lactate Current prevention and management strategies therefore
and other biomarkers in MODS management.79–82 focus on identifying at-risk patients via scoring systems or
Variations in the human DNA sequences can affect biomarkers, efficient shock resuscitation, timely treatment
the way a person responds to disease. Researchers have of infection, exclusion of secondary inflammatory insults
studied the gene code for plasminogen activator inhibitor and organ support.61,76,81

TABLE 22.2
Sequential organ failure assessment (SOFA) score69,110

S O FA S C O R E 0 1 2 3 4

Respiration >400 ≤400 ≤300 ≤200 a

≤100a
PaO2/FiO2
Coagulation platelets >150 ≤150 ≤100 ≤50 ≤20
⫻ 103/mm3
Liver <1.2 mg/dL 1.2–1.9 2.0–5.9 6.0–11.9 >12.0
bilirubin >32 micromol/L 20–32 33–101 102–204 >204
Cardiovascular MAP >70 mmHg MAP <70 mmHg Dopamine ≤5 or Dopamine >5 or Dopamine >15 or
hypotension Dobutamine (any adrenaline ≤0.1 or adrenaline >0.1 or
dose)b noradrenaline ≤0.1b noradrenaline >0.1b
CNS 15 13–14 10–12 6–9 <6
Glasgow Coma Scale
Renal creatinine <1.2 mg/dL 1.2–1.9 2–3.4 3.5–4.9 >5.0
or urine output <110 micromol/L 110–170 171–299 300–440 >440
or or
<500 mL/day <200 mL/day

a
With respiratory support.
b
Adrenergic agents administered for at least 1 hour (doses in mcg/kg per min).
FiO2 = fraction of inspired oxygen; MAP = mean arterial pressure; PaO2 = partial pressure of arterial oxygen.
 CHAPTER 22 MULTIPLE ORGAN DYSFUNCTION SYNDROME 727

Effective shock resuscitation BOX 22.1

A number of interventions have been recommended to
Surviving Sepsis campaign
reduce mortality for patients with MODS due to sepsis.
The Surviving Sepsis guidelines are based on clinical The Surviving Sepsis campaign is an international
evidence graded according to the quality of evidence collaborative formed in 2003 to reduce the mortality of
available.81 The third version of the guidelines released sepsis. Guidelines for the management of severe sepsis
in 2012 emphasises the importance of early recognition and shock were updated in 2008 and 2012 and offer a
of sepsis-induced hypoperfusion and details resuscitation comprehensive list of graded recommendations to care
goals to be achieved within the first 6 hours of resus- for these patients.81 Many of the recommendations for
citation. This treatment, known as early goal directed practice have implications for critical care nurses and
therapy (EGDT), created some controversy and dissent the multidisciplinary team (see Online resources).
when released in the 2008 version of the guidelines (see
Table 22.3) (see Chapter 21 for further discussion). Adapted from Dellinger R, Levy M, Rhodes A, Annane D, Gerlach
H, Opal SM et al. Surviving Sepsis Campaign: international
The multicentre, prospective, observational ARISE
guidelines for management of severe sepsis and septic shock:
study (Australasian Resuscitation In Sepsis Evaluation) 2012. Crit Care Med 2013;41(2):580–637, with permission.
assessed the resuscitation practices and outcomes in
patients presenting to emergency departments with
sepsis with hypoperfusion or septic shock. Overall in- mortality benefit for patients with severe sepsis/septic
hospital mortality of 23% was comparable to in-hospital shock resuscitated with the protocol using continuous
mortality reported in studies of early EGDT.85 The study central venous oxygen saturation versus lactate clearance
confirmed that protocolised central venous oxygenation as a measure of adequate tissue oxygen delivery.90 Large
saturation-directed EGDT was not routinely practised prospective clinical trials of EGDT include the US-based
in Australia or New Zealand, and recommended that ProCESS (Protocolized Care for Early Septic Shock)
EGDT not be adopted in Australia and New Zealand trial, the Australian ARISE (Australasian Resuscitation
without further multicentre randomised controlled in Sepsis Evaluation) trial and the UK ProMISe (Proto-
trials.85 While evidence of the benefits of EGDT from colised Management In Sepsis) trial.91 The ProCESS trial
a quality improvement perspective is emerging,81,86,87 showed no improvement in outcomes for patients with
these benefits may be due to increased awareness of septic shock who received protocol-based resuscitation
sepsis management rather than EGDT.88 In addition, the in the emergency department.92 Similarly, the ARISE and
complex invasive technologies that underpin EGDT are ProMISe studies also did not detect a significant decrease
not practical in resource-limited low- and middle-in- in sepsis mortality with the use of EGDT. See Chapter 21
come countries.88 Early resuscitation in severe sepsis for further discussion of resuscitation in shock.
does appear to improve patient outcomes;89 however,
evidence in relation to which components of EGDT Early treatment of infection
are effective is lacking. One study has reported no Timely treatment of infection appears important in the
prevention and management of MODS, with early anti-
microbial therapy in septic shock recommended in the
TABLE 22.3 Surviving Sepsis guidelines. The Cooperative Antimicro-
EGDT in severe sepsis: initial targets82 bial Therapy of Septic Shock Database Research Group
ITEM TA R G E T
identified that:
CVP 8–12 mmHg • inappropriate initial antimicrobial therapy was
12–15 mmHg in mechanically ventilated
associated with a five-fold decrease in survival to
patient or patient with decreased hospital discharge94
ventricular compliance • the incidence of early acute kidney injury increased
MAP ≥65 mmHg with delays in antimicrobial therapy from the onset of
Urine output ≥0.5 mL/kg/h
hypotension.94
ScvO2/ SvO2 ≥70%/≥65%
Other studies support the Surviving Sepsis guidelines
recommendation of antimicrobial therapy within the
CVP = central venous pressure; MAP = mean arterial first hour of diagnosing severe sepsis.95–97 As early anti-
pressure; ScvO2 = central venous oxygen saturation; microbial administration may be difficult to achieve
SvO2 = mixed venous oxygen saturation.
given competing patient management priorities (e.g.
Adapted from Dellinger R, Levy M, Rhodes A, Annane D, airway management, volume resuscitation, vasopressor
Gerlach H, Opal SM et al. Surviving Sepsis Campaign:
international guidelines for management of severe sepsis and
administration), systems must be developed to promote
septic shock: 2012. Crit Care Med 2013;41(2):580–637, with early administration.96 Nurses are in a pivotal position
permission. to ensure these guidelines or processes are developed,
implemented and evaluated.
728 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

has led to a number of trials that suggested some survival

Practice tip benefit for low-dose corticosteroid therapy. More research
Tips for promoting early antimicrobial administration in is required, however, because of conflicting findings from
severe sepsis/septic shock:82,96,97 individual studies.
Therapy with corticosteroids at a physiological dose,
• Ensure high priority in severe sepsis/septic shock
rather than a high dose, followed observations that patients
algorithms.
with septic shock who had a reduced response to cortic-
• Do not delay antimicrobial administration if difficulty otropin were more likely to have increased mortality, and
sampling blood cultures (cultures need to be that pressor response to noradrenaline may be improved by
collected within 45 minutes of diagnosis of severe the administration of hydrocortisone.102 A trial exploring
sepsis or septic shock). steroid use in sepsis demonstrated reduced vasopressor
• Ensure adequate supply of antimicrobials in the requirements and early lower mortality, but no difference
emergency department and ICU that fit local in 1-year survival.55 A multicentre trial demonstrated that
colonisation patterns. hydrocortisone administration did not improve survival
• Utilise appropriate antibiotics that can be given via in patients with septic shock. Shock reversal was shorter
intravenous push vs longer infusion. in patients who received hydrocortisone, but there were
more episodes of infection including new sepsis and septic
• Emphasise education of staff on the significance of
shock.102 Although the largest trial of corticosteroids in
early administration of initial antimicrobial.
patients with septic shock, the study was not adequately
• Consider other potential barriers to early powered to detect a clinically important treatment and so
antimicrobial administration in your facility. findings are to be interpreted with caution.103 It is therefore
appropriate to reserve corticosteroids for patients with
Combination antibiotic therapy may offer a survival septic shock whose blood pressure is poorly responsive
benefit in septic shock, but may be deleterious to patients to fluid resuscitation and high-dose vasopressor therapy.103
with a low mortality risk.97 Certainly, antibiotic overuse Long-term treatment with corticosteroids may result in
and misuse is of concern given the emergence of antibiotic an inadequate response of the adrenal axis to subsequent
resistance.98 Other factors that can lead to antibiotic failure stress such as infection, surgery or trauma, with resulting
in the critically ill include increased volume of distribu- onset or worsening of shock. Other studies using cortic-
tion secondary to expanded extracellular volume, transient osteroids for adrenal insufficiency in critically ill patients
increased drug clearance due to elevated cardiac output demonstrated lower mortality.8
(early sepsis) and increased free-drug levels secondary Corticosteroid administration is associated with hyper-
to reduced serum albumin. Maximum antibiotic dosage glycaemia and may affect patient outcomes, necessitating
levels on day 1 of therapy, guided by predicted volume insulin therapy to normalise blood glucose levels. A multi-
of distribution, are therefore recommended in life- centre trial (Corticosteroids and Intensive Insulin Therapy
threatening infections, as inadequate antibiotic penetration for Septic Shock [COIITS])104 demonstrated that intensive
can occur due to impaired vascularity of infected tissue insulin therapy did not improve in-hospital mortality for
(inhibits delivery of antibiotic), antibiotic antagonism patients treated with hydrocortisone and oral fludrocorti-
(uncommon but possible with combination therapy) sones for septic shock.
and coexisting unrecognised bacterial infection.81,97,99
Subsequent antibiotic dosing must be guided by drug Glycaemia control
clearance. This will be influenced by the associated organ Hyperglycaemia is common in critically ill patients as
dysfunction.100 Nursing assessment of patient response to a result of stress-induced insulin resistance and acceler-
antibiotic therapy (resolution or exacerbation of signs of ated glucose production, and excessive circulating levels
sepsis) and surveillance for sites of unrecognised infection of glucagon, growth hormone, sympathomimetics and
are also important. glucocorticoids (see Chapter 19). An increased caloric
Source control (e.g. abscess drainage, removal of infected intake from parenteral or enteral nutrition will also
necrotic tissue or potentially infected device) is also an increase glucose levels. Hyperglycaemia has undesirable
essential aspect of infection control and should be imple- effects such as fluid imbalance, immune dysfunction,
mented within the first 12 hours of diagnosing severe sepsis promoting inflammation, abnormalities in granulocyte
or septic shock. The method of source control chosen adherence, chemotaxis, phagocytosis and intracellular
should always involve a risk/benefit analysis as source killing.34 Resulting associations between hyperglycaemia
control interventions can exacerbate complications.81 and adverse clinical outcomes have been reported in many
observational studies.34,105 Potential benefits of exogenous
Steroid therapy insulin administration include normalising immune
As septic shock is a major complication of infectious function, improving oxygen delivery to ischaemic areas
processes, the relationship between the immune, coagu- of myocardium, tissue repair and preventing transfusion,
lation and neuroendocrine systems has been explored.101 dialysis and critical illness polyneuropathy.34 Intensive
The role of corticosteroids in the treatment of septic shock insulin therapy has also been suggested to improve
 CHAPTER 22 MULTIPLE ORGAN DYSFUNCTION SYNDROME 729

morbidity, reducing the risk of sepsis, excessive inflamma- Contemporary research is focusing on homogeneous
tion and multiple organ failure, transfusion requirements subgroups of critically ill patients in an effort to refine
and dependence on mechanical ventilation.106 MODS treatment, as opposed to heterogeneous groups
The Normoglycaemia in Intensive Care Evaluation where treatment impacts may be hidden by patient
and Survival Using Glucose Algorithm Regulation study diversity.76 There is a surprising dearth of literature specif-
(NICE-SUGAR) examined tight glycaemic control ically addressing the complex nursing care required by
with insulin during critical illness.106 Maintaining blood a MODS patient. These patients require highly skilled
glucose at less than 10 mmol/L resulted in 10% reduction nurses who are able to balance competing priorities via
in 90-day mortality compared to a tighter glycaemic ongoing patient assessment, care planning, monitoring
control target (4.5–6.0 mmol/L).105 Lower target blood and evaluation. The complex care required to nurse the
sugar levels are therefore not recommended for managing MODS patient is highlighted in the clinical case study.
glycaemia in critically ill patients.
Exclusion of secondary insults and Practice tip
organ support Tips for detecting haematological dysfunction in the
Prevention of secondary inflammatory insults and organ patient with MODS:48,56
support include a broad range of interventions including • Monitor the skin for significant bruising or
use of massive transfusion protocols,107 recognition of petechiae.
abdominal compartment syndrome via urine catheter • Check the sites of invasive devices such as arterial,
manometry,108 lung protective ventilation,82 early nutri- central venous access or urinary catheters for
tional support,108,109 glycaemic control,106 haemodynamic bleeding.
support using vasopressors and intropes82 and renal
replacement therapy.81 Routine evidence-based measures • Test urine or faeces for occult blood.
are also essential, including hygiene; bowel management; • Note oral bleeding during mouth care or from the
pressure area, mouth and eye care; and other processes of nose when nasal cleansing.
care (e.g. FASTHUG; see Chapter 21). • Detect progressive changes in coagulation or
Awareness of the latest evidence that underpins platelet profiles.
management of these complex patients is important.

Summary
Multiple organ dysfunction is a common presentation to critical care units across the world. Critical care nurses require
high-level knowledge of pathophysiology and early recognition of failure of individual organs and the antecedents to the
development of organ failure.The pathophysiological consequence of systemic inflammatory response and sepsis requires
understanding of individual organ function and responses to stressors so that pre-emptive strategies can be initiated
to prevent further organ failure and support individual organs. Patients with MODS are complex patients to manage,
requiring highly skilled nursing care that involves vigilant assessment, planning of intervention priorities, monitoring
and ongoing treatment evaluation. Well-developed time management skills are required to include all routine cares and
required treatment. Balancing care priorities begins on patient presentation as highlighted by the importance of initial
resuscitation and early antimicrobial therapy.

Case study
Mrs Crisp, aged 30, presented to the maternity ward in the early stages of labour. Despite an elevated
blood pressure (160/105 mmHg) on arrival, Mrs Crisp progressed to a normal vaginal delivery of a healthy
baby boy. Mrs Crisp was moved from the delivery suite to spend time bonding with her baby following the
birth. Approximately 6 hours later she began to complain of abdominal pain in the upper right quadrant.
Paracetamol was provided; however, the pain continued, radiating to the epigastrium and shoulder.
Mrs Crisp was nauseated and felt faint. Her blood pressure was noted to be 90/60 mmHg with a heart
rate of 125 beats per minute. Nursing staff called the medical officer who, in collaboration with critical
care medical staff, ordered a series of investigations. The blood results showed haemoglobin of 75 g/L,
platelets of 57,000 ⫻ 109, INR 1.6, fibrinogen of 1.4 g/L with deranged liver function tests. Chest computed
tomography revealed no evidence of pulmonary emboli.
730 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Chest auscultation revealed a decreased air entry to the right lower base; she appeared cool to the touch
with respirations of 26 per minute. Abdominal assessment revealed tenderness in the right hypochondria
and a relatively rigid abdomen. The uterus was contracting normally at this point in her postpartum period.
Mrs Crisp had not passed urine at this stage. A cannula was inserted, and fluid and oxygen therapy
commenced. Arrangements were made for urgent transfer to critical care for ongoing support. In critical
care Mrs Crisp was intubated, ventilated and continued to display signs of shock with low blood pressure,
reduced urine output and abdominal pain. She received an urgent surgical review as the CT abdomen
revealed a rupture of the liver with bleeding in the subcapsular region. Mrs Crisp was transferred to the
operating theatre for surgical repair.
On return from theatre Mrs Crisp remained intubated and ventilated with a controlled ventilation rate of
12 breaths per minute, tidal volumes of 8 mL/kg, positive end-expiratory pressure of 5 cmH2O and fraction of
inspired oxygen (FiO2) of 0.5. Her respiratory status became unstable with increasing oxygen requirements
(FiO2 0.8) and her oxygen saturation decreased to 90%. Blood gas results revealed pH 7.30, PaCO2
60 mmHg. Her inspiratory airway and plateau pressures increased and a diagnosis of acute respiratory
distress syndrome was made based on a PaO2/FiO2 ratio of less than 200 and infiltrates on her chest X-ray.
Despite therapeutic interventions Mrs Crisp continued to be haemodynamically unstable. Her blood
pressure remained low and a noradrenaline infusion of 15 mcg/min was commenced aiming to achieve
a mean arterial pressure of 65–70 mmHg. Urine output decreased on day 2 to 15 mL/h. Central venous
pressure was recorded as 14 cmH2O and fluid filling did not increase her urine output. Diuretic therapy
in the form of frusemide was trialled as a continuous infusion with some increase in her urine output.
A diagnosis of acute renal failure was made (creatinine 141 micromol/L) and continuous venovenous
haemodiafiltration renal replacement therapy commenced. Mrs Crisp had marked coagulopathy that
resulted in DIC requiring administration of blood products (platelets and fresh frozen plasma) to replace
consumed clotting factors.
Enteral feeds and a prokinetic were commenced early in the course of her admission to support nutritional
status; this was tolerated with low residual gastric volume. Over the following few days the condition of
Mrs Crisp slowly improved with lung mechanics and renal function returning to baseline levels and weaning
of therapy commenced. On day 8 Mrs Crisp was extubated and discharged to the ward to continue her
recovery and rehabilitation.

DISCUSSION
The period of time where Mrs Crisp was most at risk of multiple organ dysfunction was during the episode
of hypotension. The loss of blood from the liver tear was physiologically compensated for initially through
centralisation of cardiac output as a result of a vasomotor response resulting in vasoconstriction and
tachycardia. The respiratory system increased oxygenation uptake through augmenting respirations;
however, the reduced haemoglobin level lowered the oxygen-carrying capacity. As blood loss continued
other compensatory mechanisms came into play. The stress response triggered a cascade of neuroendocrine
and other hormonal events. Coagulation factors were consumed due to activation of tissue factor pathway
activation leading to disseminated intravascular coagulation with resulting loss of platelets and fibrinogen
levels. Microcirculatory failure and the continued vasoconstriction with altered vascular filling resulted in
renal and liver dysfunction. This was reflected by her reduced urine output, elevated creatinine levels and
deranged liver function test results.
Fortunately for Mrs Crisp, early intervention through the administration of fluids and blood products,
invasive respiratory support and surgical repair of the liver tear resulted in a short course of multiple
organ dysfunction. The critical care she received prevented many adverse effects of critical illness and
psychological care resulted in minimal disruption to the mother and baby bonding.
The case highlights the significant part that early identification of patient deterioration with appropriate and
timely management plays in averting longer periods of multiple organ dysfunction.
CASE STUDY QUESTIONS
1 Identify the organs and body systems that failed in the case of Mrs Crisp. Include in your answer the
clinical signs that indicated MODS.
2 Develop a care plan for Mrs Crisp for her stay in critical care. Ensure that you include routine cares as
well as care specifically targeted at organ support. Discuss your plan with an experienced colleague.
3 List some of the important assessment findings that influenced the care of Mrs Crisp during her stay in
critical care.
 CHAPTER 22 MULTIPLE ORGAN DYSFUNCTION SYNDROME 731

RESEARCH VIGNETTE

Andruszkow H, Veh J, Mommsen P, Zeckey C, Hildebrand F, Frink M. Impact of the body mass on complications
and outcome in multiple trauma patients: what does the weight weigh? Mediators Inflamm 2013; doi:
10.1155/2013/345702. Epub 2013 Aug 19

Abstract
Obesity is known as an independent risk factor for various morbidities. The influence of an increased body mass
index (BMI) on morbidity and mortality in critically injured patients has been investigated with conflicting results.
To verify the impact of weight disorders in multiple traumatized patients, 586 patients with an injury severity score
>16 points treated at a level I trauma center between 2005 and 2011 were differentiated according to the BMI
and analyzed regarding morbidity and outcome. Plasma levels of interleukin- (IL-) 6 and C-reactive protein (CRP)
were measured during clinical course to evaluate the inflammatory response to the “double hit” of weight disorders
and multiple trauma. In brief, obesity was the highest risk factor for development of a multiple organ dysfunction
syndrome (MODS) (OR 4.209, 95% CI 1.515–11.692) besides injury severity (OR 1.054, 95% CI 1.020–1.089) and
APACHE II score (OR 1.059, 95% CI 1.001–1.121). In obese patients as compared to those with overweight, normal
weight, and underweight, the highest levels of CRP were continuously present while increased systemic IL-6 levels
were found until day 4. In conclusion, an altered posttraumatic inflammatory response in obese patients seems to
determine the risk for multiple organ failure after severe trauma.

Critique
The researchers set the background to the work by drawing attention to the conflicting results of previous research
studies into the influence increased body mass of critically injured patients has on morbidity and mortality. The
researchers questioned the role that inflammation had on the posttraumatic systemic immune response in critically
injured obese and normal or underweight participants in the study population. The results from the study revealed
obesity as the highest risk factor for the development of MODS though it had little impact on mortality. Obese patients
were admitted with increased interleukin-6 levels for the first 4 days and showed sustained elevation in CRP levels
for the study period. Increased interleukin-6 levels were positively correlated with the incidence of MODS during the
whole study period while elevated CRP levels were positively correlated with MODS after day 3.
The authors suggest that increased adipose tissue content results in elevated pro-inflammatory adipokines, which
have a number of effects on the critically ill multiple trauma patient. These effects resulted in an increased incidence
of MODS in the obese study population. Study limitations are noted in that a substantial number of patients were
excluded due to missing weight and height data, which was noted to be comparable to other studies. BMI was also
questioned as presenting an accurate tool to determine weight disorders though this was felt by the authors to be a
safe measurement as it represented the most widely accepted parameter in the literature quoted in the study.
The final summation by the study authors advised that obesity was revealed as an independent risk factor for the
development of MODS in severely traumatised patients. The role that nutrition status plays in the post-traumatic clinical
course was put forward for consideration as important in therapeutic strategies for patients suffering from major trauma.
The study was well designed and it is a significant study in relation to the growing incidence of obesity amongst the
critically ill traumatised patients who are admitted to critical care. The relationship of obesity to MODS and mortality
outcomes for patients with trauma should encourage future prospective trials that may translate into improved
healthcare outcomes for critically ill patients.

Lear ning a c t iv it ie s
1 Identify five key elements essential in managing the patient with emergent MODS.
2 Outline four strategies that promote early antimicrobial administration and therefore the prevention and
management of MODS, in the patient with severe sepsis and septic shock.
3 Identify eight strategies that aim to minimise secondary insult and provide organ support for the MODS patient.
732 SECTION 2 PRINCIPLES AND PRACTICE OF CRITICAL CARE

Online resources
The Institute for Healthcare Improvement (IHI) is a non-profit organisation for advancing the quality and value of health care.
Search the site for sepsis-related information about improving care and severe sepsis bundles, www.ihi.org
The Surviving Sepsis guidelines webpage provides access to full text documents, references, presentations, updated
position statements and tools related to the guidelines, www.survivingsepsis.org
The US National Institutes of Health clinical trials registry. Search the site for current trials in MODS, www.clinicaltrials.gov

Further reading
Dellinger R, Mitchell M, Rhodes A, Annane D, Gerlach H, Opal SM et al. Surviving Sepsis campaign: international guidelines
for management of severe sepsis and septic shock: 2012. Crit Care Med 2013;41(2):580–637.
Fröhlich M, Lefering R, Probst C, Paffrath T, Schneider MM, Maegele M et al. Epidemiology and risk factors of multiple-
organ failure after multiple trauma: an analysis of 31,154 patients from the TraumaRegister DGU. J Trauma Acute Care Surg
2014;76(4):921–8.
Lone N, Walsh T. Impact of intensive care unit organ failures on mortality during five years after a critical illness. Am J Respir
Crit Care Med 2012;186(7):640–7.
Moore FA, Moore EE. The evolving rationale for early enteral nutrition based on paradigms of multiple organ failure:
a personal journey. Nutr Clin Practice 2009;24(3):297–304.
Nydam TL, Kashuk JL, Moore ED, Johnson JL, Burlew CC, Biffl WL et al. Refractory postinjury thrombocytopenia is
associated with multiple organ failure and adverse outcomes. J Trauma 2011;70(2):401–7.
Sauaia A, Moore E, Johnson J, Chin T, Banerjee A, Sperry JL et al. Temporal trends of postinjury multiple-organ failure: still
resource intensive, morbid, and lethal. J Trauma Acute Care Surg 2014;76(3):582–93.
Ulldemolins M, Roberts J, Lipman J, Rello J. Antibiotic dosing in multiple organ dysfunction syndrome. Chest 2011;
139(5):1210–20.

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62 Sauaia A, Moore E, Johnson J, Chin T, Banerjee A, Sperry JL et al. Temporal trends of post-injury multiple-organ failure: still resource intensive,
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63 Lone N, Walsh T. Impact of intensive care unit organ failures on mortality during five years after a critical illness. Am J Respir Crit Care Med
2012;186(7):640-47.
64 Fröhlich M, Lefering R, Probst C, Paffrath T, Schneider MM, Maegele M et al. Epidemiology and risk factors of multiple-organ failure after
multiple trauma: an analysis of 31,154 patients from the TraumaRegister DGU. J Trauma Acute Care Surg 2014;76(4):921-928.
65 Angus DC, Linde-Zwirble WT, Lidicker J, Clermont G, Carcillo J, Pinsky MR. Epidemiology of severe sepsis in the United States: analysis of
incidence, outcome, and associated costs of care. Crit Care Med 2001;29(7):1303–10.
66 Peres Bota D, Melot C, Lopes Ferreira F, Nguyen BV, Vincent J-L. The multiple organ dysfunction score (MODS) versus the sequential organ
failure assessment (SOFA) score in outcome prediction. Intensive Care Med 2002;28(11):1619–24.
67 Minei JP, Cuschieri J, Sperry J, Moore EE, West MA, Harbrecht BG et al. The changing pattern and implication of multiple organ failure after
blunt injury with hemorrhagic shock. Crit Care Med 2012;40(4):1129-35.
68 Anami EH, Grion CM, Cardoso LT, Kauss IA, Thomazini MC, Zampa HB et al. Serial evaluation of SOFA score in a Brazilian teaching hospital.
Intensive Crit Care Nurs 2010;26:75–82.
69 Minne L, Abu-Hanna A, de Jonge E. Evaluation of SOFA-based models for predicting mortality in the ICU: a systematic review. Crit Care
2008;12(6):R161.
70 Jones A, Trzeciak S, Kline J. The sequential organ failure assessment score for predicting outcome in patients with severe sepsis and evidence
of hypoperfusion at the time of emergency department presentation. Crit Care Med 2009;35(5):1649–54.
71 Vogel JA, Liao MM, Hopkins E, Seleno N, Byyny RL, Moore EE et al. Prediction of postinjury multiple-organ failure in the emergency department:
development of the Denver Emergency Department Trauma Organ Failure Score. J Trauma Acute Care Surg 2013;76(1):140-5.
72 Khwannimit B. A comparison of three organ dysfunction scores: MODS, SOFA and LOD for predicting ICU mortality in critically ill patients.
J Med Assoc Thai 2007;90(6):1074–81.
73 Heldwein M, Badreldin A, Doerr F, Lehmann T, Bayer O, Doenst T et al. Logistic Organ Dysfunction Score (LODS): a reliable postoperative risk
management score also in cardiac surgical patients? J Cardiothorac Surg 2011;6:110.
74 Sauaia A, Moore, E, Johnson J, Ciesla D, Biffi W, Banerjee A. Validation of post-injury multiple organ failure scores. Shock 2009;31(4):438-47.
75 Rice TW, Wheeler AP, Bernard GR, Hayden DL, Schoenfeld DA, Ware LB. Comparison of the SpO2/FiO2 ratio and the PaO2/FiO2 ratio in patients
with acute lung injury or ARDS. Chest 2007;4(2):410-7.
76 McConnell K, Coopersmith C. Organ failure avoidance and mitigation strategies in surgery. Surg Clin N Am 2012;92:307-19.
77 Nydam TL, Kashuk JL, Moore EE, Johnson JL, Burlew CC, Biffl WL et al. Refractory postinjury thrombocytopenia is associated with multiple
organ failure and adverse outcomes. J Trauma 2011;70(2):401-6.
78 Jansen TC, van Bommel J, Mulder PG, Lima AP, van der Hoven B, Rommes JH et al. Prognostic value of blood lactate levels: does the clinical
diagnosis at admission matter? J Trauma 2009;66:377-85.
79 Honore P, Joannes-Boyau O, Boer W, Collins V. Regional occult hypoperfusion detected by lactate and sequential organ failure assessment
subscores: old tools for new tricks? Crit Care Med 2009;37(8):2477–8.
80 Jansen T, van Bommel J, Woodward R, Mulder P, Bakker J. Association between blood lactate levels, sequential organ failure assessment
subscores, and 28-day mortality during early and late intensive care unit stay: a retrospective observational study. Crit Care Med
2009;37(8):2369–74.
81 Dellinger R, Levy M, Rhodes A, Annane D, Gerlach H, Opal SM et al. Surviving Sepsis Campaign: international guidelines for management of
severe sepsis and septic shock: 2012. Crit Care Med 2013;41(2):580-637.
82 Guyette F, Suffoletto B, Castillo J, Quintero J, Callaway C, Puyana JC. Prehospital serum lactate as a predictor of outcomes in trauma patients:
a retrospective observational study. J Trauma 2011;70(4):782-6.
83 Madách K, Aladzsity I, Szilágyi Á, Fust G, Gál J, Pénzes I et al. 4G/5G polymorphism of PAI-1 gene is associated with multiple organ
dysfunction and septic shock in pneumonia induced severe sepsis: prospective, observational, genetic study. Crit Care 2010;14(2):R79.
84 Teoh H, Quan A, Creighton AK, Bang KW, Singh KK, Shukla PC et al. BRCA1 gene therapy reduces systemic inflammatory response and
multiple organ failure and improves survival in experimental sepsis. Gene Ther 2013;20:51-61.
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85 Peake S, Bailey M, Bellomo R, Cameron P, Cross A, Delaney A et al. Australasian resuscitation of sepsis evaluation (ARISE): a multi-centre,
prospective, inception cohort study. Resuscitation 2009;80:811–18.
86 Levy M, Dellinger R, Townsend S, Linde-Zwirble W, Marshall J, Bion J et al. The Surviving Sepsis Campaign: results of an international
guideline-based performance improvement program targeting severe sepsis. Crit Care Med 2010;38(2):367–74.
87 Finfer S. The Surviving Sepsis Campaign: robust evaluation and high-quality primary research is still needed. Crit Care Med 2010;38(2):683–4.
88 Becker JU, Theodosis C, Jacob ST, Wira CR, Groce NE. Surviving sepsis in low-income and middle-income countries: new directions for care
and research. Lancet Infect Dis 2009;9(9):577–82.
89 Rivers E. Management of sepsis: early resuscitation. Clin Chest Med 2008;29:689–704.
90 Jones A, Shapiro N, Trzeciak S, Arnold R, Claremont H, Kline J et al. Lactate clearance vs central venous oxygen saturation as goals of early
sepsis therapy – a randomized clinical trial. JAMA 2010;303(8):739-46.
91 The ProCESS/ARISE/ProMISe Methodology Writing Committee. Harmonizing international trials of early goal-directed resuscitation for severe
sepsis and septic shock: methodology of ProCESS, ARISE, and ProMISe. Intensive Care Med 2013;39:1760-75.
92 The ProCESS Investigators. A randomized trial of protocol-based care for early septic shock. N Eng J Med 2014;370(18):1683-93.
93 Kumar A, Ellis P, Arabi Y, Roberts D, Light B, Parrillo JE et al. Initiation of inappropriate antimicrobial therapy results in a fivefold reduction of
survival in human septic shock. Chest 2009;136(5):1237–48.
94 Bagshaw S, Lapinsky S, Dial S, Arabi Y, Dodek P, Wood G et al. Acute kidney injury in septic shock: clinical outcomes and impact of duration
of hypotension prior to initiation of antimicrobial therapy. Intensive Care Med 2009;35:871–81.
95 Gaieski D, Mikkelsen M, Band R, Pines J, Massone R, Furia FF et al. Impact of time to antibiotics on survival in patients with severe sepsis or
septic shock in whom early goal-directed therapy was initiated in the emergency department. Crit Care Med 2010;38(4):1045–53.
96 Lily C. The ProCESS trial – a new era of sepsis management. N Eng J Med 2014;370(18):1750-1.
97 Sharma S, Kumar A. Antimicrobial management of sepsis and septic shock. Clin Chest Med 2008;29:677–87.
98 Kumar A, Safdar N, Kethireddy S, Chateau D. A survival benefit of combination antibiotic therapy for serious infections associated with sepsis
and septic shock is contingent only on the risk of death: a meta-analytic/meta-regression study. Crit Care Med 2010;38(8):1651–64.
99 Pines J. Timing of antibiotics for acute, severe infections. Emerg Med Clin N Am 2008;26:245–57.
100 Ulldemolins M, Roberts J, Lipman J, Rello J. Antibiotic dosing in multiple organ dysfunction syndrome. Chest 2011;139(5):1210-20.
101 Finfer S. Corticosteroids in septic shock. N Engl J Med 2008;358(2):188–90.
102 Sprung C, Annane D, Keh D, Moreno R, Singer M, Freivogel K et al. Hydrocortisone therapy for patients with septic shock. N Engl J Med
2008;358(2):111–24.
103 Mason P, Al-Khafaji A, Milbrandt E, Suffoletto B, Huang D. CORTICUS: the end of unconditional love for steroid use? Crit Care 2009;13(4):309.
104 Investigators TCS. Corticosteroid treatment and intensive insulin therapy for septic shock in adults: a randomised controlled trial. JAMA
2010;303(17):1694–8.
105 Vanhorebeek I, De Vos R, Mesotten D, Wouters P, De Wolf-Peeters C, Van den Berghe G. Protection of hepatocyte mitochondrial ultrastructure
and function by strict blood glucose control with insulin in critically ill patients. Lancet 2005;365(9453):53–9.
106 Finfer S, Chittock D, Yu-Shhuo S, Blair D, Foster D, Dhingra V et al. Intensive versus conventional glucose control in critically ill patients.
N Engl J Med 2009;360(13):1283–97.
107 Vincent J. Metabolic support in sepsis and multiple organ failure: more questions than answers. Crit Care Med 2007;35(9Suppl):S436–40.
108 Moore F, Moore E. The evolving rationale for early enteral nutrition based on paradigms of multiple organ failure: a personal journey. Nutrition
Clin Prac 2009;24(3):297–304.
109 Australian College of Critical Care Nurses. National Advanced Life Support Education Package: Pathophysiology of cellular dysfunction.
Melbourne: Cambridge Press; 2004.
110 Vincent J, Moreno R, Takala J, Willats S, De Mendonca A, Bruining H et al. The SOFA (sepsis related organ failure assessment) score to
describe organ dysfunction/failure. Intensive Care Med 1996;22:707–10.
Thispageintentionallyleftblank
 Section 3

Specialty practice
Thispageintentionallyleftblank
 Chapter 23

Emergency presentations
David Johnson, Julia Crilly

KEY WORDS Learning objectives

disaster After reading this chapter, you should be able to:
management • describe the uniqueness of the emergency care environment
envenomation • describe the different international triage models and outline the
extended practice development of Australasian triage models
heat illnesses • discuss the process of initial patient assessment and triage nursing
hypothermia practice
near-drowning • integrate emergency nursing principles and practice in initial patient care
poisoning • describe the various roles of extended nursing practice in the emergency
setting
retrieval
triage • describe the principles and practice of patient preparation for retrievals or
transfers
• discuss the principles for the management of disaster victims in the
emergency department
• discuss the initial nursing management of common presentations to
the ED, including respiratory or neurological dysfunction, chest pain,
abdominal pain, poisoning, envenomation, submersion and heat illness.

Introduction
Emergency nursing practice covers an enormous range of clinical presentations.
The focus of this book is critical care, and this chapter discusses conditions of
clinical presentations at the critical end of the practice spectrum. Please read
in conjunction with Chapters 24 and 25, which describe the management of
additional common presentations to the emergency department (ED): trauma
and resuscitation emergencies, respectively. Chapter 1 contains information on
extended nursing roles relevant to emergency nursing.
In this chapter the organisational systems and processes of care in an ED
environment, including triage, specifics of ED extended practice nursing roles,
multiple casualties/disaster management and transport/retrieval of critically ill
patients, are described. Details of a select group of the most common emergency
presentations and conditions related to critical care practice are then described.
The initial clinical assessment and incidences of these common presentations are
discussed, and the likely diagnoses associated with these presentations and their
740 SECTION 3 SPECIALTY PRACTICE

initial management in the ED are identified. Ongoing History of triage

management of these selected conditions is covered in
Triage was first described in 1797 during the Napoleonic
Section 2 of this text.
wars by Surgeon Marshall Larrey, Napoleon’s chief medical
Emergency nursing practice is the holistic care of indi-
officer,8 who introduced a system of sorting casualties that
viduals of all ages who present with perceived or actual
presented to the field dressing stations. His aims were
physical and/or emotional alterations. These presentations
military rather than medical, however, so the highest
are often undiagnosed and require a range of prompt
priority was given to soldiers who had minor wounds and
symptomatic and definitive interventions. Emergency
clinical practice is usually unscheduled, episodic and could be returned quickly to the battle lines with minimal
acute in its nature, and is therefore unlike any other type treatment.1,8
of nursing in the demands it places on nursing staff.1,2 In The documented use of triage was limited until World
many instances the emergency nurse is the first healthcare War I, when the term was used to describe a physical area
professional to be in contact with an acutely ill or injured where sorting of casualties was conducted, rather than a
patient. Patient presentations include a full range of acuity description of the sorting or triage process itself.9 Triage
across the spectrum of possible illnesses, injuries and ages. continued to develop into a formalised assessment process,
with subsequent adoption of initial categorising of patient
urgency and acuity within most civilian EDs.1,8–10
Background
International approaches to triage
Emergency nursing is unique, in that it involves the care
of patients with health problems that are often undiag- The triage process has evolved internationally, particu-
nosed on presentation but perceived as sufficiently acute larly over the past two decades. Four main triage scales
by the individual to warrant seeking emergency care are available and, although used in the country in which
in the hospital setting. As patients present with signs they were developed, they have also been implemented or
and symptoms rather than medical diagnoses, refined adapted in other health services.The Canadian Emergency
assessment skills are paramount. Many skills required by Department Triage and Acuity Scales (CTAS)11, the
emergency nurses are based on a broad foundation of Manchester Triage Scale (MTS) 3 and the Australasian
knowledge that serves as a guide in collecting information, Triage Scale (ATS)12,13 are the most common five-level
making observations and evaluating data, and sorting and triage scales used with the ATS being reported as the most
analysing relevant information.3–7 This foundation enables reliable.14 In the USA, three-level triage scales have histor-
an emergency nurse to communicate appropriately with ically been used; however the Emergency Severity Index
other members of the healthcare team, and to imple- (ESI),15 a five-level triage scale, was developed in the late
ment appropriate independent and collaborative nursing 1990s and has been implemented in a small number of
interventions. hospitals.7 Three-level triage scales do not fare as well as the
Emergency nurses are specialists in acute episodic five-level scales in terms of measures such as agreement,
nursing care, and their knowledge, skills and expertise discrimination, sensitivity, specificity and accuracy.16 Newer
encompass almost all other nursing specialty areas. triage systems have been developed, e.g. the four-level
Emergency nurses therefore possess a unique body of Taiwan Triage System17 and the Soterion Rapid Triage
knowledge and skill sets to manage a wide variety of System.18 These newer systems are not widely reported or
presentations across all age groups; this includes famil- implemented and require further testing.19
iarity with general physical and emotional requirements Characteristics of the ATS, CTAS, MTS and ESI
of each age group as these relate to their presenting five-level triage scales are presented in Table 23.1.7
health needs.2–4,7 ED nurses work collaboratively with Although somewhat similar, there are variations in some
pre-hospital emergency personnel, doctors and other aspects such as timeframes for which a person should wait
healthcare providers and community agencies to provide to see a doctor. For example, the ESI does not define
patient care.2,3,5 Roles in the ED include triage, direct expected time intervals to doctor evaluation, and not all
patient care, patient flow, implementing medical orders, scales are adapted to specific populations, such as paediat-
providing emotional support during crises, documenting rics, or settings, such as rural environments.The Manchester
and arranging ongoing care, admission to the hospital, Triage System differs to the ATS, CTAS and ESI in that it
transfer to another healthcare facility or discharge into the uses an algorithm approach with 52 presenting complaints
community.5,6 to derive a triage score. The other systems use a slightly
different approach where a combination of observation,
history taking and physical examination facilitates the
Triage nurse’s judgement to apply a triage score. Updates to
Central to the unique functions of an ED nurse is the role and computerisation of previous guidelines have been
of triage, perhaps the one clinical skill that distinguishes undertaken over the years.20 Educational materials to
an emergency nurse from other specialist nurses. Triage support each of the scales are available. An International
literally means ‘to sieve or sort’, and it is the first step in Triage Scale has been proposed but requires development
any patient’s management on presentation to an ED.1–3,7 and testing.20
 CHAPTER 23 EMERGENCY PRESENTATIONS 741

TABLE 23.1
Comparison of characteristics of the ATS, CTAS, MTS and ESI 5-level triage scales

CRITERION C TA S AT S ESI MTS

Time to triage assessment 10 min NS NS NS
Time to nurse assessment Based on initial triage NS NS NS
Time to doctor assessment Immediate/15/ Immediate/10/ NS Immediate/10/60/
30/60/120 min 30/60/120 min 120/240 min
Fractile response time I-98, II-95, I-97.5, II-95, NS NS
(CTAS)/performance III-90,IV-85, III-90, IV-90,
threshold (NTS) V-80 V-85
Pain scale 10-point scale NS >7/10 consider up- A major factor considered
triage to ESI level 2 for each chief complaint
Paediatrics Used in CTAS NS but generally Paediatric VS criteria Not addressed in the
recognised included to help algorithm
determine ESI level
2 vs 3; fever criteria
for <24 months
included
Sentinel diagnoses Yes Yes Not used 52 chief complaints vs
sentinel diagnosis
Expected admission rates Specified Defined using actual Benchmarking data NS
data from multiple available
sites
Education implementation Web-based training Training video; Available for Published manual:
material available for a fee Website: http://www. purchase from ENA Manchester Triage
acem.org.au/open/ (www.ena.org) Group. Emergency triage.
documents/triage.htm Plymouth: BMJ Publishing
Group; 1997
Rural setting Yes NS NS NS
Additional comments Uses acuity to Algorithmic approach that
identify level 1 and uses 52 chief complaint-
2 patients, and based flow charts; the
resources to identify triage nurse then continues
levels 3–5 an algorithmic approach
and assesses life threat,
pain, haemorrhage,
consciousness level,
temperature and acuteness
for each chief complaint

Note: the ATS performance thresholds have since been revised to: 100%, 80%, 75%, 70%, 70%.26
NS = not specified; VS = vital sign; MTS = Manchester Triage Scale.
Adapted from Fernandes CM, Tanabe P, Gilboy N, Johnson LA, McNair RS, Rosenau AM et al. Five-level triage: a report from the
ACEP/ENA Five-level Triage Task Force. J Emerg Nurs 2005;31(1):39-50; quiz 118, with permission.

Development of triage processes: EDs using random models of care; ambulance presenta-
tions were given priority and the ‘walking wounded’ seen
Focus on Australia and New Zealand in order of arrival. In the mid-1970s, staff at Box Hill
Australia is a world leader in the development of emergency Hospital in Melbourne developed a five-tiered system that
triage and patient classification systems. Because other included a time-based scale and different colours on the
triage systems (CTAS, MTS, ESI) have primarily been medical record to indicate priority.1,9,21 Subsequent modi-
adapted from the Australian system,20 the focus here is on fication and refinement led to the Ipswich Scale in the
the development of the Australian and New Zealand ATS. 1970s–80s.1,2,4,5,21 These early triage systems reinforced
In the late 1960s patients presenting to ‘casualty’ depart- the concepts developed by Larrey, and established a process
ments in Australia were not always triaged,1,2,4 with many for patient presentations to be seen in order of clinical
742 SECTION 3 SPECIALTY PRACTICE

priority rather than time of attendance. In the 1990s the characteristics of utility, reliability and validity.1,2,4,5,12,13,20,21
impacts of community expectations and national health In 1993, the NTS was adopted by the Australasian College
policy led to further enhancements of triage systems in for Emergency Medicine in its triage policy,21 and subse-
Australia, and the Ipswich triage scale was adapted into quently renamed the ATS as it was implemented in most
the national triage scale. The National Triage Scale was EDs in Australia and New Zealand (see Table 23.2).4
subsequently tested and demonstrated to have the essential

TABLE 23.2
ATS category characteristics5,13,22

AT S C O D E TYPICAL DESCRIPTION

1 Immediately life-threatening (or imminent risk of deterioration)

Patients are critically ill, and require immediate transfer to a resuscitation area for initial resuscitation, with no delay
at triage. The majority will arrive by ambulance, and will be suffering:
• multi-trauma
• shock
• unconsciousness
• convulsions
• extreme dyspnoea
• cardiorespiratory arrest
2 Imminently life-threatening
Patients ‘at high risk’ of critical deterioration or have very severe pain from any cause. Assessment and treatment
needs to commence within 10 minutes for:
• chest pain or other symptoms suggestive of myocardial ischaemia, pulmonary embolism or aortic dissection
• important time-critical treatment (e.g. thrombolysis, antidote)
• severe abdominal pain or other symptoms suggestive of ruptured aortic aneurysm
• severe dyspnoea from any cause
• altered levels of consciousness
• acute hemiparesis/dysphasia
• fever, rash, headache, suggestive of sepsis or meningitis
• severe skeletal trauma such as femoral fractures or limb dislocations
• very severe pain from any cause (practice mandates the relief of pain or distress within 10 minutes)
3 Potentially life-threatening or situational urgency
Patients have significant illness or injury and should have assessment and treatment commenced within 30 minutes
of presentation. Typical patients include those with:
• moderately severe pain from any cause (e.g. abdominal pain, acute headache, renal colic), but not suggestive of
critical illness; practice mandates relief of severe discomfort or distress within 30 minutes
• symptoms of significant infections (e.g. lung, renal)
• moderate injury (e.g. Colles’ fracture, severe laceration without active haemorrhage)
• head injury, with transient loss of consciousness
• persistent vomiting/dehydration
4 Potentially serious
The patient’s condition may deteriorate, or adverse outcome may result, if assessment and treatment is not
commenced within 1 hour of arrival. Patients have moderate symptoms, symptoms of prolonged duration or acute
symptoms of low-risk pre-existing conditions, including:
• minor acute trauma (e.g. sprained ankle)
• minor head injury, no loss of consciousness
• mild haemorrhage
• earache or other mildly painful conditions
• practice mandates relief of discomfort or distress within 1 hour
• there is a potential for adverse outcome if time-critical treatment is not commenced within 1 hour
• likely to require complex work-up and consultation and/or inpatient management
5 Less urgent
The patient’s condition is minor or chronic; acute symptoms of minor illness, symptoms of chronic disease or with a
duration of greater than 1 week. Symptoms or clinical outcome will not be significantly affected if assessment and
treatment are delayed up to 2 hours from arrival. Examples include:
• chronic lower back pain with mild symptoms
• minor wounds: small abrasion/minor lacerations
• most skin conditions
• clinical administrative presentations (e.g. results review, medical certificates, repeat prescriptions)
 CHAPTER 23 EMERGENCY PRESENTATIONS 743

The process of triage Practice tip

All patients presenting to an ED should be triaged on
arrival by a suitably experienced and trained registered Triage decisions must be accurate, ensure the patient’s
nurse.2,12,15,22,23 This assessment represents the first clinical safety and be reproducible across clinicians and
contact and the commencement of care in the department. departments. The decision regarding triage urgency
The ideal features of a triage area are: a well-signposted should not be clouded by factors other than the patient’s
location close to the patient entrance; ability to conduct clinical condition.7,22 If it is unclear what triage category
should be assigned, the patient should be allocated a
examination and primary treatment of patients in privacy;
higher category.
close proximity to the acute treatment and resuscitation
areas; and appropriate resources including an examination
table, thermometer, a sphygmomanometer, stethoscope, The premise for a triage decision is that utilisation of
glucometer and pulse oximetry.2,4,12 Access to emergency valuable healthcare resources should provide the greatest
equipment, communication devices (such as telephone, benefit for those most in need, and that persons in need
of urgent attention always receive that care.13,25 Triage
emergency buzzer), standard precaution equipment (such
encompasses the entire body of emergency nursing
as gloves and hand-wash) and paper/electronic recording
practice, and nurses complete a comprehensive triage
facilities are also important.24
education program prior to commencing this role. Formal
As the first clinician in the ED to interview the patient, triage training resources have been developed that provide
the triage nurse gathers and documents information from the essential education components to promote consis-
the patient, family and friends, or pre-hospital emergency tency in application of the triage score, depending on the
personnel. Professional maturity is required to manage scales used.7,13,15,25
the stress inherent in dealing with an acutely ill patient
and family members (under significant stress themselves), Triage categories
while rapidly making informed judgement on priorities After triage assessment is undertaken on arrival, patients
of care for a wide range of clinical problems.7,12 are allocated one of five triage categories depending on
The triage nurse receives and records informa- the triage scale used (see Tables 23.1 and 23.2). Prompt
tion about the patient’s reason for presentation to the assessment of airway, breathing, circulation and disability
ED, beginning with a clear statement of the complaint, remains the cornerstone of patient assessment in any
followed by historical information and related relevant clinical context, including triage.
details, such as time of onset, duration of symptom/s
and what aggravates or relieves the symptom/s. A brief, Triage assessment
focused physical assessment including vital signs may be Patient assessment at triage has three major components:
undertaken to identify the urgency and severity of the quick, systematic and dynamic. Speed of assessment is
condition, and may be collected as part of the triage required in life-threatening situations, with the focus on
process to inform decision making.5,12,13 Triage assessment airway, breathing, circulation and disability, and a quick
generally should be no longer than 2–5 minutes, balancing decision on what level of intervention is required. A
between speed and thoroughness.13 From the informa- systematic approach to assessment is used for all patients
tion collected, the triage nurse determines the need for in all circumstances, to ensure reproducibility. Finally,
immediate or delayed care,1–3,7 and assigns the patient a the triage assessment must be dynamic, in that several
1–5 ATS category in response to the statement: This aspects can be undertaken at once, and acknowledges
that a patient’s condition can change rapidly after initial
patient should wait for medical assessment and treatment no
assessment. Various assessment models are available, but
longer than … .13
fundamentally they all include components of obser-
Patients with acute conditions that threaten life or
vation, history taking, primary survey and secondary
limb receive the highest priority while those with minor survey.1–4,6,13,15,25
illness or injury are assigned a lower priority. It may
not be possible to categorise the patient correctly in all Patient history/interview
instances, and it is better to conservatively allocate priority The triage interview provides the basis for data gathering
to ensure the patient is seen sooner, if the triage category and clinical decision making regarding patient acuity.
is unclear.3,8,12,13 Importantly, a triage allocation is flexible After an introduction, the triage nurse asks person-spe-
and can be altered at any time.5–8,13 If a patient’s condition cific, open-ended questions. Use of close-ended questions
changes while awaiting medical assessment/treatment, or summative statements enables clarification and confir-
or if additional relevant information becomes available mation of information received, and a means of checking
that impacts on the patient’s urgency, the patient should understanding by the patient.26 Privacy is important
be re-triaged to a category that reflects the determined to ensure that the patient is comfortable in answering
urgency.13,25 Frequent, ongoing observation and assessment questions of a personal nature. Most EDs need to balance
of patients is therefore routine practice following the providing an area that is private and accessible, yet safe for
initial triage assessment. staff to work in relative isolation.
744 SECTION 3 SPECIALTY PRACTICE

A large component of the triage assessment may be

based on subjective data, which are then compared and TABLE 23.3
combined with objective data obtained through the senses Aids to triage assessment8
of smell, sight, hearing and touch to determine a triage
MNEMONIC COMPONENTS
category. If time permits, vital signs such as pulse, blood
pressure, respiratory rate, oxygen saturation, tempera- SOAPIE Subjective data
ture and blood glucose level can be measured to assist Objective data
Assessment (to enable formulation of a …)
in estimating urgency.24 One aspect of the history that is
Plan (that is …)
difficult to quantify is intuition. This is that ‘sixth sense or
Implemented (and …)
gut feeling’ that tells us that something not yet detectable is
Evaluated (as to its success)
wrong with the patient. This unexplained sense is difficult
to outline or apply scientific research models to, but has a AMPLE Allergies
role to play in patient assessment and should be acknowl- Medications
edged when something ‘doesn’t feel right’.6,13,25 Past medical history
Last food and fluids ingested
Primary survey Environmental factors and Events leading
to presentation
While taking a patient history, the triage nurse also simul-
taneously conducts a primary survey. As noted earlier, PQRST Provoking or Precipitating factors
airway, breathing, circulation and neurological function are Quality and Quantity (severity) of the
observed. If any major problem is observed (or a patient is symptom
identified as ATS Category 1 or 2), the interview is ceased Region/Radiation
Symptoms associated
and the patient is transferred immediately to the acute
Time of onset and duration of episode, and
treatment or resuscitation area.8,24
Treatment
Secondary survey and physical
examination system, cardiovascular system, respiratory system, gastro-
A secondary survey, involving a concise, systematic physical intestinal system etc).6,13,15 Detailed descriptions of systems
examination, is conducted after the patient history and assessment are available elsewhere in the text.
primary survey have been completed.The equipment used
includes a thermometer, stethoscope, oxygen saturation Triage assessment of specific patient
monitor and sphygmomanometer, in combination with groups
clinical skills. This examination is not comprehensive but While triage assessment is a complex process for a range
focuses on the presenting complaint while avoiding tunnel of patient presentations, some specific groups are more
vision and wrong conclusions.3,26 Remember that the demanding, such as mental health, paediatric, older and
patient may not be able to lie down or be exposed for an mass casualty patients.
examination in the triage area, and may be distressed. The
triage process should reflect a system of rapid assessment Mental health presentations
that is reproducible and adaptable to a variety of presen- Patients with psychiatric problems presenting to an
tations. The secondary survey may be performed by the ED should be triaged, assessed and treated as for other
triage nurse if time permits or by another registered nurse presenting patients, with particular attention to appropri-
who may be able to initiate appropriate investigations ate initial medical assessment and management.6,13,22,26,27
(such as X-rays) or initial management (such as analgesia), Resources outlining specific mental health triage
according to hospital protocols.24 Further information category descriptors are readily available and relate specific
regarding advanced practice roles such as the clinical aspects of mental health presentation with clinical urgency
initiatives nurse is presented in Chapter 1. and triage categories (see Table 23.4),27 including an outline
of suggested responses, such as patient placement require-
Practice tip ments based on the level of risk and urgency.6,13,22,25–30
The triage physical assessment should be quick,
Although the triage process has the same underlying
accurate and concise, focusing on the presenting
principles, factors associated with mental health presen-
complaint.
tations may vary between geographical settings and
countries where there are differences in health system
structure, financing and sociocultural contexts.27,31,32
Approaches to triage assessment
A range of approaches to nursing assessment is applicable Paediatric presentations
to triage assessments (see Table 23.3).8 Body systems Children presenting to the ED are assessed and assigned
approach enables systematic examination of each body a triage category as for adults, although vital differ-
system to discover abnormalities (i.e. central nervous ences in paediatric anatomy, physiology and clinical
 CHAPTER 23 EMERGENCY PRESENTATIONS 745

TABLE 23.4
Examples of a mental health triage tool26

AT S O B S E R VAT I O N ACTION

1 Immediate Severe behavioural disorder with immediate threat of • Provide continuous visual observation in safe
dangerous violence to self or others environment
• Ensure adequate personnel to provide restraint/
detention
2 Emergency Severe behavioural disturbance with probable risk of • Provide continuous visual observation in safe
danger to self and others environment
• Use defusing techniques
• Ensure adequate personnel to provide restraint/
detention
3 Urgent Moderate behavioural disturbance or severe distress • Provide safe environment, frequent visual
with possible danger to self and others observations every 10 minutes
4 Semi-urgent Semi-urgent mental health problem with no • Regular visual observations at a maximum of
immediate risk to self or others every 30 minutes
5 Non-urgent No behavioural disturbance or acute distress with no • Regular visual sighting at a maximum of 1-hour
danger to self or others intervals

presentations should be considered (see Chapter 27).The Older persons

reliance on information from parents or primary carers With the ageing population globally, there is a trend
and their capacity to identify deviations from normal towards an increase in the use of emergency services
are important, particularly in supporting recognition of by older persons. While older persons should be triaged
often subtle indicators of serious illness in infants and according to their presenting complaint, this can be
young children. Paediatric triage resources are available complicated by a number of factors.35 It is therefore
to assist in identifying physiological alterations and important to consider additional comorbidities, place
applying a triage category based upon identified physio- of residence, medications and cognitive function when
logical discriminators.3,15,26,33 Other important points to triaging older adults.36 Evidence-based recommenda-
consider include the following: tions37–39 and policy guidelines40 for the management
• Children may suffer rapid decompensation due to of older persons in the ED are available with additional
limited physiological reserves.13,22,34 recommendations provided by key organisations.36,37
• Children are less able to tolerate13,22,34
pain in either Important points to remember when triaging the elderly
physical or psychological terms. are the following:
• It is difficult to rationalise long waiting periods with • Older persons have an increased medical complexity
a child or parent of a sick child. The longer they wait, and nursing dependency.39
the more difficult an examination becomes.13,22,34
• Be attuned to the potential signs of elder abuse,39 and
• Parents are much less tolerant of waiting times the presence of pressure sores.
for their sick child than they would be for
themselves.13,22,34 • Note the use of aids such as hearing aids, glasses
and walking sticks that assist with activities of daily
• The spectrum of childhood illnesses presenting to living.
EDs varies between countries that are developing
and those that have more established health • The older person (particularly if from an aged
systems.33,34 care facility) may have an advanced medical
directive that should be used to ensure their wishes
Practice tip are respected in the event of a life-threatening
illness.39
A short time is a long time in the life of a child; they may
develop serious illness in a much shorter time than for Practice tip
an adult.
When triaging older people important considerations
Adapted from Durojalve L, O’Meara M. A study of triage in
include other illnesses they may have, where they live,
paediatric patients in Australia. Emerg Med 2002;4: 67-76, medications they are on and changes in their cognitive
with permission. function.
746 SECTION 3 SPECIALTY PRACTICE

Chemical, biological and radiological back to the 14th century.45 Biological agents are living
organisms or toxins that have the capacity to cause disease
events in people, animals or crops. Toxins are a special type of
Since the Japanese doomsday cult Aum Shinrikyo released poisonous chemical categorised as biological agents
sarin nerve gas on the Tokyo subway in March 1995, killing because they were created by living organisms. They
12 people, terrorist incidents and hoaxes involving toxic generally behave like chemical agents and serve the same
or infectious agents have been on the rise. The ease of function: to poison people.
obtaining non-nuclear radioactive material may mean that Biological agents are relatively inexpensive to produce
‘dirty bombs’41,42 are more likely to be used as an explosive and have the potential to be devastating in their effects.
device. The availability and the impact of chemical and Organisms such as anthrax, plague and smallpox have been
biological threat materials are both relatively high, with the agents of greatest concern from a potential terrorist use
potentially devastating impact.43–46 Because biological and perspective.43 Table 23.6 presents an outline of biological
chemical agents are so dissimilar, each category will be agents, clinical presentations and treatments.
dealt with separately but there are common elements or
characteristics. Radiological agents
Radiological materials can pose both an acute and
Chemical agents long-term hazard to humans. In many ways, they behave
Chemical agents are supertoxic chemicals used for the like some of the chemical agents in that they cause cellular
purpose of poisoning victims.They are similar to hazardous damage. A major difference is that radiological agents do
industrial chemicals, but hundreds of times more toxic.44 not necessarily have to be inhaled or come in contact with
For example, the 1995 sarin attack in Tokyo caused the skin to do damage.41
1039 injuries and at least 4000 people with psychogenic The deployment of a nuclear weapon would be cata-
symptoms.44 Sarin is approximately 60 times more toxic strophic, as evidenced by events such as Hiroshima or
than methylisocyanate. To put this in perspective, a leak of industrial accidents as occurred at Chernobyl. While very
methylisocyanate from a factory in Bhopal, India, in 1984 different, both events produced immediate injury and had
caused 200,000 people to be effected, 10,000 severely long-term effects of ionising radiation on large popula-
affected and 3300 deaths.47 Relatively small quantities tions.43 The event of highest risk is likely to be a ‘dirty
of a military grade chemical agent could have the same bomb’ that combines conventional explosives with any
capability to produce large numbers of casualties (sympt- available radioactive source.43
omatic and psychological).44,45
Table 23.5 provides a summary of the more common Psychological effects
chemical agents, their effects, clinical presentations and A chemical, biological or radiological terrorism incident
treatments. It needs to be stressed that specialised personal may or may not result in mass casualties and fatalities
protective equipment (PPE) and specialist training are as intended. However, large numbers of psychologi-
required to manage these situations.48 cal casualties are very likely and, therefore, regardless of
the effectiveness of the attack and number of people
Biological agents actually exposed to the agent, there will most likely be
The use of biological weapons is not a recent concept.44,45 a mass casualty situation.43 The psychological implica-
Biological agents have the longest history of use, dating tions of chemical and biological weapons may be worse

TABLE 23.5
Summary of common chemical agents, effects, clinical presentations and treatments42–45

TYPE OF CLINICAL
CHEMICAL EFFECT EXAMPLE P R E S E N TAT I O N A N T I D O T E S / T R E AT M E N T

Nerve agent Inhibits the Sarin Muscarinic and nicotinic Atropine

activation of VX signs 2-Pyridine aldoxime methyl chloride
acetylcholinesterase Soman Benzodiazepines
Tabun
Blood agents Binds with Cyanide Hypoxia Cyanide kit
cytochrome oxidase, Sodium nitrite
causing hypoxia Sodium thiosulfate
Vesicants Chemical burns Mustard gas Burns and blisters Decontamination with soap and water
Lewisite
Pulmonary agents Irritation to the Chlorine Respiratory distress Oxygen
respiratory tract phosgene Pulmonary oedema
 CHAPTER 23 EMERGENCY PRESENTATIONS 747

TABLE 23.6
Summary of biological agents, clinical presentations and treatments43,44,46,47

BIOLOGICAL GROUP EXAMPLE C L I N I C A L P R E S E N TAT I O N T R E AT M E N T

Virus Smallpox (variola) Supportive care

Bacteria Anthrax (Bacillus anthracis) Inhalational Antibiotics
• Respiratory failure
• Widened mediastinum
• Severe sepsis
Plague (Yersinia pestis) Pneumonic plague Antibiotics
• Respiratory failure
• Haemoptysis
• Painful lymph nodes
Toxin Botulism (Clostridium botulinum) Supportive care
Botulism immune globulin

than the physical ones. Chemical and biological weapons Nurse-initiated radiology
are weapons of terror; part of their purpose is to wreak
Nurse-initiated radiology ordering enables radiolog-
destruction via psychological means by inducing fear,
ical investigations of extremities,54 joints such as hips
confusion and uncertainty in everyday life.49
The long-term social and psychological effects of an and shoulders, the chest and abdomen according to
episode of chemical or biological attack, real or suspected, clinical protocols that list inclusion and exclusion
would be as damaging as the acute ones, if not more so.50 criteria55 based on findings from the patient’s history
and clinical examination. The inclusion criteria reflect
Major challenges for chemical, well-established clinical indicators. While nurse-initiated
biological or radiological responders radiology ordering is often undertaken as an extended
triage nurse function, it can be performed by any accredited
A well-delivered chemical or biological event would be
nurse. The use of nurse-initiated radiology, especially in
catastrophic and exposure for emergency workers likely,
association with extremity injuries, is safe and accurate,
as occurred previously when 110 staff developed signs
and symptoms of exposure following the 1995 sarin attack reducing both waiting time and department transit time
in Tokyo.51 and improving both patient and staff satisfaction.53–57
To protect staff, there must be clear procedures for Nurse-initiated analgesia
dealing with potentially exposed or contaminated patients.
Although pain is a common complaint in the majority
This begins with proper assessment of a patient in need of
of patients presenting to the ED,58,59 timeliness, adequacy
isolation or decontamination and includes understanding
and appropriateness of analgesia administration have been
of what PPE is appropriate and the capability of staff to
suboptimal58,59 and contribute to poor patient satisfaction.58
effectively use the PPE. Emergency personnel must also
have immediate access to the PPE that they need to limit Consequently, many EDs have developed nurse-initiated
their risk of exposure. However, the issue is complex: analgesia protocols, standing orders or pathways to enable
advanced levels of PPE require advanced training and designated emergency nurses to implement analgesia
special skills to be used safely. Decontamination of regimens before medical assessment. These protocols are
patients with chemical exposure is a high-risk activity for locally derived and note patient inclusion and exclusion
untrained staff.51,52 criteria for managing mild, moderate or severe pain in both
adult and paediatric patients, and often include administra-
tion of an antiemetic.58,59 A numerical pain rating scale or
Advanced clinical skills a visual analogue scale is used to direct the type and route
Within the ED, there has been an evolution of advancing of analgesia administration. Severe pain protocols outline
the clinical roles and skill set for nurses. This has come intravenous (IV) narcotic administration, including incre-
about largely in response to an increasing number of mental and total maximum administration dosages. After
emergency presentations, and to improve performance administration of the initial dose, the administering nurse
in patient flow, waiting times, length of stay and patient gives subsequent doses in response to patient assessment
satisfaction.51–53 Within the ED, advanced clinical roles, as of pain score and vital signs (pulse, blood pressure and
discussed in more detail in Chapter 1, mean that registered respiratory rate). Protocols directed towards moderate and
nurses with advanced clinical skills can progress patient minor pain may include either single or incremental IV
assessment and management through nurse-initiated or oral analgesia. Nurse-initiated analgesia protocols are
radiology and nurse-initiated analgesia. safe and effective, shortening the time ED patients wait
748 SECTION 3 SPECIALTY PRACTICE

for analgesia,59–61 which should assist in improving patient including assessment of airway, breathing, circulation and
outcomes and satisfaction. suitable IV access.62,68,70
If potential airway compromise is suspected, careful
Retrievals and transport of consideration should be given to an elective intubation
prior to transport rather than an emergency airway inter-
critically ill patients vention in a moving vehicle or a radiology department.
A laryngeal mask airway is not an acceptable method of
The care of an acutely ill patient often includes transport,
airway management for critically ill patients undergoing
either within a hospital to undergo tests and procedures
transport because of the problems associated with move-
or between hospitals to receive a higher level of care or
ment.68 A nasogastric or orogastric tube is inserted in all
to access a hospital bed. The movement of critically ill
patients requiring mechanical ventilation.
patients places the patient at a higher risk of complica-
Fluid resuscitation and inotropic support are initiated
tions during the transport period62–65 because of condition
prior to transporting the patient. Planning for the trip
changes, inadequate availability of equipment or support
needs to include adequate reserves of blood or other IV
from other clinicians or the physical environment in the
fluid for use during transport. If the patient is combative
transport vehicle. For this reason the standard of care
or uncooperative, the use of sedative and/or neuromus-
during any transport must be equivalent to, or better than,
cular blocking agents and analgesia may be indicated.68 A
that at the referring clinical area.62,66,67 Safe transport of
syringe pump with battery power is the most appropri-
patients requires planning and stabilisation by staff with
ate method for delivering medications for sedation and
appropriate skills and experience. This section focuses on
pain relief. A urinary catheter is inserted for transports of
the movement of critically ill patients between hospitals. extended duration and all unconscious patients.68,69
Retrievals Equipment essential for transport includes:
Although there are a variety of retrieval or transport • equipment for airway management, sized
models, most retrieval teams comprise doctors, nurses appropriately and transported with each patient
and paramedics with specialised training in critical care. (check for operation before transport)
The skills of the escort personnel need to match the • portable oxygen source of adequate volume
acuity of the patient, so that they can respond to most to provide for the projected timeframe, with a
clinical problems.68,69 Thus, retrieval team staff need to 30-minute reserve
deliver high-level critical care equal to the standard of • a self-inflating bag and mask of appropriate size
the receiving centre, but need to be familiar with the
challenges associated with working outside the hospital • handheld spirometer for tidal volume measurement
environment. Standards and guidelines for the transport of • available high-pressure suction
critically ill patients have been established by the College • basic resuscitation drugs, and supplemental
of Critical Care Medicine and the Australasian College medications, such as sedatives and narcotic analgesics
for Emergency Medicine,62 the Intensive Care Society,69 (considered in each specific case)
American College of Critical Care Medicine68 and the • a transport monitor, displaying electrocardiogram
Association of Anaesthetists of Great Britain and Ireland.70 (ECG) and heart rate, oxygen saturation, end-tidal
When transporting an unstable patient it is essential CO2 and as many invasive channels as required for
that a minimum of two people focusing solely on the pressure measurements.
clinical care aspects of the patient are present, in addition
The patient’s identification bracelet should be checked
to other staff transporting the patient and equipment. The and verified, medical records and relevant information
transport team leader is usually a medical officer with such as laboratory and radiology findings are copied for
advanced training in critical care medicine or, for the the receiving facility, and other documentation includes
transport of critical but stable patients, a registered nurse initial medical evaluation and medical officer to medical
with critical care experience. The precise composition of officer communication, with the names of the accepting
the transport team can depend on the clinical circum- doctors and the receiving hospital.67–69
stances in each case.The skill set includes advanced cardiac
life support, arrhythmia interpretation and treatment and Patient monitoring during transport
emergency airway management.68 Critically ill patients undergoing transport receive the
Preparing a patient for inter-hospital same level of monitoring as they would have in a critical
care unit. Monitoring equipment should be selected
transport for its reliable operation under transport conditions, as
Adequate and considered preparation for the transport of monitoring can be difficult during transport; the effects of
a critically ill patient from one hospital area to another motion, noise and vibration can make even simple clinical
should be appropriately planned and not compromised observations (e.g. chest auscultation or palpation) difficult,
by undue haste. Appropriate evaluation and stabilisation if not impossible.71 The monitor should have a capacity
are required to ensure patient safety during transport, for storing and reproducing patient bedside data and
 CHAPTER 23 EMERGENCY PRESENTATIONS 749

printouts during transport.62,68,71 As transport of mechan- be given a low treatment priority, though this will almost
ically ventilated patients is associated with risk,62,68,71,72 certainly ensure their death. These decisions are therefore
consistent ventilation and oxygenation should be a goal; best made by an experienced doctor. In a situation with a
transport ventilators provide more constant ventilation than large number of casualties, one or more doctors should be
manual ventilation. An appropriate transport ventilator present at the site to lead the triage effort. Further, it is not
provides full ventilatory support, monitors airway pressure within the scope of practice of non-physician emergency
with a disconnect alarm and should have adequate battery personnel to pronounce a patient dead, but properly
and gas supply for the duration of transport.62 trained ambulance or rescue personnel can recognise the
Adverse events during transport of critically ill patients signs of death for the purposes of triage until doctors can
fall into two categories:62,72,73 1) equipment dysfunction, formally declare death.63,64
such as ECG lead disconnection, loss of battery power,
loss of IV access, accidental extubation, occlusion of the Emergency department response
endotracheal tube or exhaustion of oxygen supply (at least to an external disaster: receiving
one team member should be proficient in operating and
troubleshooting all equipment), and 2) physiological dete-
patients
riorations related to the critical illness. Mechanisms for Disasters may produce mass victims on a scale that means
audit, quality improvement and teaching purposes should routine processes and practices in the ED and hospital will
be in situ to allow for feedback, performance review and be overwhelmed. The ED response to an external disaster
service improvements.62,68–71 forms part of the overall hospital response, outlined in
a hospital disaster plan. The ED response plans also sit
within the larger context of other health disciplines where
Multiple patient triage/disaster there is a consideration of the prevention of, preparedness
Disaster triage is a process designed to provide the greatest for, response to and recovery from the health problems
benefit to multiple patients when treatment resources arising from a disaster.64 These plans are reviewed regularly
and facilities are limited. Disaster triage systems differ for currency, and practised for preparedness.The following
from the routine triage system used within the ED aspects form part of ED planning and response to receiving
(e.g. the ATS, MTS): system care is focused on those patients from an external disaster.64,65,74
victims who may survive with proper therapy, rather
than on those who have no chance of survival or who Department preparation
will live without treatment. The system was first devised If the disaster site is close to the hospital, a significant
during war as a method of managing large numbers of number of disaster victims will self-evacuate from the site
battlefield casualties. Today it is applicable for treating and arrive at the hospital without any prehospital triage,
multiple victims of illness or injury outside and within treatment or decontamination before any formal notifica-
the hospital setting. Variations exist between states and tion has been received. In this instance the ED will need
countries regarding disaster victim triage classifications. to declare the incident and commence the notification
It is therefore important to be familiar with local plans process required.64 The ED may be quickly overwhelmed
and policy.13,22,74 with arriving patients; the closest local medical facility
Triage of mass victims may be necessary in common may receive up to 50–80% of the disaster victims within
situations, such as vehicle collisions with multiple 90 minutes of the incident.65 On notification of a disaster
occupants, as well as other large-scale disasters, such as response a number of key positions should be allocated
earthquakes, floods, bushfires, damaging storms, public (medical coordinator, nursing coordinator, triage nurse,
transport incidents or explosions. The principles of triage medical triage officer). These personnel are senior staff
vary little, though the methods used to communicate with specific disaster training and knowledge of the
triage information and to match victims with available hospital’s disaster plan.63,64,74 Nursing and medical coordi-
resources may differ.Triage at the scene of a major incident nators are responsible for allocating staff to specific duties;
or disaster is commenced by the first qualified person to all designated roles are outlined on action cards available
arrive (i.e. the one with the most medical training). This for staff to read prior to commencing their roles.65
person is initially responsible for performing immediate The capacity of the ED to accommodate a large influx
primary surveys on all victims and for determining and of patients needs to be maximised. Patients currently in the
communicating the numbers and types of resources department are reviewed for a decision to admit. Patients
needed to provide initial care and transport.8 requiring admission are transferred out of the department
In Australia, New Zealand, the United Kingdom to a suitable location in the hospital. Patients suitable for
and the United States of America disaster systems have discharge or referral to their local medical officer, including
up to five triage categories (depending on jurisdictional patients with minor complaints currently waiting, should
and local protocols), usually with corresponding colours. be discharged or referred to community resources. A small
Despite slight variation, the aim is similar: to provide number of patients may need to remain in the ED, and
the best level of care and ensure the highest number of their care will need to be prioritised in conjunction with
survivors. Those who are mortally injured but alive may arriving disaster victims.62–65
750 SECTION 3 SPECIALTY PRACTICE

Areas of the department are designated to accommodate Respiratory presentations

the expected severity of the victims (e.g. resuscitation room
for priority 1 patients, observation areas for priority 2). Patients with respiratory dysfunction are common pres-
Walking wounded casualties with relatively minor injuries entations to the ED and are seen across all age groups.
and who are unlikely to require admission to hospital are Respiratory symptoms can be associated with a broad
best accommodated in a treatment area outside the ED, as range of underlying pathologies. This section will discuss
this reduces congestion and increases the capacity for more the initial assessment and treatment of several common
significantly-injured victims to be managed.64 respiratory diseases seen in the ED. Chapter 14 provides
Additional staff members are notified from the current more detailed information regarding respiratory diseases.
staff lists to participate in the disaster management. Staff
members are allocated to teams to manage bed spaces
Presenting symptoms and incidence
within designated treatment areas. Additional staff from Patients presenting with respiratory complaints may
outside the ED may be deployed to assist; these staff display a range of symptoms. These symptoms will vary
should be teamed with routine ED staff because of their based upon the age of the patient, the underlying cause
familiarity with the layout and location of equipment of the symptoms and the severity of the underlying
and other resources. It is important to recognise the need condition. A list of frequently encountered respiratory
to replace staff to avoid fatigue, especially in incidents signs and symptoms can be found in Box 23.1.75–77
of a protracted nature. Therefore, not all staff should be
called in initially. Where possible, staff who usually work BOX 23.1
together on a daily basis should work in teams during the
disaster period.64,65,74 Signs and symptoms commonly associated with
respiratory presentations75,76
Triage and reception • Shortness of breath
Routine, day-to-day triage and reception processes will • Dyspnoea (painful or difficulty breathing)
be ineffective when receiving large numbers of disaster
• Decreased SaO2
victims. A registration process for disaster victims generally
involves collecting minimal personal information from the • Cyanosis
patients, where possible, and the allocation of a prepared • Alteration in respiratory rate – tachypnoea/
disaster hospital number used for identification and bradypnoea
ordering investigations.8,74 Triage assessments will often be • Alterations in respiratory depth or pattern
undertaken by both a medical officer and a nurse, and the
• Use of accessory muscles
process will be brief and focused. Most victims will have
been allocated a triage tag in the field, but are reevaluated • Intercostal and/or subcostal recession
for any changes, as their condition may have deteriorated. • Inability to speak in full sentences
Triage assessment is based on observations of the nature • Wheeze
and extent of the victims’ injuries. Patients present in the • Stridor (upper airway respiratory disorders)
ED prior to disaster notification are considered part of
the disaster event and triaged in the same manner.4,8,65 • Alterations in level of consciousness
• Anxiety/feeling of impending doom
Treatment
Treatment provided during a disaster will not reflect
routine practices; priorities focus on resuscitation, iden- Shortness of breath or dyspnoea is a frequent symptom
tification of serious injuries, identification of patients or complaint on presentation to the ED. Respiratory
requiring urgent surgery and stabilisation of patients for presentations are not isolated to any one specific patient
transfer out of the ED. The best overall outcomes during population or age group and are frequently encountered
a disaster are achieved when the routine principles of in patients across the lifespan. Dyspnoea, while commonly
resuscitation and management are adapted to reflect the associated with respiratory conditions such as asthma,
resources available.64,65 pneumonia, chronic obstructive pulmonary disease and
cardiac conditions, has multiple aetiologies and can be
Transfer from the ED caused by disease in almost any organ system. Shortness
Patients are triaged, stabilised and transferred out to the of breath is a significant symptom and is commonly
operating theatre or other clinical areas as soon as possible associated with the need for hospital admission.77–79
using designated transfer staff and a coordinated process Assessment, monitoring and
outlined in the hospital plan. This will maintain the
effectiveness and efficiency of the department as victims diagnostics
continue to arrive. During and after the incident, oppor- On arrival, patients with respiratory complaints should
tunity for staff to debrief is an important aspect to manage be quickly assessed utilising a systematic approach to
staff psychosocial wellbeing.8,74 determine whether there is any potentially life-threatening
 CHAPTER 23 EMERGENCY PRESENTATIONS 751

disturbance to the airway, breathing or circulation that time-dependent having a slow onset, which allows time
requires immediate medical assessment and/or resuscita- for monitoring with pulse oximetry, arterial blood gas
tive intervention. analysis and clinical review.79
Initial assessment should include a thorough history
focused on the presenting complaint/s. A detailed history Patient diagnoses and management
may often identify the underlying process; however, The common diagnoses related to patients who present
the emergency clinician should maintain a high index with shortness of breath are asthma, respiratory failure and
of suspicion of other potential causes during the initial pneumonia.78
assessment.77,78 The history should focus on the nature of
symptoms, the timing of the onset of symptoms, associated Asthma
features, the possibility of trauma or aspiration and past Asthma is a very common reason for patients presenting
medical history, especially the presence of chronic respi- to Australasian emergency departments. Over 2.2 million
ratory conditions. After obtaining a history, a physical Australians have asthma: up to 16% of children and 12% of
assessment of the respiratory system should be undertaken adults are affected by the condition.81–85 In other developed
(see Chapter 13 for a detailed description of respiratory countries like the USA asthma is the most common
physical assessment). respiratory disease affecting between 4% and 5% of the
Patients with significant respiratory symptoms are best population.85 Asthma is a chronic inflammatory disease of
managed in an acute monitored bed or resuscitation area of the airways in which many cells and cellular elements play
the emergency department.A set of observations including a role, including mast cells, eosinophils, T lymphocytes,
heart rate, respiratory rate, blood pressure, temperature and macrophages, neutrophils and epithelial cells. The inflam-
oxygen saturation should be completed and the patient’s matory changes cause recurrent episodes of wheezing,
heart rate and oxygen saturation can be continuously breathlessness, chest tightness and coughing associated
monitored. Pulse oximetry plays an important role in the with widespread reversible airflow obstruction of the
monitoring of the patient with a respiratory complaint. airways. This airflow obstruction or excessive narrowing is
The recognition of hypoxaemia is significantly improved a result of airway smooth muscle contraction and swelling
with the use of pulse oximetry.80 of the airway wall due to smooth muscle hypertrophy,
IV access should be obtained and venous blood samples inflammatory changes, oedema, goblet cell and mucous
may be collected for full blood count, urea, electrolytes gland hyperplasia and mucus hypersecretion.84,85
and creatinine where clinically indicated. A chest X-ray Normally, airways widen during inspiration and
(CXR) should be ordered in most instances. The CXR is narrow in expiration. In asthma, the above responses
one of the most useful investigations in the patient with a combine to severely narrow or close the lumen of the
respiratory presentation. Interpretation of the CXR does bronchial passages during expiration, with altered ventila-
not provide 100% accuracy in distinguishing between tion and air trapping.84,85 The causes of asthma are related
possible underlying pathologies, and may appear normal to many factors, including allergy,81 infection (increased
in some instances. Therefore, interpretation of the CXR reaction to bronchoconstrictors such as histamine),81–85
should always be performed in light of the clinical history irritants (e.g. noxious gases, fumes, dusts, dust mites,
and other examination findings.79 An arterial blood gas powders) or heredity, although the exact role or importance
is often indicated in patients with a significant respira- of any hereditary tendency is difficult to assess.85
tory presentation. The arterial blood gas will provide A patient usually has a history of previous asthma
useful information that assists in identifying alterations to attacks. Often, an acute episode follows a period of exercise
oxygenation, ventilation and acid–base status.79 Spirometry or exposure to a noxious substance, or a known allergen.
or peak flow measurements may also be utilised in the The onset of the asthma may be characterised by vague
assessment of the patient. Peak expiratory flow rate, forced sensations in the neck or pharynx, tightness in the chest
vital capacity and forced expiratory volume in 1 second are with breathlessness, loose but non-productive cough with
useful in determining the nature of the underlying respi- difficulty in raising sputum, difficulty breathing, particu-
ratory condition and, when the values are compared to larly on expiration, with increasing severity as the episode
predicted normal values, are useful in determining severity. continues; apprehension and tachypnoea may follow as the
These tests are, however, effort- and technique-dependent patient becomes hypoxic, with audible wheezing.84,85
and may not be able to be performed by the patient who The characteristics and initial assessment of acute mild,
is acutely short of breath.79 moderate and severe/life-threatening asthma in adults are
Oxygen therapy should be commenced early in outlined in Table 23.7.The associated clinical management
patients presenting with signs of acute respiratory guidelines for acute asthma are outlined in Table 23.8. Be
compromise, including patients known to have chronic alert to the high-risk patient whose ability to ventilate
obstructive pulmonary disease. Patients with acute is impaired: this is a life-threatening condition. Such
hypoxia require oxygen. The often mentioned compli- patients will exhibit an inability to talk, central cyanosis,
cations associated with oxygen, especially in the patient tachycardia, use of respiratory accessory muscles, a silent
with known chronic obstructive pulmonary disease, are chest on auscultation and a history of previous intubation
uncommon. Such complications are concentration- and for asthma.81–88
752 SECTION 3 SPECIALTY PRACTICE

TABLE 23.7
Initial assessment and characteristics of acute asthma84,85

S E V E R I T Y O F AT TA C K
SEVERE OR
SYMPTOMS MILD M O D E R AT E L I F E - T H R E AT E N I N G

Able to talk in Sentences Phrases Words

Physical exhaustion No No Yes, may have paradoxical
chest wall movement
Pulse oximetry (room air) >94% 90–94% <90%; cyanosis may be
present
Pulse rate <100/min 100–120/min >120/min; below 60/min
Level of consciousness Normal May be agitated Confused, drowsy or
agitated
Wheeze intensity Variable Moderate–loud Often quiet
Central cyanosis Absent May be present Likely to be present
Peak expiratory flow (% predicted) >75% 50–75% <50% or an inability to
perform the test
Arterial blood gases Test not necessary If initial response is poor Yes

TABLE 23.8
Initial clinical management in acute asthma84,88

MILD M O D E R AT E SEVERE OR
L I F E - T H R E AT E N I N G

Hospital admission necessary Probably not Likely to be required Yes, consider ICU
Oxygen High flow of at least 8 L/min, titrated to maintain SaO2 >90%, preferably >94%. Monitor effect
by oximetry. Frequent measurement of arterial blood gases in severe asthma if not responding
Beta-2-agonist via a metered- Salbutamol 8–12 puffs Salbutamol 8–12 puffs Salbutamol 8–12 puffs every
dose inhaler and spacer or or 15–30 min
or Salbutamol 5 mg Salbutamol 5–10 mg every or
nebulised solution with 1–4 hours Salbutamol 5–10 mg every
8 L/min O2 15–30 min
If no response to aerosol give
salbutamol 250 mcg IV bolus
and then 5–10 mcg/kg/h
Ipratropium bromide metered Not necessary Optional 6 puffs (20 mcg/puff) with
dose inhaler or spacer salbutamol every 2 hours
or Not necessary Optional 2 mL 0.05% (500 mcg)
nebulised solution ipratropium bromide with
salbutamol 2-hourly
Steroids Yes (consider oral) Yes, oral 0.5–1.0 mg/kg IV hydrocortisone 250mg
6-hourly
Other agents Not indicated Not indicated For life-threatening and no
response, magnesium sulfate
2 g IV over 10 min may help
CXR (and other investigations Not usually necessary Not necessary unless Necessary if no response
focal signs present, or no to initial therapy or suspect
improvement with therapy pneumothorax/infection
Check for hypokalaemia
Observations Regular Continuous Continuous
 CHAPTER 23 EMERGENCY PRESENTATIONS 753

Acute respiratory failure cell count (i.e. leucocytosis). Blood cultures and sputum
Acute respiratory failure exists when the lungs do not cultures will also be acquired to assist in identifying the
provide sufficient gas exchange to meet the body’s need for causative organism. Arterial blood gases will assist in deter-
oxygen consumption, carbon dioxide elimination or both. mining the degree of impaired gas exchange. Hypoxaemia
Acute respiratory failure results from a number of causes.89 and often hypocarbia may be present.76
When alveolar ventilation decreases, arterial oxygen tension Initial treatment involves administration of oxygen
falls and carbon dioxide rises. The rise in arterial carbon therapy via face mask. Oxygen therapy should be evaluated
dioxide produces increased serum carbonic acid and pH frequently in response to arterial blood gas results and
falls, resulting in respiratory acidosis.90 If uncorrected, pulse oximetry. Treatment will routinely require IV fluid
low arterial oxygen combines with low cardiac output to therapy to ensure adequate hydration, and administra-
produce diminished tissue perfusion and tissue hypoxia. tion of antibiotics orally or parentally in accordance with
Anaerobic metabolism results in increased lactic acid, aggra- existing antibiotic guidelines or suspected infective agent
vating the acidosis caused by carbon dioxide retention. In (see Chapter 14). Ventilatory support may be required
the process, a wide range of symptoms develop, involving in some cases; in spontaneously breathing patients non-
the central nervous and cardiovascular systems.84 Arterial invasive ventilation via a face mask should be utilised
blood gases confirm the diagnosis, with hypercarbia and before invasive ventilation. Mechanical ventilation is not
a partial pressure of carbon dioxide in the arterial blood normally required unless there is some underlying cardio-
>45 mmHg and hypoxaemia evidenced by a partial pressure pulmonary disease.76,87
of oxygen in the arterial blood <80 mmHg, and a low
pH evident. A CXR identifies the specific lung disease.89 Chest pain presentations
Clinical management focuses on correction of hyper-
capnia, treatment of hypoxaemia, correction of acidosis Chest pain or chest discomfort is a common presenting
and identification and correction of the specific cause89 complaint to the ED and can be associated with a number
(see Chapter 14). For a spontaneously breathing patient, of different clinical conditions, several of which are
administer oxygen by Venturi mask (24%) or nasal cannula. associated with life-threatening pathology.92 The identifica-
Adjust oxygen therapy, according to arterial blood gas tion of cardiac-related chest pain is important. During an
findings at 15–20-minute intervals, to achieve a partial initial assessment it may be difficult to differentiate between
pressure of oxygen in the arterial blood of 85–90 mmHg. non-cardiac and cardiac causes of chest discomfort based on
For a patient with inadequate respiratory effort, non- pain characteristics such as intensity, location, radiation and
invasive ventilation may be instituted (see Chapter 15). In other associated symptoms.92,93 Therefore, it is important to
an apnoeic situation, initiate ventilatory assistance with consider any presentation in which chest pain is a feature as
bag–mask ventilation (see Chapter 15) prior to endo- cardiac in origin until a cardiac cause has been ruled out or
tracheal intubation, and then commence mechanical another cause has been confirmed.
ventilation.
Description of presenting symptoms
Pneumonia and incidence
Pneumonia is an acute inflammatory condition of The incidence of acute chest pain presentations appears to
lung tissue caused by a variety of viral and bacterial
be increasing as patients are more aware of the importance
organisms, fungi and parasites.76,87,91 These organisms
of early treatment for myocardial infarction due to public
cause an inflammatory response from the cells involved
awareness campaigns.92,94 In American EDs up to 7% of all
in the affected segment of lung tissue. Pneumonia may
presentations are for complaints of chest pain.95 The pain
occur in previously healthy patients, but more often it is
or discomfort associated with chest pain presentations is
associated with conditions that impair the body’s defence
often described in a variety of ways in terms of onset,
mechanisms76,87,91 (see Chapter 14). The predominant
symptoms associated with pneumonia are a combination intensity, duration and radiation (see Table 23.9).
of cough, chest pain (usually pleuritic), dyspnoea, fever Up to 9% of patients who will go on to be diagnosed
(with or without chills) and mucoid, purulent or bloody with an acute coronary syndrome (ACS) may present with
sputum, with an abrupt or gradual onset.87,91 A physical a number of these associated symptoms but without chest
examination demonstrates tachypnoea, fever, tachycardia, pain. These patients tend to be elderly, female, diabetic
possible cyanosis, diminished respiratory excursion due and non-white minorities.96–98 Therefore, it is important
to pleuritic pain, end-respiratory crackles or rales on to consider the possibility of a cardiac presentation in
auscultation with bronchial breathing over areas of consol- patients presenting with these associated symptoms even
idation76,87,91 (see Chapter 14). in the absence of chest pain.9
Investigations include a CXR, which may reveal Assessment, monitoring and
varying infiltrates – interstitial, segmental or lobar. The
CXR, however, may initially be clear until later in the diagnostics
illness and following adequate rehydration.79 Venous Any patient presenting with a complaint of chest pain
blood samples will be analysed to identify a raised white requires urgent assessment, generally within 10 minutes of
754 SECTION 3 SPECIALTY PRACTICE

TABLE 23.9
Features of chest pain92,94–97

C H E S T PA I N F E AT U R E DESCRIPTION

Description Typical: pressure, a weight on the chest, tightness, constriction about the throat, an aching feeling
Less typical: epigastric, indigestion, stabbing, pleuritic, sharp
Onset Unprovoked or gradual
With physical exertion or emotional stress
Intensity Mild to severe
Radiation To one or both arms, neck, jaw or back
Associated symptoms Shortness of breath, nausea, vomiting, weakness, dizziness, anxiety, feeling of impending doom,
palpitations, diaphoresis

arrival to the ED. Any patient with evidence of a distur- damage to the myocardial cells. A time-critical obstruction
bance to airway, breathing or circulation requires close results in death or necrosis of a segment of myocardial cells
monitoring, immediate medical assessment and resuscita- resulting in an AMI.93
tive interventions. The initial assessment should include a ACS collectively describes unstable angina and AMI.
12-lead ECG and a history of the presenting complaint Coronary heart disease is the largest single cause of death
including an evaluation of the pain utilising a systematic and the commonest cause of sudden death in Australia
approach. The ECG should be rapidly evaluated for the and New Zealand.100 It is the leading cause of premature
presence of ST-segment elevation or a new left bundle death and disability in both countries, although death
branch block suggestive of an acute myocardial infarction rates have fallen since the 1960s. Over half of all coronary
(AMI) so that time-critical treatment can be initiated. heart disease deaths were from AMI.101 ACS is the most
If the initial ECG is non-diagnostic and symptoms common life-threatening condition seen in the ED and
continue, repeat ECGs should be performed at 15-minute therefore represents an important area of clinical practice
intervals.92,95,96 in the ED.101,102 Chapters 10 and 11 provide additional
The patient should have cardiac monitoring information about presentations of cardiac dysfunction,
commenced in order to identify any life-threatening including pathophysiology, clinical manifestations and
arrhythmias. Supplemental oxygen should also be treatment of cardiac conditions. This section summarises
commenced if indicated to potentially improve PaO2 and clinical management processes in the ED.93
increase oxygen availability, especially in the presence of The initial management in the ED is focused on rapid
myocardial ischaemia;99 however this is a routine inter- identification of patients with AMI and their suitability
vention currently being reviewed. An IV cannula should for reperfusion therapy. Reperfusion therapy consists of
be inserted and routine venous blood samples collected the administration of thrombolytic drugs with or without
for troponin T or troponin I, cardiac enzymes that, when percutaneous coronary intervention (angioplasty ± stent).
elevated, suggest myocardial injury. Cardiac enzymes are Percutaneous coronary intervention is generally only
usually repeated within 6–8 hours of ED presentation.99 available to patients in larger centres where there is access
A physical examination should also be performed. The to such resources. If percutaneous coronary intervention
physical examination may be of limited value in iden- is not available, suitable patients should be managed with
tifying cardiac causes of the pain but will be beneficial thrombolysis.93
in identifying non-cardiac causes of the pain or compli- The ongoing management in the ED for patients
cations associated with cardiac-related conditions.92,94,96 with ACS includes oxygen therapy, administration of
The examination should also include assessment of the aspirin 300 mg – if not already administered by pre-
abdomen as a number of significant abdominal complaints hospital personnel – and pain relief. Pain relief management
may also present with chest pain as a feature.92–94 A CXR generally includes the administration of IV morphine in
should also be performed in order to identify any potential small incremental doses. Pain relief may also include the
causes for the patient’s pain. administration of nitrates initially via the sublingual route;
Patient diagnoses and management however, if pain persists despite IV morphine, the adminis-
tration of IV nitrates may be indicated.102 The patient and
Acute coronary syndromes their family should also be provided reassurance, informa-
Chest pain of cardiac origin results from reduced or tion and emotional support.
obstructed coronary blood flow, commonly due to athero- Patients without initial evidence of AMI are subse-
sclerosis, although coronary artery spasm or an embolism quently stratified into high-, intermediate- and low-risk
may also be involved.92–94 Angina, whether stable or groups based upon the presence of a number of clinical
unstable, is a temporary condition in which there is no features associated with the presentation including the
 CHAPTER 23 EMERGENCY PRESENTATIONS 755

significance and duration of pain, ECG findings, past history, Assessment, monitoring and
cardiovascular disease risk factors and cardiac enzyme
results.99 Specific ongoing treatment and management is diagnostics
then guided by the associated risk pathway.93,99 Patients presenting with abdominal pain are assessed
quickly for any disturbance to airway, breathing or circu-
Thoracic aortic dissection lation requiring close monitoring, immediate medical
Thoracic aortic dissection (TAD) occurs when there is a assessment and/or resuscitative interventions. Abnormal
tear in the intimal layer of the vessel wall. Blood passes vital signs are suggestive of clinically significant abdominal
through the tear, separates the intima from the vessel media pain.109 A thorough history includes location and timing
or adventitia and results in a false channel. Shear forces of onset; quantity, quality and radiation of pain; associated
lead to dissection propagation as blood flows through the symptoms, previous history and general state of health.
false channel.96,103 The incidence of TAD is quite low; A complaint-specific history and physical examination
ACS is 80 times more common. Identification of this is performed for a differential diagnosis.105,106,109 Physical
life-threatening condition in the patient presenting with assessment includes visual inspection of the abdomen with
chest pain is important as patients often require immediate the patient in a supine position, followed by auscultation,
surgery. TAD is most commonly seen in men aged 50 to then gentle palpation and percussion of all four quadrants
70 years who have a history of hypertension. Other risk of the abdomen, working towards the area of reported
factors include Marfan’s disease and other connective tissue pain.110,111 While location of the pain is important, it can be
disorders, cocaine or ecstasy use, pregnancy and aortic misleading, as various pathological processes can localise
valve replacement.98 TAD is associated with an acute and to different areas of the abdomen (see Figure 23.1).112 An
sudden onset of severe pain that is maximal at symptom ECG is considered to rule out myocardial ischaemia or
onset. Pain is usually located in the midline and may be infarction, as some cardiac patients may present with upper
present in the back and rarely radiates. The pain is often abdominal pain as the predominant symptom. Myocardial
described as sharp, tearing or ripping in nature.98 Patients ischaemia may also be caused by the physiological stress of
may also have pulse deficits or blood pressure differences the intra-abdominal pathology.105
(>20 mmHg) between the upper arms. CXR will be Administration of narcotic analgesia in acute abdominal
abnormal in 80–90% of cases with a widened mediastinum pain does not hinder assessment or obscure abdominal
seen in approximately 50% of cases.103,104 Patients will most findings, nor cause increased morbidity or mortality,
commonly have the diagnosis confirmed using contrast and may allow for a better abdominal examination.113,114
computed tomography. The management of TAD is aimed Incremental doses of a narcotic can minimise pain but not
at aggressive control of blood pressure and pulse with palpation tenderness. Analgesics enable relaxation of the
sodium nitroprusside and beta-blockers, relief of pain with patient’s abdominal muscles and decrease anxiety, poten-
narcotic analgesia and referral and/or transport to cardio- tially improving information obtained from the physical
thoracic services for definitive surgical intervention.103,104 examination.61,113
Venous blood samples are collected for full blood
count, urea, electrolytes, creatinine and amylase and
Abdominal symptom lipase.111 A dipstick urinalysis can suggest specific disease.
presentations For example, leucocytes and/or blood in the urine can
suggest a urinary tract infection and haematuria can suggest
Acute abdominal pain is a common complaint, accounting renal colic, but should be considered in the context of
for 5–10% of all presentations to the ED.105–107 Specific other clinical findings and formal microscopy.111 Women
cause for the presenting abdominal pain will not be found of child-bearing age with abdominal pain provide the
in 30–40% of patients of all ages;105 for children, a diagnosis challenge of a broader range of potential causative pathol-
of non-specific abdominal pain accounts for up to 60% of ogies, although history and physical examination are
cases.108 About 20% of adult patients presenting will require unreliable in determining pregnancy.111 If pregnancy or a
surgical intervention and/or hospital admission.108,109 pregnancy-related disorder is possible, a urine beta-human
Common causes in the elderly include biliary tract chorionic gonadotrophin test is performed. Test sensitiv-
disease (25%), diverticular disease (10%), bowel obstruc- ity is extremely high; a positive finding occurs within a
tion (10%) or malignancy (13%).110 Elderly patients are few days of conception, and accuracy is comparable to
more likely to have catastrophic illnesses rarely seen in blood sampling. An ectopic pregnancy may be missed
younger patients, including mesenteric ischaemia, leaking if pregnancy is not considered; an ectopic pregnancy is
or ruptured abdominal aortic aneurysm and myocardial extremely unlikely if the beta-human chorionic gonado-
infarction.105,106,109 Up to a third require surgical interven- trophin result is negative.111
tion,108 while 15% will not have a cause for their abdominal
pain found.110 Presentations by elderly patients are often Patient diagnoses and management
complicated by delays in seeking medical attention, Common abdominal diagnoses for acute abdominal pain
atypical presentations, associated medical conditions and are abdominal aortic aneurysm, appendicitis and bowel
comorbidities, medications and cognitive function. obstruction.
756 SECTION 3 SPECIALTY PRACTICE

FIGURE 23.1 An algorithm for triaging commonly missed causes of acute abdominal pain.

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Adapted from Dagiely S. An algorithm for triaging commonly missed causes of acute abdominal pain. J Emer Nurs 2006;32(1):9,
with permission.

Abdominal aortic aneurysm aneurysms are surgically repaired more than any other type
Abdominal aortic aneurysm is more likely to develop in of aneurysm. Unless a patient receives immediate resus-
men than women,115 is a common cause of death in all citation and surgical intervention, a ruptured abdominal
aortic aneurysm is fatal.116
patients over the age of 65 years and is responsible for
0.8% of all deaths.108,116 The traditional presentation is Appendicitis
acute pain in the back, flank or abdomen, with hypoten- Appendicitis is the most common acute abdominal
sion and a palpable abdominal mass in the older patient.116 pain presentation worldwide that requires a surgical
Missed diagnoses primarily occur because physical exam- intervention. About 8% of people in Western countries
ination is frequently unreliable.116 Many patients with will have appendicitis during their lifetime.117 Along
dissecting abdominal aortic aneurysm are misdiagnosed with pain (usually in the right lower quadrant),
with renal colic because of haematuria present, no palpable other presenting symptoms may include nausea and
pulsatile mass and flank pain.116 Other common misdiag- vomiting.117 Diagnosis is based on clinical assessment as
noses include diverticulitis, gastrointestinal haemorrhage, there is no specific test available to confirm diagnosis.118
AMI and musculoskeletal back pain.116 Abdominal aortic Appendicitis can mimic almost all acute abdominal
 CHAPTER 23 EMERGENCY PRESENTATIONS 757

pain presentations, and is frequently misdiagnosed as in persons aged over 75 years.125 The two general stroke
gastroenteritis during the initial ED visit, pelvic inflam- classifications are:
matory disease or urinary tract infection.111 Although • Ischaemic strokes are precipitated by disrupted blood
it is a well-studied disease, appendicitis continues to be flow to an area of the brain as a result of arterial
difficult to diagnose in ED because of its varied presen- occlusion. Acute ischaemic stroke presentations are
tations. Elderly patients require careful consideration due now referred to as a ‘brain attack’, to promote early
to associated comorbidities117 and women of childbear- presentation for access to time-critical treatments126–128
ing age are commonly misdiagnosed due to anatomical and because the pathophysiology and current
changes associated with pregnancy. Treatment includes treatment of acute ischaemic stroke mimics that of
management of pain-related symptoms and provision of AMI. From an ED perspective, serious long-term
IV hydration.118 Definitive treatment is surgical removal disability can be minimised if ischaemic stroke is
of the appendix.118 recognised and treated promptly; that is, within
3 hours of symptom onset.127,129
Practice tip
• Haemorrhagic strokes are caused by rupture of a
Elderly patients require careful consideration due to blood vessel, which produces bleeding into the
associated comorbidities and age-related changes brain parenchyma. (Chapter 17 details the
to their response to illness. pathophysiological processes.)
For patients diagnosed with an ischemic stroke,
Bowel obstruction 13–25% will die within the first 30 days and 60% within
10 years.130–132 Permanent disability requiring care in a
A bowel obstruction commonly results from impaired peri-
nursing home or other long-term facility is required for
staltic movement, hernias, adhesions and neoplasms.119,120
around 10%.125,130
Presentation includes poorly localised colicky pain that
increases in intensity and location, with subsequent Assessment, monitoring and
abdominal swelling and vomiting of faecal fluid.119,120
Management includes both conservative options
diagnostics
(management of symptoms, placement of a nasogastric Symptoms of stroke are common amongst patients
tube and replacement of IV fluids) and surgical therapy presenting to the ED; presenting signs vary from profound
for neoplasms or hernias.119,120 alterations in level of consciousness and limb hemiplegia
to mild symptoms affecting speech, cognition or coordi-
Ectopic pregnancy nation. Symptoms may include confusion, dizziness, ataxia,
An ectopic pregnancy is implantation outside the uterus, visual disturbances, dysphasia or receptive and expressive
most commonly in the fallopian tubes. Ectopic preg- aphasia, dysphagia, weakness and numbness or tingling of
nancies in the developed world occur at a rate of about the face, arm or leg, which is usually unilateral.125,129,131 Many
11:1000 diagnosed pregnancies.121 The incidence is disorders resemble a stroke presentation so emergency
thought to be higher in developing countries but specific clinicians must quickly determine if another condition is
numbers are unknown.122 Presenting symptoms can responsible for the patient’s neurological deficits. Other
include lower abdominal pain that can become severe, conditions include post-ictal phase following seizures,
feeling faint, bleeding or shoulder tip pain. Management migraine with neurological deficits, hypoglycaemia or
is guided by the patient’s haemodynamic state. Stable hyperglycaemia, systemic infections, brain tumours, hypo-
patients with no tubular ectopic may be managed with natraemia and hepatic encephalopathy.124,129
observation and drugs such as methotrexate; haemo- The focus of initial assessment is airway, breathing,
dynamically unstable patients will require resuscitation circulation and disability. Of note, for airway assessment,
and surgical intervention.122 stroke symptoms include altered muscle function, affecting
swallowing and speech functions. A patient with a Glasgow
Coma Scale (GCS) score of 9 or less may require intubation
Acute stroke to protect and secure the airway.123 The patient’s breathing
Cerebrovascular disease is highly prevalent in developed pattern should be assessed and continually monitored.
countries. In some countries that have seen continuing Hypertension is common, with the increase improving
industrialisation (such as Asia and Africa) the increasingly any cerebral ischaemia so this should not be lowered unless
unhealthy lifestyle is being reflected in diseases including dangerously high or contraindicated.126 Hypotension or
cerebrovascular disease.123 In China, different epidemiolog- dehydration decreases cerebral blood flow and perfusion
ical changes, such as an ageing population, high prevalence and should be corrected, although fluid replacement is
of smoking and hypertension, are expected to result in instituted with caution.131 Vital signs are documented
an increase in stroke rates.123 In Australia, cerebrovascu- every 15 minutes during drug therapy to identify changes
lar disease is the third-largest cause of death.124 Around suggestive of internal bleeding. Maintaining blood pressure
60,000 acute cerebrovascular accidents or recurrent less than 185/110 mmHg during fibrinolytic infusion
strokes are reported each year with around half occurring decreases the risk of intracerebral haemorrhage.128
758 SECTION 3 SPECIALTY PRACTICE

A thorough assessment of neurological disability drug and alcohol misuse in the age group between 15 and
should be undertaken, including a GCS (see Chapter 16). 29.133–138 In developed counties up to 25% of successful
An ECG is recorded to detect any abnormal rhythm such suicides are due to poisoning.135 In Australia and New
as atrial fibrillation, which may be associated with stroke Zealand, poisoning accounts for 1–5% of admissions to
presentation.123 IV access is obtained to administer medica- public hospitals.133–135,137
tions, and collect blood for electrolytes, haematology and Current clinical management with supportive and/or
coagulation studies. Assessment of blood glucose will rule symptomatic control has resulted in death rates as low as
out hypoglycaemia or hyperglycaemia as a cause of the 0.5% for overdose admissions to hospitals in developed
presenting symptoms. Abnormal glucose levels adversely countries.135
affect cerebral metabolism.126 After obvious alternative The usual types of poisoning encountered as ED
diagnoses are excluded, a brain computed tomography presentations include self-poisoning with prescribed
scan determines whether a stroke is haemorrhagic or drugs, ingestion of illicit drugs and common dangerous
ischaemic in origin. While a new-onset ischaemic stroke substances (e.g. detergents, cleansers; psychotropic agents;
may not be evident for up to 24 hours, blood in the cranial analgesics; insecticides; paracetamol, aspirin).139 A range of
cavity will be apparent immediately. Patients with any sign artificial and naturally occurring substances can produce
of haemorrhage are excluded for fibrinolytic therapy.127 acute poisonings. The toxicity of a substance depends on
Management numerous factors, such as dose, route of exposure and
the victim’s pre-existing conditions. Poisoning, whether
Acute ischaemic stroke management includes timely intentional or unintentional, can occur at any time, and
administration of a fibrinolytic agent in appropriately may involve single or multiple substances.133–137
selected patients (see Box 23.2), which facilitates reper- The vast amount of knowledge required concerning
fusion, minimises tissue damage and reduces long-term all poisons prompted the development of poison control
stroke sequelae. Longer times between symptom onset information centres to provide specific information and
and fibrinolytic infusion are associated with higher rates of
guidance for healthcare providers and the general public
morbidity and mortality.125 Early presentation is therefore
on the management of a poisoned patient; to collect
essential to instigate appropriate assessments and investi-
statistics on toxic substances; and to educate the public on
gations, including computed tomography scanning, and
the prevention or recognition of toxic exposures.136 Other
then thrombolytic administration and still fall within the
initiatives to limit the incidence and severity of acute
narrow treatment window. Acute stroke unit care, with
poisoning include the control of drugs, specific infor-
specialised teams dedicated to the rapid assessment and
management of presentations, can significantly reduce mation on labels, the introduction of blister packs and
death and disability125 (see Chapter 17). enforced safety standards such as childproof caps.136,140,141
Assessment, monitoring and
Overdose and poisoning diagnostics
Poisoning is a common clinical presentation throughout The poisoned patient may present with a wide range
the world. Worldwide up to 9% of deaths are related to of clinical features from no symptoms through to a

BOX 23.2

Criteria for administering fibrinolytic therapy in ischaemic stroke127

Inclusion criteria (all must be positive): • Patient received heparin within 48 h and had an
• Age ≥18 years elevated activated partial thromboplastin time (PTT)
• Clinical diagnosis of ischaemic stroke with • Current use of oral anticoagulants (e.g. warfarin)
measurable neurological deficit • Recent use of anticoagulant and elevated
• Time of symptom onset <180 min and well international normalised ratio (INR) or prothrombin
established time (>15 s) or
Exclusion criteria (all must be negative): • Intracranial surgery or serious head trauma, or
• Evidence of intracranial haemorrhage on non- previous stroke within 3 months
contrast head computed tomography • Major surgery or serious trauma within 14 days
• Only minor or rapidly improving stroke symptoms • History of intracranial haemorrhage, arteriovenous
• High suspicion of subarachnoid haemorrhage, even malformation, or aneurysm
with normal computed tomography • Witnessed seizure at stroke onset
• Active internal bleeding • Recent acute myocardial infarction
• Known bleeding condition, including but not limited • Systolic blood pressure >185 mmHg or diastolic
to platelets <100,000/mm3 blood pressure >110 mmHg at time of treatment
 CHAPTER 23 EMERGENCY PRESENTATIONS 759

life-threatening condition or the potential to deterio- are often complicated by coexisting medical conditions,
rate rapidly, and should always be assessed immediately. which may exaggerate the effects or impair the excretion
Triage decisions should be based on the potential for of the substances involved. Boys are more likely to be the
rapid deterioration and the need for urgent interven- victims of poisoning than girls. Adult women attempt
tion. Resuscitation may be necessary before any further suicide with poisons more often than men, but men’s
definitive care can be commenced. The priorities of care suicide intentions are associated with a higher mortality
for all patients include the assessment and maintenance rate.135,137,139
of an airway, adequate ventilation and circulation.134,136
Successful resuscitation may require removal of the Practice tip
toxin, counteraction of the poisoning by an antidote if
Poisonings in the aged population are often compli-
available, and the treatment or support of symptoms.133–137
cated by coexisting medical conditions, which may
It is extremely important to note that many drugs such as
exaggerate the effects or impair excretion of the
paracetamol may have limited initial effects but serious, substances involved.
potentially fatal consequences if not treated in a timely
manner.134,141
An accurate history is often the most significant aid Previous history
in directing care. If a history is unobtainable or uncertain, Patients with existing medical conditions often have
there are several general guidelines that may prove helpful multiple medications that could be either intentionally
for dealing with the patient who has an altered mental or unintentionally ingested. The use of multiple drugs
state or conscious level133–137 (see Table 23.10). may cause untoward reactions. A patient with a history
Poisoning should always be considered when dealing of depression may attempt suicide with psychotropic
with a patient who has a sudden-onset, acute illness. drugs.133–137 A quick onset and acute illness or condition
If there is a strong suspicion of poisoning, a clinician should raise the level of suspicion of a poisoning, especially
should attempt to compare the patient’s presentation if there is no history of previous signs or symptoms that
with symptoms caused by the suspected toxin and the suggest another cause.
likelihood of exposure. Suspected toxin
Accidental poisonings are the commonest cause of
medical emergencies in the paediatric patient population. Rescue personnel, family or friends should bring any
Childhood ingestions tend to be accidental and to involve container, plant product or suspected toxin with the
a single substance. Intentional poisonings occur more patient to the hospital, as long as the substance presents
no risk of contamination to the person retrieving it. A
often with adults, and are more likely to involve multiple
child’s play area should be inspected for possible sources
substances.135,137,139 Poisonings in the aged population
of toxins.133–137

TABLE 23.10
Time of poisoning
Acronyms outlining potential causes of altered levels History should include time of exposure, onset of
of consciousness133–136 symptoms and time since treatment began. Alcohol is
the commonest drug taken with other intentional self-
ACRONYM CAUSE ACRONYM CAUSE poisonings, and can potentiate a range of medication
T Trauma A Alcohol and effects and increase the incidence of vomiting and
other toxins potential aspiration.134,136 Poisonings in children tend to
I Infection E Endocrine
occur most often just prior to mealtimes, when they are
hungry. Adults may take substances late in the evening, fall
Encephalopathy asleep and be found several hours later.134
P Psychogenic Electrolyte A thorough assessment may provide clues about an
abnormality unconscious, uncooperative or suspicious presentation.
Porphyria Assess for respiratory effort, skin colour, pupil size and
I Insulin/diabetes
reactivity, reflexes and general status. Auscultation of the
lung fields, the apical pulse and presence of active bowel
S Seizure sounds provide a baseline for further assessment and clues
Syncope O Oxygen: about current problems. Check blood pressure as often
hypoxia of any as necessary to determine cardiovascular stability. Percuss
cause the thorax and abdomen to detect accumulations of fluid
Space- Opiates or air.134,136 Needle marks, pill fragments, uneaten leaves
occupying or berries or drug paraphernalia assist in a diagnosis.134,136
lesion The presence of pressure areas on the skin may indicate
U Uraemia how long the patient has been unresponsive. Any odours
are important to note. An oily-garlicky smell may be due
760 SECTION 3 SPECIALTY PRACTICE

to pesticides. Other odours may indicate chronic medical gastrointestinal absorption, increasing plasma levels.144 Also,
disorders (e.g. fruity odour with diabetic ketoacidosis) or consider the effects of substances on tissue. Corrosives, such
neglect of personal hygiene.142,143 as acids, alkalis and iron supplements, produce irritation
and tissue breakdown when in contact with the skin or
Practice tip mucous membranes. Recognition is important, as therapy
may cause further injury. Emesis could be contraindicated,
Odours are important to note, as they may reflect not and a lavage tube may further traumatise injured tissue.145
only poisoning but other medical disorders, for example Ipecac syrup and vomiting are generally ineffective against
a fruity odour may reflect diabetic ketoacidosis. a substance with an antiemetic property, such as phenothi-
azines.134,136 Waiting for emesis also causes further delay in
Toxicology screens include an analysis of serum definitive treatment. Other substances have natural emetic
and urine to determine the presence and amount of a qualities if taken in sufficient doses (e.g. hand soaps and
substance. Laboratory levels are helpful but must be liquid soap detergents).136
considered according to the nature of the substance and Evaluate other substances on an individual basis. Most
its rate of metabolism. Certain substances are sequestered petroleum distillates, such as furniture polish or cleaning
in fatty tissues or are bound to serum proteins, and may be fluids, present a greater hazard for chemical pneumonitis
present with a misleadingly low serum level.133,136 Serum than a systemic intoxication.133 Even very small amounts
electrolytes, non-electrolytes, osmolality, arterial blood can quickly disperse over the lung surface if accidentally
gases and urine electrolytes are used to determine the introduced into the trachea. Avoid emesis or lavage when
patient’s overall status or response to therapy. Continuous the chance of aspiration is high.133 There are situations,
cardiac monitoring supplemented with a 12-lead ECG however, when the amount, character or additional
or invasive monitoring devices may be required to help chemicals present make it necessary to remove the ingested
provide symptomatic care.134,136 substance from the stomach. Occasionally, therapy is based
Initial and ongoing care of the victim follows three on the reported amount taken or time since ingestion.
principles:134,136 Time since ingestion is important in order to rule out
1 preventing further absorption of the toxin the benefit of therapy. The stomach tends to empty its
2 enhancing elimination of absorbed toxin from the contents after 1 hour, unless a substance that slows gastric
body motility has been ingested. For example, narcotics can
slow peristalsis and may be found in the stomach several
3 preventing complications by providing symptomatic
hours after ingestion.134,136 A patient may also underreport
or specific treatments, including psychiatric
the dosage to avoid an obviously unpleasant experience.
management.
Although conservative management with observation is
Management: Preventing toxin appropriate in certain situations, the risk of not treating
might be greater in others.134,136,146 If a large number of
absorption tablets or pills are consumed at one time, they may clump
Ingested poisons are best removed while still in the upper together in the stomach and form a mass that is too large
gastrointestinal tract when possible. Emesis and gastric to pass out of the pylorus (e.g. aspirin).146
lavage were utilised in the past to empty the stomach, Once a substance enters the lower gastrointestinal
although a significant body of evidence now suggests that tract, it can be absorbed into the mesenteric circulation.
these are relatively ineffective and effectiveness decreases As absorption can vary according to substance, slow-
rapidly after 1 hour.134,136 Both the patient and substance release characteristics, rate of peristalsis and the presence
should be evaluated for appropriateness of gastric of other substances, it is possible for a poison to be present
emptying.134,136 in the bowel for an extended period of time. If intestinal
The patient’s consciousness level, gag reflex and ability motility can be stimulated or the toxin permanently bound
to vomit while protecting the airway from aspiration until excretion, then further absorption is reduced.134,136
should be considered. Any central nervous system depres- Activated charcoal is a refined product with an enormous
sants are capable of obtunding the protective gag or surface area that binds to a large range of substances to
cough reflex. If the ingested substance has a rapid onset enhance elimination, and is the most effective decontami-
of action, such as with benzodiazepines, it is safer to avoid nating agent currently available.134,136
emetics because of the risk of a sudden fall in the level of A solution of either water or sorbitol is mixed with
consciousness.134,136 approximately 15–30 g of activated charcoal to form a
thick, liquid slurry that can be given to a compliant patient
Ingested poisons orally or through a nasogastric tube. It may be mixed with
Evaluate the substance ingested to determine whether a cathartic, which reduces the time the substance or the
gastric emptying is appropriate. The physical properties of charcoal is in contact with the bowel wall, although there
a drug may make it more responsive to a particular type of is no evidence that this improves clinical outcome.134,136
gastric emptying. For example, the antimuscarinic effect However, there is no clinical evidence that adding cathartic
of tricyclic antidepressants on gut motility can prolong agents such as sorbitol improves the clinical outcome.134
 CHAPTER 23 EMERGENCY PRESENTATIONS 761

It has been suggested that effectiveness can be improved Management: Enhancing elimination
through repeated administration of activated charcoal, by
ensuring that the entire drug is absorbed, as well as by inter- of the toxin from blood
rupting the reabsorption of any drug in the enterohepatic After a substance has entered the bloodstream, it is
circulation.134 Cathartic agents such a sorbitol and poly- normally excreted from the body either in an unchanged
ethylene glycol reduce gastric transit time, reducing the time form or after liver metabolism and detoxification. Various
a drug spends in the gastrointestinal tract, in theory limiting metabolic byproducts are eliminated in the bile and faeces
the time available for drug absorption; however, this has not or urine. Urinary excretion of substances can be enhanced
been demonstrated to significantly improve outcomes.134,136 by increasing the filtration process by forcing diuresis and
Unfortunately, not all poisons ingested can be bound by the administration of large volumes of IV solutions and/or
charcoal, such as alcohol and heavy metals.134,136 diuretics. Enhanced secretion can also occur by inhibiting
absorption in the renal tubules or by stimulating the
Inhaled poisons secretion of substances into the urine.134,136,146
A patient poisoned by inhalation of toxic gases or powders Alkalinisation of urine
should be removed from the source as soon as it is safe to Manipulation of the absorption or secretion process of a
do so. Attempts to remove the substance, which is usually a drug can be assisted by chemically altering the structure
vapour, gas or fine particulate matter, from the lung are not of some substances. All substances break down into ions at
normally useful.134,136 The history of a patient suspected of a specific pH for that substance. Altering the pH of urine
an inhaled poison should include time of exposure, the with acidifying or alkalising drugs allows the poison to be
duration of exposure, the onset of symptoms, suspected forced into an ionic state and then excreted in the urine.
inhalant and time since treatment began. This ion trapping process is effective only for substances
Staff involved in direct care of the patient should take that are primarily eliminated by the kidneys,134,136 for
precautions to avoid unprotected contact to reduce the example salicylates and tricyclic antidepressants.134
risk of self-contamination with unknown substances. For
many inhaled poisons clothing may contain significant Haemodialysis or haemoperfusion
amounts of the poison and serve as a continuous source If a dangerous amount of a poison is present or if renal
of the toxin. Contaminated linen and clothes should be failure is evident, haemodialysis or haemoperfusion may be
removed carefully, sealed in a bag and destroyed.134,136 used to enhance excretion. Dialysis is effective in removing
substances that are reversibly bound to serum proteins,
Contact poisons or not stored in body fat, only. This is a highly invasive
Contact poisons are dangerous because of their ability to approach and is normally reserved for life-threatening cases
enter the body via the skin or mucous membranes. All (see Chapter 18 for further discussion).133,136
clothing and all of the toxic substance should be carefully
removed, preferably with an irrigating and neutralising Management: Preventing complications
solution. Precautions to avoid direct skin contact and and specific symptomatic care
reduce the risk of self-contamination should be used. Supportive care is the key element in managing an acutely
Clothing may contain significant residual amounts of poisoned patient. Once a patient has either ingested or
the poison and serve as a continuous source of the toxin. been exposed to many poisons, there are limited options
Contaminated linen and clothes should be sealed in a bag other than to treat the symptoms as they appear or become
and destroyed.134,136 clinically significant (see Table 23.11).

TABLE 23.11
Summary of the management of poisoning victims133–136

AIM ACTION
Prevent absorption • Ingested toxins: activated charcoal is the most effective method of reducing adsorption
of toxin • Inhaled toxins: remove victim from source of contamination and administer oxygen or provide fresh air
• Contact toxins: remove any substances from the body surface, preferably with copious amounts of
irrigating fluid. Remove clothing and place in a sealed bag to reduce vapour hazards. Use special
caution with corrosive materials and pesticides
Enhance elimination Ingested or injected toxins: administer an antidote or antagonist if available (e.g. naloxone for opiates;
of the toxin from the flumazenil for benzodiazepines). Employ forced diuresis, for acidification or alkalinisation of the urine;
blood and haemodialysis
Prevent complications Carefully monitor all vital systems. Continually reassess patient for changes or response to therapy.
by providing Administer antidotes as prescribed. Provide symptomatic care as needed for: cardiac arrhythmias, CNS
symptomatic or depression or stimulation, fluid and electrolyte imbalances, acid–base disturbances, renal function,
specific treatment effects of immobility
762 SECTION 3 SPECIALTY PRACTICE

nervous system (CNS). The clinical findings associated

TABLE 23.12 with CNS alteration can vary a great deal from drug
Common emergency antidotes133–136 class to class or within the same drug family, as physical
effects are dependent on the chemical structure of
POISONING ANTIDOTE
the drug, the dose, the route of exposure, any other
Benzodiazepines Flumazenil co-ingested drugs and the rate of drug metabolism. In
Opioids Naloxone addition, the chemical structure and/or purity of illicit
Paracetamol N-Acetylcysteine drugs may be affected by variations or deliberate aber-
rations in the manufacturing process.147–149 Drugs in
Organophosphates Atropine and pralidoxime
this section include sedatives, hypnotics, tranquillisers
Tricyclic antidepressants Sodium bicarbonate and narcotics.
Carbon monoxide Oxygen
Assessment
Insulin Dextrose
The predominant observed effect is an altered level of
CNS function.147–149 A spectrum of physical findings is
Antidotes act to antagonise, compete with or override possible with the selective action of the specific drug on
the effects of the poison, although few specific antidotes inhibitory or excitatory centres of the brain: effects can
exist for toxins (see Table 23.12). In some cases, an vary from mild euphoria to convulsions, or mild sedation
absorbed toxin can be rendered benign by the use of to coma, dependence, addiction and tolerance. Narcotics
an antidote (e.g. the interaction between naloxone and constrict the pupil, and some patients experience nausea
opiates). For chelating agents, such as desferrioxamine for and vomiting due to a stimulation of the chemoreceptor
iron poisoning, a non-toxic compound is formed that is trigger zone in the medulla.142,147–149
then safely eliminated from the body.133–136 The effect of A narcotic overdose is distinctive, with a set of readily
an antidote may be only temporary if the antidote has identifiable features. These features include a decreased
a shorter half-life than the poison. Most antidotes are respiratory rate and tidal volume, constriction of the pupil,
given either in a specific dose or at a response to dose hypotension and an altered level of consciousness.147–149
rate.133−136 For many poisonings, symptomatic care involves Other factors may, however, affect these findings as
support and protection of vital organ systems. Routine outlined in Box 23.3.
and frequent physical assessment of respiratory, cardiovas- Patients with an altered level of consciousness are
cular and renal function enables identification of potential subject to injury from decreased sensory ability or
problems. If large volumes of fluids or drugs that alter prolonged immobilisation. Reddened areas over bony
serum pH are administered, the patient’s electrolyte and prominences or pressure points appear within a short
acid–base balance are also monitored.
A poisoning may be the physical manifestation of
an emergency or crisis that requires emotional support. BOX 23.3
A patient may have underlying emotional conflict/s Factors confounding diagnosis of narcotic
or mental health problems, regardless of whether the overdose142,147–149
poisoning was intentional or accidental. Psychological
• A decreased respiratory effort may produce
care is, therefore, an important component for all patients
hypercarbia, which in turn may cause pupil dilation.
presenting with poisoning.133–136 Many facilities offer the
services of a mental health worker while the patient is • Chronic narcotic users tend to have multiple
still in the ED. If the patient’s condition is stable and the problems associated with their drug use or lifestyle,
poisoning has not altered their mental state, early inter- which may modify findings.
vention is appropriate. • CNS depressants in sufficiently high dose cause
For adult patients, the desire for treatment is not as depression of vital regulatory centres in the brain.
important as the manner in which treatment is received. • Altered respirations cause hypoventilation, stasis
Even though patients may initially refuse care, if approached of secretions and atelectasis. The resultant hypoxia
in a non-threatening way and given some form of control, serves to further aggravate the sensorium and
they will usually comply. If threatened with force or cerebral functioning.149
restraints, they are placed in the position of either submitting
• Narcotics may produce idiopathic pulmonary
to coercion or resisting therapy in order to ‘protect’
oedema.142,147–149
themselves. A paediatric patient may be too young either to
fully understand or to effectively cooperate with staff. • CNS depressants often possess the ability to cause
peripheral vasodilation, with a resultant hypotension
Central nervous system depressants and tachycardia.
A large number of common medications are capable of • Arrhythmias may occur because of cardiac
depressing levels of consciousness, thought processes or conduction effects or tissue hypoxia.142,147–149
important regulatory centres located within the central
 CHAPTER 23 EMERGENCY PRESENTATIONS 763

time. Skin blisters indicate altered blood flow, usually due Central nervous system stimulants
to excessive pressure. Actual skin breakdown can occur
CNS stimulants increase the activity of the reticular
within 3 hours. If external pressure or altered circulation
activating system, promoting a state of alertness and
to an extremity is allowed to continue for over 4 hours,
affecting the medullary control centres for respiratory and
compartment syndrome may develop.147–149
cardiovascular function. Many illegal stimulants are poorly
Effects of multiple drug use manufactured, with no guarantee of purity or consis-
tency in dosage. The possibility of overdose is therefore
A patient who ingests a combination of drugs may
always present, producing profound CNS excitation.147–149
experience toxicity because of additive or synergistic
Commonly used stimulants include amphetamines,
effects.147–149 Illicitly produced drugs will most likely have
dextroamphetamine, methylphenidate, lysergic acid diet-
had substances added (e.g. glucose powders, icing sugar,
hylamide (LSD), phencyclidine (PCP), caffeine, cocaine
talcum powder) to dilute or ‘cut’ them, to increase the
and methamphetamines147,150 (see Table 23.13).
volume of their supply and thus profit to the supplier.147–149
Users may also intentionally inject other drugs (e.g. anti- Assessment
histamines, amphetamines, benzodiazepines) to modify or Both psychological and physical symptoms are produced.
potentiate the effects of narcotics.147–149 A patient may demonstrate repetitive, non-purposeful
movements, grind their teeth and appear suspicious of or
Potential for acute or active infections paranoid about others. Physiological stimulation causes an
The use of non-sterile solutions and equipment and the increase in metabolism, with flushing, diaphoresis, hyper-
sharing of injection equipment significantly increase pyrexia, pupillary dilation and vomiting evident. Dizziness,
the likelihood of acute or active infections. Frequent loss of coordination, chest pains, palpitations or abdominal
exposure and a depressed immune response also predispose cramps may also occur. During the acute phase of poisoning,
a patient to severe infections, such as hepatitis, osteomy- severe intoxication and loss of rational mental functioning
elitis, infective bacterial endocarditis and encephalitis/ may lead individuals to behave irrationally and even attempt
meningitis.147–149 suicide. Anxiousness and a general state of tension may also
Management lead the affected person to attempt to harm others.147,150
Death is possible from cardiovascular collapse or as a sequela
General principles for the management of a patient with to convulsions and acute drug toxicity.147,150
ingestion of a toxic substance with a reduced level of
consciousness apply. Prevent continued absorption by Management
administering activated charcoal for oral ingestions, and If a patient has ingested the drug, emesis or lavage is of
provide symptomatic care (see Table 23.13).147–149 little value, and an individual risk–benefit assessment is

TABLE 23.13
Assessment and management of specific drug overdoses147–149,153–155

TYPE OF POISONING GENERAL MANAGEMENT ANTIDOTE C L I N I C A L C O N S I D E R AT I O N S

CNS depressants Supportive care of airway, Naloxone Action of naloxone may be much shorter
(morphine, heroin, breathing, circulation hydrochloride (Narcan); than the duration of effect of the drug; the
methadone, oxycodone) specific reversal agent patient may need to be observed for return of
unconsciousness
CNS stimulants Supportive care of airway, Benzodiazepines may Reduce stimulation in the surrounding
breathing, circulation be used to reduce environment; monitor cardiovascular status
symptoms and temperature
Salicylate Observe for hyperventilation Nil; charcoal may be Monitor electrolyte changes and increases in
and acid–base disturbances used fever
Paracetamol Careful history required N-Acetylcysteine Antidote must be given within the specified
to determine time and time range; consider the effects of other drugs
amount taken; initially vague (i.e. paracetamol and codeine combinations);
symptoms monitor for signs of hepatotoxicity
Carbon monoxide Supportive care of airway, High concentrations of Hyperbaric oxygen may be required; monitor
breathing, circulation oxygen therapy carboxyhaemoglobin; oxygen saturation
monitors will give erroneously high readings
Organophosphates Decontamination; supportive Pralidoxime chloride; Maintain careful decontamination and
care of airway, breathing, benzodiazepines personal safety considerations
circulation
764 SECTION 3 SPECIALTY PRACTICE

required. Gastric emptying may precipitate more severe of events or other people. The patient’s physical and
agitation with a concomitant rise in blood pressure, mental responses may be dulled and slow, or abusive and
pulse rate and metabolism.147,150 Activated charcoal and delusional. Intoxication is marked by paranoid thoughts,
cathartics may be administered to promote elimination. with the patient responding to therapeutic or friendly
Ongoing emergency management includes: gestures with behaviours ranging from apprehension to
• support of vital functions147,150 aggressive hostility. To avoid stimulating the patient and
thereby intensifying the behaviour, a quiet environment
• reduction of external stimulation by placing the should be provided for initial assessment and treatment,
patient in a quiet, non-threatening environment
where a supportive person can attempt to calm and although this is often difficult in the ED.147,150
‘talk the person down’ while observing for untoward
reactions Practice tip

• sedating when necessary, although it is not desirable Noxious environmental stimulation such as bright
to give more medications in a precarious situation; lighting, loud noises and activity can provoke these
sedation may be needed to control seizures or keep patients to become anxious and uncooperative.
the patient from self-harm.147,150

Practice tip
Management
Gastric emptying is normally ineffective due to delays
Note that there are no specific antidotes for CNS in seeking treatment. If a patient presents early, activated
stimulants. charcoal and cathartics are useful in preventing further
absorption. Noises, sights and sounds provoke paranoid
Amphetamines and designer drugs ideation and may present a risk to staff and other patients.
‘Talking down’ is usually not successful and probably
Amphetamines and designer drugs have been drugs of only serves to exacerbate the situation. If the patient is
abuse for a number of years. Originally, many of them demonstrating hostile or self-abusive forms of behaviour,
were designed and introduced as anaesthetic agents, restraints may be needed to protect him/her and any
decongestants or for other legitimate purposes. Amphet- others present.The use of physical restraints is not without
amines are chemically related to the anaesthetic ketamine,
danger, and they should never be used as a substitute for
with a similar CNS response.147,150 Most drugs in this
a more desirable environment. If the threat of danger
group were discontinued or controlled because of the
or psychosis is significant, sedatives such as diazepam or
delirium and agitation experienced by the patients who
haloperidol may be necessary to control the patient’s
had received them; paradoxically, these effects led to their
behaviour. IV diazepam is also used to control frequent
popularity as recreational drugs.147,150 Amphetamines are
synthetic sympathomimetic drugs; they are available in seizure activity.147,150
oral, intranasal or IV forms; crystalline rock forms such Salicylate poisoning
as ‘ice’ are smoked. Death may occur from overdose, self-
Aspirin is the commonest form of salicylate in the home
mutilation or dangerous activities such as diving or
and is found in many over-the-counter medications,
walking on roads.147,150,151
such as combination analgesic and topical ointments.152
Assessment Aspirin may be ingested orally, absorbed through the
Depending on the dose, route and time since exposure, rectal mucosa, or applied to the skin in topical prepara-
a person exhibits characteristic behavioural and physical tions. Under normal circumstances, the kidneys serve as
changes. With high-dose intoxication, the patient has the principal organ of excretion. At one time, aspirin was
pronounced CNS involvement – altered levels of cons- the commonest form of poisoning in children.140,152,153 In
ciousness, seizure activity or a loss of protective gag, response to the problem, legislation has been implemented
corneal and swallow reflexes. Nystagmus is a classic sign, to limit the number of tablets per pack and to introduce
along with hypertension and an elevated body tempera- packaging with childproof caps. In Australia salicylate
ture. A significant rise in arterial pressure presents a risk poisoning is now relatively uncommon, accounting for
for intracerebral haemorrhage. One of the distinguishing about 0.3% of calls to poison information centres.154 The
features of amphetamines is their ability to produce coma three common types of aspirin overdose are: accidental
without affecting respirations.147,150 The patient may risk ingestion (more common in young children); intentional
dehydration and renal failure if muscle breakdown has ingestion (more common in adults); and chronic toxicity
occurred. A high urine output should be maintained and (occurs in any age group).146,154
serum urea and creatinine levels monitored to detect a
decrease in renal function.147,150
Assessment, monitoring and
Lower dose intoxications do not produce uncon- diagnostics
sciousness but typically cause behavioural patterns that Intentional or accidental ingestion is straightforward, with
reflect depersonalisation and distorted perceptions a clear history of poisoning. Chronic toxicity is, however,
 CHAPTER 23 EMERGENCY PRESENTATIONS 765

often unrecognised. Many individuals are not aware of by carefully monitoring fluid output and providing
correct dosages, may combine multiple drugs, each of adequate fluid replacement and monitoring serum elec-
which contains aspirin, or may have impaired excretion trolytes for imbalance and replacing as needed. Evaluate
due to dehydration. The symptoms of chronic aspirin arterial blood gases to determine whether the patient
overdose include dehydration, lethargy and fever and continues to have an effect from aspirin toxicity or
resemble the original problem being treated, and some is not responding to therapy. Temperature elevations
people will continue treating themselves with aspirin for should be controlled with external cooling methods if
these symptoms. Chronic toxicity has a higher mortality fever develops.
than acute ingestion.146,154
Toxicity may result if aspirin is ingested in amounts Paracetamol poisoning
greater than 150 mg/kg. Aspirin toxicity can result in The incidence of paracetamol, also known as acetamino-
tachypnoea, fever, tinnitus, disorientation, coma and phen, toxicity is associated with approximately half of all
convulsions.146,154 Acid–base disturbances arise from a Australasian toxic ingestions, due in part to its common
direct stimulatory effect on the respiratory centre in the availability as an analgesic/antipyretic agent.140,152 The drug
CNS. An increased rate and depth of respirations causes is absorbed in the stomach and small bowel, with 98%
hypocarbia and respiratory alkalosis, with renal compensa- metabolised by the liver using one of two mechanisms:
tion by bicarbonate elimination. However, salicylates also most is via a pathway that breaks down into non-toxic
alter metabolic processes, resulting in metabolic acidosis. byproducts; the second hepatic pathway usually metab-
Blood gases can therefore reflect acidosis, alkalosis or a olises about 4% of the drug, but the process has a toxic
combination of the two. Tinnitus is a symptom of the byproduct. The liver is capable of detoxifying the toxic
effect of aspirin on the 8th cranial nerve.146,154 byproduct by combining it with a naturally occurring
Aspirin interferes with cellular glucose uptake, causing substance, glutathione. In an overdose or when the minor
initial hyperglycaemia. Cellular levels of glucose become pathway has already been stimulated (e.g. concomitant
depleted and the patient then demonstrates hypoglycae- barbiturate use), more paracetamol is metabolised by the
mic effects, particularly those related to the central nervous secondary pathway and the toxic byproduct accumulates,
system. Later, serum levels may be either normal or hypo- quickly consuming the available glutathione, resulting in
glycaemic.146,154 Patients may be nauseated and vomit after liver tissue destruction.140,152,155
ingestion, causing fluid and electrolyte imbalance.146,154
Aspirin use is also associated with local tissue irritation
Assessment, monitoring and
and gastrointestinal bleeding. Normal platelet function is diagnostics
altered by aspirin, with an increased tendency for bleeding. The amount of paracetamol ingested is best determined
Concomitant use of anticoagulants increases the risk of from the patient history, as serum levels, although helpful,
haemorrhage.146,154 can be easily distorted. A nomogram is used to plot
measured levels against time post-ingestion as a relative
Management indicator of toxicity. A relatively small dose of 200 mg/kg
Absorption can be reduced with activated charcoal. Repeat paracetamol is considered to be toxic, although hepato-
doses should be given for patients with signs of ongoing toxicity occurs after an ingestion of 140 mg/kg or 10 g in
absorption.146,153,154 Urine alkalisation and forced diuresis a single dose.152,155–157
can significantly increase elimination, as salicylates are Liver function studies are helpful to recognise the
weak acids excreted by the kidneys.146,153,154 Haemodialysis development of hepatic dysfunction or damage. These
is reserved for extreme cases with profound acidosis, high include liver enzymes, serum bilirubin, protein, prothrom-
blood levels, persistent CNS symptoms or renal failure.146,154 bin time, partial thromboplastin time and platelets.140,152,155
As salicylates have no known specific antidote,146,153,154 Three phases of toxic damage resulting from excess
supportive therapy includes prevention of dehydration paracetamol are presented in Table 23.14.140,152,155–157

TABLE 23.14
Phases of toxic damage resulting from an excess of paracetamol140,152,155–157

PHASE TIMEFRAME SYMPTOMS

Phase 1 First 24 hours Vague symptoms of nausea, vomiting and malaise
Phase 2 24–48 hours Vague symptoms subside; onset of right upper quadrant pain due to hepatic injury; urine output
may decrease as paracetamol potentiates the effect of antidiuretic hormone; liver enzymes,
bilirubin, proteins and clotting studies may be abnormal
Phase 3 60–72 hours Liver impairment becomes more obvious, with jaundice, coagulation defects, hypoglycaemia and
hepatic encephalopathy; renal failure or cardiomyopathy may also occur;
death from hepatic failure occurs in approximately 10% of severe overdose
766 SECTION 3 SPECIALTY PRACTICE

Management Mild-to-moderate poisoning can be managed without the

Absorption can be reduced with activated charcoal when use of hyperbaric oxygen, as hyperbaric oxygenation is not
the patient presents to hospital early; however, following available at every facility. Treatment depends on carboxy-
periods of 2 hours or greater since ingestion activated haemoglobin serum levels, time since exposure, transport
charcoal is unlikely to be very effective. Haemodialysis time to the hyperbaric chamber and the clinical symptoms
with a charcoal dialysate has been used in an attempt to of the patient.156,158,159 Patients should be monitored for
remove unchanged paracetamol from the liver, but this adverse effects of hypoxia, as they may have convulsions,
does not remove the toxic byproduct. Forced diuresis is cardiac arrhythmias and acid–base disturbances.
also not effective, because little paracetamol (about 2%) Corrosive acids
is removed by the kidneys.140,152,155
The specific therapy for paracetamol poisoning is A number of substances are discussed here due to their
administration of the antidote, N-acetylcysteine, which similar ability to cause local tissue injury. Some common
is structurally similar to glutathione and binds to the acids involved in toxic emergencies are acetic acid (vinegar),
toxic byproduct. When given within 24 hours of an acute carbolic acid (phenol disinfectants), chlorine (swimming
ingestion, N-acetylcysteine is effective in preventing pools, sanitising agents), hydrochloric acid (pools, cleaning
hepatic damage. 140,152,155 agents), hydrofluoric oxalic (laundry agents), sodium
bisulfate (toilet cleaning agents that become acidic when
Carbon monoxide poisoning added to water) and sulfuric acid (car battery acid).
Carbon monoxide is a gaseous byproduct of incomplete Ingested corrosives can produce immediate or late
fuel combustion, and is present where there is a flame in a life-threatening complications. In general, acids dissolve
confined space with improper ventilation or air exchange. tissue and destroy haemoglobin.160 Swallowing a strong
Levels of carbon monoxide can accumulate rapidly, and the acid can produce ulceration and perforation of oral and
gas is dangerous as it is colourless, odourless, tasteless and oesophageal mucosa, presenting a danger for haemorrhage
non-irritating156,158,159 Common sources of carbon monoxide and mediastinitis, and cardiac arrest as a result.160,161 The
are faulty radiant heaters, kerosene lamps, cooking stoves, late sequelae of swallowing a corrosive substance involve
engine exhausts and fireplaces. Acute carbon monoxide mucosal scarring with constriction and mechanical
poisoning is the commonest form of successful poisoning in obstruction of the oesophagus.
three of the world’s most developed countries.156,158,159
Assessment
Assessment, monitoring and diagnostics Physical findings are site-specific and relate to the type
Haemoglobin has a 210–240-fold greater affinity for of exposure – ingestion, inhalation or contact (see
carbon monoxide than for oxygen, and shifts the oxygen– Table 23.15). Ingested acids present as burns to the mouth
haemoglobin curve to the left (see Chapter 13). As carbon and pharynx. Patients able to vocalise complain of pain,
monoxide displaces oxygen from red blood cells, the gastric irritation with vomiting and haematemesis. Fumes
patient experiences hypoxaemia and hypoxia.156,158,159
Headache, nausea and vague pains are often experienced
TABLE 23.15
at onset of poisoning, and the patient may feel increas-
Summary of assessment and management of acid
ingly tired and sleepy, have difficulty concentrating and and alkali exposure160–162
fail to recognise the onset of poisoning.With higher levels
of inhalation, the patient may be tachypnoeic, tachycardic CORROSIVE ACIDS OR
and experience loss of consciousness. A characteristic red CORROSIVE ALKALIS
colour presents in the lips with skin flushing.156,158,159 The Assessment • Burns to skin, mouth, pharynx or
most important factors in determining carbon monoxide oesophagus
poisoning are a history of exposure with an elevated blood • Gastric irritation with nausea and vomiting
carboxyhaemoglobin level.156,158,159 Management • Airway
• Breathing
Management • Circulation
As CO is an inhaled toxin, the patient should be removed • Decontamination
from the contaminated environment to prevent further Prevent • Do not induce vomiting
absorption and allowed to breathe fresh air until 100% absorption • Remove contaminated clothing
oxygen can be administered, although this may be inef- • Flush the skin with copious amounts of
fective because of the bond between carbon monoxide water
and haemoglobin. High flow high concentration oxygen Enhance • Administer chelating agents if they
administration will, however, substantially reduce the elimination exist, such as calcium gluconate for
half-life of carbon monoxide.159 Hyperbaric oxygenation is hydrofluoric acid
used to treat severe cases of carbon monoxide poisoning, as Symptomatic • Protect burnt skin with sterile dressings
pressurised oxygen reduces the half-life of the carboxyhae- management • Monitor respiratory status
moglobin molecule and shortens the duration of its effects.
 CHAPTER 23 EMERGENCY PRESENTATIONS 767

from an ingested substance may cause pneumonitis. contain sodium carbonate; and laundry bleaches that
Contact with skin or eyes is similar to other types of burns, contain sodium hypochlorite.160
with a sharply defined blister or wound, inflammation, pain
and ulceration. Hypotension and cardiovascular collapse Assessment
are also possible when damage occurs to underlying vital The immediate response to ingestion is increased secretions,
structures.160,162 pain, vomiting or haemoptysis. Signs of perforation include
Inhalation irritates respiratory tissues, producing direct fever, respiratory difficulty or peritonitis. Approximately
damage, oedema and alterations in ventilation. Patients 98% of patients develop strictures.145,160,161 Alkalis and skin
may initially experience coughing, choking, gasping for contact produce a soap-like substance because of the inter-
air and increased respiratory secretions. Clinicians should action with tissue fats, giving a slimy, soapy feeling.145,160,161
assess and monitor any obvious tissue injury, impaired
respiratory function and subsequent effects of hypoxia and Management
pulmonary oedema, which may occur up to 6–8 hours Induced vomiting or gastric lavage should not be
later.145,160,162 Arterial blood gases, ventilation studies, serial attempted for ingested alkalis, as these will be neutralised
chest X-rays and frequent physical assessments are used to by stomach acid. Lavage tubes may cause further tissue
monitor for changes. damage.145,160,161 External contact with alkalis necessi-
tates copious irrigation of the point of contact. Continue
Management irrigation for at least 15 minutes; in the case of the eye,
Contaminated clothing should be removed to prevent irrigation may be necessary for up to 30 minutes. Cover
recontamination. Patients with external contamination all wounds after irrigation with sterile dressings to reduce
should be washed thoroughly to remove any remaining the risk of infection.
surface material that may come into contact with treating A patient should be nil by mouth until an inspection
staff. For acid contact with skin or eyes, begin immediate of the mouth and throat is conducted to determine the
flushing with a non-reactive liquid and continue to do amount and extent of burns. An oesophagoscopy will
so for at least 15 minutes to guarantee complete removal. identify the degree of injury and enable direct irrigation
In most cases water will be the safest and best available of any affected areas of mucosa.145 Alkalis that contain
liquid. Provide skin or eye protection with a sterile phosphates may produce a systemic hypocalcaemia, and IV
dressing.145 calcium gluconate may be required. Continue to monitor
For ingested acids, emesis or lavage should not be for systemic effects of perforation or tissue injury.145
attempted, as the substance will cause additional damage
when ejected from the stomach. A gastric tube may also Petroleum distillates
cause structural damage by penetrating or irritating friable Petroleum distillates are common substances, and account
tissues.145,160 Do not attempt to neutralise the acid, as this for 7% of all poisonings.163 Typical petroleum products
may result in a chemical reaction and generate heat as a are benzene, fuel oils, petrol, kerosene, lacquer diluents,
byproduct, with potential further burning and damage to lubricating oil, mineral oil, naphthalene, paint thinners and
the patient.145,160 Suctioning of oral secretions should be petroleum spirits. Toxicity depends on: route of exposure
done carefully and with as much visualisation of tissues as (ingestion or aspiration); volatility (ease with which the
possible. A patient may be given water or milk to irrigate substance evaporates); viscosity (density or thickness);
the upper gastrointestinal tract, although extreme care is amount ingested; and presence of other toxins.163
required to ensure that the airway is adequately protected Products with a low viscosity are more likely to be
because there is a risk of aspiration.160 aspirated and can quickly spread over the lung surface.
Substances with low viscosity and high volatility, for
Corrosive alkalis example benzene, kerosene, and turpentine, are toxic
Alkalis produce tissue destruction on contact by interact- in doses as low as 1 mL/kg, with death from doses of
ing with tissue component fats and proteins and producing 10–250 mL. Mortality is increased if an additional toxic
necrotic tissue. Erosion of the oesophagus and stomach substance is present, or if accidental aspiration occurs.163
occurs if ingested orally, and peritonitis or mediastinitis
may develop as sequelae. Late effects are similar to those Assessment
produced by acids. Oesophageal strictures due to scarring Aspiration causes pneumonitis with low-grade fever,
are common post-ingestion. About 25% of patients who tachypnoea, coughing, choking, gagging and pulmonary
ingest a strong alkali will die from the initial insult.160 oedema as a late effect.163,164 As petroleum distillates are
Skin contact and ingestion are the commonest types fat solvents and rapidly cross the lipid-rich cell membrane,
of injury from an alkali; however, ingestion is the most nerve tissue is especially sensitive to injury. A patient may
immediately life-threatening form of contact. Alkalis exhibit local effects, such as depressed nerve conduction,
involved in toxic emergencies include many substances or varied central effects, such as feelings of wellbeing,
found around the house, such as detergents and cleaning headache, tinnitus, dizziness, visual disturbances, through
agents that contain ammonia; cement and builder’s lime; to respiratory depression, altered levels of consciousness,
low-phosphate detergents; dishwasher detergents that convulsions and coma.164
768 SECTION 3 SPECIALTY PRACTICE

Management Assessment, monitoring and

In the awake and alert patient, the decision to treat is based diagnostics
on the physical properties of the substance, the likelihood The clinical findings of organophosphate poisoning can
of aspiration or other complications and the amount be divided into three broad categories: muscarinic effects,
consumed.163,164 When preventing absorption, careful con- nicotinic effects and effects on the central nervous system.
sideration needs to be given to gastric emptying, as neither Common muscarinic manifestations are summarised
induced vomiting nor gastric lavage is recommended. by the mnemonic SLUDGE: Salivation, Lacrimation,
The patient’s respiratory status should be immediately Urination, Defecation, GI upset, Emesis.133,143,165 Other
assessed for possible aspiration. A patient that is coughing, symptoms include bradycardia, hypotension, broncho-
has cyanosis or appears hypoxic may have aspirated or spasm, cough, abdominal pain, blurred vision, miosis and
developed chemical pneumonitis.145 If the patient is sweating. Nicotinic effects include muscle fasciculations,
lethargic or unconscious, an endotracheal tube must be cramping, weakness and diaphragmatic failure. Autonomic
placed for adequate airway protection,145,163,164 although effects include hypertension, tachycardia, pupillary dilation
this heightens the risk of aspiration as hydrocarbons and pallor.
adhere to the tube and increase the risk of chemical pneu- CNS effects include anxiety, restlessness, confusion,
monitis.145,163,164 ataxia, seizures, insomnia, dysarthria, tremors, coma and
paralysis. The three types of paralysis that may result
Organophosphates from organophosphate poisoning are described in
Organophosphates are a large and diverse group of Table 23.16.133,143,165,166
chemicals used in domestic, industrial and agricultural Laboratory diagnosis is based on the measurement of
settings (e.g. insecticides, herbicides).133,143 The primary cholinesterase activity using either erythrocyte or plasma
effect of organophosphates is binding and inactivation of levels; erythrocyte cholinesterase is more accurate, but
acetylcholinesterase, a neurotransmitter that metabolises plasma cholinesterase is easier to test and is more widely
acetylcholine.133,143 available. Erythrocyte acetylcholinesterase is found in
Organophosphates can be absorbed through the skin, the grey matter of the central nervous system, red blood
cells, peripheral nerve and muscle. Plasma cholinester-
ingested or inhaled. Although most patients become
ase circulates in plasma and is found in white matter of
symptomatic soon after ingestional exposure, the onset
the central nervous system, pancreas and heart.133,143,165,166
and duration of action depend on the nature and type of
Mild poisoning is when the cholinesterase activity
compound, the degree and route of exposure, the mode is reduced to 20–50% of normal; moderate poisoning
of action of the compound, its lipid solubility and rate of occurs when activity is 10–20% of normal; and severe
metabolic degradation.133,143,165 poisoning occurs at less than 10% of normal cholines-
Mortality rates range from 3% to 25%, with organo- terase enzyme activity. Levels do not, however, always
phosphate poisonings the commonest mode of suicide correlate with clinical illness.143
in some developing countries, including Sri Lanka and
Fiji.166 In one Australian study, 36% of patients had Management
suicidal intentions, compared with 65–75% in developing Initial priorities in managing organophosphate poisoning
countries.166 Men aged 30–50 years were more likely to are airway, breathing and circulation, incorporating D for
attempt suicide with organophosphates. Common compli- danger, as organophosphates also present considerable risk
cations include respiratory distress, seizures and aspiration to staff caring for the patient, especially during the initial
pneumonia, with respiratory failure the commonest cause phases of management. All of the patient’s clothing should
of death.166 be removed and considered as hazardous waste.The patient’s

TABLE 23.16
Types of paralysis that may result from organophosphate poisoning133,143,165,166

TYPE ONSET P R E S E N TAT I O N DUR ATION OF SY MP TOMS

Type 1 Occurs shortly after exposure Acute paralysis secondary to persistent

depolarisation at the neuromuscular junction
Type 2 24–96 hours after resolution of acute Paralysis and respiratory distress Up to 3 weeks
cholinergic poisoning Proximal muscle groups are involved, with
relative sparing of distal muscle groups
Type 3 2–3 weeks after exposure to large Distal muscle weakness with relative sparing Up to 12 months
doses of certain organophosphates of the neck muscles, cranial nerves and
proximal muscle groups
 CHAPTER 23 EMERGENCY PRESENTATIONS 769

decontamination with soap and water is a priority, as soap presence of a red, orange or brownish stripe on its char-
with a high pH breaks down organophosphates.143,165 Staff acteristic black, globular abdomen. The female is much
must use personal protective equipment, such as neoprene larger than the male; generally only the female is considered
or nitrile gloves, and gowns are worn when decontami- dangerous. Juveniles are smaller, more variably coloured
nating patients. Charcoal cartridge masks for respiratory and may lack any spots or stripes. Bites from both male
protection are useful, although recent evidence suggests and juvenile spiders may result in symptoms, although these
that the nosocomial risk to staff may not be as significant tend to be less significant than bites from females.168
as was once thought.165 Intubation is commonly required The redback spider has also become established
after significant exposure, due to respiratory distress from outside Australia, including in New Zealand, Japan and
laryngospasm, bronchospasm or severe bronchorrhoea. South America.168,169 Although bites are rare, small popu-
Continuous cardiac monitoring and an ECG are used to lations of redback spiders have been reported in Central
check for bradycardias. Activated charcoal is used for gastric Otago (South Island) and New Plymouth (North Island)
decontamination for those patients who have ingested since the early 1980s.168,169 The only other venomous
organophosphate. The mainstay of treatment is atropine spider in New Zealand is the katipo (Latrodectus katipo)
and pralidoxime, with a benzodiazepine used for seizure from the same genus as the redback. The katipo has a
control.165,166 Atropine blocks acetylcholine receptors and black, rounded body, slender legs and a red stripe on the
halts the cholinergic stimulation. Very large doses of atro- abdomen. Adult males and juveniles are black and white
pine are usually required, 1–2 g IV, and repeated if muscle and are smaller than females.170 Symptoms of katipo spider
weakness is not relieved or the signs of poisoning recur. bite are similar to those of the redback spider and, where
Clearing of bronchial secretions is the end point of atropine indicated, redback antivenom is used to treat bites.
administration, not pupil size or the absolute dose.133,165,166 A redback spider bite is a frequent cause for ED presen-
Pralidoxime hydrochloride reactivates acetylcholinesterase tations and the most clinically significant spider bite in
and is effective at restoring skeletal muscle function, but Australia.168,171 Most bites are minor, with either minimal
is less effective at reversing muscarinic signs. Over time, or no symptoms and requiring no antivenom. In approxi-
the bond between organophosphate and cholinesterase mately 20% of cases, significant envenomation occurs and
becomes permanent and the effectiveness of pralidoxime antivenom administration is generally indicated, although
diminishes165,166 The current recommendation is adminis- death is extremely unlikely in untreated cases.172 Redback
tration within 48 hours of organophosphate poisoning.166 antivenom is the most commonly administered antivenom
Benzodiazepines are clinically indicated through their in Australia.168
binding to specific receptor sites, potentiating the effects of Clinical manifestations
gamma-aminobutyrate and facilitating inhibitory transmit-
ters for management of seizures.133,143,165,166 Envenomation by a redback spider is known as latro-
dectism; the venom contains excitatory neurotoxins that
Envenomation stimulate release of catecholamines from sympathetic
Venomous animals can be land-based or marine-based, nerves and acetylcholine from motor nerve endings.168,172
and their distribution ranges from broad to very specific Signs and symptoms associated with a significant enven-
locations. Exposure of humans to venom produces a large omation are distinctive, and diagnosis is by clinical findings.
and varied range of symptomatology, which often results Initially, there is a minor sting at the bite site, where the
in an emergency presentation. It is therefore important spider may or may not have been seen. Over the first hour
for critical care nurses to be familiar with the types of the bite becomes progressively painful to severe, spreading
potentially venomous animals inhabiting the catchment proximally with and involving swollen and tender local
area of their health setting. From a first aid perspective lymph nodes. Localised sweating at the bite site or limb
it is vital nurses are familiar with the presentation and or generalised sweating may appear, associated with
hypertension and malaise. Pain eventually becomes gener-
management of specific life-threatening or injury causing
alised and may be expressed as chest, abdominal, head or
envenomations, including the use of antivenom when
neck pain suggestive of other acute conditions such as
one exists. Most countries have local poison information
myocardial infarction.171
centres for advice from expert toxicologists (see Online
Progression of symptoms generally occurs in less than
resources). Common envenomations across Australia and
6 hours but may take up to 24 hours. People with minor
New Zealand are described below.
untreated bites may experience symptoms for several
Redback/katipo spider bite weeks.168,172 Other less common signs and symptoms
include local piloerection, nausea, vomiting, headache,
Description and incidence fever, restlessness/insomnia, tachycardia and neurological
The redback spider (Latrodectus hasseltii) is found throughout symptoms such as muscle weakness or twitching.168,172,173
Australia but more commonly in temperate regions.
Tasmania has the lowest frequency of reported bites, while Assessment
areas around Alice Springs, Perth and Brisbane are especially Patients presenting with pain from a bite who have the
infested.167 The redback spider is easily identifiable by the offending spider with them are straightforward in terms of
770 SECTION 3 SPECIALTY PRACTICE

initial assessment. Identification of the spider is confirmed administration over IM administration was demonstrated
and a history of the event obtained, including the time of in a randomised controlled trial, so there is little evidence
the bite and any first aid initiated. A brief assessment of the to justify one route of administration over another.176
bite site and the involved limb is undertaken, including Redback spider antivenom administration in various
the extent of pain, presence of sweating and painful tender stages of pregnancy has not been associated with direct or
lymph nodes, and a baseline set of vital signs. Patients are indirect harmful effects to the fetus.168,172
then placed in a suitable area for medical assessment and
ongoing observation.173 Practice tip
Adult patients presenting with vague limb pain, or
preverbal children who are ‘distressed’ and ‘cannot be Observations for the development or progression
settled’, may be unaware that they have been bitten by a of symptoms of a redback envenomation focus on
redback.The pain may not have been felt at the time of the development of local pain that spreads proximally and
bite and no spider may have been seen. Thorough history increases in intensity, development of sweating (either
taking, physical assessment and knowledge of the effects of local or generalised) and hypertension.
latrodectism enable detection of a suspected spider bite.173
Funnel-web spider bite
Management
There is no recommended definitive first aid for a redback Description and incidence
spider bite. Application of cold packs to the bite site and Funnel-web spiders are the most venomous spiders to
administration of simple analgesia, such as paracetamol, humans worldwide,173,177 and Australian funnel-web
may assist with local pain relief. The use of a pressure spiders (Atrax or Hadronyche genera) are found primarily
immobilisation bandage is not necessary, as symptom along the east coast. The Sydney funnel-web spider (Atrax
progression is slow and not life-threatening,168,172–174 and robustus) is found mainly around Sydney, while other
will cause further pain only in the affected limb. Remove species are found in eastern New South Wales and central
any pressure bandage that was applied during first aid after and southern Queensland. The spider is large, black or
identification of the spider is confirmed.168 dark brown and approximately 3 cm long in the body.
Presence of the above symptoms (pain, swelling, localised Male spiders have smaller bodies and are significantly
sweating at the site) indicates systemic envenomation more toxic than females.177
requiring administration of redback spider antivenom.168,172
Prior to administration, the patient should be placed in a Clinical manifestations
clinical area with readily available resuscitation equipment Funnel-web spider bites are potentially rapidly lethal;
to treat any anaphylactic reaction, although this is rare. An however, only 10–20% of bites result in systemic enven-
IV cannula is inserted and adrenaline 1:1000 is prepared for omation, with the majority being minor and not requiring
the possibility of anaphylaxis. antivenom. The bite is extremely painful, and fang marks
The initial dose of Redback Spider Antivenom is may be seen. Signs and symptoms of systemic enven-
2 ampoules administered intramuscularly (IM) (500 units; omation may appear within 10 minutes, and include
approximately 1.5 mL each ampoule), and symptoms perioral tingling and tongue fasciculation, increased
should subside over the next 30–60 minutes. Complete salivation, lacrimation, piloerection, sweating; nausea,
resolution of symptoms requires no specific further vomiting, headache; hypertension, tachycardia; dyspnoea,
treatment. If there has not been complete resolution of pulmonary oedema; irritability, decreased consciousness
symptoms after 2 hours a further 2 doses of antivenom and coma.172,178 Regardless of the presence of symptoms,
are given. If after a further 2 hours there is incomplete all possible funnel-web spider bites are managed as a
resolution of symptoms or no discernable response after medical emergency.172
4 ampoules of antivenom, expert advice should be sought
via the local poison information centre. Patients who are
Assessment
symptom-free after 6 hours of observation or the admin- Patients with suspected funnel-web spider bites are rapidly
istration of antivenom can be discharged home with assessed for the presence of any signs and symptoms of
instructions to re-present should any symptoms return. envenomation and allocated an ATS triage category of
Antivenom may be effective days after the bite, and 1–3, based on presenting symptoms. A pressure immobili-
possibly longer; however, a larger amount of antivenom sation bandage is applied if this was not done during initial
is usually required.168,172 IV administration has been first aid. Patients with signs of envenomation are moved
advocated in severe cases or where there is poor response to a resuscitation area for immediate treatment, including
to IM administration.168,172 The manufacturer recommends urgent antivenom administration and management of
that, for life-threatening envenomation, the IV route may the clinical effects of envenomation. Monitoring and
be used after first diluting the antivenom to 1:10 with assessment for potentially serious manifestations focus on:
Hartmann’s solution and the antivenom administered over • airway compromise due to decreased level of
20 minutes.172,175 IV administration is safe with reactions consciousness, requiring airway protection with an
uncommon (less than 5%).176 No significant benefit of IV airway adjunct or endotracheal intubation
 CHAPTER 23 EMERGENCY PRESENTATIONS 771

• breathing for respiratory compromise due to residential and metropolitan areas, especially when in close
pulmonary oedema, requiring continuous positive proximity to bush land and in periods of drought. The
airway pressure or intubation/ventilation with incidence of snakebite is estimated at 500–3000 each year,
positive end-expiratory pressure (see Chapter 15) with approximately 200–500 cases requiring treatment
• circulatory compromise due to profound with antivenom.180 There are on average 1–3 deaths per
hypotension, although a late sign with hypertension year, although this may be higher due to unrecognised
more commonly seen, requires IV access and volume snake bites.180
replacement. Circulatory compromise/failure may
Clinical manifestations
lead to cardiac arrest requiring cardiopulmonary
resuscitation (see Chapter 25). The majority of snake bites do not result in significant
envenomation.181 Bites are generally recognised by the
All patients require full monitoring with constant patient at the time because of associated pain, although
nursing observation. A patient with no signs of envenom- some bites are unrecognised. The bite site may show
ation on arrival has a detailed history taken regarding the minimal to obvious signs of punctures or scratches, with
circumstances of the bite, the time of bite, a description of accompanying swelling and bruising. Multiple bites
the spider and any first aid undertaken.The patient is then are possible and are generally associated with major
regularly assessed for any symptoms suggesting systemic envenomation.172,181 Australian snake venoms contain
envenomation. After thorough medical assessment, if there various toxins that are responsible for the systemic
are no signs of systemic envenomation, any first aid such effects172,181,182 (see Table 23.17). Renal damage may
as a pressure immobilisation bandage is removed and occur as a consequence of myoglobinuria from severe
the patient observed for 6 hours.172 With no diagnostic rhabdomyolysis or haemoglobinuria associated with
test for funnel-web spider envenomation and no venom coagulopathies,181 leading to acute renal failure (see
detection procedure available,172 clinical diagnosis is based Chapter 18).180
on the history and symptoms.
Assessment
Management Patients presenting with snake bite(s) are allocated a
For signs of systemic envenomation, 2 ampoules of high priority for assessment and treatment even if they
funnel-web spider antivenom are administered slowly IV appear well on arrival. Patients who present without
over 15–20 minutes;177,178 premedication is not required,172 effective first aid measures (the application of a pressure
although the patient is observed closely for anaphy- immobilisation bandage and splint) have these applied
laxis. In severe envenomation associated with dyspnoea, immediately.181 The pressure immobilisation bandage
pulmonary oedema or decreased level of conscious- is applied with a broad (15-cm) bandage, commencing
ness, the initial antivenom dose should be doubled to over the bite site with the same pressure that would be
4 ampoules.177,178 More antivenom may be required until used for a sprained ankle. The bandage is then extended
all major symptoms have resolved (severe bites often to cover the whole limb, including fingers/toes, and the
require 8 ampoules).172,177,178 The antivenom dose for limb is splinted and immobilised.183 Correct application
children is the same as the adult dose.172,177,178 First aid of the pressure bandage is important, as any benefit is
measures such as a pressure immobilisation bandage lost with bandages that are too loose, not applied to the
can be removed after antivenom administration and the whole limb or with no splinting or immobilisation.183
symptoms have stabilised; this may take several hours.172 Elasticised bandages are superior to crepe bandages in
obtaining and maintaining adequate pressure.184 Do not
Snake bites wash the wound prior to applying the pressure immobil-
Worldwide there are a variety of snakes that have the isation bandage, as swabbing of the bite site is used when
capacity to envenomate humans and cause life-threatening performing venom detection. The patient should not
clinical features; broadly these snakes fall into three groups, mobilise to minimise distribution of any injected venom.
elapids, pit vipers and cobras. Elapids are mostly encoun- Once applied, the pressure immobilisation bandage is
tered throughout Australasia, pit vipers in the Americas not removed until the patient is in a healthcare location
and cobras in Africa and south Asia.167,179,180 that is stocked with antivenom.180
The focus of this section will be on the life-threaten-
ing Australasian elapid species. Practice tip

Description and incidence Pressure immobilisation may be contraindicated or

ineffective in bites from exotic snake species. Many of
Australasia is inhabited by a large number of snakes (over these non-Australasian species of snake have venoms
140 recognised snakes from 30 different species; 25% of that cause local tissue destruction. For example, pit
all known venomous snakes, and 40% of all dangerous vipers and cobras can both cause extensive localised
front-fanged snakes or elapids).167,179,180 New Zealand tissue damage. Immobilisation is the mainstay of first
has no known venomous terrestrial snakes.167 Australian aid.180,181
venomous snakes are found in both rural areas and
772 SECTION 3 SPECIALTY PRACTICE

TABLE 23.17
Characteristics and clinical manifestations of snake venom172,181,182

TOXIN EFFECTS SIGNS AND SYMPTOMS

Neurotoxin Blocks transmission at the neuromuscular junctions, causing • Ptosis (drooping of upper eyelids)
skeletal and respiratory muscle flaccid paralysis, presynaptic • Diplopia (double vision)
and/or postsynaptic • Ophthalmoplegia (partial or complete
paralysis of eye movements)
• Fixed, dilated pupils
• Muscle weakness
• Respiratory weakness, paralysis
Haemotoxin Causes coagulopathies, resulting in either: • Bleeding from bite wounds
• defibrination with low-fibrinogen, unclottable blood, but usually • Bleeding at venipuncture sites
with a normal platelet count • Haematuria
or
• direct anticoagulation with normal fibrinogen and platelet count
Both cause an elevated prothrombin ratio and international
normalised ratio
Myotoxin Causes myolysis, resulting in generalised destruction of • Muscle weakness
skeletal muscles with high serum creatine kinase and leading to • Muscle pain on movement
myoglobinuria and occasionally severe hyperkalaemia • Red or brown urine, which tests
positively to blood

A brief and focused history explores the time and should be inserted for close monitoring of urine output
circumstances of the bite, a description of the snake and presence of any myoglobin in urine.
(colour, length), geographical location and the application To identify the likely snake involved and thus the
of any first aid.The patient is assessed for general symptoms correct antivenom required, a bedside snake venom
including headache, nausea, vomiting, abdominal pain, detection kit is used at the bite site or with a urine sample.
collapse, convulsions and anxiety, although these alone A swab of the washings from the bite area is collected
do not indicate envenomation.180,181 Additional signs by leaving the pressure immobilisation bandage on and
and symptoms include blurred or double vision, slurred creating a window over the bite site to expose the bitten
speech, muscle weakness, respiratory distress, bleeding area. Testing takes about 25 minutes. If there are signs of
from the bite site or elsewhere and pain and swelling at systemic envenomation, urine can be used to perform the
the bite site and associated lymph nodes. test; blood should be avoided, as it is unreliable. A positive
Patients with suspected snake bite are located in an result indicates that venom from a particular snake is
acute area with full monitoring available, with symptom- present, but does not mean that systemic envenomation
atic patients placed in a resuscitation area. The patient has occurred, while a negative result does not exclude
requires insertion of IV access devices and collection of systematic envenomation.179,181
blood for pathology tests including full blood count, urea,
electrolytes, creatine, creatinine kinase and full coagulation Practice tip
studies. Unnecessary venipunctures should be avoided,
including sites where it may be difficult to control Whole blood clotting time is performed by drawing
bleeding should it occur. Healthcare settings without ready 10 mL venous blood and placing in a glass test tube. If the
access to pathology services may need to perform whole blood has not clotted within 10 minutes, a coagulopathy
blood clotting time testing at the bedside to assess for any is likely to exist, suggesting envenomation.182
coagulopathy.
All probable snake bites require observation for at least In patients with known snake bite and systemic
12 hours, as some serious symptoms may be delayed.180,181 envenomation, antivenom administration is required if
Patients should be assessed for tachycardia, hypotension or there is any degree of paralysis, significant coagulopathy,
hypertension, and falling oxygen saturation, altered respi- any myolysis (myoglobinuria or creatinine kinase >500
ratory rate, forced vital capacity or peak expiratory flow micrograms per litre), unconsciousness and/or convul-
rate, indicating respiratory muscle paralysis.181 Frequent sions. In an asymptomatic patient with normal pathology
neurological observations focus on identification of and a negative or positive snake venom detection result,
muscle weakness and paralysis; clinicians should note any it is likely that envenomation has not occurred. In this
ptosis, diplopia, dysphagia, slurred speech, limb weakness case, the pressure immobilisation bandage can be removed
or altered levels of consciousness. An indwelling catheter under close observation in a resuscitation area.The patient
 CHAPTER 23 EMERGENCY PRESENTATIONS 773

is fully reevaluated including repeat blood tests, assessing The tentacles are covered with millions of stinging
coagulation parameters, within 1–2 hours after removal nematocysts, each a spring-loaded capsule that contains
of the pressure bandage. If the patient’s condition remains a penetrating thread that discharges venom. Threads are
unchanged, further observation and repeat blood tests at 1 mm in length and capable of penetrating the dermis of
6 and 12 hours are required. Patients with no evidence of adult skin. The tentacles also produce a sticky substance
envenomation after 12 hours may be discharged.179,181 that promotes adherence to a victim’s skin, causing some
tentacles to be torn off and remain attached to the person,
Management where the nematocysts remain active.167
A patient with evidence of systemic envenomation requires
antivenom administration; monovalent antivenom is used Description and incidence
in preference to polyvalent antivenom when identity of Most stings occur during the summer months (December,
the snake species is known. Polyvalent antivenom is a January) in the tropical waters of northern Australia, from
mixture of all monovalent antivenoms, and is therefore Gladstone in Queensland around to Broome in Western
used for severe envenomation where the identity of the Australia, on hot, calm and overcast days when the
snake is unknown and the patient’s condition does not jellyfish moves from the open sea to chase prey in shallow
allow time for a snake venom detection kit result, or where water.167,186,187 The exact incidence of stings is difficult to
there is insufficient monovalent antivenom available.179,181 determine, but they are common in children. One ED
Expert advice from a poison information centre may assist reported 23 confirmed C. fleckeri stings in a 12-month
in identifying the snake, based on known habitats and period.188 There have been at least 63 confirmed deaths
distribution as well as presenting symptoms. Antivenom from envenomation by Chironex fleckeri in the Indo-
is always administered IV in a diluted strength of 1:10 (or Pacific region.
less if volume is a concern) via an infusion. Administra-
tion is commenced slowly while observing for signs of any Clinical manifestations
adverse reaction. The infusion rate can be increased if no Most stings are minor, with clinically significant stings
reaction occurs, with the whole initial dose administered occurring from larger jellyfish. Stings generally occur
over 15–20 minutes. The dose will vary depending on the on the lower half of the body, and are characterised by
type of antivenom, type of snake and number of bites; the immediate and severe pain. Pain increases in severity
use of 4–6 ampoules is not uncommon in severe enven- and may cause victims, especially children, to become
omation.172,181 Use of premedication before antivenom incoherent. While mechanisms of toxicity remain poorly
administration is controversial; at present the antivenom understood, death is thought to occur from central respi-
manufacturer does not recommend any premedication to ratory failure, or cardiotoxicity leading to atrioventricular
reduce the chance of anaphylaxis. Regardless of whether a conduction disturbances or paralysis of cardiac muscle.
premedication is used, prepare to treat anaphylaxis.179,181,185 Victims may become unconscious before they can leave
When the patient’s condition has stabilised after the the water following envenomation, and death can occur
initial dose of antivenom, the pressure immobilisation within 5 minutes.167,186,187
bandage is removed, with continuous close observation Multiple linear lesions, purple or brown in colour, are
for any clinical deterioration caused by the release of seen on the area where tentacle contact occurs. A pattern
venom contained by the pressure bandage. If deteriora- of transverse bars is usually seen along the lesions, along
tion is evident, further antivenom and reapplication of with an intense acute inflammatory response, initially as
the pressure immobilisation bandage may be required.182 a prompt and massive appearance of wheals, followed by
Patients without signs of deterioration still require oedema, erythema and vesicle formation, which can lead
ongoing observation in a high dependency unit/intensive to partial- or full-thickness skin death.167,189
care unit and repeat testing of coagulation at 3 and 6 hours
post-antivenom administration should be done. Ongoing Assessment
observation and pathology studies will occur for at least Patients presenting to ED after potential box jellyfish sting
24 hours.181 are easily diagnosed based on the history, the presence of
In children, management for snake bite is similar, with pain and their skin lesions as outlined above. Generally,
antivenom dosages the same as for an adult. Dilution some form of pre-hospital management or first aid will
volume can be reduced (from 1:10 to 1:5) for children.180 have been instituted. On arrival, patients with signs of
clinically significant stings, alteration in consciousness,
Box jellyfish envenomation cardiovascular or respiratory function, or those with severe
Chironex fleckeri (box jellyfish) is one of the world’s pain are seen immediately.
most dangerous venomous animals.167 The jellyfish is a
cubic (box-shaped) bell measuring 20–30 cm across and Management
weighing up to 6 kg. Four groups of tentacles, with up to Treatment focuses on appropriate first aid, administra-
15 tentacles in each group, can stretch up to 2 m and total tion of adequate pain relief, symptomatic management
length can exceed 60 m. Importantly, the animal is trans- of cardiovascular and respiratory effects and the admin-
parent in water and is therefore difficult to identify.186,187 istration of box jellyfish antivenom when indicated. First
774 SECTION 3 SPECIALTY PRACTICE

aid measures include liberal application of vinegar to Assessment

the sting area for 30–60 seconds. Vinegar inactivates the People stung by an Irukandji may have no symptoms
undischarged nematocysts, so removal of any remaining initially, but may develop symptoms up to 1 hour after
tentacles should occur simultaneously to prevent further being stung. Irukandji syndrome produces clinical features
envenomation.167,189,190 Mild stings respond to the appli- of severe lower back pain, muscle cramps; raised blood
cation of ice packs and simple oral analgesia, after the pressure, pulse; and respiratory compromise, vomiting
application of vinegar.167,188 Patients with moderate-to- and anxiety.194 A patient with suspected Irukandji enven-
severe pain require IV narcotic analgesia. For patients with omation is placed in an acute area with full monitoring
continuing severe pain, antivenom is administered along available.
with continued parenteral analgesia.187
Patients are observed for the development of cardio- Management
respiratory symptoms, including arrhythmias. Management The mainstays of patient management are pain control
focuses on specific clinical effects, ranging from oxygen and symptom management. Application of vinegar has
administration and IV fluid resuscitation through to been part of first aid treatment but, due to delay in the
intubation/mechanical ventilation or cardiopulmonary presentation of symptoms following a sting, this may
resuscitation.167,189 Antivenom is indicated in patients with be of limited value.190 Evidence is emerging indicating
cardiorespiratory instability, cardiac arrest or severe pain that washing the area with either fresh or salt water may
unrelieved by narcotic analgesia.187 Antivenom is carried also be effective. Pain is severe, and opioid analgesia may
by prehospital personnel, and administration may occur be required; if requirements for opioids are very high,
prior to ED presentation. A 20,000-unit ampoule of box fentanyl is considered.194 There is anecdotal evidence that
jellyfish antivenom is diluted in 10 mL isotonic saline magnesium sulfate may have a role in the management of
and administered IV over 5–10 minutes.188 The number Irukandji syndrome not responsive to the above treatments,
of ampoules used varies with clinical status: at least one but this remains unproven.190
for cardiorespiratory instability; up to three for life-
threatening situations with an inadequate response; and at Ciguatera
least six for a cardiac arrest.167,189 Ciguatera is a type of seafood poisoning caused by the
While the application of a pressure immobilisation consumption of fish, especially certain tropical reef fish,
bandage to affected limbs after vinegar application was which contain one or more naturally-occurring neuro-
previously recommended as a first aid intervention, there toxins from the family of ciguatoxins. Ciguatera is
is little current evidence supporting this in box jellyfish reported as the most common form of seafood poisoning
stings, and its application may promote additional venom in the world,196 and is considered a mild non-fatal disease,
release and therefore be potentially dangerous.187,191 Some with a worldwide mortality rate ranging from 0.1–20%.197
animal research has suggested a role for magnesium Ciguatera as a tropical disease confined to latitudes
sulfate in management for patients not responding to 35°North–35°South is no longer tenable, as tropical fish
antivenom.192 are now marketed throughout the world and some species,
such as tuna, mackerel and dolphin fish, also migrate
Practice tip considerable distances. In Australia, there have been
numerous outbreaks of ciguatera poisoning in Sydney and
The Australian Resuscitation Council currently recom- as far south as Melbourne.197,198
mends that a pressure immobilisation bandage not be Ciguatera toxins (ciguatoxins) are among the deadliest
used in the management of jellyfish stings. poisons known, reportedly 1000 times more potent
than arsenic.199 These heat-stable toxins originate from
Adapted, with permission, from Australian Resuscitation
a microorganism that attaches to certain species of algae
Council. Guideline 8.9.6. Envenomation – jellyfish stings,
<http://resus.org.au/download/9_4_envenomation/guideline-
in tropical areas around the world; these toxins become
9-4-5july10.pdf>; 2005 (updated July 2010) [accessed 12.14]. altered after ingestion by progressively larger fish up the
food chain.191,197
Irukandji envenomation Clinical manifestations and diagnosis
The Irukandji is a small marine jellyfish, with stinging Ciguatera poisoning typically presents as an acute gastro-
tentacles capable of causing intense pain and catechol- intestinal illness, followed by a neurological illness with
amine release.194 classical symptoms of heat and cold reversal of sensation
that may last for a few days after consumption of contam-
Description and incidence inated fish191 (see Table 23.18).
Irukandji syndrome is a poorly-understood marine enven- A patient may become sensitive to repeated exposure
omation encountered in far northern and northwestern to ciguatoxins;191,197 additional exposure to poisoning
areas of Australia. Death is uncommon and attributed from ciguatera may be more severe than the first episode.
to cerebral haemorrhage and is associated with other Importantly, patients exposed to ciguatera suffer recur-
comorbid conditions.195 rences following the consumption of seemingly innocuous
 CHAPTER 23 EMERGENCY PRESENTATIONS 775

TABLE 23.18
Symptoms of ciguatera191,197

GASTROINTESTINAL NEUROLOGICAL C A R D I O VA S C U L A R OTHER SYMPTOMS

Abdominal pain Paraesthesias in extremities and around Bradycardia Dermatitis

Nausea the mouth, tingling, burning and pain Tachycardia Rash
Vomiting Painful extremities Hypotension Arthralgia and myalgia
Diarrhoea Paradoxical temperature reversal where Hypertension General weakness
hot feels cold and cold feels hot Arrhythmia Salivation
Temperature sensitivity Dyspnoea
Vertigo Neck stiffness
Dental pain where teeth feel loose Headache
Blurred vision Ataxia
Tremor Sweating
Metallic taste in the mouth

foods (e.g. nuts, nut oils, caffeine, alcohol or animal protein scombrotoxin to be eliminated from the patient’s system.
foods),197,199 with relapses months or years after the initial Importantly, while this may appear to have the clinical
poisoning.199 features of an allergic reaction, drugs such as adrenaline
Diagnosis is made on a patient’s history and clinical and corticosteroids do not play a role in management.
features: consumption of fish followed by an acute gastro-
intestinal and neurological illness. There is no conclusive Near-drowning
diagnostic test for the presence of ciguatoxins.197,199
Description and incidence
Management Submersion incidents are often preventable events
Treatment of ciguatera poisoning is supportive care and associated with significant mortality and morbidity in both
symptom management. Mannitol has been recommended, adults and children, usually necessitating an ED presenta-
although this is only effective if used in the first 48–72 tion and subsequent hospital admission. Worldwide, there
hours of the illness.191,197 are an estimated 359,000 drowning deaths annually with
children, males and those with increased access to water
Scombroid fish poisoning most at risk.201 The location of drowning varies from
Scombroid poisoning is a form of food poisoning caused country to country. In the USA, artificial pools and natural
by the combination of inadequately cooled fish and the bodies of freshwater were common drowning locations,
bacterial decomposition of the fish flesh resulting in a particularly for children.202 In Australia, drowning often
release of histamine. The active component of scombro- occurred in non-tidal lagoons, lakes and surf beaches.203
toxin is histamine. The main groups of fish associated In Uganda, lakes and rivers were common sites particu-
with this type of poisoning are the Scombridae, that is tuna larly for young males.204 A bimodal distribution of deaths
and mackerels; however, other fish such as mahi-mahi is seen in children, with a peak in the toddler age group
have also been known to have illness-causing potential.200 (0–4 years) and a second peak in young adolescent males
Scombrotoxin is not inactivated by the cooking process. (15–19 years).201,205–207
It is estimated that, for every drowning death, there
Clinical manifestations and diagnosis are 4–5 near-drowning hospital admissions and 14 ED
People normally start feeling unwell in about 30 minutes presentations.205,206,208 Near-drowning is also associated
after eating fish affected with scombrotoxin, with with high-impact injuries, especially boating or personal
flushing, development of a rash and urticaria. This may be watercraft incidents and shallow-diving-related injuries.
followed by more profound symptoms such as tachycardia, Associated cervical spine injury is seen in 0.5% of
pounding headaches, difficulty breathing and collapse due near-drowning cases.205
to hypotension.200 Deaths have been recorded from this;
recently, two Australian tourists died from the same meal Clinical manifestations
while travelling in Bali. The sequence of events in drowning has been identified
primarily by animal studies, highlighting an initial phase
Management of panic struggling, some swimming movements and
The mainstays of treatment are controlling the histamine sometimes a surprise inhalation. There may be aspiration
reaction with antihistamines and supportive nursing care of small amounts of water at this time that produces
for symptoms. Histamine-2 receptor blockers have been laryngospasm for a short period. Apnoea and breath-
shown to be useful for up to 24 hours following the devel- holding occur during submersion and are often followed
opment of symptoms.This prolonged treatment allows the by swallowing large amounts of water with subsequent
776 SECTION 3 SPECIALTY PRACTICE

vomiting, gasping and fluid aspiration. This leads to severe of fluid aspiration often progress to develop severe acute
hypoxia, loss of consciousness and disappearance of airway respiratory distress syndrome within a very short time.205
reflexes, resulting in further water moving into the lungs No significant effects on electrolytes are noted in humans,
prior to death.205,209,210 as rarely more than 10 mL/kg and commonly no more
Approximately 80–90% of submersion victims suffer than 4 mL/kg of water is aspirated, while clinically signif-
‘wet drowning’ as described above, with aspiration of icant electrolyte disturbances occur when over 22 mL/kg
water into the lungs resulting from loss of airway reflexes has been aspirated.205,208,209
and laryngospasm. Approximately 10–15% of victims Cardiovascular effects are influenced by the extent
have sustained laryngospasm, and no detectable amount and duration of hypoxia, derangement of acid–base
of water will be aspirated (known as ‘dry drowning’), status, the magnitude of the stress response and hypo-
with the resulting injury secondary to anoxia.205,206 thermia.205 Ventricular arrhythmias and asystole may
Pre-existing medical conditions predispose a person to result from hypoxaemia and metabolic acidosis. Acute
drowning and should be considered during management, hypoxia results in release of pulmonary inflammatory
including seizures, arrhythmia (especially torsades de mediators, which increase right ventricular afterload and
pointes associated with long Q-T interval), coronary decrease contractility.205,208,209 Hypotension is commonly
artery disease, depression, cardiomyopathy (dilated or seen due to volume depletion secondary to pulmonary
hypertrophic obstructive), hypoglycaemia, hypothermia, oedema, intracompartmental fluid shifts and myocardial
intoxication or trauma.209 dysfunction.205
Pulmonary manifestations after aspiration of fresh or Severe hypoxic and ischaemic injury is the most
salt water differ, as fresh water is hypotonic and when important factor related to outcome and subsequent
aspirated moves quickly into the microcirculation across the quality of life. Other factors influencing the extent of
alveolar–capillary membrane. With fresh water aspiration, injury include water temperature and submersion time,
surfactant is destroyed, producing alveolar instability, stress during submersion and coexisting cardiovascu-
atelectasis and decreased lung compliance and resulting lar and neurological disease.205,208,209,211,212 Prediction of
in marked ventilation/perfusion mismatching.205,206,208,209 death or persistent vegetative state in the immediate
In contrast, salt water has 3–4 times the osmolality of period after near-drowning is difficult. Patients awake or
blood and, when aspirated, draws damaging protein-rich with only blunted consciousness on presentation usually
fluid from the plasma into the alveoli, resulting in both survive without neurological sequelae. A third of patients
interstitial and alveoli oedema, with associated broncho- admitted in coma or after cardiopulmonary resuscitation
will survive neurologically intact or with only minor
spasm and subsequent shunting and ventilation/perfusion
deficits, while the remaining two-thirds of patients will
mismatch.205,208,209
either die or remain in a vegetative state.205
Despite these different physiological effects from
Hypothermia is a well-documented feature in sub-
aspirated fresh and salt water, the resulting clinical mani-
mersion victims.205,208,209,212 Incidents of submersion times
festation is the same: profound hypoxaemia secondary
of greater than 15 minutes where victims recovered with
to ventilation/perfusion mismatch with intrapulmonary a good neurological outcome all occurred in very cold
shunting (see Figure 23.2).205,208,209 Patients with evidence water (<10°C). While the exact mechanisms in these
outcomes are unclear, acute cold submersion hypo-
FIGURE 23.2 Pathophysiology of respiratory failure thermia may be protective against cerebral insult by: very
due to fluid aspiration.205,206,208,209 rapid cooling in victims with low levels of subcutaneous
fat who have aspirated a large amount of very cold water;
(ZWPYH[PVU induced muscle paralysis leading to minimal struggling
)UHVKZDWHU 6DOWZDWHU and very little oxygen depletion; and the heart gradually
slowing to asystole in the presence of profound hypo-
%URQFKRVSDVP $OYHRODU thermia.205,208,209,212 In these cases prolonged resuscitative
6XUIDFWDQW efforts may be warranted, including active and aggressive
$FXWHHPSK\VHPD RHGHPD
re-warming interventions, that should not be abandoned
until the patient has been re-warmed to at least 30°C.208
94PLVPDWFK
$WHOHFWDVLV Assessment
&RPSOLDQFH :2% Continuously monitor heart rate, blood pressure and
oxygen saturation, and assess neurological status, including
any seizure activity. Deterioration is evident with a falling
level of consciousness, a high alveolar–arterial gradient,
+\SR[LD respiratory failure evidenced by a partial pressure of carbon
$FLGRVLV dioxide in the arterial blood >45 mmHg or worsening
94PLVPDWFKYHQWLODWLRQSHUIXVLRQPLVPDWFK:2%ZRUNRIEUHDWKLQJ blood gas results.208 Caution should be taken to avoid
activities that may cause a rise in intracranial pressure.
 CHAPTER 23 EMERGENCY PRESENTATIONS 777

A 12-lead ECG identifies any arrhythmias that result from rapid volume expansion (crystalloid or colloid) and
acidosis and hypoxia rather than electrolyte abnormali- an indwelling catheter for hourly urine measurement.
ties. The patient should be managed conventionally (see Patients with persistent cardiovascular compromise may
Chapter 11).208 All patients require serial CXR, as lung require inotropic support in conjunction with invasive
fields often worsen in the first few hours. In clinically haemodynamic monitoring.205,208,212,213
significant submersions, the CXR will typically show Patients presenting with associated high-impact or
bilateral infiltrates undifferentiated from other causes of shallow-diving mechanisms should have cervical spine
pulmonary oedema. immobilisation instituted with the application of a rigid
cervical collar, especially for complaints of neck pain or
Management an altered level of consciousness (see Chapter 17). The
The condition of the patient, the environment and the management of hypothermia and re-warming methods
skill of the attending rescue personnel will influence outlined below are appropriate for the management of
prehospital management of the post-submersion patient, near-drowning.
and the adequacy of initial basic life support at the
scene is the most important determinant of outcome.213 Hypothermia
The Heimlich manoeuvre should not be performed in
an attempt to remove aspirated water, as it is ineffec- Description and incidence
tive and likely to promote aspiration of gastric contents. Hypothermia is a core body temperature that is lower than
Supplemental oxygen 100% is administered as soon as 35°C (measured centrally by oesophageal or rectal probe)
possible.211–213 and occurs with exposure to low ambient temperatures
For patients presenting to the ED in cardiac arrest, that are influenced by low environmental temperatures,
active resuscitation measures continue (see Chapter 25), humidity, wind velocity, extended exposure time or
although the need for continued cardiopulmonary resus- cold water immersion.214–216 Cold injury is a common
citation is generally associated with a poor neurological occurrence in those climates with cooler ambient
outcome; however, patients experiencing submersions in conditions; however, when body heat is lower than the
very cold water may have a better outcome.213 The focus surrounding environmental conditions, it can easily
of management for patients with spontaneous circu- develop so it is not an uncommon problem in Australia
lation includes respiratory support and the correction and New Zealand, despite the relatively warm weather
of hypoxia, neurological assessment and maintenance of zones in the former.The very young and very old are most
optimal cerebral perfusion, cardiovascular support and susceptible to injury.214,217 A normal core temperature
maintenance of haemodynamic stability, correction of of 37°C has a variation of 1–2°C. Temperature mainte-
hypothermia and management of other associated injuries. nance is essential for normal homeostatic functioning, and
All patients require 100% supplemental oxygen normal adaptive mechanisms can respond to reductions in
via a non-rebreathing mask initially, unless mechanical ambient temperature.
ventilation is required. Patients without any respira-
tory symptoms should be observed for 6–12 hours, until Clinical manifestations
there is a GCS greater than 13, normal CXR, no signs of When skin temperature is reduced after exposure to the
respiratory distress and normal oxygen saturation on room cold, sympathetic stimulation occurs causing peripheral
air.205,208,212,213 Alert patients unable to maintain adequate vasoconstriction, decreased skin circulation and shunting
oxygenation should be considered for continuous positive of blood centrally to vital organs. Blood pressure, heart
airway pressure or bi-level positive airway pressure prior rate and respiratory rate rise, and shivering (involun-
to intubation provided they are able to maintain their own tary clonic movements of skeletal muscle) stimulates
airway, with its effect on circulation monitored closely metabolic activity to produce heat and blood flow to
(see Chapter 15). striated muscles214 to maintain a normal core temperature.
While cerebral oedema and intracranial hypertension If continued exposure to cold occurs these compensatory
is often seen in hypoxic neuronal injury, only general functions fail, and hypothermia results.214,216
supportive measures are recommended as there is insuf- Ambient temperatures need not be particularly low, as
ficient evidence to indicate that invasive intracranial other contributing factors such as wind or a person having
pressure monitoring and related management improve wet clothing may be significant. A patient with a decreased
outcomes.205,208,212,213 Any seizures should be promptly level of consciousness may present with hypothermia after
treated with appropriate measures (see Chapter 17). Acute lying on a cool surface.214 As a person’s core temperature
respiratory distress syndrome should be managed with drops, progressive cardiac abnormalities occur; normal
non-invasive ventilation if possible.209 Barbiturate-induced sinus rhythm may progress to sinus bradycardia, T-wave
coma or corticosteroids are not recommended as there is inversion, prolonged P–R and Q–T intervals, atrial fibril-
no evidence of improvement in outcome.209,211 lation and ventricular fibrillation.214 A QRS abnormality,
Cardiovascular support may require a multifaceted the Osborn wave, represented by a positive deflection at
approach, initially by improving hypoxia and correct- the junction of the QRS and ST segments, is frequently
ing circulating volume. Hypotensive patients require described as being characteristic of cold injury.218
778 SECTION 3 SPECIALTY PRACTICE

TABLE 23.19
Physiological effects of hypothermia214–216,218–221

DEGREE OF HYPOTHERMIA
PHYSIOLOGICAL
EFFECTS MILD (32–35°C) M O D E R AT E ( 2 8 – 3 2 ° C ) SEVERE (<28°C)

General metabolic Shivering Raised oxygen consumption Normal metabolic functions fail
Raised oxygen consumption Acidosis
Hyperkalaemia
Cardiac Vasoconstriction Atrial arrhythmias Ventricular arrhythmias
Tachycardia Bradycardia Decreased cardiac output
Increased cardiac output
Respiratory Tachypnoea Decreased respiratory drive Apnoea
Bronchospasm
Neurological Confusion Lowered level of consciousness Coma
Hyperreflexia Hyporeflexia Absent reflexes
Coagulation Platelet dysfunction Increased haematocrit Lower bleeding times due to
Impaired clotting enzyme function failure of clotting systems
Increased blood viscosity

Metabolic acidosis and blood-clotting abnormal- that being approximately 7.5°C per hour.217,219 While the
ities are common, as well as hypoglycaemia, which technique is efficient, it is obviously more invasive and
occurs because of depletion of glycogen stores caused carries associated risks, and so is reserved for profoundly
by excessive shivering. Hyperglycaemia can be present hypothermic patients.214
because of inhibition of insulin action due to the lowered External warming is indicated only if the core
temperature.214–216,218–221 The physiological alterations that temperature is above 32°C, as this may cause vasodilation
accompany lowering of core temperature to below 30°C and hypovolaemic shock. Shunting of cold peripheral
are summarised in Table 23.19.214–216,218–221 blood to the core may also lead to further chilling of the
myocardium and ventricular fibrillation.214,216 External
Management warming using warm blankets, forced warm air blankets
A patient with severe hypothermia may appear dead: and heat packs in contact with the patient’s body should
cold, pale, stiff, with no response to external stimula- raise body temperature by approximately 2.5°C per
tion. Successful resuscitation of patients has occurred at hour.214,216 Inhalation rewarming with oxygen warmed to
temperatures as low as 17°C, due to the low body tempera- 42–46°C is also effective, as around 10% of metabolic heat
ture protecting vital organs from hypoxic injury.215,216,218,219 is lost through the respiratory tract.219
This is reflected in the anecdotal phrase, ‘patients are not
dead until they are warm and dead’.215 In most cases, Practice tip
therefore, resuscitation should continue until the patient’s
core temperature reaches 30°C.215,216,218,219 Always measure the blood glucose of hypothermic
patients to exclude hypoglycaemia as a reason for an
Practice tip altered conscious state.

Removing wet clothing and drying the patient is an Recovery of patients with temperatures as low as
extremely important first aid measure for a cold wet to 13.7°C has occurred, so death in hypothermia is defined
prevent further cooling. as failure to revive with rewarming. Hence unless there
are other factors preventing survival, resuscitation should
If a patient’s core temperature is below 32°C, ‘core continue until the patient’s temperature reaches at least
rewarming’ is indicated. This approach is favoured, as 30°C–32°C.216
experimental evidence indicates that return to normal
cardiovascular function is more rapid with tempera- Hyperthermia and heat illness
ture rises of up to 7.5°C per hour.214,216 A number of
invasive internal warming options are available, including Description and incidence
peritoneal lavage, although the most effective of all internal Potentially one of the more significant environmental fears
methods is cardiopulmonary bypass, as it transfers heat at a expressed by many scientists is the issue of climate change
rate several times faster than any other methods available, and the consequence of heat-related illness worldwide.
 CHAPTER 23 EMERGENCY PRESENTATIONS 779

Global warming and events such as recurrent prolonged to excessive sweating; the patient’s temperature may range
hot weather days have recently caused numerous deaths between normal and below 40°C.217,222 Combined water
through Europe, the USA and Australia and scientists are and salt losses cause muscle cramps, nausea and vomiting,
predicting the events will become more common.217,222 headache, dizziness, weakness, fainting, thirst, tachycar-
Heat-related illness is common in Australia and represents dia, hypotension and profuse sweating, but with normal
a significant public health risk, although there are only neurological function.217
limited deaths compared to what has happened in the Heat stroke is the most severe and serious form of
USA and Europe.217,222 heat-related illness, with temperatures above 41°C
Heat-related illness can affect any age group; however and impaired neurological function. Heat stroke is a
it is the very young, because of their larger surface area, profound disturbance of the body’s heat-regulating
reduced sweating capacity and inability to access their ability, and is often referred to as ‘sunstroke’, although
own fluids, and the older person, who may have fluid it relates to the body’s inability to dissipate heat, loss of
restrictions because of other health reasons or taking medi- sweat function and severe dehydration, rather than actual
cations that affect their capacity to sweat and a tendency sun exposure.217,222,223
to layer clothing, who are at the highest risk.217,222 The
other vulnerable group is those in the younger age groups Management
undertaking physical activity during hot weather periods Initial management of the hyperthermic patient focuses
whether because of work or sports. on airway, breathing and circulation,217,222,224 correction
Alterations in thermoregulatory function cause of urgent physiological states such as hypoxia, severe
varying degrees of heat illness, categorised as three potassium imbalances and acidosis. A heat-stressed patient
types: heat cramps, heat exhaustion and heat stroke.217,222 can have large fluid losses and require prompt fluid resus-
Excessive exposure to heat substantially increases fluid citation, preferably isotonic sodium chloride solution.217,222
and electrolyte losses from the body.217,222 The loss of Total water deficit should be corrected slowly; half of
both fluids and electrolytes in addition to impaired organ the deficit is administered in the first 3–6 hours, with the
function leads to the complications of heat illnesses. remainder over the next 6–9 hours.222
Factors contributing to heat illness include elevated Rapid cooling is the second priority: lowering core
ambient temperature, increased heat production due temperature to less than 38.9°C within 30 minutes
to exercise, infection and drugs such as amphetamines, improves survival and minimises end-organ damage.222
phenothiazines or other stimulants.217 The ideal goal is to reduce the core temperature by
0.2°C/min.222 Non-invasive external methods of cooling
Clinical manifestations include removal of clothing and covering the patient with
Environmental heat illness is more likely to develop a wet, tepid sheet. Ice packs can be placed next to the
when the ambient temperature exceeds 32–35°C and patient’s axillae, neck and groin. Invasive cooling measures
the humidity is greater than 70%.217,222 Assessment of the such as iced gastric lavage and cardiopulmonary bypass are
patient’s physical state and vital signs including GCS score reserved for the patient who fails to respond to conven-
provides some evidence of hypovolaemia and potential or tional cooling methods.217,222 Core body temperature
impending shock. should be monitored using a continuous rectal or tympanic
Heat exhaustion is a more severe form of heat illness probe. No randomised clinical trials have compared the
and is associated with severe water or salt depletion due effectiveness of different cooling methods.222

Summary
This chapter has provided an overview of important emergency systems and processes, outlining the practice of initial
assessment and prioritisation of patients presenting to the ED through the unique nursing process of triage. The role of
the emergency nurse in the initial assessment, intervention and management of the patient has been described.The initial
ED management of common emergency presentations was outlined, reflecting current practice and based on the latest
available evidence.
The emergency environment is dynamic, and it was beyond the scope of this chapter to describe the full extent of
emergency nursing practice and the clinical entities that are frequently managed. It is therefore important for a critical
care nurse to be familiar with the content provided in the other chapters in this text, as well as other resources. As noted
at the beginning of this chapter, other common presentations to the ED, such as trauma and cardiorespiratory arrest, are
described in Chapters 24 and 25.
Emergency nursing is a demanding specialty area of practice, as are all areas of specialty practice.The challenges with
emergency nursing come with the volumes of predicable patient groups, changing demographics in our community and
the unpredictable or unusual presentations. Emergency nurses need to prepare themselves with a broad knowledge base,
adaptability to change and resilience to meet these demands.
780 SECTION 3 SPECIALTY PRACTICE

Case study
0750 h: Maria Baxter, a 42-year-old woman, presented to the ambulance bay of the ED in a private car and
accompanied by her family for evaluation after a suspected overdose of insecticide. Maria’s partner and
sister approached the triage area stating that the patient had taken ‘another overdose and was vomiting’.
The triage nurse questioned Maria’s sister who revealed that she had deliberately drunk approximately one
cup of ‘insect killer’.

The triage nurse protected herself with a pair of gloves and a patient gown, then went to assess Maria, who
was sitting in the backseat of the car. On initial triage assessment, Maria was alert and able to talk, stating
that she ‘felt unwell’. The triage nurse noted that she had vomited and that there was a strong smell of a
garlicky oily-type substance coming from the car. The triage nurse immediately removed herself from the
area and contacted the shift coordinator of the ED to inform her of the incident, the need for assistance and
that staff should adopt a standard approach to a chemically contaminated patient.

Maria remained in the car while staff prepared a treatment area that was isolated from the department (a
single room with negative-pressure air flow and high-volume air extraction). Staff also applied personal
protective equipment to guard themselves from contamination. Three suitably-clothed nursing staff helped
Maria from the car. After minimal assessment, she was taken to an external shower, where she had her
clothing removed and placed in a sealed contaminated-waste bag. The patient was then given a shower
using warm, soapy water. It was noted at this point that an oily substance on and around her mouth and
hands turned white when water was applied. This was thoroughly removed and Maria was placed in the
isolation room of the ED.

0803 h: Maria was formally triaged with an ATS of 2, meaning she should be seen by a doctor within
10 minutes, based on her exposure to the chemical and the level of response required. Her initial observations
were: alert with pink, warm and dry skin; pulse 72 beats per minute; blood pressure 117/71 mmHg;
oxygen saturation 100%. Cardiac monitoring and supplemental oxygen therapy (6 L/min via Hudson
mask) were commenced. An IV cannula was inserted by an ED nurse and venous blood samples were
collected.

0810 h: Initial medical assessment noted the following additional history:

• Maria vomited twice, once in the car and once in the ED; this was followed by an episode of diarrhoea.
• Maria had taken an intentional ingestion of chlorpyrifos, estimated to be approximately half a cup at
0630–0645 h. Maria stated that she wanted to kill herself.
• The family members who had accompanied her appeared asymptomatic: that is, they had no physical
signs of organophosphate adsorption at this time; however, they were complaining of headaches and
feeling ill from the smell.
• On the container supplied by the family, the information label read ‘Super Buffalo Fly Insecticide, 20%
chlorpyrifos, 65% liquid hydrocarbon’.

0815 h: The Poisons Information Hotline was contacted for advice, with the following information
provided:
• Symptoms may have a delayed onset.
• The solution contains active metabolites.
• A serum cholinesterase level should be collected.
• An oral dose of activated charcoal should be administered.
• A dose of atropine may be given as a heart rate response test.
• Administration of pralidoxime was suggested if there was no response to atropine or an exacerbation
of symptoms was seen.

0825 h: Maria’s pulse rate was noted to be 110 beats per min. A dose of atropine 0.5 mg IV was administered
and her pulse rate rose to 125 beats per min. A CXR was also ordered.

0830 h: Maria developed mild sweating of the face and forehead. There was no increase in salivation but a
large amount of clear saliva was noted on the tongue. No muscle fasciculations were evident, and Maria’s
 CHAPTER 23 EMERGENCY PRESENTATIONS 781

pupils fluctuated from 4 mm to 1 mm in size. On auscultation her chest was clear, and good power was
evident in all limbs. At this time, staff discussed Maria’s progress with her concerned family, including the
potentially serious nature of the ingestion, and offered emotional support.

0845 h: Maria developed widespread muscle tremors but retained good muscle strength, including the
ability to cough and maintain adequate respiratory function. Her pulse rate rose to 144 beats per minute
with a blood pressure of 140/90 mmHg. A pralidoxime loading dose was ordered (1 g in 100 mL isotonic
saline) and commenced over 30 minutes, followed by a pralidoxime infusion (at 400 mg/h).

0850 h: An ICU review was requested and Maria was seen by the intensive care consultant. The consultant
agreed with the current management plan and accepted Maria as a suitable admission to the ICU. At
that time a bed was available and ready. The earlier CXR was reviewed and noted to be clear. The ICU
consultant also noted that the ECG showed a sinus tachycardia with no rhythm disturbances. At this time,
emergency staff caring for Maria began complaining of nausea and headaches. A rotation of the staff caring
for Maria was commenced.

0900 h: Maria had an increase in sweating, further diarrhoea, had developed a cough and increased
salivation, which required suctioning. But Maria was still able to talk, and her GCS remained at 15.
Other observations were: heart rate 130 beats per min, respiratory rate 24 breaths per min, blood pressure
140/95 mmHg and oxygen saturation 99%.

0910 h: With an ICU bed available, a transfer to the ICU was undertaken. Maria was transferred with full
monitoring and resuscitation equipment and with the ICU consultant, emergency doctor and an emergency
nurse escort.

0915 h: Maria’s condition suddenly deteriorated during transport to the ICU. Her level of consciousness
decreased, along with her respiratory effort. She was noted to be profoundly weak, with widespread
piloerection and muscle tremors. Assisted ventilation with bag–valve–mask resuscitator commenced.

0920 h: On arrival in the ICU Maria was unable to protect her airway due to profound weakness and a
reduced GCS. She was intubated with midazolam 3 mg and vecuronium 10 mg given for induction.

Summary of ICU admission: Maria required 3 days of ventilation. A pralidoxime infusion was required
for 2 days due to depleted cholinesterase levels. On extubation, Maria complained of a headache and
generalised weakness, but was able to eat, drink and mobilise. She spent a total of 5 days in the ICU before
being discharged to the mental health service.

Mental health admission summary: Maria was diagnosed as having a maladaptive situational response
and moderate depression with ongoing suicidal thoughts. She stated to staff that she would not use insect
killer again and had no other formal plan of how she might harm herself. The mental health admission was
for a total of 5 days. At hospital discharge Maria had no suicidal ideation. A community mental health team
follow-up was arranged.

CASE STUDY QUESTIONS

1 Why did Maria have her clothing removed and then her body washed with soapy water before entering
the ED?
2 Outline the physiological effects of atropine administration in the context of this poisoning. What are the
clinical end points for atropine therapy and how should this be monitored?
3 Pralidoxime is one pharmacological agent available to treat patients with symptomatic organophosphate
exposure. How does this drug work?
4 Maria’s family members requested to visit her during the initial management phase in the ED. How
would you handle this request?
Please consider the following issues:
a the current clinical safety for the patient
b management of family exposure to this substance/poisoning
c containment of the potential distribution of the substance within the ED.
782 SECTION 3 SPECIALTY PRACTICE

RESEARCH VIGNETTE

Muntlin A, Carlsson M, Safwenberg U, Gunningberg L. Outcomes of a nurse initiated IV analgesic protocol for
abdominal pain in an emergency department: a quasi-experimental study. Int J Nurs Stud 2011;48(1):13–23

Background: Abdominal pain is one of the most frequent reasons for seeking care in an emergency department.
Surveys have shown that patients are not satisfied with the pain management they receive. Reasons for giving
inadequate pain management may include poor knowledge about pain assessment, myths concerning pain, lack of
communication between the patient and healthcare professional and organizational limitations.

Objectives: The aim of the study was to investigate the outcome of nursing assessment, pain assessment and nurse-
initiated IV opioid analgesic compared to standard procedure for patients seeking emergency care for abdominal
pain. Outcome measures were: (a) pain intensity, (b) frequency of received analgesic, (c) time to analgesic, (d) transit
time, and (e) patients’ perceptions of the quality of care in pain management.

Design: A quasi-experimental (before–during–after) design was used.

Setting: The study was conducted in an emergency department at a Swedish university hospital.

Participants: Patients with abdominal pain seeking care in the emergency department were invited to participate.
A total of 50, 100 and 50 patients, respectively, were included for the three phases of the study. The inclusion criteria
were: ongoing abdominal pain not lasting for more than 2 days, ≥18 years of age and oriented to person, place and
time. Exclusion criteria were: abdominal pain due to trauma, in need of immediate care and pain intensity scored
as 9–10.

Methods: The patients’ perceptions of the quality of care in pain management in the emergency department were
evaluated by means of a patient questionnaire carried out in the three study phases. The intervention phase included
education, nursing assessment protocol and a range order for analgesic.

Results: The nursing assessment and the nurse-initiated IV opioid analgesic resulted in significant improvement in
frequency of receiving analgesic and a reduction in time to analgesic. Patients perceived lower pain intensity and
improved quality of care in pain management.

Conclusions: The intervention improved the pain management in the emergency department. A structured
nursing assessment could also affect the patients’ perceptions of the quality of care in pain management in the
emergency department.

Critique
This paper described the effect of introducing a nurse-led analgesia protocol for patients who presented to an ED in
Sweden with abdominal pain. Pain management in the ED in this and other groups is often poorly done everywhere.
In order to improve care delivery for this group of patients, a strategy that focused on nurse assessment, pain
assessment and nurse-initiated IV opioid analgesia was introduced. Educational sessions were delivered over a
one-month period prior to the introduction of the intervention. Most (n = 47) of the 50 registered nurses participated
in this requirement to use the analgesic order that was developed based on the literature and clinical experience.
It was also validated by the head of the ED, specialists in general surgery and registered nurses working in the
ED for relevance and clinical applicability. The order was based on a pain score range, following assessment of
the patient, and considered inclusion and exclusion criteria (e.g. allergy to morphine, pregnant, pain intensity >8,
circulation or respiratory condition) to assure patient safety and prevent adverse events (of which there were none).

Outcomes measures included: pain intensity, frequency of received analgesic, time to analgesia, transit time in the
ED and patients’ perceptions of the quality of care in pain management. These outcomes were measured before
(phase A1), during (phase B) and after (phase A2) the introduction of the intervention. This was a strong design given
the inability to undertake a randomised controlled trial (the optimal design choice to study the effect of an intervention)
due to practical and financial reasons. The authors provide justification for their sample size requirements (n = 50
in A1, 100 in B, 50 in A2) that was based on a power calculation and previously documented evidence of clinical
 CHAPTER 23 EMERGENCY PRESENTATIONS 783

significance. The tools and outcomes used in the study were based on previous research and, where indicated, have
been validated with minor adaption made in this study to suit the ED setting. The analysis, consisting of descriptive
and inferential statistics, was clear, thorough and considered, including Bonferroni correction to avoid reporting mass
significance when using the one-way analysis of variance test. Recognising potential areas where bias may occur,
the authors present important information such as: dropouts were not different in terms of age and gender to the
group that was included and there were no significant differences between patients in the three phases with respect
to background information.

Results from the study indicate that a structured nurse assessment protocol and nurse initiated IV opioid analgesic
can increase the frequency of pain assessment and received analgesia while also reducing the patient’s waiting time
for analgesia in the ED (median times: A1, 1.8 h; B, 1.0 h; A2, 1.7 h). Although there were some limitations to this study,
such as some external dropouts and incompleteness of questionnaires, there is some degree of generalisability of the
results to other settings with similar findings noted elsewhere.

Overall, this is a good example of a well-conducted study demonstrating how an evidence-based approach to
changes in nursing care can result in positive patient and service outcomes at a relatively low cost.

Lear ning a c t iv it ie s
These learning activities will require you to investigate plans that exist in your clinical areas, and demonstrate an
understanding of an approach to a chemically contaminated patient, important emergency interventions and aspects
of personal protection for the responder and the clinical unit where the patient has presented.

1 Review your department’s plan for the management of a potentially chemical-contaminated patient.
2 Outline what PPE your department has available for staff use.
3 Describe the routes by which organophosphates can be absorbed and how inadvertent staff exposure can be
minimised.

Online resources
American Emergency Nurses Association, www.ena.org
Australasian College for Emergency Medicine, www.acem.org.au
Australian College of Emergency Nursing, https://acen.com.au
Australian Institute of Health and Welfare, www.aihw.gov.au
Australian Venom Research Unit, www.avru.org
Best Bets, www.bestbets.org
Clinical Toxinology Resources, Women’s and Children’s Hospital, Adelaide, www.toxinology.com
College of Emergency Nursing Australasia, www.cena.org.au
College of Emergency Nursing New Zealand, www.nzno.org.nz/groups/colleges/college_of_emergency_nurses
Commonwealth Serum Laboratories Antivenom Handbook eMedicine, www.emedicine.com
Emergency Nursing World, http://enw.org
National Asthma Council of Australia, www.nationalasthma.org.au
National Institute of Clinical Studies, Emergency Care Community of Practice Project, www.nicsl.com.au
New Zealand Health Information Service, www.nzhis.govt.nz
New Zealand Ministry of Health, www.moh.govt.nz
784 SECTION 3 SPECIALTY PRACTICE

Poisons Information Australia, telephone: 131126

Poisons Information New Zealand, phone: 0800 POISON or 0800 764766
The Cochrane Centre, http://acc.cochrane.org

Further reading
White J. A clinician’s guide to Australian venomous bites and stings: Incorporating the updated CSL Antivenom Handbook.
CSL Ltd, <http://www.toxinology.com/fusebox.cfm?staticaction=generic_static_files/cgavbs_avh.html>; 2013.

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208 Shepherd S. Submersion injury, near drowning, <http://www.patient.co.uk/doctor/Drowning-and-near-drowning.htm>; 2010 [accessed 12.14].
209 Moon R, Long R. Drowning and near-drowning. Emerg Med 2002;14(4):377-86.
210 World Health Organization. Guidelines for safe recreational water environments: Drowning and injury prevention, <http://www.who.int/water_
sanitation_health/bathing/srwe1/en/> [accessed 05.14].
211 Ibsen L. Submersion and asphyxial injury. Crit Care Med 2002;30(11 Suppl):402-8.
212 Handley AJ. Drowning. BMJ 2014;348:g1734.
213 Fiore M. Near drowning, <http://www.emedicine.com/ped/topic2570.htm>; 2009 [accessed 12.14].
214 Rodgers I. Hypothermia. In: Cameron P, Jelinek G, Kelly A, Murray L, Heyworth J, eds. Textbook of adult emergency medicine. Edinburgh:
Churchill Livingstone; 2009, pp 852-4.
215 Ko C, Alex J, Jefferies S, Parmar J. Dead? Or just cold?: profound hypothermia with no signs of life. Emerg Med J 2002;19:478-9.
216 Bressen H, Ngo B. Hypothermia. In: Tintinalli J, Stapczynski J, Ma J, Cline D, Cydulka R, Meckler G, eds. Emergency medicine; A
comprehensive study guide. American College of Emergency Physicians. 7th ed. New York: McGraw-Hill; 2011, pp 1335-9.
217 Rodgers I, Williams A. Heat related illness. In: Cameron P, Jelinek G, Kelly A, Murray L, Heyworth J, eds. Textbook of adult emergency
medicine. Edinburgh: Churchill Livingstone; 2009, pp 848-51.
218 Krantz M, Lowery C. Giant Osborne waves in hypothermia. N Engl J Med 2005;352(2):184.
219 Tsuei B, Kearney P. Hypothermia in the trauma patient. Injury 2005;35(1):7-15.
220 Sessler D. Complications and treatment of mild hypothermia. Anesthesiology 2001;95(2):531-43.
221 Hildebrand F, Giannoudis P, van Grievensen M, Chawda M, Pape H-S. Pathophysiologic changes and effects of hypothermia on outcome in
elective surgery and trauma patients. Am J Surg 2004;187(3):363-71.
222 Waters T, Al-Salamah M. Heat emergencies. In: Tintinalli J, Stapczynski J, Ma J, Cline D, Cydulka R, Meckler G, eds. Emergency medicine;
A comprehensive study guide. American College of Emergency Physicians. 7th ed. New York: McGraw-Hill; 2011, pp 1339-44.
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224 Yeo T. Heat stroke: a comprehensive review. AACN Clin Issues 2004;15(2):280-93.
 Chapter 24

Trauma management
Catherine Bell, Kerstin Prignitz Sluys

KEY WORDS Learning objectives

abdominal trauma After reading this chapter, you should be able to:
burns • identify the benefits and limitations of an organised trauma system
chest trauma • describe the rationale for a systematic approach to the patient who has
damage-control sustained injuries
surgery • discuss the benefits of appropriate management of the patient with
fractures serious injury and/or multitrauma
multitrauma • describe the acute management of the patient with multiple serious
fractures
transport
• describe the acute management of patients with burn injuries, abdominal
trauma
injuries and chest trauma
• describe the nurse’s role in managing the trauma patient undergoing
interim damage-control surgery.

Introduction
Trauma is one of the leading public health problems and the most common
avoidable cause of death among children and adults under 45 years of age
throughout the world.1–5 The World Health Organization (WHO) reports that
almost 6 million people die every year and 100 million are admitted to hospital
after traumatic injury, accounting for 16% of the world’s disease burden.2,4
Survivors incur temporary or permanent impairments and disabilities resulting
in human suffering, major social consequences and economic cost for the
individual, families and society. The most common cause of death from trauma
worldwide is traffic accidents, and more than 90% of the deaths occur in low
and middle income countries.6
The injury epidemiology for trauma differs with severity. The majority of
trauma patients requiring admission to an ICU are those with more serious
injuries that are associated with motor vehicles, motorbikes and pedestrian
collisions. Falls, self-inflicted injuries and assaults are less common, but still
frequent, causes of trauma requiring critical care admission. A significant
proportion of injured patients admitted to critical care have experienced
neurotrauma (see Chapter 17), while other common injuries include multiple
fractures and injury to internal organs in the thorax and abdomen.
792 SECTION 3 SPECIALTY PRACTICE

The systematic organisation of trauma systems, major initial reduction observed when a trauma system is first
changes in practice and delivery of time-critical interven- implemented.9
tions have made the traditional boundaries more seamless
between pre-hospital emergency medical service and Pre-hospital care
hospital-based emergency, surgery, radiology and intensive There are multiple purposes of pre-hospital care, including:
care services, improving the survival of trauma patients in • providing appropriate care at the scene
recent years. Consequently, a greater number of patients
with severe multiple injuries are now admitted to critical • transporting the patient to the most appropriate
healthcare facility for further management
care units. These patients generally require complex
nursing care, often for lengthy periods, both within the • reducing the occurrence of preventable death and
critical care unit and beyond. The common traumatic disability associated with trauma.
injuries that result in admission to critical care and the The optimal pre-hospital trauma care model is in doubt
principles of management are outlined in this chapter. with the debate of whether pre-hospital time or initial
treatment occurring in a hospital is the more relevant
Trauma systems and to decreasing mortality in the trauma population.17 The
focus of treatment should be on:
processes • rapid primary assessment
A trauma system can be defined as: • maintaining a patent airway
an assembly of health care processes intended to improve survival • immediate control of external haemorrhage
among injured patients by reducing the time interval between
injury and definitive treatment, and by assuring that appropriate
• immobilisation of the patient
resources and personnel are immediately available when a patient • rapid transfer to an appropriate trauma centre.18
presents to a hospital’.7 The principle of the ‘golden hour’ is commonly referred
Trauma systems should be ‘designed to provide citizens to in trauma literature, with the belief that trauma patients
with prompt, safe and effective access to the health-care have better outcomes if they are provided definitive care
system in times of urgent need. Each system must be within 60 minutes of injury. This is the basis for concepts
defined by local needs and assessments of capacity and such as ‘scoop and run’, aeromedical transport and trauma
developed with due regard for local culture, legislation, centre designation with trauma teams in place that are
infrastructure, health-system capacity, economic consider- seen to have an impact on the management of the injured
ations and administrative resources’.8 p 13 patient.19 In the USA a reduction in mortality in those
Over the last 30 years there has been significant patients transported by air rather than traditional methods
evolution of trauma systems and planning for how major has been seen,20 whereas others have suggested that the
trauma is managed.9 The World Health Organization timely triage of the injured to the closest most appropriate
(WHO) suggest that pre-hospital trauma care systems facility is essential.21
cannot function in isolation and must be fully integrated In countries with large distances to designated trauma
into existing public health and healthcare infrastructure to centres this can pose a problem; however, it has been
be effective.8,10 shown that the disadvantage of spending more time at the
Trauma systems are inclusive of all areas of health care scene is possibly diluted by the delivery of high standards
that are involved in the management of the trauma patient of care using the principles of Advanced Life Support
from injury through to discharge or death, to enable the (ALS). There is controversy about whether treating
scope of improvement to be targeted at any area across the life-threatening events at the scene or first hospital rather
continuum of care.11,12 Although many studies have found than at a trauma centre reduces mortality or not.17,20,22
that regionalisation of trauma care has been associated with Treatment at the scene may be delivered by personnel
reduced mortality,13 the impact on the quality of survival with differing levels of expertise worldwide, with some
of trauma patients has not been systematically explored.14 countries in Europe having doctors at the scene while
One possible explanation for improved outcome in those countries such as Australia, the USA and UK have highly
patients who are admitted to a major trauma service is the trained paramedics.21 Other countries may rely on first
expertise and experience of all staff caring for this cohort responders who may only have the capacity to administer
and the greater access to rehabilitation services, which Basic Life Support (BLS).10
may contribute to improved functional outcome.14,15 In areas where trauma systems have been implemented
Despite the lack of empirical evidence supporting processes are in place to facilitate advance notice being
the benefits of implementing trauma systems,16 interna- given to the trauma centre to enable the assembly of a
tionally it is suggested that the mortality rate is reduced multidisciplinary group of health professionals who can
by 15–40% when a trauma system is implemented.9 In provide immediate assessment, resuscitation and treatment
developed countries where trauma systems have been of the injured patient.23–25 Such trauma teams have been
established the likelihood of continued improvement shown to provide benefit in the early management of
in mortality is seen to be small in comparison to the trauma patients, and are reviewed later in this chapter.25,26
 CHAPTER 24 TRAUMA MANAGEMENT 793

Transport of the critically ill trauma The following principles apply during such phases
of care:
patient
Transporting severely injured patients directly from the
• There must be adequate preparation of the patient
and equipment.
scene of injury to a designated trauma centre is considered
optimal;12,27 however, there are risks involved in any
• Transport must occur by personnel with appropriate
levels of expertise.
transfer and the goal should be to provide the best care
possible while reducing those risks to the patient.21,23 In • Necessary equipment, including batteries and pumps,
should be secured.
general, with any patient transfer the level of health care
available should be maintained or increased at each stage.13 • Patients should be stabilised prior to transport (while
Transport of critically injured patients occurs at two balancing the need for timely transport).
stages in the patient’s care. Primary transport occurs from • Monitoring of relevant aspects of the patient’s care is
the scene of injury to the first healthcare facility that essential.
provides care to the patient; this is sometimes referred • Adequate vascular access and airway control must be
to as pre-hospital transport. Secondary transport occurs secured prior to commencing transport.
between healthcare facilities; this is sometimes referred • Effective communication is mandatory between
to as inter-hospital transport. This chapter concentrates referring, transporting and receiving personnel.
on secondary transport, although many of the principles • Documentation, including X-rays and scans, should
are similar for both stages of transport. Secondary accompany the patient and should cover the patient’s
transport principles are also relevant for critically status, assessment and treatment before, during and on
injured patients being transferred within departments completion of the transport.
in a healthcare facility (see Chapter 6). Transport of a • Relatives should be informed of the transfer, including
patient between healthcare facilities may occur for destination, and provided with assistance for their own
clinical reasons, such as specialist or higher levels of care travel arrangements.32 Checklists itemising many of
being required, or for non-clinical reasons, such as bed these principles, sometimes attached to an envelope
availability. It is preferable for patient transfer to be for containing all transfer documentation, are often used to
clinical reasons only. ensure that all necessary actions are undertaken.30
Secondary transport of critically injured patients
may occur via ground or air (by fixed-wing aircraft or Trauma reception
helicopter).28 The decision as to what form of transport to Reception of the trauma patient at the emergency
use will depend on: department of the hospital is generally performed by
• the condition of the patient the triage nurse, with patients managed in a designated
resuscitation area and received by a trauma team.13 In the
• the potential impact of the transport medium on the severely injured patient it is usual for a multidisciplinary
patient
team to receive the patient and commence assessment
• the distance to be covered and treatment concurrently. In the setting of a mass-
• the urgency of the transport casualty incident, triage may be performed in the field.
• the environmental conditions Despite documented benefits, such as shorter emergency
department (ED) time, ED to computed tomographic
• the resources available imaging time, ED to operating room time and improved
• the expertise of the respective transport teams. survival, having a trauma team is not universal, even within
Amenities such as landing sites, particularly for heli- advanced trauma systems.33 For example, only 20% of UK
copters, being in close proximity to healthcare facilities hospitals have a trauma team available.13
must also be considered. Different jurisdictions activate In the ED, the trauma team receives the patient after a
air retrieval using helicopters when the distance for the comprehensive, clear handover that is heard by the entire
transport is beyond a certain point, with the minimum team. The importance of a handover from the paramedics
distance ranging from 16 to 80 km.11,27,29,30 cannot be overestimated.34
It is essential that the standard of care is not The formal process of triage provides a means of
compromised during transport of critically injured categorising patients based on threat to life. Although
patients. Minimum standards exist that outline the there are many different triage systems in use the most
requirements for transport of critically injured patients, commonly used ones are the MTS, the Canadian Triage
and these should be referred to for full details.27,31,32 Assessment Scale and the Australasian Triage Score (ATS).
Consideration should be given to both the conscious The Canadian Triage Assessment Scale and the ATS are
patient and the restless, anxious or combative patient in similar as they both use a time-to-treatment objective
ensuring adequate preparation prior to transfer. These scale, while the MTS is an algorithm-based approach
preparations might include anti-emetics and sedation to to decision making involving the selection of one of
ensure the safety of both the patient and the personnel 52 algorithms.35,36 See Chapter 23 for further description
involved in the transport.21 of the ATS.
794 SECTION 3 SPECIALTY PRACTICE

Primary survey is activated on notification of the imminent arrival of a

Priorities of care are similar to those in all health settings, severely injured trauma patient. Radiological investiga-
with airway, breathing and circulation taking precedence tion is dependent on the type of injury sustained, but will
during the primary survey (see Chapter 23). Disability and generally consist of a portable X-ray of the injured area/s
exposure/environment are essential elements that should if these include the chest, cervical spine or pelvis. Other
follow.37 These components of care will often occur X-rays at this stage are rarely beneficial, or rarely change
simultaneously rather than sequentially and are designed the course of treatment.
to identify immediately life-threatening injuries.37 If the patient is sufficiently stable after the secondary
Compromise to airway and breathing may result from survey, more extensive investigation in the radiology
direct injury, for example to the trachea, or indirectly department should be undertaken. This will include CT
through decreased level of consciousness. Compromise to scans. It is essential that clinicians consider investigations
circulation is usually as a result of significant blood loss carefully, to ensure that all necessary imaging is undertaken;
although it may occur as a result of injuries, such as cardiac for example, where a CT scan of the brain is required it is
contusions in chest trauma, or the patient’s pre-existing often prudent to also undertake a CT scan of the cervical
disease. The evaluation of patients after trauma must be spine. However, care should be taken to avoid investi-
rapid, systematic and organised, and include: gations that will not change the planned treatment but
may delay urgent interventions such as surgery. Current
• airway with cervical spine precautions controversies in radiation exposure and lifetime-associated
• breathing cancer risks need to also be considered.21
• circulation with control of external haemorrhage Furthermore, there are not insignificant implica-
tions of moving the patient on and off imaging tables for
• disability, including brief neurological assessment repeated imaging. The patient should be accompanied
• exposure/environment, including prevention of and monitored by a competent nurse during all transfers
hypothermia when removing clothing37 for investigation. Where the patient is requiring ongoing
• prevention of complications or further compromise. advanced life support such as fluid resuscitation or airway
monitoring, it may also be appropriate for a medical
Secondary survey officer to accompany the patient.
Following stabilisation of the life-threatening problems Further radiological investigation may be required
identified during the primary survey, patients should as part of the tertiary survey. This will depend on the
undergo a secondary survey (see Chapter 23). This is a radiological examinations that have been undertaken
systematic examination of the body regions to identify as part of the secondary survey, the treatment that has
injuries that have not yet been recognised. It is essential already been administered and the current condition of
that both the front and the back of the patient, as well as the patient.
areas covered by clothing, are examined during this process.
Focused assessment with sonography for trauma
Tertiary survey Where abdominal trauma is suspected, a focused
A tertiary survey should be conducted upon the arrival assessment with sonography for trauma (FAST) exam-
of trauma patients in the ICU, or soon after. The purpose ination22,23 is likely to be used as part of the secondary
of this third survey is to identify injuries that have not yet survey to determine whether free fluid is present in
been detected, assess initial response to treatment and plan the abdominal cavity. The abdomen is scanned in four
assessment and management strategies for future care. zones – pericardial, Morison’s pouch (right upper
The tertiary survey consists of another head-to-toe quadrant), splenorenal (left upper quadrant) and pelvis
physical examination, assessment of the patient’s condition (Douglas’ pouch).This generally takes 1–2 minutes when
in the context of his/her earlier condition and the performed by an experienced, credentialled clinician.
treatment that has been administered, a full review of all Findings are regarded as positive (fluid [blood] observed),
diagnostic information gained so far and acquisition of the negative or equivocal. Technical difficulties can be expe-
patient’s past health history if family members or friends rienced with obese patients. While a positive FAST is
are available. A systematic approach will minimise the useful in identifying if a patient should receive urgent
number of injuries that are not identified during the first surgical intervention, a negative FAST does not rule out
24 hours of care. It is also important to repeat the tertiary significant abdominal trauma, and the low sensitivity of
survey after the patient regains consciousness and begins FAST remains a concern for trauma clinicians.22 Where
to mobilise. Joint injuries may only become apparent a patient is undergoing a prolonged trauma resuscitation
during weight-bearing movements. phase, there may be an indication to repeat the FAST
after 20 minutes. The use of FAST examination outside
Radiological and other investigations the trauma resuscitation and reception phase is occurring
Initial radiological investigations will usually be performed more often and can be undertaken in any clinical setting
in the emergency department using portable equipment. where there is a suspicion of internal haemorrhage or
A radiographer is often a member of the trauma team that pneumothorax.24
 CHAPTER 24 TRAUMA MANAGEMENT 795

Trauma teams from burns. Specific considerations relating to penetrat-

ing injuries have been covered separately, although the
There are a number of different ways to organise the early
majority of care for patients with penetrating injuries will
care of trauma patients. The most common method used
follow the principles of the area of injury. For example,
is through the establishment of multidisciplinary trauma
a patient with a penetrating injury of the abdomen will
teams that can provide immediate, expert assessment, generally be cared for in the same way as all patients with
resuscitation and treatment of traumatised patients, abdominal trauma.
especially those with multiple injuries.38 The purpose of Patients with multi/poly-trauma will also be cared for
the trauma team is to provide a coordinated and collab- according to the principles of care for each specific injury,
orative approach by relevant specialists to the injured although consideration of priorities is essential. Care
trauma patient in a designated resuscitation area10,38,39 with should follow the common principles of airway, breathing
the performance of the team being greater than the sum and circulation as developed by the American College
of the individuals. of Surgeons over 30 years ago,23 hence concentrating
Many hospitals that receive trauma patients operate on respiratory and circulatory compromise first, before
trauma teams that are either activated or placed on standby, moving on to the treatment of other injuries. The relative
via pagers or telephone, based on communications from importance of other injuries, for example neurological
paramedic personnel in the pre-hospital setting.40 This trauma or skeletal trauma, will vary for each individual
activation is based on a combination of physiological and patient and will be dependent on the physiological impact
injury criteria (Table 24.1). Age is sometimes added to the of the injuries. Neurological and spinal cord injury are
patient criteria, with those under 5 years or over 65 years reviewed in Chapter 17.
receiving particular attention. A number of hospitals have
two levels of trauma team activation, with patients with Mechanism of injury
more severe injuries activating the full trauma team and Trauma refers to the physical injury that is caused by a
those with less severe injuries activating a partial team.The mechanism of injury or kinetic injury. The principles of
use of two-tiered trauma team activation has not been kinetic energy associated with blunt trauma are generally
shown to affect patient outcomes.25 those of acceleration and deceleration forces that can lead
to shearing or compression injuries, while penetrating
TABLE 24.1 injury is proportional to the velocity of the object striking
Criteria for activation of trauma teams131,130 tissue and the associated energy dissipation leading to
either permanent or temporary cavitation.37
PHYSIOLOGICAL CRITERIA I N J U RY C R I T E R I A The most common mechanisms of injury are either
Heart rate <50 or Penetrating injury to head, blunt or penetrating injury. The third, less common
>120 beats/min neck or torso mechanism of injury is blast injury, usually as a result of
Respiratory rate <10 or Burn to ≥20% body surface explosions that can be related to industrial or recreational
>29 breaths/min area accidents or terrorist acts.The mechanisms of blast injuries
Systolic blood pressure Fall ≥5 metres include:
<90 mmHg
Glasgow Coma Scale
Multiple trauma
Crush or degloving injury to
• primary blast injury – blast overpressure reaches the
person and transmitted forces exert their effects on
score <10 extremity the body, causing direct tissue damage
Skin pale, cool or moist Amputation proximal to the
Paralysis wrist or ankle • secondary blast injury – created by debris that is
Trauma arrest Motor vehicle crash with
physically displaced by the blast overpressure
ejection • tertiary blast injury – caused when the person is
physically displaced by the force of the peak over-
Adapted with permission from: pressure and blast winds leading to blunt traumatic
Richards CE, Mayberry JC. Inital management of the trauma injuries being sustained
patient. Crit Care Clin 2004;20(1):1–11.
• quaternary blast injury – miscellaneous blast injuries
Kohn MA, Hammel JM, Bretz SW, Stangby A. Trauma team caused directly by the explosion including injuries
activation criteria as predictors of patient disposition from the such as burns, toxic substance exposure
emergency department. Acad Emerg Med 2004;11(1):1–9.
• quinary blast injury – a hyperinflammatory state
manifested by hyperpyrexia, diaphoresis, low CVP
and positive fluid balance.41
Common clinical presentations In 2008 traumatic injury was ranked as the ninth
Trauma generally occurs to a specific area of the body leading cause of unintentional injury, and by 2030 it is
(e.g. the chest or the head) or consists of an injury predicted to be the fifth leading cause of injury.6 Leading
caused by a specific external cause (e.g. burns). This causes of injury include road traffic crashes, drowning,
section has been arranged according to these specific burns, poisoning and falls.42 The mechanism of injury is
types of injury, including skeletal, chest, abdominal and recognised as affecting both survival and requirements
796 SECTION 3 SPECIALTY PRACTICE

for admission to ICU. The largest proportion of serious The principles of positioning and mobilisation are
injuries is related road crashes and makes up approxi- generally not different from those in other critically ill
mately 33% of unintentional injury deaths.42,43 Patients patients, and should incorporate the need to:
who are injured in a road traffic crash experience a similar • promote the patient’s comfort
mortality to those injured through falls (approximately
3% in all patients and 10–17% in major injury patients), • maintain the patient’s and staff members’ safety
with both groups having a higher mortality than patients • prevent complications
injured in assaults and collisions with objects (<1% in • facilitate delivery of care.
all patients and 12% in major injury patients).41,42 While Difficulty in positioning and mobilisation is often
motor vehicle related deaths in Australia and many experienced when there is concern for the stability
developed countries have fallen, the numbers of pedal of the patient’s spine, in particular the cervical spine in
cyclist deaths and drownings have increased over the the unconscious patient. Specific protocols such as the
same period.42 Falls account for one-third of injuries in NEXUS criteria and the Canadian C-Spine Rule21 are
the over-65-years age group or approximately 11% of used for confirming the absence of injury to the cervical
unintentional injury deaths,40 with approximately 20% spine. Patients are considered to be at extremely low risk
requiring healthcare attention. of cervical spine injury if the following criteria are met:
Injuries sustained in road traffic crashes tend to • no midline cervical spine tenderness
be more severe given the high velocity of the trauma
and account for the greatest number of major injuries, • no focal neurological deficit
including those injuries that require admission to a • no evidence of intoxication
critical care unit.43 In addition, they are associated with • no painful distracting injuries
a higher proportion of disability life-years lost annually • no altered mental status.44
with road traffic injuries accounting for approximately For those patients who exhibit any of the above criteria a
17.5% in comparison to 12.2% for falls as reported clinical examination is unreliable and radiographic assessment
by the World Health Organization.42 is advised.The debate continues as to whether these protocols
The older age group, with associated comorbidities, should be used in any patient who is unconscious, intox-
is likely to account for many of the deaths in the group icated or complaining of cervical soreness or abnormal
injured through falls. In addition, patients injured in road neurology. The following principles should be incorporated
traffic crashes tend to spend longer in the intensive care into confirming the presence or absence of injury:21,44
unit than patients injured through falls or assaults and
collisions, and experience a greater number of injuries.43 • Obtain a detailed history of the injury wherever
possible, including specific investigation of
Generic principles of management of mechanisms of injury that might exert force on the
cervical spine. A high index of suspicion should
the injured patient remain, particularly in the setting of injuries often
Nursing care of trauma patients is characterised by the associated with cervical spine injury, including
need to integrate practices directed towards limiting the craniofacial trauma, rib fractures, pneumothoraces and
impact of the injury and healing injuries to multiple body damage to the great vessels and/or trachea.
areas in a complex process. The delivery of critical care
services must be systematic and must cross both team and
• Undertake plain X-rays of the full length of the spine,
interpreted by a radiologist.
departmental barriers to achieve a coordinated approach.
This section outlines the principles of care relevant to • Where any abnormality exists in clinical or
radiological assessment, or the patient remains
all trauma patients, including positioning, mobilisation
unconscious, a CT or MRI may be undertaken,
and prevention or minimisation of the trauma triad and this must be reported on by a radiologist.
components of hypothermia, acidosis and coagulopathy.
• A correctly fitted hard collar should remain in place
Positioning and mobilisation only until the patient is appropriately reviewed and the
Appropriate positioning and mobilisation can be a signif- chance of a cervical spine injury is eliminated. If a collar
icant challenge, especially in those patients with multiple is required for more than 4 hours, a long-term collar
injuries that create competing needs. Positioning refers (e.g. Philadelphia, Aspen or Miami J) should be used.
to the alignment and distribution of the patient in the • Maintain appropriate pressure area care to areas under
bed, for example supine, Fowler, semirecumbent or prone. the hard collar as well as the usual pressure points
In addition to these fundamental nursing postures, there until cervical clearance is gained.45
is positioning of the limbs (i.e. elevated arms and legs). The practice of maintaining a patient in a hard collar for
Mobilisation refers to the movement of joints by the days without active attempts to gain cervical clearance
patient, to shift from one place to another.This movement should be avoided at all costs.
may be restricted to rolling within the bed, or moving out The two methods available for moving the trauma
of the bed. patient are staff manual handling and lifting hoists.
 CHAPTER 24 TRAUMA MANAGEMENT 797

Generally, trauma patients can be log-rolled (see Figure

24.1 for initial care) as frequently as required for nursing Practice tip
care. Any restrictions to patient positioning and weight The NEXUS low-risk criteria have been widely accepted
bearing due to injuries or physiological status must be as identifying patients in whom further examination is
considered through this process; it is essential that care unnecessary and cervical spine injury can be excluded
be taken to prevent any worsening of injuries due to on the basis of clinical examination.44
handling of the patient. Although the benefits of immobil-
isation of the cervical spine have not been demonstrated Adapted with permission from Ackland H. Spinal clearance
through research, it is a practice that is supported by years management protocol. Melbourne: Alfred Health, <http://www.
of cumulative trauma and triage clinical experience45 and alfred.org.au/Assets/Files/SpinalClearanceManagement
should be used to prevent worsening of injuries. Protocol_External.pdf>; updated 24.11.09.
Knowledge of the position restrictions for each limb,
including all weight-bearing joints and the vertebrae, is The ‘trauma triad’
imperative to avoid secondary iatrogenic injury. Certain The critically injured patient can experience the ‘trauma
injuries will impose position and mobility restrictions (see triad’ of hypothermia, acidosis and coagulopathy. These
Table 24.2). pathophysiological conditions can occur individually;
however, they often occur simultaneously. Hypothermia
Practice tip
is a known contributor to the development of acidosis
When planning positioning and mobilisation of the and coagulopathy. This relationship between the three
trauma patient, ascertain the weight-bearing status of conditions can contribute to a mortality rate of 35–90%
each injured limb/body region, then determine positions in severe trauma patients.46,47
or methods of mobilisation that are appropriate. Acidosis has been discussed in earlier chapters so is
Consultation with allied health professionals such as reviewed here only as it interacts with hypothermia and
physiotherapists may aid in planning. coagulopathy in the trauma setting. Low cardiac output,
hypotension, hypoxia, hypothermia and rhabdomyolysis

FIGURE 24.1 Spine movement precautions.123

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Modified from Howard PK, Steinmann RA, Sheehy SB. Sheehy’s emergency nursing: Principles and practice. St Louis: Mosby
Elsevier; 2010, with permission.
798 SECTION 3 SPECIALTY PRACTICE

Accidental hypothermia can occur without thermo-

TABLE 24.2 regulatory dysfunction, and generally occurs in the trauma
Position and mobility restrictions in trauma patients patient as a result of environmental exposure either at the
injury site or during transport to, or between, healthcare
TYPE OF
I N J U RY RESTRICTIONS
facilities, as a result of large-volume fluid resuscitation46
or during prolonged surgical procedures. The patho-
Traumatic • Nurse head up 15–30° physiological changes associated with hypothermia vary
brain injury • Side-lying as tolerated
depending on the severity, and are outlined in Chapter 23.
• Full tilt on bed if cervical spine not yet
Of particular relevance, shivering leads to increased
cleared of injury
oxygen consumption and acidosis; platelet dysfunc-
• Occasionally nursed flat if ICP
problematic
tion leads to impaired clotting,50,52,54 while haemorrhage
reduces the circulating volume, which in turn may lead
Facial trauma • Generally nurse in head-elevated to a reduction in core body temperature and hypoper-
position to reduce swelling, using either
fusion of tissues. Hypoperfusion may cause hypoxia and
full bed tilt or back rest elevation
subsequent production of lactic acid, which in turn slows
Chest trauma • Nurse in varying positions from semi- the clotting cascade allowing haemorrhage to continue.46
Fowler to side-lying Measures to reduce the incidence of hypothermia – or
• Postural drainage (head down) usually to correct it when it is present – in the trauma setting
beneficial if not contraindicated by other include:
injuries (e.g. head or facial)
Abdominal • Nurse in varying positions from semi-
• ensuring the patient is adequately covered during
transport and hospital care
trauma Fowler to side-lying
• Preferable to have some degree of hip
• warm intravenous fluids
flexion when lying supine to reduce • using warm blankets or electrical warming blankets
abdominal suture line tension • adjusting the temperature in the operating room
Pelvic trauma • Position restrictions are dependent on
where feasible.53
severity of fracture(s), use of external In extreme cases of hypothermia methods of rewarming,
fixateurs and degree of stabilisation such as cardiopulmonary bypass and peritoneal dialysis or
• Some patients may sit out of bed and lavage, might be used.
ambulate with external pelvis fixateur in
situ Coagulopathy
• Position restrictions require regular Coagulopathy is a term used for a group of conditions
review, as changed or loss of fixation in which there is a problem with the process of blood
may affect recovery clotting.46 These are widespread in the trauma setting,
Extremity • Significant position restrictions may ranging from mild defects in coagulation function to
trauma include limb elevation, avoidance of life-threatening coagulopathy. Defects in coagulation may
side-lying or limited movement be caused by dilution, hypothermia, acidosis, tissue damage
or the effects of the underlying disease.46,53,55
ICP = intracranial pressure.
Dilution results from the transfusion of either crystal-
loid or colloid fluids, and occurs as the concentration of
coagulation factors in the patient’s blood is diluted with
are common causes of acidosis in the trauma setting. the transfused fluid. It should be remembered that trans-
The increased recognition of the importance of this fusion of red blood cells has the same effect, as whole
triad in the trauma setting has led to the development of blood or packed cells have undergone some dilution and
damage-control surgery.48 The principle of this surgery is have reduced viability of platelets.56
reviewed below. Preventing or intervening early in acute traumatic
Hypothermia coagulopathy is an important goal for all major traumas,
but may be even more important in the elderly or chronic
Hypothermia is defined as a core temperature <35°C46,49
disease population who are on anticoagulants and anti-
and is associated with high morbidity and mortality. Even
platelet agents.47,57
in subtropical environments, hypothermia is identified
in approximately 10% of major trauma cases during the
Practice tip
pre-hospital or in-hospital phase of care.50,51
Uncontrolled causes of hypothermia can be endogenous Check whether trauma patients are on anticoagulant
or accidental.51–54 Endogenous causes include metabolic or antiplatelet agents, particularly those patients who
dysfunction with decreased heat production or central have chronic disease or are elderly. If patients are taking
nervous system dysfunction with insufficient thermoregu- these medications, be on the alert for complications
lation such as in neurological trauma. Dermal dysfunction, associated with coagulopathy.
such as a burn, is another endogenous cause of hypothermia.
 CHAPTER 24 TRAUMA MANAGEMENT 799

Hypothermia causes coagulopathy because many of Damage-control surgery

the enzymatic reactions in coagulation are temperature- The goals of controlling haemorrhage and prevention of
dependent.53 Platelet and thromboplastin function both contamination while limiting the stress of surgery to the
decline with even moderate (34°C) hypothermia, while patient are the underlying principles of damage-control
hypothermia stimulates fibrinolysis.46,53 surgery (DCS).55 Initially, DCS was used for injuries
Acidosis reduces the activity of both extrinsic and sustained in the abdomen but this has now expanded to
intrinsic coagulation pathways, as well as platelet function. include thoracic, skeletal and vascular injuries.61
This is particularly pronounced with a pH below 6.8.53
DCS can be seen as encompassing up to five stages
Tissue damage causes endothelial disruption and defi-
including: 1) the early recognition of relevant patients,
brination, which promote the systemic activation of
2) repair of structures to achieve haemostasis and restore
coagulation; this is particularly profound in patients with
distal vascularity, 3) correction of physiological insult from
brain injury due to the high level of thromboplastin in
the initial trauma and subsequent surgery, 4) secondary
brain tissue.51,53,58
return to theatre for definitive surgical procedures and
The final cause of coagulopathy in trauma is the
5) final closure of injury once the visceral oedema has
underlying disease present in many patients. Patients may
have a coagulation defect, such as haemophilia or von subsided in those patients where it is required.55,62 This
Willebrand’s disease, or liver disease with resultant approach to surgical correction of traumatic injuries gained
compromise to coagulation on an ongoing basis. Alterna- favour through the latter part of the 1990s and is intended
tively, patients may be taking anticoagulants, such as aspirin to reduce the development of the triad of complications
or warfarin, as treatment for other health conditions.51,59 of hypothermia, acidosis and coagulopathy.55,61 Mortality
Treatment of coagulopathy should focus first on among patients in the 1990s who received traditional
prevention of coagulopathy and then on amelioration as definitive surgery versus the newer concept of DCS was
required. Prevention strategies include:56 similar, although a subset of patients with multiple visceral
injuries and a vascular injury showed improved survival
• maintaining normothermia in critically injured with DCS (77% vs 11%).61
patients through the use of blankets and warming Other adjuncts to DCS and damage-control resus-
devices and minimisation of exposure and theatre citation include topical haemostatic agents and now
time
tranexamic acid after the results of the CRASH-2
• administering as little resuscitation fluid as is necessary (Clinical Randomisation of an Antifibrinolytic in Signifi-
to maintain adequate circulation cant Haemorrhage 2) trial demonstrated benefit.32,48 Other
• achieving control of haemorrhage as soon as possible, pharmacological agents may emerge as future therapies;
through techniques such as low-pressure resuscitation however, the utilisation of interventional radiology for
and damage-control surgery. endovascular management of bleeding is proving useful in
Traumatic injury often necessitates large volume the massively injured patient.55,61
replacement of blood volume to increase perfusion. Even Nursing a patient who undergoes damage-control
protocols such as Advanced Trauma Life Support do surgery requires recognition of the principles and aims of
not provide clear guidance on the administration of the surgery, as well as flexibility in the care of the patient
pro-coagulation products to optimally resuscitate patients after the initial surgery but before definitive surgery. In the
while also maintaining the ability to form clots.60 There is emergency department setting there is a need to undertake
a strong need to ensure that patients are not overtransfused, a rapid, systematic evaluation of the patient and prepare
and regular monitoring of coagulation factors including him or her for rapid transfer to the operating room. It is
haematocrit, platelet count, prothrombin time (PT), essential to implement all measures possible to preclude
activated partial thromboplastin time (APTT), thrombin the components of the trauma triad, while avoiding any
time (TT) and fibrinogen levels will assist in achieving delays to surgery.When the patient is admitted to the ICU
this aim. The international normalised ratio (INR) should postoperatively, the standard mechanisms for the treatment
be measured at the beginning of the process and repeated of hypothermia, acidosis and coagulopathy, as discussed
if abnormal. above, should be implemented. After damage-control
Treatment includes transfusion of platelets, fresh frozen surgery, patients may also have an open abdomen with
plasma (FFP) and cryoprecipitate, as well as the plasma temporary dressings or skeletal fractures with external
derivatives showing promise in this area of treatment.60 fixateurs in situ and may require multiple return trips to
While transfusion of platelets is specifically directed theatre to achieve final closure.
towards increasing the circulating concentration of
platelets, administration of FFP is directed at increasing the Skeletal trauma
levels of fibrinogen and other coagulation factors. Cryo- Skeletal trauma involves injury to the bony structure of
precipitate is made by freezing and thawing individual the body. Although skeletal injuries alone rarely result
units of FFP and collecting the precipitate, a process that in the patient being admitted to critical care, damage
concentrates fibrinogen, von Willebrand factor, factor VIII to surrounding blood vessels and nerves, as well as
and factor XIII. potential complications such as fat embolism syndrome63
800 SECTION 3 SPECIALTY PRACTICE

and rhabdomyolysis, may cause the patient to become to the site, such as in screwing or wiring, primary healing
seriously ill. Patients with skeletal trauma who require takes place.71 When a fracture is fixed in a manner that
admission to ICU include those with multiple injuries, reduces but does not eliminate movement around the
severe pelvic fractures (often associated with significant fracture site, secondary healing takes place.71
blood loss), long bone fractures (often associated with fat In primary healing, also referred to as direct union,
embolism syndrome [FES]) and thoracic injuries such as the haematoma that initially formed is eliminated by the
flail segment. A small number of people with crush injuries apposition of fracture ends during reduction. Once the
that cause significant damage to muscles, often resulting in bone ends are intact, osteoclasts form cutting cones that,
rhabdomyolysis, also require admission to the ICU.64,65 in turn, form new haversian canals across the fracture
Skeletal trauma is the form of trauma that causes the gap.68 These contain blood vessels that are essential to
highest number of patients to be admitted to hospital for primary bone healing. By 5–6 weeks after the fracture,
24 hours or more, with approximately 50% of patients osteoblasts will fill the canals with osteons, which are the
experiencing a fracture as their main injury.66 More than basic structure of the new bone. Although the bone is now
70% of all patients with major trauma need at least one formed, the strength and shape continues to develop over
surgical procedure, with survivors experiencing poor coming weeks. Clinical evaluation of whether a fracture
functional outcome or quality of life, especially those with has healed is based on both radiographic and clinical
lower limb injury.64 findings; however, associated injuries may confound the
ability to use clinical criteria.64,71
Pathophysiology In contrast to primary healing, secondary healing is
Bone is composed of an organic matrix as well as bone characterised by an intermediate phase, where a callus
salts. The majority of the organic matrix is collagen of connective tissue is first formed and then replaced
fibres and the remainder is ground substance, a homo- by bone.68 The secondary healing phase begins with an
geneous gelatinous medium composed of extracellular inflammatory phase in which the haematoma clots and
fluid plus proteoglycans.67,68 Calcium and phosphate provides initial support, then inflammatory cells invade
are the primary ions in bone salts, although there are the haematoma to remove necrosed bone and debris.
smaller amounts of magnesium, sodium, potassium and The reparative phase begins 1–2 weeks after the fracture
carbonate ions. These ions combine to form a crystal and consists of immature woven bone being laid down
known as hydroxyapatite. and strengthened through a process known as mineralisa-
A fracture is simply defined as a break in the continuity tion. The final remodelling stage consists of replacement
of a bone. Fractures generally occur when there is force of the woven bone by lamellar bone, through osteoblasts
applied that exceeds the tensile or compressive strength secreting osteoid that is mineralised and forms intersti-
of the bone. In patients sustaining a major injury tial lamellae.68 The remodelling of these structures occurs
(injury severity score ≥16 [1998 version] or ≥12 [2008 in response to appropriate levels of mechanical loading
version]),69 fractures are the primary injury in more during this phase.64
than 15% of cases, although many patients experience a
fracture in addition to other serious injury resulting in Fat embolism
ICU admission.66 Fat embolism syndrome63 may occur in patients who
Fractures are classified as either complete or incomplete. have experienced a fracture of a long bone, particularly if
A complete fracture is where the bone is broken all the multiple fractures or fractures to the middle or proximal
way through, while incomplete fractures only involve part parts of the femur are experienced. Fractures to the pelvis
of the bone. Fractures are also classified according to the can also lead to a fat embolism. Incidence of FES is
direction of the fracture line, and include linear, oblique, low (<1%). FES consists of fat in the blood circulation
spiral and transverse fractures. Finally, fractures are classified associated with an identifiable pattern of clinical signs
as either open or closed, with those patients who sustain and symptoms that include hypoxaemia, neurological
an open fracture having a higher risk of delayed healing symptoms and a petechial rash.65 Patients generally present
or non-union compared with closed fractures. Loss of the 12–72 hours after they have experienced a relevant
haematoma that initiates the inflammatory phase of fracture fracture and often require admission to a critical care
healing and contamination leading to infection are causative unit for assessment and treatment, including mechanical
influences behind delayed healing or non-union.70 ventilation.72
A fracture causes disruption to the periosteum, blood Internationally, there continues to be disagreement
vessels, marrow and surrounding soft tissue, resulting in a regarding the pathophysiological changes associated
loss of mechanical integrity of the bone. When a fracture with FES, although there is general consensus on the
occurs, there is initial bleeding and soft tissue damage following principles. It has been accepted that there is a
around the site, with haematoma formation within the mechanical component to the changes that take place in
medullary canal.70 The healing sequence that follows FES, where fat is physically forced into the venous system
a fracture depends on the type of fracture fixation that and causes physical obstruction of the vasculature.72
is used. When a fracture is fixed using a method that Although marrow pressure is normally 30–50 mmHg, it
eliminates the interfragmentary gap and provides stability can be increased up to 800 mmHg during intramedullary
 CHAPTER 24 TRAUMA MANAGEMENT 801

reaming (the process where the medullary cavity of the example amputation of a thumb by a bandsaw.
bone is surgically enlarged to fit a surgical implant such as Traumatic amputations vary in severity and ongoing
a tibial nail), consequently reaching a pressure significantly compromise, with a clean-cut amputation more likely
above pressures throughout the vasculature.72 to be successfully reattached than a crushed extremity.
A second theory, associated with the biochemical Criteria that inform the surgical decision-making
changes that occur during trauma, proposes that trauma process include: the amount of tissue loss; location
is associated with a higher level of circulating free fatty on the body at the connection site; damage to
acids, which cause destabilisation of circulating fats and/or underlying and surrounding tissues, bones, nerves,
direct toxicity to specific tissues, including pulmonary and tendons/muscles and vessels; and condition of the
vascular endothelium.72 amputated part.
Rhabdomyolysis • Fractures of the pelvis – the pelvis is the largest
combined bony structure in the body and serves
Rhabdomyolysis is a potentially life-threatening condition to provide an essential supporting framework
and is caused by either acquired or inherited factors. Nine for ambulation and protection of pelvic organs.
percent of cases occur as a result of trauma, 34% are due Major blood vessels and nerves traverse the pelvic
to substance abuse and 11% from medications.73 Rhabdo- bones, supplying the lower limbs and pelvic organs.
myolysis is the breakdown of muscle fibres resulting in the Therefore, injury to any part of the pelvis is serious.
distribution of the cellular contents of the affected muscle The three bones that comprise the pelvic ring are the
throughout the circulation, and occurs during the reper- two innominate bones (ilium and pubic rami) and the
fusion of injured muscle. There are two phases of injury sacrum. Due to its reinforced structure, the amount
that are essential for the development of rhabdomyolysis: of force required to fracture the pelvis is substantial.
the first is when muscle ischaemia occurs and the second Fractures of the pelvis can affect one or both sides
is with reperfusion of the injured muscle. The length of of the pelvis, and be stable or unstable. A variety of
time that muscle is ischaemic affects the development of classification systems exist to describe the severity
rhabdomyolysis, with periods of less than 2 hours generally of pelvic fractures, the most common being the Tile
not producing permanent damage whereas periods longer classification (see Figure 24.2).
than 2 hours can result in irreversible anatomical and
functional changes.74 Presentation varies widely across • Fractures of the spinal column (see also Chapter 17) –
patient groups and ranges from asymptomatic elevated the spinal column includes all of the bony
creatinine kinase (CK) to life-threatening conditions with components in the cervical, thoracic and lumbar
electrolyte disturbances, cardiac arrhythmias, acute renal vertebral regions. Fractures of the vertebra are
failure and disseminated intravascular coagulation (DIC).73 common in trauma patients, but the actual incidence
of fracture without spinal cord injury in multitrauma
Clinical manifestations patients is not well described. Not all fractures cause
Common forms of skeletal trauma include the following: vertebral column instability with the subsequent risk
of spinal cord damage. A spinal column fracture will
• Long bone fractures – the long bones are the be diagnosed as mechanically stable or unstable and
humerus, radius, ulna, femur, tibia and fibula. Fractures
this will affect the positioning and possible activity
of these bones are serious and can carry a high level
of the patient.
of morbidity, especially if they involve a joint such
as a trimalleolar fracture of the ankle (distal tibia and • Discoligamentous injuries of the spinal column
fibula). In many cases definitive surgical management (see also Chapter 17) – the soft tissue components
is required, with internal fixation. of the spinal column include the spinal cord, the
intervertebral discs and the spinal ligaments. An
• Dislocations – all joints are at risk of traumatic injury to the spinal column can disrupt one or more
dislocation, depending on the mechanism of injury.
of these structures with or without fracture. These
Dislocations can be limb-threatening if they cause
injuries can be highly unstable and the nurse must be
neurovascular compromise. Reduction of traumatic
vigilant with spinal precautions and the fitting and
dislocation is a medical emergency.
management of the patient requiring a spine orthosis
• Open fractures (compound) – any break in the (see Figure 24.1).
skin that communicates directly with the fracture is
classified as an open fracture. Open fractures carry a Patient management
higher infection risk and require surgical treatment There are several major considerations for the nurse
within 8 hours.70,75 managing the critically ill patient with skeletal trauma.
• Traumatic amputation – amputation refers to These include appropriate assessment as well as appli-
an avulsion in which the affected limb or body cation of traction, management of any amputated parts
appendage is completely separated from the body. and stabilisation of pelvic fractures and spine precautions.
This can occur when a digit or extremity is sheared These latter aspects of care will be conducted in collabo-
off by either mechanical or severing forces, for ration with medical and allied health colleagues.
802 SECTION 3 SPECIALTY PRACTICE

FIGURE 24.2 Tile classification for pelvic fractures.124

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Reproduced from Kobziff L. Traumatic pelvic fractures. Orthopaed Nurs 2006;25(4):235–41; quiz 42-3, with permission.

Bones are very vascular structures and can be the

cause of substantial blood loss in the trauma patient. TABLE 24.3
The critical care nurse should therefore be cognisant Potential blood loss caused by fractures37
of the potential for extensive blood loss in common FRACTURE BLOOD LOSS (ML)
fractures (Table 24.3).
Humerus 500–1500
Given the potential for extensive blood loss, as well as
Elbow 250–750
the frequent close proximity of nerves and blood vessels
to bones, neurovascular assessment of the patient with Radius/ulna 250–500
skeletal trauma is essential (Table 24.4). Pelvis 500–3000
Femur 500–3000
Splinting
Tibia/fibula 250–2000
One of the major emergent management strategies for Ankle 250–1000
haemorrhage control in the patient with skeletal trauma
Adapted with permission from McQuillan KA, Makic MBF,
is splinting. Splinting is a potentially life-saving inter-
Whalen E. Trauma nursing: from resuscitation through
vention and is generally undertaken by nursing staff. rehabilitation. St Louis, Mo: Saunders/Elsevier; 2009.
The purpose of splinting is to align and immobilise the
 CHAPTER 24 TRAUMA MANAGEMENT 803

TABLE 24.4
Neurovascular observations of the skeletal trauma patient

Note: should be undertaken on all injured limbs both pre- and postoperatively as required.

O B S E R VAT I O N PROCESS COMMENTS

Skin colour State the skin colour of the area inspected Pink: normal perfusion
as it compares with the unaffected part Pale: reduced perfusion
NB: distal limb pulses may be difficult to Dusky, purple or cyanotic discolouration: usually indicating
palpate in the injured limb; a warm pink significantly reduced perfusion
limb is a perfused limb Demarcated: a distinct line where the skin colour changes to
dusky (usually follows the vessel path)
Skin temperature to State the ambient temperature of the skin Normal: not discernibly cold to touch
touch to touch as it compares with normally Reduced skin temperature indicates reduced perfusion
perfused skin at room temperature
Voluntary movement The patient should be able to move the It is important to assess range of motion where that
non-immobilised distal part of any injured is possible, provided this will not aggravate the injury.
limb (i.e. fingers and toes of a plastered Reduced movement may indicate compromise to either the
limb) nerve or blood supply to the limb
Sensation The patient should be able to report Sensation should be assessed in nerve distributions
normal sensation to touch (i.e. all fingers and toes). Reduced sensation may indicate
compromise to either the nerve or blood supply to the
limb

bone, which alone has remarkable haemorrhage control complications, such as pressure sores or displacement
properties. Every fractured bone that has not undergone of fractures.
definitive orthopaedic management requires splinting. • Traction – may be required as part of fracture
Examples of intermediate stabilisation of fractures management, and involves the application of a pulling
include: force to fractured or dislocated bones. There are three
• Positioning of injured limbs – all patients who have types of traction:
any form of splint in situ may need to have it elevated skeletal, where traction pins are anchored into the
to promote venous return and minimise tissue bone (i.e. Steinmann pin)
oedema. In the ICU the trauma patient will often skin, where the body is gripped, as in the use of
be nursed flat, with the bed on tilt for a head- slings and bandages
elevation position. In these circumstances, the manual, applied by a clinician pulling on a body
injured dependent limb must be elevated on pillows. part, such as in the reduction of dislocation. It may
Care must be taken to ensure that elevation does also be applied to maintain the traction during
not place pressure on any part of the limb: for such nursing care manoeuvres as log-rolling or
example, a hand sack made from a pillowcase tied repositioning of the traction.
to an IV pole should not be used, as it places direct The principles of traction are to achieve the goal of
pressure on the path of the median nerve and can alignment of bones while preventing complications.
cause an iatrogenic neurapraxia. Remember that incorrectly applied traction is painful
• Wooden/air splints – are padded appliances that and can exacerbate the injury. The following should guide
are strapped to the injured limb. Ideally, no patient management of the patient with traction:
should remain in wooden splints for longer than 1 The grip or hold on the body must be adequate and
4 hours, as pressure may build up on pressure secure.
points.
2 Provision for counter-traction must be made.
• Plaster backslab – limbs with fractures will often swell 3 Minimise friction.
as a physiological response to injury; a plaster backslab
composed of layered plaster of Paris is the preferred 4 Maintain the line and magnitude of the pull, once
treatment, as it accommodates swelling and can easily correctly established.
be loosened by nursing staff at any time of day. It is 5 Frequently check the apparatus and the patient to
imperative that this be adequately padded within the ensure that: 1) the traction set-up is functioning as
limitations of providing structural support to the limb. planned and 2) the patient is not suffering any injury
Poorly made or ill-fitting backslabs can cause major as a result of the traction treatment.
804 SECTION 3 SPECIALTY PRACTICE

surgical intervention, or they can be serious enough to

Practice tip be the primary cause of death from exsanguination.76
No patient should remain in a wooden splint longer than The mortality rate from pelvic fracture ranges from 18%
4 hours. Wooden splints must be changed to a resting to 40% with death usually occurring within 24 hours
backslab if prolonged immobilisation is required; this of injury, frequently as a result of haemorrhage.76,77
will maintain the injured limb in anatomical fracture Appropriate assessment and management of pelvic
alignment. fractures is essential and should encompass diagnostic
evaluation, non-invasive pelvis stabilisation, abdominal
evaluation, the requirement for surgical intervention and
Traumatic amputations
angiography.78
Traumatic amputation is the separation of a limb or The initial management of the patient with a fractured
appendage from the body. During the pre-hospital phase pelvis involves assessment and splinting. Assessment should
any amputated body part should be wrapped in a clean or encompass the following two aspects:77
sterile (if available) cloth and placed in a plastic, waterproof
1 haemodynamic status – to identify signs of ongoing
bag inside an insulated cooler with ice. It is important
that the ice does not come into direct contact with the blood loss and determine fluid resuscitation
amputated part.When managed using these principles, the requirements
amputated part may be viable for up to 6–12 hours before 2 stability of the pelvic ring – assessed with the aid
reattachment. Depending on any additional injuries, and of clinical examination and diagnostic imaging.
the cardiovascular status of the patient, surgery for limb Palpation and inspection of the anterior and posterior
salvage will be scheduled as soon as possible. pelvis for signs of trauma, including tenderness in the
Postoperative management will be guided by the type conscious patient, is generally adequate.77
of surgery that was performed, specifically whether or The orthopaedic surgeon may elect to undertake
not amputation occurred. Principles of postoperative care further clinical assessments incorporating ‘springing’ of the
include: pelvis, although it should be noted that this may aggravate
• appropriate positioning of the affected limb, usually the injury and cause additional bleeding.77 Nursing staff
based on surgical orders would not normally conduct such assessment, unless
under appropriate specialist guidance in a setting such as
• frequent neurovascular observations, particularly remote area trauma nursing or tele-health consultation.
observing for reperfusion injury, which manifests as
an acute compartment syndrome or vascular trashing Non-invasive pelvic binding, in the form of either a
of distal vessels from a clot bedsheet or a proprietary pelvic binder, may make a signif-
icant impact on patient morbidity and mortality.76,78 Such
• implementing changes in treatment initiated in a manoeuvre will stabilise the pelvis and assist in approx-
response to altered perfusion in a timely manner
imating bleeding vessels, thereby assisting in haemostasis
• psychological support to assist the patient in dealing (see Figure 24.3).
with the injury. Pelvic binders are temporary devices,76–78 and ideally
will not be left in situ for longer than 4 hours. If a patient
Practice tip

Where there are any signs of deterioration of the re- FIGURE 24.3 Application of a pelvic binder.
implanted part, communication should occur directly
between the nursing staff and the surgical consultant
to ensure timely implementation of changes to optimise
salvage of the amputated part.

Practice tip

For patients with amputations, on arrival in the

emergency department:
1 Inspect the amputated part.
2 Clean with 0.9% saline solution and return to a
clean plastic bag wrapped in 0.9% saline-soaked
gauze. Surround with ice in a thermal cooler.

Pelvic stabilisation
Pelvic fractures can occur in 5–16% of patients with Courtesy Ferno Australia
blunt trauma and can be uncomplicated and require no
 CHAPTER 24 TRAUMA MANAGEMENT 805

is to remain in the binder longer than 4 hours, nursing staff • analgesia – based on patient reports of pain and taking
must take care to minimise pressure. Conscious patients into account planned activities such as mobilisation
should be advised to report signs of increasing pressure, and physiotherapy
such as positional paraesthesia. Increasing abdominal • mobilisation – based on stability of the pelvis, and in
swelling may indicate a need to reposition the binder. consultation with the surgeon
Position restrictions should be clarified by all members
of the healthcare team, especially if the patient will
• patient education – particularly regarding the safety
of the procedure and mobilisation and rehabilitation
be in the binder for a lengthy period. The patient may be plans.
able to be log-rolled and side-lain with a pelvic binder
in situ. Release of a pelvic binder should by undertaken Pelvic embolisation involves interventional radiology
only with caution and as part of definitive care (e.g. within to control haemorrhage in patients with pelvic fractures.
the operating theatre), with all relevant members (particu- Because of the large arteries that traverse the pelvis,
larly the orthopaedic or trauma surgeon) of the healthcare arterial bleeding can be the cause of substantial blood loss
team present.77 in 10–20% of cases. The timing of embolisation, particu-
Invasive pelvic fixation uses an external fixateur larly in relation to stabilisation, remains controversial, and
(Figure 24.4) to achieve pelvic stabilisation.77,78 The appli- is dependent on the availability of appropriately trained
cation of an external bridging frame (either anterior or staff and resources.78
posterior) to stabilise the pelvis may be an interim or Spine orthoses
definitive treatment measure that may be in situ for days
The cervical collar or orthosis is the most commonly
or weeks. Patients in external fixation may be permitted to used splint to immobilise the cervical spine. It commonly
mobilise, although the extent of mobilisation will depend remains in situ for >24 hours in an ICU setting. This
on the stability of the fracture. While the external fixateur particular type of splinting is associated with an increased
is in place, the following nursing care is required: risk of pressure ulceration in immobile patients due to
• pin site care – usually cleaned with isotonic saline and unrelieved pressure, shearing forces, moisture or foreign
left open unless there is a large amount of exudate, bodies beneath the collar. Collar care is an essential
in which case the pin sites may be covered with dry component of critical care practice. Any dirt, grit, glass
absorbent dressing; care should be taken to identify and road grime must be removed from under the collar,
gaping or stretched skin around the site, as this may particularly in the occipital regions. The patient should
require surgical intervention side-lie as much as possible and the collar should be

FIGURE 24.4 External fixateur: pelvis.128

Reproduced from Wiss DA, Ovid Technologies I. Fractures. Philadelphia: Lippincott Williams & Wilkins; 2006: Figure 37.21, p 634,
with permission.
806 SECTION 3 SPECIALTY PRACTICE

TABLE 24.5
Spinal precautions44

ACTION R AT I O N A L E AIM METHOD

Head hold To maintain the To prevent flexion, extension 1 Nurse holds head from head of bed – the head is held
cervical spine in and lateral head tilting during firmly by placing one hand around the patient’s jaw with
a neutral position any movement fingers spread to cup the jaw and hold the endotracheal
during any position tube as necessary. The forearm is used to support the side
change of the head
2 Nurse holds head from side of bed – nurse stands on side
of bed that the patient will be rolled towards. One hand is
placed firmly under the patient’s occiput. Ensure nurse is
in a position to support the weight of the head.
The other hand holds the jaw and endotracheal tube
as necessary. The patient is rolled onto the forearm
of the nurse holding the head, which completes the
biomechanical support for the head thus immobilising the
cervical spine during the rolling
Log roll To maintain the To prevent rotational torsion The patient is rolled in one smooth motion with assistants
entire spine on the spinal column by supporting the shoulder and pelvic girdles. Another assistant
in anatomical minimising twisting of the supports the legs so the patient moves in one plane
alignment position craniocervical, cervicothoracic The patient is rolled in one smooth motion with the nurse
during any position and thoracolumbar junctions holding the head issuing the command to start and stop the
change of the spinal column manoeuvre

removed while maintaining spinal precautions (see up of two structures, including a bony cavity consisting
Table 24.5) and the underlying skin integrity assessed of the ribs, sternum, scapulae and clavicles, and the
at least every 4 hours. Other examples of spine orthoses second muscular structure of the respiratory muscles and
include a halothoracic brace and thoracolumbar/truncal diaphragm. The organs contained in the chest include
anti-flexion bracing. the lungs, airways, heart, blood and lymph vessels and
oesophagus.
Chest trauma As in all trauma, chest trauma can be penetrating or
Chest trauma is recognised as a severe, potentially blunt in nature. Penetrating trauma is generally caused by
life-threatening form of injury that may require admission blades or bullets and results in damage to the structures
to critical care. Chest trauma may be blunt in nature, often and organs in the chest, as well as disruption of the normal
being experienced during road traffic crashes, and can negative intrapleural pressure leading to a pneumothorax.
be associated with injuries to other areas of the body or Blunt chest trauma generally occurs as a result of road
penetrating in nature. Penetrating injuries are often expe- traffic crashes, falls and assaults or collisions.
rienced during gunshot or stabbing injuries.79 Chest trauma can be separated into injury to the
Chest trauma represents approximately 10% of injuries thoracic structure, including the ribs and diaphragm;
that require admission to hospital for more than 24 hours, injury to the lung, airways and associated tissue; injury to
although this proportion grows to over 15% when only the heart and associated tissue; or injury to the vascular or
patients with major injury (injury severity score >15) are digestive system located in the chest.
considered. Chest trauma represents approximately 15% Chest trauma covers a broad array of injuries and
of the injured patients requiring admission to the ICU. severity, and ranges from relatively minor injuries (e.g.
The incidence of chest trauma varies, depending on the abrasions and fracture of a single rib) to major, imme-
external cause of the injury, with approximately 20–30% diately life-threatening injuries (e.g. cardiac rupture
of road traffic crash injuries occurring to the chest,80 30% or tension pneumothorax). In 70–90% of patients who
of stabbing injuries occurring to the chest and 10–15% of sustain a severe chest injury there are associated injuries to
assault and fall injuries resulting in injuries to the chest. other regions of the body, including the head, neck, spine,
Associated mortality ranges from 20% to 25% with reported abdomen and limbs.83,84
mortality rates up to 60% in America and Europe.79,81–83 Chest trauma includes the following:

Pathophysiology
• Rib fractures – a very common form of chest
trauma, often a source of severe pain and often
The chest consists of the thoracic cavity and the associated with other injuries such as haemothorax,
organs contained within. The thoracic cavity is made pneumothorax and pulmonary contusion.83
 CHAPTER 24 TRAUMA MANAGEMENT 807

• Flail chest – fractures to two or more ribs, in two of occult pneumothorax (pneumothorax detected
or more places, resulting in a freely-moving section on CT scan that was not diagnosed on X-ray) has
of the rib cage. The production of a flail segment appeared, with a reported incidence of 2–7%. Up
is dependent on a number of factors, including the to 76% of pneumothoraces have been identified
extent of adjacent soft tissue support.80 Usually such as occult when the CXR was read in the acute
fractures occur in the anterior or lateral sections of resuscitation setting by the trauma team.83
the rib cage, where there is less muscle protection. • Haemothorax – the accumulation of blood in the
The significant impact of this injury is paradoxical pleural space. Blood may collect from the chest
movement of the flail segment during spontaneous wall, the lung parenchyma or major thoracic
ventilation, so that when a patient inspires, the vessels.88 Breath sounds are usually reduced on the
flail segment moves inwards with the negative side of the haemothorax and percussion is noted
intrapleural pressure instead of expanding with to be dull rather than hyper-resonant.79 Small
the rib cage. Compromised respiratory function haemothoraces (<200 mL blood) may not be
is caused by the increased work of breathing that apparent on clinical or radiological investigation,
this ineffective flail segment creates as well as the although respiratory compromise is likely to be
contused lung that normally occurs underneath the present. Initial management of a haemothorax is the
flail segment.80 insertion of a chest tube to allow for drainage of
• Diaphragmatic injuries – generally consist of the accumulated blood. Optimal evacuation
diaphragmatic rupture when there has been a of residual clots and breakdown of adhesions
significant rise in intra-abdominal pressure, usually and loculated effusions is important to prevent
with compression injuries.85 When the rupture complications such as empyema or fibrothorax and
is sufficiently large, protrusion of the abdominal can be achieved using a surgical approach in the
contents into the thoracic space, resulting later phase of care.88
in respiratory compromise, is likely. Bilateral • Cardiac trauma – encompasses a number of
diaphragmatic injury is uncommon, with the different injuries, ranging from relatively mild
majority involving the left hemidiaphragm, with 75% bruising of the heart muscle to rupture of the
of injuries caused by blunt trauma.86 heart wall, septum or valves or damage to the
• Pulmonary contusion – consists of bruising to the coronary arteries.89 The right side of the heart is
lung tissue, usually as a result of mechanical force. most commonly injured,83 probably as a result of
This bruising is followed by diffuse haemorrhage and the anterior placement of this side of the heart
interstitial and alveolar oedema, resulting in impaired in the thorax.
gas exchange due to shunting and leading to hypoxia • Aortic injuries – generally, injuries to the
and increased oxygen requirements.85 This injury brachiocephalic, left subclavian or right subclavian
represents the most common internal injury after branches of the aorta are associated with high
blunt thoracic trauma and has been estimated to affect mortality at the scene. Aortic injury is divided into
30–70% of injured patients.80,84 minor and significant injuries. Minor injuries
• Pneumothorax – the accumulation of air in the usually involve a small intimal tear with small
pleural space.84 A pneumothorax may be closed peri-aortic haematoma, while significant injuries
(no contact with the external atmosphere) or open include the intima and full thickness of media with
(a communicating channel with the atmosphere).87 associated high risk of rupture.79 Aortic transection
Closed pneumothoraces are generally caused by and rupture is associated with >80% mortality
blunt chest trauma and result from a fractured within the first 30 minutes of injury;89 those who
rib puncturing the lung parenchyma. Open do survive to hospital frequently have a significant
pneumothoraces generally occur in the setting injury.79
of penetrating trauma, where air is able to move • Tracheobronchial injuries – tend to occur as a result
from the external atmosphere to the pleural space of direct blunt trauma and in close proximity to the
during inspiration. If not all of the inspired air is carina, but are relatively rare.83 Larger defects result in
able to escape during expiration, due to a tissue dyspnoea (with or without respiratory distress) while
flap or similar obstruction covering the opening, smaller injuries may initially go unnoticed. Many
the volume of the pneumothorax will gradually subtle presentations will manifest as mediastinal air
expand and cause collapse of the adjacent lung, on CT scan.83
with resultant hypoxaemia. Where air is not able to
escape at all from the pleural space, this is referred to Clinical manifestations
as a tension pneumothorax, and rapidly becomes a Injuries to the thoracic cavity can manifest according to
life-threatening event due to the increasing pressure the structures and systems involved (see Table 24.6).When
on the lungs, heart and trachea.79,87 With the use of multiple organs and systems are involved, the combined
imaging modalities such as CT scan the phenomenon injuries pose an increased threat to life.
808 SECTION 3 SPECIALTY PRACTICE

TABLE 24.6
Clinical manifestations of chest trauma

SYSTEM M A N I F E S TAT I O N CLINICAL SIGNS AND SYMPTOMS

Respiratory Any sign of respiratory compromise, noting Abnormal respiratory rate (<12 or >20 breaths/min)
• Airways that serial observations are an important Abnormal chest wall movement, including asymmetrical
• Lungs indicator of imminent decompensation chest wall expansion
• Diaphragm Reduced breath sounds
Obstructed airway
Hypoxia (<94%)
Hypercarbia
Apnoea
Dyspnoea
Orthopnoea
Crepitus/surgical emphysema
Cardiovascular Circulatory insufficiency resulting in decreased Abnormal heart rate (<60 or >100 beats/min)
• Heart tissue perfusion Arrhythmia
• Great vessels In severe cases, pulseless electrical activity (see Chapter 9)
Pulsus alternans
Decreased cardiac output
Lowered blood pressure (systolic <100 mmHg)
Reduced peripheral perfusion
Confusion and reduced consciousness level
Gastrointestinal Perforation and contamination of mediastinum Crepitus
• Oesophageal Haemopneumothorax
rupture Pain
Cough
Stridor
Bleeding
Sepsis (late)
Systemic May occur in response to injury of a vessel that Varied depending on location, but may include:
• Air embolism traverses an air space; manifestations will vary • Focal neurological sign
depending on location and associated injuries • Cardiac deterioration

Patient management elevated heart rate

Given the underlying structures of heart, lungs and great reducing pulse pressure, with falling systolic BP and
vessels, chest trauma can cause rapid deterioration in the rising diastolic BP
patient. Ongoing and thorough assessment, particularly in increased preload (CVP and/or PCWP)
relation to the signs and symptoms outlined in Table 24.6, distended neck veins
is essential. Other essential aspects of care include patient signs of reduced cardiac output, including lower
positioning and management of pain relief. level of consciousness, poor peripheral perfusion
and reduced urine output.
Assessment
Initial assessment in the emergency department should be
• Tension pneumothorax – the lung or lungs collapse
as the pleural space fills with air that cannot escape
conducted on an ongoing basis, with formal documentation (see Figure 24.5). As the volume of air grows
of these findings occurring every few minutes until stabil- with each breath, the thoracic cavity contents are
isation. The frequency of ongoing assessment will then be compressed or pushed against the opposite side of
based on the patient’s condition, but is likely to be needed the chest. Signs of tension pneumothorax include:
every 15 minutes initially, reducing to hourly with transfer elevated heart rate
to the critical care unit. Signs of chest trauma that represent increased respiratory rate
life-threatening emergencies include the following. decreased air entry, particularly over the affected
• Cardiac tamponade – as blood collects in the lung
pericardium, the venous return to the heart is tracheal deviation
impeded, resulting in reduced cardiac output. distended neck veins
Signs of cardiac tamponade include: surgical emphysema.
 CHAPTER 24 TRAUMA MANAGEMENT 809

Pain relief will normally include IV opioids, but may

FIGURE 24.5 Right tension pneumothorax. also include intercostal or epidural analgesia and non-
steroidal anti-inflammatory agents in selected patients (see
Chapter 7). Non-pharmacological means such as the use
of supplemental oxygen, use of cold packs early and heat
packs late in the treatment course, massage, relaxation and
diversion techniques should also be considered. Providing
and maintaining a comfortable posture for the patient that
includes the elevation and support of injured limbs has
remarkable analgesic properties. A confident, competent
and efficient nurse who engenders trust from both the
patient and family is very comforting.
Surgical management of injury
Surgical intervention in the chest trauma patient is
generally limited to repair of tears and lacerations, for
example repair of vessel injuries including rupture, lung
lacerations, heart injuries including lacerations and valvular
injury. A ruptured diaphragm or oesophageal perforation
will also be repaired surgically.
Courtesy The Alfred, Melbourne. The emergency thoracotomy has proven beneficial
in a select group of patients with penetrating trauma
and less than 15 minutes of cardiopulmonary resuscita-
Practice tip tion; however, it is generally recognised as not providing
benefit in patients with blunt chest trauma.While different
Unexplained hypotension in a patient with chest trauma techniques are used in different settings, the main access
may indicate a tension pneumothorax; an urgent chest to the thoracic cavity is via a left thoracotomy, a midline
X-ray is required for diagnosis. sternotomy or a ‘clam shell’ incision. Initial assessment of
the patient is used to determine the need for a thora-
Positioning cotomy in either the emergency department or the
Early mobilisation of the patient with chest trauma is vital operating room. Nurses working in a trauma reception
to prevent the complications of prolonged bed rest and facility that has the capacity for emergency thoracotomy
immobility. Patients should be nursed side-to-side and in should be familiar with the equipment and process for
a variety of positions, including sitting upright.The extent this procedure. Postoperative nursing care of these patients
to which the patient can be mobilised is dependent on should follow the same principles as for patients who have
other injuries. Patients should be mobilised to sit out of undergone routine cardiothoracic surgery.
bed as soon as they are conscious and their injuries permit. Chest drainage
Care must be taken to accommodate the increased
work of breathing that is associated with injuries to the When injury to the pleura occurs, air or blood collects
lungs. Appropriate use of supplemental oxygen will assist between the two layers of the pleura, causing collapse
the patient’s exercise tolerance. Further, if the patient is of the underlying area of lung and loss of the negative
mechanically ventilated, additional mechanical support intrapleural pressure. Insertion of an intercostal catheter
(i.e. transient increase in pressure support) may be applied drains the air and/or blood from between the pleura,
to assist the patient’s exercise tolerance. Being unable to resulting in reinstatement of the negative intrapleural
catch their breath is a terrifying experience that is likely to pressure and reinflation of the underlying lung.
result in increased levels of anxiety for patients, and should A central principle in the treatment of chest trauma is
be avoided wherever possible. the use of the intercostal catheter (ICC) for chest drainage
purposes. The principles of chest drainage include the
Pain relief following:
The principles of managing pain in chest trauma • The lungs are encased in a potential space.The
patients are similar to those for other patients, although visceral pleura attaches to the parietal pleura via
the potential severity of pain, particularly as a result of surface tension, creating a negative intrapleural pressure
fractured ribs, should not be underestimated. Effective and attaching the lung to the chest wall. During
pain management in the chest trauma patient is a major inspiration the rib cage moves out and the diaphragm
determinant of maintaining adequate spontaneous contracts and moves down, increasing the size of the
breathing. Avoiding mechanical ventilation is a major intrathoracic space. Air moves from an area of higher
goal in the less-severe group of chest trauma patients, so pressure in the environment to an area of lower
effective deep-breathing and coughing must be promoted. pressure within the lungs along a pressure gradient.
810 SECTION 3 SPECIALTY PRACTICE

• An intercostal catheter is inserted into the pleural

TABLE 24.7
space, passing between the ribs. The ICC is designed
Assessment of chest drainage
to drain both air and fluid as required.
• The drainage system and seal provides an ongoing CHARACTERISTIC DESCRIPTION
means of removing air and/or fluid from the pleural Water seal Ensure there is sufficient water in
space, while preventing air from the atmosphere the water seal chamber
entering via the ICC. If the traditional glass bottle Bubbling Continued bubbling indicates an
system is being used, the seal is provided by placing air leak
the distal end of the ICC under water (usually 2 cm).
Drainage Observe the nature and volume of
The catheter should not be placed under excessive
fluid exudate (NB: >1500 mL stat
levels of water, as this creates resistance and will limit
or 200/mL/h for 2–4 hours; surgical
air and fluid escaping from the pleural space.
exploration may be required)
• Suction is often added to the drainage system to Patency Ensure the intercostal catheter is not
promote drainage of fluid. blocked, remove any blood clots
Care of the chest trauma patient with intercostal Swinging Oscillation of fluid in the ICC
drainage is directed towards ensuring sterility and patency confirms patency, as this reflects
of the system and assessing the amount and type of the changes in intrapleural pressure
drainage, as well as the impact on the patient (Table 24.7). with respiration; such oscillation
Additional considerations include the following: should continue even when the lung
• ICC may be positional, or alternatively haemo/ has re-expanded
pneumothoraces may be loculated. Repositioning of Suction If suction is ordered, check the
either the patient or the catheter may be necessary. appropriate level is being delivered
• Side-lying or lifting the patient, especially with a
frame, may kink or disconnect the ICC.
• Surgical emphysema around the site of the ICC may • Airway injury – initiation of positive pressure
ventilation in the chest trauma patient may identify
dislodge the tip of the catheter out of the pleural
damage to a small airway that previously went
cavity as the emphysema swells. Ongoing assessment,
unnoticed (damage to a large airway will usually
including a chest X-ray, is required to confirm the
position of the ICC. have been detected early in the assessment phase).
Treatment will depend on the severity and location
• Movement of the patient, including sitting upright, of the rupture, but usually requires decompression of
will assist with fluid drainage; the volume of drainage the pleura with an ICC, possibly surgical intervention
should be assessed after moving the patient. and advanced respiratory support such as independent
• Monitoring of respiratory function should continue lung ventilation.
after removal of the ICC to detect recollection of air
or fluid. • Use of tracheostomy – this may be required for
patients with injury to the trachea and is managed
using the same principles as with any patient with a
Practice tip
tracheostomy.
Fresh, brightly-coloured blood drained from the ICC
Allied health interventions
indicates continued active bleeding, while dark blood
usually indicates older blood that has been resting in Physiotherapy is generally required for chest trauma
the pleural space for some time. patients.The primary aspects of care include chest physio-
therapy, given the often extended episodes of mechanical
Ventilatory support ventilation and bed rest that are required, as well as mobility
exercises. Occupational therapy particularly offers benefits
Ventilatory support is often required for patients with to the long-term ventilated patient in terms of diversion
chest trauma (see Chapter 15 for general principles). The activity, while social work is often beneficial for patients
following specific considerations apply:
with ongoing disability and financial and social problems.
• Non-invasive ventilation – care should be taken Early referral of selected patients to allied health profes-
based on associated injuries, with contraindications sionals has the potential to significantly influence patient
including fractured base of skull or facial fractures. outcome.
• Intubation – haemoptysis is relatively common in Abdominal trauma
patients with lung injury, and care must be taken to
ensure removal of blood clots from the endotracheal Any organ or structure in the abdominal cavity can be
tube (ETT). Heated, humidified air and regular injured. Abdominal trauma presents unique challenges to
suctioning will assist with maintaining ETT patency. clinicians due to the abdominal cavity’s high diversity of
 CHAPTER 24 TRAUMA MANAGEMENT 811

organs and structures. Approximately 10–15% of blunt Contusion/laceration

trauma patients experience intra-abdominal injury63,90 with Sudden deceleration of moving body tissues can result in
high associated morbidity and mortality;63,91 hence the need laceration or haemorrhage into the tissues (contusion).
for early, accurate diagnosis and treatment is paramount. This is related to the tearing of the tissues that occurs due
Recent advances in diagnostic and treatment tech- to inertia, or the tendency of tissues to resist changes in
niques for abdominal trauma have seen an increased speed or direction (e.g. to keep moving forwards when the
emphasis on non-operative management for solid organ body has stopped moving, resulting in a tearing action to
injury, with more recent increases in the use of angioem- the tissues). Any structure in the abdomen is susceptible to
bolisation. These two clinical treatment innovations place this type of injury. Commonly, the liver and spleen are the
an emphasis on excellent patient monitoring and, in some worst-affected organs, largely related to a seatbelt injury
instances, higher ICU utilisation for selected cases.92 in motor vehicle collisions. Laceration of a solid organ
Pathophysiology can be a minor injury that is appropriately monitored
and managed conservatively; alternatively, a similar injury
The abdominal cavity consists of a range of tissues
can lead to exsanguination (e.g. a liver laceration into the
and organ structures, including musculoskeletal, solid
hilum that involves the inferior vena cava). Hollow viscus
and hollow organs, vessels and nerves. Musculoskeletal
can be contused, as can the mesentery and peritoneum.
structures include the major abdominal muscle groups
forming the abdominal wall, as well as the lumbar Perforation
vertebrae and pelvis. Solid organs include the liver, Full-thickness injury, or perforation, to a hollow viscus
spleen, pancreas, kidneys and adrenal glands (and ovaries organ is life-threatening. Perforation of the intestine can
in women). Hollow organs include the stomach, small result in peritoneal soiling and ischaemic bowel. Small
and large intestines, gallbladder and bladder (and uterus in bowel injuries are particularly difficult to diagnose;92 if
women). Finally, the vessels and nerves include a complex diagnosis is delayed, morbidity can be severe.The abdominal
array of all abdominal blood vessels (arterial and venous), seatbelt sign – in other words, bruising across the anterior
lymphatics and nerves including neural plexuses and the abdominal wall that follows the path of the lap and sash
spinal cord. Traumatic abdominal injuries are classified of the seatbelt – is a sentinel sign for hollow viscus perfo-
as being extraperitoneal, intraperitoneal and/or retro- ration.93,94 A high index of suspicion should be given to
peritoneal. Importantly, a patient can have any mix or passengers of motor vehicle crashes who present with a seat
multiples of these. The classification of injury guides belt sign as it has been shown that they have twice the odds
clinical decision making. of sustaining an abdominal injury. One thought behind this
The pathophysiology of abdominal trauma is largely finding is that adult passengers tend to sit further back from
related to the structure(s) injured. Careful serial assessments the instrument panel where the frontal airbag deploys, and
are essential to identify changing clinical manifestations. may have different safety belt force loading characteristics.95
The most common clinical manifestation of abdominal Importantly, patients with this type of abdominal trauma
trauma is haemorrhage and/or signs of an acute abdomen, can present late (by days). If presenting late, the usual clinical
such as pain, tenderness, rigidity and bruising. Importantly, manifestations are pain, peritonitis and sepsis.93,94
these are life-threatening signs and require immediate
surgical intervention. Secondary injury: Abdominal compartment syndrome
The most significant sign of abdominal trauma in The abdominal viscera are highly vascular and subject to
the conscious patient is thought to be pain, although vascular engorgement during massive fluid resuscitation.
in a recent systematic review abdominal pain along with Where this occurs, there is an acute rise in intra-abdominal
abdominal tenderness with palpation were less predictive pressure (IAP). In severe cases, the IAP will rise to the point
in identifying intra-abdominal injuries than other investi- where cardiorespiratory function is compromised. This is
gations.90 Where hollow viscus perforation has occurred, a surgical emergency and the abdominal cavity requires
such as bruising across the area of the abdominal seatbelt, decompression immediately. The incidence of abdominal
small bowel perforation may be present. These patients compartment syndrome is difficult to determine because of
are characterised by pain out of proportion to that the different assessment and measurement techniques used,
expected with superficial abdominal wall contusions. but has been reported to be 6–14% in trauma patients.96
Other signs of abdominal trauma can be related to the A high level of suspicion for abdominal compart-
structure that has been injured. For example, haematuria ment syndrome should be retained for all patients with
demonstrates trauma to some part of the urinary tract, abdominal trauma as well as those who have had abdominal
including the kidneys. surgery for other reasons. Clinical examination, looking
The abdomen is susceptible to injury from a variety of for a distended and firm abdomen, is insensitive in the
external causes, both blunt and penetrating (see discussion early stages of abdominal compartment syndrome with
of penetrating injuries below). A key aspect to remember detection in only 40–60% of cases;96 however, these signs
with any abdominal injury is that the superficial injury should be identified if abdominal compartment syndrome
does not always reflect what lies below. For example, it progresses to a late state. Proactive detection of abdominal
is not possible to be certain of the trajectory that a bullet compartment syndrome is more effectively carried out
took after it passed through the skin. through the use of routine IAP measurements in patients
812 SECTION 3 SPECIALTY PRACTICE

with the potential to develop abdominal compartment undergone an abdominal surgical procedure. The specific
syndrome. While agreement regarding the level of IAP nursing care elements will depend on what organ has been
that indicates abdominal compartment syndrome does not injured and the surgical procedure undertaken. Careful
exist, values above 20 mmHg generally require investiga- attention must be paid to general nursing care elements
tion; and pressures above 25 mmHg, in association with for all patients (see Chapter 6).
other clinically relevant findings such as firm or distended Postoperative feeding and bowel care should be
abdomen and the systemic effects outlined above, often discussed with the healthcare team and plans made early
indicate a need for urgent surgery.97 It may also be appro- to avoid delays and adverse events such as constipation
priate to monitor the abdominal perfusion pressure,98 (see Chapter 19 for principles of feeding). A paralytic ileus
which is the mean arterial pressure minus the IAP. is a common manifestation of the critically-ill abdominal
Although not validated it is recommended to maintain an trauma patient. Ensuring that the gut is decompressed, with
arterial perfusion pressure between 50 and 60 mmHg or a functional enterogastric tube that is correctly positioned,
higher if possible.96 See Chapter 20 for a detailed review is essential. Because constipation is a common problem,
of abdominal compartment syndrome including IAP early intervention and implementation of a bowel care
monitoring and subsequent management. protocol for trauma should be considered (see Chapter 6).
Diagnosis in the trauma setting consists of a thorough
Patient management clinical assessment, the potential use of FAST, diagnostic
Recent trends have seen an increasing use of non- peritoneal lavage (DPL), abdominal computed tomography
operative care of patients with abdominal injury. In these (CT)68 and laparotomy or laparoscopy. Clinical assessment
patients, monitoring for deterioration is essential, as is the may reveal clinical signs such as skin bruising, lacerations,
ability to activate surgery and care for patients accordingly. signs of abdominal rigidity and guarding. The various
Care of patients after abdominal trauma also includes locations of clinical signs are clues to potential abdominal
effective diagnosis, surgical or radiological interventions, injury. The results of this phase of the investigation will
and associated care. Damage-control surgery is now a determine what additional diagnostic tests are undertaken.
mainstay in management. FAST is rapidly becoming an extension of the clinical
With the high use of non-operative management assessment in abdominal trauma patients.
techniques for solid organ injury, the role of monitoring
of patients with abdominal trauma is pivotal. Nurses must Diagnostic peritoneal lavage
be cognisant of the clinical signs of abdominal injury, Diagnostic peritoneal lavage (DPL) is a procedure that
especially haemorrhage, and act on these immediately (see can be undertaken rapidly to assess for intra-abdominal
Table 24.8). Specific aspects of nursing care for patients after bleeding, although it is frequently only used where FAST
abdominal trauma include pain management, monitoring or CT is not available.99 DPL may be performed on a
and postoperative care. Patients often experience severe patient with unexplained persistent signs of shock (hypo-
pain as a result of both the primary trauma and any surgical tension ± tachycardia); where the abdominal clinical
intervention for repair (see Chapter 7). examination and FAST is inconclusive; or where there is
Vital sign monitoring is a mainstay of nursing a high index of suspicion of intra-abdominal injury. DPL
management in patients with abdominal trauma, and all can identify the presence of haemorrhage but gives no
patients should have appropriate monitoring (as outlined indication of its source.92,100 Disadvantages of DPL include:
in trauma reception). It is also essential that patients receive
a urinalysis after incurring abdominal trauma in order to • high level of invasiveness and associated complications
identify trauma to the urinary system. • inability to detect retroperitoneal injuries
Where the patient has undergone a trauma laparotomy, • potential interference 92with the interpretation of
postoperative care is standard as for any patient who has subsequent CT scans.

TABLE 24.8
Common signs of abdominal injury133

SIGN DESCRIPTION S U S P E C T E D I N J U RY
Grey Turner’s sign Blueish discolouration of the lower abdomen and Retroperitoneal haemorrhage
flanks 6–24 hours after onset of bleeding
Kehr’s sign Left shoulder tip pain caused by diaphragmatic Splenic injury, although can be associated with any
irritation intra-abdominal bleeding
Cullen’s sign Bluish discolouration around the umbilicus Pancreatic injury, although can be associated with
any peritoneal bleeding
Coopernail’s sign Ecchymosis of scrotum or labia Pelvic fracture or pelvic organ injury
Adapted with permission from Eckert KL. Penetrating and blunt abdominal trauma. Crit Care Nurs Q 2005;28(1):41–59.
 CHAPTER 24 TRAUMA MANAGEMENT 813

Abdominal computed tomography organs without the need for surgery, which in turn may
Abdominal computed tomography68 is recognised as reduce the resuscitation period and requirements for
having high sensitivity and specificity in the setting of transfusion.103 In patients with vascular injuries within the
abdominal trauma and is therefore accepted as a diagnostic abdominal cavity the treatment of choice is percutane-
mainstay in this group of patients, particularly for patients ous selective embolization, which is directed to the injury
with blunt trauma who are haemodynamically stable.90,92 site by the previously performed CT examination.103 The
The main exception to this is where the results of a patient undergoing embolisation for the control of haem-
FAST examination are positive and the patient is taken orrhage requires meticulous monitoring and an ability to
to surgery urgently. The use of abdominal CT in patients respond immediately to hypovolaemic shock should the
with a penetrating injury has an accuracy rate >90% when bleeding worsen.
combined with the administration of oral, rectal and intra- Management of the patient with an open
venous contrast with some evidence suggesting that triple
abdomen
contrast CT may reduce the need for operative investi-
gation of these injuries.101 An important pitfall for CT In cases of severe abdominal trauma, the abdominal trauma
imaging in abdominal trauma occurs when the patient has patient may be returned to the ICU with an open abdomen,
arrived at the scanner so quickly after the injury that major or laparotomy, covered with a temporary wound-clo-
blood loss is not apparent and the extent of the injury is sure system. There are various types of open abdominal
missed or underevaluated. A high index of suspicion in the dressings with negative pressure therapy techniques
setting of a negative CT and extensive abdominal trauma becoming the most extensively used. The principal aim
should remain, particularly if signs of shock develop. of the dressing is to provide coverage for the contents of
Debate currently exists as to the role of oral contrast in the peritoneum if these are too swollen to fit beneath the
the trauma patient who must remain supine and immo- closed skin or where there is a need for repeated opening
bilised in a cervical collar. It is essential that nursing of the abdomen.104 Ultimately, the aim is to close the skin
assessment for the risk of aspiration be conducted, and to as soon as possible, when the patient’s physiological status
be prepared to manage the vomiting patient. Any supine normalises. It is possible for these abdominal dressings to
patient given radiographic contrast should not be left cause a secondary abdominal compartment syndrome if
unattended, and there should be sufficient staff available they are too restrictive. Another challenge for the patient
at short notice to roll the patient onto their side if he/ with the open abdomen is the potential for the develop-
she vomits. The healthcare team should discuss the risk of ment of enteroatmospheric fistulas.104,105
vomiting prior to ordering the test so that an informed The primary aims of managing a patient with an open
decision can be made regarding the risk–benefit ratio on an abdomen include minimising complications of prolonged
individual case basis. Oral contrast has been demonstrated immobility, observing for signs of ongoing abdominal
to be highly effective in revealing hollow viscus injury, compartment syndrome, restoring the patient’s physiology
and therefore has a place in the diagnostic evaluation of to normal and supporting the patient and family through
abdominal trauma. a psychologically distressing time. Understandably, both
the patient and their family can be distressed by the
Laparotomy/laparoscopy appearance of an open abdomen. There are no specific
The role of diagnostic operations such as laparotomy/ position restrictions for a patient with an open abdomen,
laparoscopy is well described in the literature,102 and is but haemodynamic status is often labile so that care must
essential to aid diagnosis (laparoscopy) and provide appro- be taken with side-lying and hygiene care.
priate treatment to control haemorrhage and repair organ
injury (laparotomy). When this procedure is considered Splenic injuries
appropriate, rapid transit to the operating room should The spleen is the solid organ most commonly injured in
be undertaken. As the consequences of missed or delayed blunt trauma.92,103 Its location (under the ribs) also makes it
diagnosis of abdominal injury can be catastrophic for the vulnerable to secondary injury from fractured ribs. Splenic
patient, opening the peritoneal cavity to exclude injury injury should always be suspected in those patients who
in selected cases is a necessity. In an analysis of 51 studies have sustained a direct blow to the abdomen, as it is a large
the conversion rate from laparoscopy to laparotomy was organ. The most common sign of splenic injury is pain
33.8%, of which 16% were non-therapeutic and 11.5% over the left upper quadrant. There may be no changes to
were negative.102 vital sign parameters until the patient has incurred signif-
icant circulating blood loss. Splenic injury is categorised
Embolisation in a scale consisting of five levels; this scale is designed to
Interventional radiology is an option in the management aid classification for management and research purposes105
of abdominal trauma. Via an arterial approach, the inter- (see Table 24.9).
ventional radiologist can insert cannulae to identify The spleen has an immunological function that is
arterial blushes (bleeders). Once identified, the vessel can not well understood. After splenectomy, patients are
be ligated via mechanical coiling or blocked chemically. at increased risk of infection and therefore require
Embolisation aims to achieve haemostasis and salvage careful education regarding lifelong risks. The role of
814 SECTION 3 SPECIALTY PRACTICE

immunisation after splenectomy is very important, and The overwhelming aim of the management of liver
the patient must be counselled regarding the necessity for injuries is to preserve liver function. This is achieved by
follow-up on immunisations.106 Prior to discharge from controlling haemorrhage, resting the patient and close
the hospital, the patient should be administered the first monitoring. Most liver injuries can be managed non-
round of immunisations.The current recommendation for operatively. In these cases it is imperative that the patient
predischarge immunisations includes: be closely monitored for signs of haemorrhage and that
the capacity for laparotomy is available at short notice if
• pneumococcal vaccine required. In some cases, embolisation may be considered
• meningococcal vaccines for arterial haemorrhage.92 Late complications of liver
• influenza vaccine.107 injury include infection, haematoma, bile leak and late
The patient will also be commenced on antibiotic haemorrhage.
prophylaxis and should be advised to wear a medi-alert Penetrating injuries
disk or card and consult specialist travel advice when
Trauma is broadly categorised according to whether the
travelling.107
external cause of injury was blunt or penetrating. Pene-
Liver injuries trating trauma refers to a mechanism of injury where the
skin has been cut through the insertion of a foreign object.
The liver is a vital organ, with liver failure being a fatal
The most common examples include knife and gunshot
condition unless reversible. After the spleen, the liver is the wounds, although solid objects such as fences, signposts and
next most common solid organ injured.103 Any injury to tools can cause penetrating trauma. Penetrating trauma is
this highly vascular organ is serious and requires surgical significantly different from blunt trauma in that the injury is
review. As the largest abdominal solid organ traversing the largely localised to a single body region. Exceptions to this
midline, the liver is susceptible to injury from any external may occur: for example, with firearm wounds if there are
forces applied to the abdomen, for example seatbelt multiple bullet-entry wounds or multiple knife-stab sites.
injuries and abdominal blows from an assault. Liver Care must be taken when caring for patients with
injuries are graded using the six-level liver injury scale105 penetrating injury to prevent injury to staff. This is partic-
(see Table 24.10). The treatment of liver injuries is largely ularly important when the patient presents with a knife in
dependent on the nature of the injury or injuries to the situ or a large, protruding foreign object in their body. It
liver itself, presence of concomitant injuries, premorbid should also be noted that some penetrating trauma occurs
status and overall injury severity. The treatment options as a result of a criminal act, and it is essential to observe
may also be guided by the services and expertise that your rules governing forensic evidence. Police should be
health agency can offer the patient. notified by the senior clinician involved in providing care.

TABLE 24.9
Spleen injury scale134

GRADEa I N J U RY T Y P E D E S C R I P T I O N O F I N J U RY

I Haematoma Subcapsular, <10% surface area

Laceration Capsular tear, <1 cm parenchymal depth
II Haematoma Subcapsular, 10–50% surface area
Intraparenchymal, <5 cm in diameter
Laceration Parenchymal depth 1–3 cm not involving a trabecular vessel
III Haematoma Subcapsular, >50% surface area or expanding
Ruptured subcapsular or parenchymal haematoma
Intraparenchymal haematoma >5 cm or expanding
Laceration Parenchymal depth >3 cm or involving trabecular vessels
IV Laceration Laceration involving segmental or hilar vessels producing major devascularisation
(>25% of spleen)
V Laceration Completely shattered spleen
Vascular Hilar vascular injury that devascularises spleen
a
Advance one grade for multiple injuries, up to grade III.
Adapted with permission from Olthof DC, van der Vlies CH, Scheerder MJ, de Haan RJ, Breenen LFM, Goslings JC, van Delden
OM. Reliability of injury grading systems for patients with blunt splenic trauma. Injury 2014;45(1):146–50.
 CHAPTER 24 TRAUMA MANAGEMENT 815

TABLE 24.10
Liver injury scale37

GRADEa I N J U RY D E S C R I P T I O N

I Haematoma Subcapsular, <10% surface area

Laceration Capsular tear, <1 cm parenchymal depth
II Haematoma Subcapsular, 10–50% surface area
Intraparenchymal, <10 cm in diameter
Laceration Parenchymal depth 1–3 cm, <10 cm in length
III Haematoma Subcapsular, >50% surface area or expanding
Ruptured subcapsular or parenchymal haematoma
Laceration Parenchymal depth >3 cm
IV Laceration Parenchymal disruption involving 25–75% of hepatic lobe or 1–3 Couinaud’s segments within a single lobe
V Laceration Parenchymal disruption involving >75% of hepatic lobe or >3 Couinaud’s segments within a single lobe
Vascular Juxtahepatic venous injuries; i.e. retrohepatic vena cava/central major hepatic veins
VI Vascular Hepatic avulsion
a
Advance one grade for multiple injuries, up to grade III.
Adapted with permission from McQuillan KA, Makic MBF, Whalen E. Trauma nursing: from resuscitation through rehabilitation.
St Louis, Mo: Saunders/Elsevier; 2009.

Clinical manifestations In the emergency setting the following considerations

The clinical manifestations of penetrating injuries are are generally unique to the patient with a penetrating
dependent on where in the body the penetrating injury injury:
has occurred, the underlying organs and the amount of • Stabilise the foreign object. This may require
force and dispersion caused by the injury. For example, a padding and/or taping an object, for example a
high-velocity bullet will cause substantial tissue damage knife, to ensure minimal movement and prevent
in a wider area than just the bullet’s track. The clinical further damage until definitive care to remove
manifestations of penetrating trauma can be divided into the object.
two broad types: • Care for the patient in a non-standard position.
1 conspicuous – where the penetrating article is grossly This will be dependent on how and where any
visible (e.g. a shard of glass, a branch or a knife); care foreign object is protruding from the body. For
must be taken not to focus solely on the visible cause example, it may be necessary to care for a patient in
of injury but to continue to undertake a systematic the side-lying or prone position until the object is
trauma assessment removed.
2 inconspicuous – where the penetrating article is • Use minimal volume resuscitation. This describes
not immediately visible and may become apparent the practice of only resuscitating a patient
only during the systematic trauma assessment of the sufficiently to maintain adequate perfusion to
patient (e.g. with gunshot wounds and projectiles); essential organs until definitive repair of the
in these injuries the visual signs on the external skin wound can be undertaken.108
may not reflect the catastrophic injury underlying it • Provide psychosocial care of the patient and
(e.g. ventricle lacerations or serious vascular injury). family. It is possible that patients with penetrating
injury will need specific psychosocial care,
Patient management particularly when the injury has occurred as a
Patients with penetrating injury will be cared for based result of assault.
on the severity and area of injury they have sustained.
Surgical intervention is usually more urgent than that Burns
seen with blunt injury, as bleeding may be occurring from Recent improvements in both shock and sepsis
a ruptured organ or vessel either into a body cavity or management have resulted in patients with severe and
externally. For this reason, the incidence of procedures extensive burn injuries spending long periods of time
such as laparotomy and thoracotomy is high in patients in the critical care environment. Burn injuries occur
with a penetrating injury. as a result of thermal, electrical or chemical injury and
816 SECTION 3 SPECIALTY PRACTICE

cause both local and systemic changes to a patient. An Pathophysiology

understanding of these changes will assist with planning The skin is the largest organ in the human body and
appropriate care for this group of patients. accounts for 15% of its weight. The skin has multiple
In recent years, improved survival, reduced hospital purposes, including protection from infection, regulation
length of stay and a decrease in morbidity and mortality of body heat and function as a vapour barrier.
has been seen in burns patients. This is primarily due The skin consists of three layers: the epidermis, the
to a better understanding of burns pathophysiology dermis and subcutaneous tissue.39 The epidermis is the
and advancements in care that include improvements outer layer, and is composed of stratified epithelial cells
in resuscitation protocols, improved respiratory support, that protect against infection and conserve moisture. This
management of the hypermetabolic response, rigid layer is characterised by having regenerative ability. The
infection control monitoring, early excision and burn dermis, as the middle layer, is between 1 and 4 mm thick,
wound closure, use of skin substitutes and early nutri- although thinner in the elderly and the very young. It
tional support. is composed of an outer papillary dermis and an inner
Burn injuries are highly variable and individual injuries reticular dermis, and supplies nutrients to the epidermis.
that affect all ages and social groups. In general terms, The dermis contains all the accessory structures including
assessment is based on the size, depth and anatomical site blood vessels, nerve endings, the sweat and sebaceous
of the injury, mechanism of injury and the presence of glands and the hair follicles. The dermis itself does not
coexisting conditions. The World Health Organization have regenerative ability, but because the glands, vessels
estimates that more than 300,000 deaths are fire- and follicles are lined with epidermis, burns that involve
related every year, the majority occurring in developing this layer may still regenerate. The innermost layer, the
countries.109 Due to improvements in both surgical subcutaneous tissue, consists of adipose and connective
treatment and intensive care management strategies the tissue. This layer has no regenerative ability.
outcomes of burn patients have continued to improve;
however, they still require complex interdisciplinary thera- Local changes
peutic approaches to optimise management.110 Local changes include the zones of coagulation, stasis and
All patients with a serious burn injury should be hyperaemia (see Figure 24.6) and the specific changes are
referred to a specialised burns unit that is staffed and outlined below.21,39,111
equipped appropriately to manage burns. The Australian • Zone of coagulation: occurs at the point of maximum
and New Zealand Burns Association (ANZBA) criteria damage. Irreversible tissue loss occurs in this zone due
outline which burns patients require treatment in a to coagulation of the constituent proteins.
specialised burns unit (see Box 24.1).
• Zone of stasis: surrounds the zone of coagulation
and is an area of decreased tissue perfusion. Changes
BOX 24.1 that contribute to this stasis include microthrombus
formation, neutrophil adherence, fibrin deposition
Criteria for treatment in a specialised burn centre113 and endothelial swelling. Tissue in this zone is
• Burns greater than 10% of total body surface area potentially salvageable if sufficient resuscitation is
(TBSA) achieved to increase tissue perfusion. If insufficient
• Burns to special areas: face, hands, feet, genitalia,
resuscitation occurs, or if there are additional insults
perineum, major joints
of hypotension, infection or oedema, tissue within
this zone may convert to the zone of coagulation.
• Full-thickness burns greater than 5% of TBSA
• Electrical burns
• Zone of hyperaemia: is the outermost zone. It
experiences increased tissue perfusion as a result of
• Chemical burns local inflammatory response, which results in local
• Burns with an associated inhalation injury vasodilation and an increase in vascular permeability.
• Circumferential burns of the limbs or chest Tissue in this zone will usually recover, unless there
are prolonged or severe periods of hypotension,
• Burns in the very young or very old
infection or oedema.
• Burns in people with pre-existing medical
disorders that could complicate management, Systemic changes
prolong recovery or increase mortality With a burn injury of >30% total burn surface area (TBSA),
• Burns with associated trauma microcirculation vessel wall integrity is altered resulting in
• The possibility of non-accidental injury in children
fluid and protein loss into the interstitium. The protein
loss results in a reduction in osmotic pressure that further
insults circulating volume. Changes to the cardiovascular,
Adapted with permission from Australian and New Zealand Burns
Association. Early management of severe burns (EMSB). Albany
respiratory, metabolic and immunological systems occur as
Creek: Australian and New Zealand Burns Association; 2013. a result of the release of cytokines and other inflammatory
mediators in response to the injury (see Table 24.11).
 CHAPTER 24 TRAUMA MANAGEMENT 817

pulmonary shunting, augmented microvascular pressure

FIGURE 24.6 Zones of burn damage.127 gradient and severe hypoxaemic respiratory failure. Other
than traditional ventilation strategies extracorporeal life
=RQHRI =RQHRI support could be considered as a respiratory support option
FRDJXODWLRQ VWDVLV although the evidence clarifying benefits and limita-
=RQHRI tions is limited (extracorporeal life support is discussed
(SLGHUPLV K\SHUDHPLD further in Chapter 15).113 Diagnosis of an inhalation burn
'HUPLV injury remains problematic, but it should be suspected if
the injury was sustained in a closed spaced as well as if
$GHTXDWH =RQHRI ,QDGHTXDWH there are facial burns, singed nasal hairs or carbonaceous
UHVXVFLWDWLRQ FRDJXODWLRQ UHVXVFLWDWLRQ debris in the mouth or pharynx or in the sputum.39,112 The
specific changes are dependent on the types of substances
inhaled at the time of injury. In addition, the size of the
smoke particles that are inhaled will affect the location of
any injury. If coarse smoke particles are inhaled, these will
primarily be deposited in the upper tracheobronchial tree,
=RQHRIVWDVLVSUHVHUYHG =RQHRIVWDVLVORVW while fine smoke particles will usually be lodged in the
alveoli. Patients with inhalation burn injury will usually
Reproduced from Stehan H, Peter D. ABC of burns. Br Med J experience upper airway oedema and bronchospasm in the
2004;328(7452):1366, with permission. early stages, with the airway disease progressing to the small
airways in subsequent days.112,114 Bronchoscopy is useful to
reveal injury to the large bronchi and therefore is recom-
TABLE 24.11
mended in the early evaluation of upper airway burn.112,115
Systemic changes that occur with burn injuries135 Clinical manifestations
SYSTEM The most prominent clinical manifestations of burn injury
AFFECTED PAT H O P H Y S I O L O G I C A L C H A N G E are the dermal signs of injury. ANZBA uses the principles
Cardiovascular • Increased capillary permeability
of the Early Management of Severe Burns (EMSB) course,
system leading to capillary leak of intravascular which has been adopted internationally and categorises
proteins and fluids to interstitial burns:111,116
compartment 1 Epidermal burns are limited to injury to the
• Peripheral and splanchnic epidermis and tend to be very painful, with a
vasoconstriction common example being sunburn. The skin is pink
• Reduced myocardial contractility to red in colour and remains intact. The surrounding
• Systemic hypovolaemia due to above, tissues may be oedematous and there is no blistering.
plus fluid loss from burn This burn injury will usually heal within 7 days.
Respiratory • Bronchoconstriction 2 Superficial partial-thickness burn injury involves the
system • Adult respiratory distress syndrome
epidermal and superficial dermal layers and is generally
Metabolic • Increased basal metabolic rate (up to red or mottled in appearance and the underlying skin
system 3 times normal) will blanch with pressure, demonstrating that perfusion
• Above, plus splanchnic is intact; blisters are a hallmark symptom. This degree
vasoconstriction, will lead to catabolism of burn injury is very painful and healing may take up
if patient not fed early and aggressively
to 14 days. There is usually a lot of wound exudate in
Immunological • Downregulation of immune response the first 72 hours where the skin is broken.
system
3 Mid-dermal partial-thickness injuries extend a
Adapted with permission from Grunwald TB, Garner WL. part way into the dermis. They have a large zone
Acute burns. Plast Reconstr Surg 2008;121(5): 311e-319e. of damaged non-viable tissue extending into the
dermis, with damaged but viable tissue at the base.
Preservation of the damaged but viable tissue
Inhalation injury (particularly in the initial period following injury)
The presence of an inhalation injury will increase mortality is pivotal to preventing burn wound progression.
and morbidity in people with a dermal burn injury.112 As some of the nerve endings remain viable, pain
Inhalation injury consists of three components that may is present but is less severe when compared to
occur independently but often occur simultaneously, and superficial burns. Similarly, as some of the capillaries
include heat injury to the upper airways, effects of smoke remain viable, capillary return is present, albeit
on the respiratory system and inhalation of toxic gases.112 delayed. Blisters may be present and the underlying
This type of burn injury results in airway inflammation, dermis is a variable colour (pale to dark pink).
818 SECTION 3 SPECIALTY PRACTICE

4 Deep partial-thickness burns extend into the deep

dermal layer. The tissue is a characteristic pink to FIGURE 24.7 Diagram of the ‘rule of nines’: A, adult;
pale ivory in appearance. It can also have a blotchy B, child.128
red base due to extravasation of red blood cells. The
underlying tissue does not blanch and the hair is
easily removed; sensation is reduced. These burns 
usually take in excess of 3 weeks to heal and are
managed with surgical excision and closure.
5 Full-thickness burns destroy both layers of skin
(epidermis and dermis) and may penetrate more
deeply into underlying structures. These burns have 

a dense white, waxy or even charred appearance. The
)URQW
sensory nerves in the dermis are destroyed in a full
thickness burn, and so sensation to pinprick is lost.   
The coagulated dead skin of a full thickness burn, 
which has a leathery appearance, is called eschar.
%DFN  )URQW
 
Assessment of the total body surface area (TBSA) 
of burns %DFN
The extent of injury is best described using the percentage
of the total body surface area that sustained burns. The  
measurement of burn surface area is important during the
initial management of people with burns for estimating 
fluid requirements and determining the need for transfer 
to a burns service. Erythema should not be included when
calculating burn area.
There are several methods that provide a reproducible
estimation of the area of surface area burns. These are: $ %
• Rule of nines – for the adult population, the most
widely known and easily applied method of estimating Reproduced from Sheehy SB, Newberry L. Sheehy’s
TBSA is the ‘rule of nines’ (see Figure 24.7). The emergency nursing: Principles and practice. St Louis: Mosby;
2003, with permission.
principle of this assessment method is that most areas
of the body constitute 9% (or multiples of 9%) of the
TBSA. then be cooled to minimise the burden of injury. ANZBA
• Palmar surface – the surface area of a patient’s palm recommends the application of cool running water for
(including fingers) is about 1% total body surface 20 minutes.111 This is most useful immediately after injury
area. This method of estimating TBSA is commonly but can be instigated up to 3 hours post-injury. The
taught but is yet to be validated. The palmar surface wound and the patient should then be covered to reduce
method can be used to estimate relatively small burns risk of hypothermia. Adequate analgesia must be provided
(<15% of total surface area) or very large burns early in patient care.
(>85%, when unburnt skin is counted), but is
inaccurate for medium-sized burns. Airway
All patients with burn injury require supplemental oxygen.
Patient management Facial burns or carbonaceous sputum (sputum with signs
Care can be considered in two phases. The first is the of smoke or charcoal) may indicate a burn injury to the
immediate priorities of care (outlined below) and includ- airway. A carboxyhaemoglobin of >10% within the first
ing emergency principles, assessment and management hour post-injury is strongly indicative of inhalation injury.
of airway, breathing and circulation, and minimisation of Classic signs of obstruction including stridor, dyspnoea and
hypothermia and hyperkalaemia. The second phase of hoarse voice warrant immediate intubation and should be
care is that provided throughout the first 24 hours (see considered early as worsening oedema can make intubation
Table 24.12). Care of the burn patient beyond that time difficult. Airway stability is mandatory for safe transfer.111
will follow the general principles for critically ill patients,
with additional considerations relating to wound care. Breathing
Carbonaceous pulmonary secretions are a hallmark of
Emergency principles of care airway injury. Dyspnoea and tachypnoea are signs of respir-
The patient should be removed from danger and the atory distress, while pulmonary oedema will often ensue
burning process should be stopped. The wound should with airway burns.
 CHAPTER 24 TRAUMA MANAGEMENT 819

TABLE 24.12
Acute nursing care after burn injury (first 24 hours)

ELEMENT OF CARE MINOR BURN INJURY (<10%) M A J O R B U R N I N J U RY C R I T I C A L LY I L L

Fluid replacement Generally not fluid loaded Fluid replacement as per Major fluid replacement
relevant formula
Need for intubation and Supplemental oxygen therapy. Supplemental oxygen therapy. Mandatory
mechanical ventilation Only if airway burns are Intubation and mechanical
suspected or comorbidities ventilation may be required with
require it analgesia and in burns shock.
Any airway burn in this group
requires intubation
Respiratory and Hourly TPR, BP, SpO2 adapted Continuous ECG, SpO2, Continuous invasive
cardiovascular according to patient status temperature, urine output (hourly haemodynamic, respiratory
observations observations if not continuously and urine output monitoring,
monitored) including core temperature
Neurovascular Assess neurovascular status of Assess neurovascular status of Assess neurovascular status of
observations circumferential burns to chest circumferential burns to chest circumferential burns to chest
and limbs (including fingers and and limbs (including fingers and and limbs (including fingers and
toes) toes) toes)
Analgesia Continuous, intermittent or Continuous intravenous Continuous intravenous
patient-controlled (if patient analgesia ± conscious sedation analgesia + sedation
capable) analgesia ± conscious for dressings
sedation for dressings
Arterial blood gas, Baseline and as indicated by Baseline and as indicated by Baseline and minimum 4-hourly
serum potassium; patient’s condition patient’s condition depending on patient’s
chloride and condition, including temperature
haemoglobin and ventilatory requirements
Haematology Baseline and as indicated by Baseline and as indicated by Baseline and as indicated by
patient’s condition patient’s condition, noting that patient’s condition, noting that
more frequent assessment will more frequent assessment will
be needed if coagulopathy is be needed if coagulopathy is
present present
Feeding Oral intake should be monitored Enteral or oral intake should Enteral feeding should
and encouraged commence within 24 hours of commence within 24 hours of
injury (NB: burns of >20% TBSA injury
require enteral feeding)
General burn dressings Primary debridement Primary debridement undertaken Primary debridement undertaken
undertaken by nursing staff by nursing staff with theatre by nursing staff with theatre
with theatre debridement if debridement if indicated due to debridement if indicated due to
indicated due to burn depth burn depth burn depth
Burn escharotomy as Burns escharotomy as indicated Burns escharotomy as indicated
indicated (unlikely unless (likely with circumferential injury) (highly likely)
circumferential injury)
BP = blood pressure; ECG = electrocardiogram; SpO2 = peripheral oxygen saturation; TBSA = total body surface area;
TPR = temperature, pulse respiration.

Circulation of evidence there is still considerable variability in resus-

The massive interstitial and intracellular fluid shifts citation protocols.110
associated with acute burn injury will deplete circulating Early intravenous cannulation (with two wide-bore
volume and result in shock if it remains uncorrected. Fluid cannulae) and the administration of high-volume fluids
resuscitation aims to anticipate and prevent rather than must begin immediately. ANZBA recommends crystalloid
treat shock. ANZBA and EMSB guidelines recommend solution in the first 24 hours, with fluid administration
IV resuscitation in adults with burns >15% TBSA and titrated to patient response. One of the most widely accepted
children with burns >10% TBSA, although due to a lack resuscitation formulas is the Modified Parkland formula,
820 SECTION 3 SPECIALTY PRACTICE

which recommends delivery of Hartmann’s solution at The multitrauma burns patient

the rate of 3–4 mL/kg/% TBSA over the first 24 hours The combination of traumatic injury and burn injury is
commencing at the time of burn injury, with half the fluid not common, with an incidence of 5–7%, however the
administered within the first 8 hours and the remainder mortality and morbidity is significantly higher than in
over the next 16 hours. Time delays for implementation those patients who sustain an isolated traumatic or burn
of fluid resuscitation should be corrected by increasing injury.117 It is essential to combine the principles of care
infusion rates to reach targets. Fluid resuscitation should be of the burns patient with those of the relevant injury as
guided by predetermined end points in combination with outlined below:
fluid volumes dictated by the formula. Precise end points
for burns resuscitation remain debatable; at present ANZBA • Spinal injury – if the patient has potential spinal
recommends urine output of 0.5–1 mL/kg/h in adults and injuries in addition to the burn, spinal precautions
0.5–2 mL/kg/h in children. The evolution of ‘fluid creep’ must be maintained; however, cervical collars should
has been reported due to over-resuscitation in the early not be used over a burnt neck or upper chest due to
phases of shock, which can result in complications such as the potential for swelling and subsequent restriction.
acute lung injury, abdominal and extremity compartment If a collar is used, changing to an appropriate size as
syndrome, multi-organ failure and death.109,110 the swelling worsens or goes down is essential.
Patients with circumferential full thickness burn injury • Skeletal injury – skin traction cannot be used in a
may require escharotomies due to the extensive oedema patient with burn injury over a limb that also has a
formation and the inelasticity of burn eschar. Delayed skeletal fracture; this will necessitate early internal
capillary return, a cool limb and increased pain manifest fixation or the use of an external fixateur.
earlier than loss of palpable pulse. • Electrocution injuries – electrocution burns are
The use of invasive monitoring in the burns patient largely internal burns that potentially cause devastat-
is controversial, as the relevant catheters often require ing multiple internal injuries. The electrical current
insertion through a burn and therefore provide a portal causes a burn at both the entry and exit sites. Where
of entry for infection. However, all serious burns patients electrocution is confirmed or suspected the body
require an indwelling catheter for monitoring. Relevance must be inspected to identify all injuries. These may
of other monitoring capability will be determined on an be in obscure places such as the hands and feet or
individual patient basis based on cardiovascular status, need even the back and scalp. Close monitoring for cardiac
for inotropic support, extent of the burn and potential for damage and rhabdomyolysis is essential.
infection.
Burn dressings
Minimising hypothermia
Mitigating infection is the primary aim of good burns
Skin is an essential component of the body’s natural
nursing.116 The greatest challenge is minimising the risk
thermoregulation mechanism, so loss of skin integrity,
for cross-contamination, and patients should be nursed
coupled with such treatment strategies as cooling the
in a single room where possible. Burn dressings present
burn and administering high-volume fluid replacement,
a physical challenge, particularly when large areas of the
exposure of wounds following injury and during dressing
body are affected.
changes, places the patient at high risk of hypothermia.
The traditional burn dressing in the ICU is undertaken
Continuous temperature monitoring is essential, and
as a surgically clean technique. As part of the management
strategies to maintain normothermia should be imple-
of the burn injury, there are a number of specific issues
mented immediately and continuously. Strategies include
that require attention. The following is a guide to specific
minimising exposure, warming fluids and warming
aspects of burn management:
the patient’s environment. Warm blankets and heated
humidified supplemental oxygen are also valuable adjuncts. • Debridement – this refers to the excision of dead
skin. Gentle scrubbing is generally used to remove
Hyperkalaemia loose tissue and burst blisters. Forceps and scissors
Cell destruction from the burn injury can result in high may be required to lift and remove smaller areas of
serum potassium levels, which should be monitored tissue. Extensive areas of debridement will usually be
closely. Metabolic acidosis will exacerbate the hyper- undertaken in the operating room.
kalaemia, as intracellular exchange of hydrogen ions with
potassium ions takes place.
• Blisters – small blisters should be left intact whereas
large blisters may be aspirated or deroofed during
Nutrition debridement, although it should be noted that
Supplemental feeding is mandatory and should commence evidence regarding blister management is poor.
as soon as possible following severe burn injuries due to the Blisters over joints that are restricting movement
hypermetabolism.39 Patients with >20% TBSA are unable should also be debrided.
to meet their nutritional requirements orally. ANZBA and • Escharotomy – an escharotomy is undertaken to a
EMSB recommend enteric feeding in adults with burn limb or side of the trunk for circumferential burns
injury >20% and >10% TBSA in children. that are contracting and creating vascular compromise
 CHAPTER 24 TRAUMA MANAGEMENT 821

to the underlying and distal tissues. The escharotomy includes leaving the site intact and immobilising
is an incision through the eschar, and does not involve the graft site, applying the appropriate wound care
opening muscle fascia. The escharotomy immediately regimen, preventing shearing injury to the graft site
relieves the compression and is a limb-/life-saving and minimising the risk for infection. With autografts,
surgical manoeuvre. The escharotomy is dressed as a wound care will also be required for the donor site.109
burn to prevent infection. • Skin substitutes – some products are available to
• Skin grafts – these are required to cover the skin cover partial-thickness wounds that provide a moist
defect. They may be full-thickness or partial-thickness environment that stimulates epithelialisation. These
grafts, and may be harvested from the patient or, are best reserved for ‘clean’ wounds. Some products
in some cases, obtained from a cadaver donor. are able to act as full-thickness substitutes that provide
Regardless of the type of skin graft, nursing care wound closure, protection from mechanical trauma
remains the same, with the aim being to maximise and bacteria and a vapour barrier. Once the new
adherence. Specific nursing care of the graft site dermis is created the substitute is removed.109

Summary
Care of the trauma patient presents the critical care nurse with multiple challenges. With the introduction of trauma
systems the outcome and survival of injured patients has improved dramatically. The severity of injury and patient
outcome are dependent on effective pre-hospital care, resuscitation and definitive surgical management on arrival at the
hospital. Principles of resuscitation of the trauma patient are the same as for all patients, with a primary, secondary and
tertiary survey being undertaken, and maintenance or correction of airway, breathing and circulation taking precedence.
Prevention of the ‘trauma triad’ of hypothermia, acidosis and coagulopathy has the potential to significantly influence
patient outcome. Consideration of the specific injury, with its resultant pathophysiological changes, is necessary to care
effectively for patients with abdominal, chest, multiple or burn injuries. It is challenging work as trauma patients are
largely a young and healthy population prior to injury and may experience significant ongoing compromise.

Case study
Helen is a 45-year-old, 70-kg woman from Hong Kong who has been working in Australia for several months.
Her husband and son both reside in Hong Kong. Helen was a pedestrian walking with her headphones on
and had stopped at an intersection where she was struck by a concrete mixer and dragged 200 metres.
Glasgow Coma Score (GCS) was initially 3; however, it improved to 9 pre-hospital.
Helen met the major trauma triage criteria and was transferred via road to a major trauma hospital. Trauma
team activation occurred prior to Helen’s arrival. When Helen arrived in the emergency department (ED), a
full team was present to assess and treat her. This team included a trauma surgeon, trauma nurse leader,
emergency doctor, orthopaedic surgeon, anaesthetist, specialist nurses and support staff.
On arrival of the ambulance personnel Helen’s vital signs were as follows:
• HR was 140 (sinus tachycardia), BP unrecordable, respiratory rate (RR) not recorded, unconscious
GCS 3, SpO2 92% on room air.
• IV cannula was inserted with 1 L normal saline administered during transport. Helen received O2 and
morphine for pain; her spine and left leg were both immobilised.
• First ABGs were: pH 7.03, pCO2 56 mmHg, pO2 447 mmHg, HCO3− 15 mEq/L, SpO2 99%, Na 138
mmol/L, K 6.8 mmol/L. Cl−109 mmol/L, glucose 17.0 mmol/L; lactate was unavailable.
• Duration at scene was 8 minutes.
Ongoing assessment and treatment in the ED consisted of the following:
• HR was 76, SBP 60–70, RR not recorded, GCS fluctuating from 9 to 3, SpO2 97% decreased to 79%.
• Primary survey was conducted.
• Initial resuscitation with 1 L normal saline, FAST negative, massive transfusion protocol activation, right
subclavian CVC inserted, 7 units RBC administered, intubation, left lower leg splint, left thigh pressure
bandage, pelvic binder applied.
• Duration in ED was 28 minutes.
822 SECTION 3 SPECIALTY PRACTICE

Observations and treatment in the operating theatre included:

• SBP was <100, HR >100, initial temp 33°C, increased to 37°C.
• Operations were trauma laparotomy and vacuum dressing, external fixateur and C-clamp to pelvis,
external fixateur to left knee and right femur, left thigh exploration and repair left iliac artery, laparotomy
and control iliac vein bleeding (avulsion injury), left lower eyelid canthotomy, repair facial and lip
laceration, repair left hand laceration, left leg wound repair and vacuum dressing, left illiofemoral bypass,
fasciotomy and haemostasis; indwelling catheter (IDC) insertion
• Duration in theatre was 11 h.
Injuries included: right tentorial subdural haemorrhage; left orbital fracture (#); left ribs # 3–12th; bilateral
sacroiliac joint diastasis and left sacral alar #; left superior pubic rami #; left inferior ischial rami #; right
femur #; dislocated left knee, pancreatic, duodenal and jejunal oedema and mesenteric haematoma;
left subcostal artery injury; left inferior gluteal and left external iliac artery injury; left hand laceration; full
thickness graze to mid back and sacral area; scalp haematoma.
On arrival in intensive care Helen had already received a total of 54 units red blood cells (RBC), 40 units
fresh frozen plasma (FFP), 7 pooled units platelets, 750 mL cryoprecipitate, Novo 7 (noted in anaesthetics
documentation, with dose not recorded), and cell saver had been used in theatre.
In ICU Helen was initially reported as being able to roll for pressure care; however, subsequently this was
changed by the orthopaedic team to Jordan frame lift only due to pelvic fracture instability. Post fixation of
her pelvic fracture and removal of external fixateurs this changed and Helen was only allowed to log roll to
the left side with no side lying at all.
During day 1 Helen had rising creatine kinase (CK) levels (<30,000) and decreasing urinary output resulting in
commencement of dialysis post insertion of a right internal jugular vascular catheter. She had high inotropic
requirements (both noradrenaline and adrenaline) to maintain her mean arterial pressure >70 mmHg. An
echocardiogram showed normal cardiac function. A warming blanket was used as Helen had hypothermia
(temp 35°C) on arrival in ICU, no doubt as a result of the prolonged theatre time.
Consultation with trauma, orthopaedics and vascular teams occurred on day 1 regarding the viability of
Helen’s left leg. Discussion then occurred with Helen’s family – her son was present, but other family
members including Helen’s husband were in Hong Kong. A decision was made to return Helen to theatre
for a left hindquarter amputation.
A social worker worked with Helen’s son to support him and to make travel arrangements for Helen’s
husband to come to Australia from Hong Kong; the social worker and nursing team continued to support
the family throughout Helen’s ICU stay.
Within ICU members of the multidisciplinary team who contributed to Helen’s care included nursing and
medical staff who provided patient and family care and support; physiotherapists delivering ongoing
respiratory assessment, passive limb movements and assessment for increasing tone in all limbs; and the
dietitian to assess nutritional requirements and provide total parenteral nutrition and enteral nutrition.
Other teams who contributed to Helen’s care included:
• trauma team, which undertook the FAST in the ED and performed some of the surgical procedures
initially and on an ongoing basis
• orthopaedic team, which undertook the orthopaedic surgical procedures and provided ongoing
management in this area of her care
• vascular team, who were involved in the management of all arterial injuries including her amputation
• haematology team, who were involved in the management of her coagulopathy
• plastics team, which contributed expertise related to the management of full thickness graze and burn injuries
• faciomaxillary team, which completed an open reduction and internal fixation of her left orbit # on day
16 of admission
• renal team, who were involved with management of intermittent dialysis via a perma-cath
• speech therapy, who assessed Helen’s swallow post extubation to ensure that she was safe to
commence oral intake
• occupational therapy, who assessed Helen for post traumatic amnesia and contributed to her discharge
planning, including the possibility of musculoskeletal and acquired brain injury rehabilitation.
 CHAPTER 24 TRAUMA MANAGEMENT 823

Commencing on day 12 Helen was gradually woken. She had slow improvements in her conscious state
and was able to tolerate a slow wean of her mechanical ventilation support. She was successfully extubated
on day 13 of her admission.
Helen was initially confused and not speaking English, although she did recognise her husband and son
when they visited and was often more settled during these times. Helen required frequent orientation to
time and place and what had happened to her. Fortunately, she was able to speak and understand English,
although this was not her native language, which was difficult for her. Helen was assessed for delirium and
was treated for this during the days leading to her discharge to the ward; she also experienced depression
in response to the injury and subsequent loss of independence. A plan was instituted for the ongoing
assessment and management of this while in ICU and post discharge to the ward.
The social worker supported Helen and her family to assist with the many adjustments required as a result
of her injury and subsequent loss of independence and changes to living arrangements as Helen previously
lived in a first floor apartment with stair access only.

CASE STUDY QUESTIONS

1 Discuss the components of the ‘trauma triad’ and outline the practices that would prevent or ameliorate
the triad.
2 Identify the likely causes of Helen’s renal failure and discuss the preventative and treatment approaches
that are available.
3 Discuss the management of massive blood transfusion and the treatment approaches that are available.
4 What is ‘damage-control surgery’ and why is this so important to survival in trauma patients? Describe
the implications of the type of accident experienced by Helen and her likely injuries and treatment in
relation to DCS.
5 Describe the practices that could be incorporated into Helen’s care to reduce her psychological distress
both during the initial weeks post injury and in the rehabilitation/discharge phase of her recovery.

RESEARCH VIGNETTE

Hyllienmark P, Brattstrom O, Larsson E, Martling CR, Petersson J, Olner A. High incidence of post-injury pneumonia
in intensive care-treated trauma patients. Acta Anaesthesiol Scand 2013;57:848–54

Abstract
Introduction: Trauma patients are susceptible to post-injury infections. We investigated the incidence, as well as
risk factors for development of pneumonia in intensive care unit (ICU)-treated trauma patients. In addition, we report
pathogens identified in patients that developed pneumonia.

Methods: The study cohort consisted of 322 trauma patients admitted to the ICU at a level-one trauma centre
following initial resuscitation. Patients 15 years or older with an ICU stay of more than 24 h were included. We
investigated pre-hospital and hospital parameters during the first 24 h after admission and their possible association
with pneumonia within 10 days of ICU admission.

Results: Majority of the patients were male (78%) and the median age was 41 years. The overall degree of injury was
high with a median Injury Severity Score of 24. Overall 30-day mortality was 9%. Eighty-five (26%) patients developed
pneumonia during their first 10 days in the ICU. Univariate logistic regression revealed that intubation in the field, shock,
Glasgow Coma Scale (GCS) 3–8, major surgery within 24 h after admission, massive transfusion and injury severity
score >24 were all risk factors for subsequent development of pneumonia. In the multivariable model, only GCS 3–8 was
identified as an independent risk factor. In 42 out of the 85 cases of pneumonia, the diagnosis was defined by significant
growth of at least one pathogen where Enterobacteriaceae and Staphylococcus aureus were the most common.

Conclusion: Pneumonia is a common complication among ICU-treated trauma patients. Reduced consciousness is
an independent risk factor for development of pneumonia after severe injury.
824 SECTION 3 SPECIALTY PRACTICE

Critique
This investigation was a single site study with an exploratory research design. The setting for the study was a mixed
13-bed ICU in a designated level 1 trauma centre in a university hospital in Stockholm, Sweden. The trauma centre
served as the only referral centre for severe trauma cases in a region with a population of approximately 2 million
inhabitants. This makes this study cohort a representative sample of severe trauma across urban and rural settings
in this country. However, patients were excluded if they were admitted to the ICU from other receiving units, and it is
not clear why the transferred patients were excluded; this may limit the generalisability of the results.

The study has several strengths. One is that all clinical data were entered prospectively into the databases, which likely
minimised missed values and increased the accuracy and validity of the data. Another strength was that pneumonia
was clearly and thoroughly defined based on radiographic criteria together with clinical or microbiological criteria as
established by the Swedish intensive care registry (SIR); these are the same criteria developed by the CDC National
Health and Safety Network with the exception that microbiological criteria are optional.119 Pneumonia occurring after
more than 48 hours of invasive mechanical ventilation was classified as ventilator-associated pneumonia (VAP). Other
assessment requirements and interventions were also clearly described, e.g. massive transfusion was defined as
more than 10 units of blood during the first 24 hours after admission.

The study included 322 patients for analysis. The characteristics of the cohort, with relatively low median age,
male dominance and limited number of penetrating injuries, was representative of other European trauma ICU
cohorts.120,121 One-quarter of the patients developed pneumonia during their first 10 days post-injury, which is
consistent with other studies. The key finding in this study was that reduced level of consciousness (GCS 3–8) was
the single greatest independent risk factor for the development of post-injury pneumonia. Although the risk factors
of intubation in the field, shock, major surgery, massive transfusion and severe injury had a univariate relationship
with the outcome of pneumonia, they did not retain significance in the multivariable model. The investigators
suggest that factors other than decreased consciousness, for example immobilisation, may contribute to the
development of post-injury pneumonia.

This study was generally well designed. Further prospective, multicentre research is needed to address the
complexity in the pathophysiology of multiple injuries and the association with pneumonia and VAP in trauma
patients. The implications for clinical nursing are significant, as 25% of severe trauma patients have the potential of
developing pneumonia and VAP in the first 10 days after a major trauma event. Trauma management includes the
use of VAP bundle strategies containing different components such as body position, oral care, daily interruption
in sedation and assessment of readiness for extubation, and use of specialised endotracheal tubes.122 The efficacy
and validity behind the components in the VAP bundle need to be investigated as there is a lack of evidence.
Nurses, using their clinical expertise, can identify at-risk patients for developing VAP and play a vital role in the
innovation and critical evaluation of the evidence behind interventions and contribute to improving trauma patients’
safety and outcome.

Lear ning a c t iv it ie s
1 Briefly describe why the mechanism of injury is important information in diagnosing injuries.
2 Describe the implications of the type of accident experienced by Helen and her likely injuries and treatment.

Online resources
American College of Surgeons, www.facs.org
Australasian College for Emergency Medicine, www.acem.org.au
Australasian Trauma Society, www.traumasociety.com.au
Australian and New Zealand Burn Association, www.anzba.org.au
 CHAPTER 24 TRAUMA MANAGEMENT 825

Eastern Association for the Surgery of Trauma, www.east.org

European Society for Trauma and Emergency Surgery, www.estesonline.org
NSW Trauma Management Guidelines, www.itim.nsw.gov.au/go/itim-trauma-guidelines
NSW Trauma System, www.itim.nsw.gov.au/index.cfm
Royal Australasian College of Surgeons, www.surgeons.org
Society of Trauma Nurses, www.traumanurses.org
Trauma.org, an independent, non-profit organisation providing global education, information and communication resources
for professionals in trauma and critical care, www.trauma.org
Victorian State Trauma System, www.health.vic.gov.au/trauma
World Health Organization, www.who.int/topics/injuries/en/

Further reading
McQuillan K, Whalen E, Flynn-Makick M. Trauma nursing: From resuscitation through rehabilitation. 4th ed. Philadelphia:
Saunders, 2008.
Moloney-Harmon PA, Czerwinski SJ. Nursing care of the paediatric trauma patient. Cambridge: Elsevier, 2003.
Skinner DV, Driscoll PA. ABC of major trauma. 4th ed. West Sussex: Wiley, 2013.
Spahn DR, Bouillon B, Cemy V, Coast TJ, Duranteau J, Fernandez-Mondejar E et al. Management of bleeding and coagulopathy
following major trauma: an updated European guideline. Crit Care 2013;17:R76. <http://ccforum.com/content/17/2/R76>.
Wolf SJ, Bebarta VS, Bonnett CJ, Pons PT, Cantrill SV. Blast injuries. Lancet 2009;374(9687):405–15.

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to the emergency department with acute blunt abdominal trauma. Ann Emerg Med 2011;57(4):387-404.
64 Balogh ZJ, Reumann MK, Gruen RL, Mayer-Kuckuk P, Schuetz MA, Harris IA et al. Advances and future directions for management of trauma
patients with musculoskeletal injuries. Lancet 2012;380(9847):1109-19.
65 Panteli M, Lampropoulos A, Giannoudis PV. Fat embolism following pelvic injuries: a subclinical event or an increased risk of mortality? Injury
2014;45(4):645.
66 Aitken LM LJ, Bellamy N. Queensland Trauma Registry: description of serious injury throughout Queensland, 2003. Herston: Centre of National
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67 Guyton AC, Hall JE. Textbook of medical physiology. Philadelphia: Elsevier Saunders; 2006.
68 Little N, Rogers B, Flannery M. Bone formation, remodelling and healing. Surgery (Oxford) 2011;29(4):141-5.
69 Association for the Advancement of Automotive Medicine. Abbreviated Injury Scale 2005: update 2008. Barrington: Association for the
Advancement of Automotive Medicine; 2008.
70 Copuroglu C, Calori GM, Giannoudis PV. Fracture non-union: who is at risk? Injury 2013;44(11):1379.
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72 Sinha P, Bunker N, Soni N. Fat embolism – an update. Curr Anaesth Crit Care 2010;21(5):277-81.
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74 Bosch X, Poch E, Grau JM. Rhabdomyolysis and acute kidney injury. N Engl J Med 2009;361(1):62-72.
75 Lenarz CJ, Watson JT, Moed BR, Israel H, Mullen JD, Macdonald JB. Timing of wound closure in open fractures based on cultures obtained
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76 Chesser TJS, Cross AM, Ward AJ. The use of pelvic binders in the emergent management of potential pelvic trauma. Injury 2012;43(6):667.
77 Walker J. Pelvic fractures: classification and nursing management. Nurs Stand (Royal College of Nursing (Great Britain): 1987) 2011;26(10):49.
78 Eckroth-Bernard K, Davis JW. Management of pelvic fractures. Curr Opin Crit Care 2010;16(6):582-6. doi: 10.1097/MCC.0b013e3283402869.
79 Roodenburg O, Roodenburg B. Chest trauma. Anaesth Intensive Care Med 2011;12(9):390-2.
80 Kiraly L, Schreiber M. Management of the crushed chest. Crit Care Med 2010;38(9 Suppl):S469-77.
81 Ahmad M, Sante ED, Giannoudis P. Assessment of severity of chest trauma: is there an ideal scoring system? Injury 2010;41(10):981-3.
82 Martínez RJA, Fernández CM, Alarza FH, Serna IM, de Alba AM, Bedoya MZ et al. Evolution and complications of chest trauma. Arch Bronchol
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83 Bernardin B, Troquet JM. Initial management and resuscitation of severe chest trauma. Emerg Med Clin North Am 2012;30(2):377-400.
84 Turkalj I, Stojanović S, Petrović D, Brakus A, Ristić J. Blunt chest trauma: an audit of injuries diagnosed by the MDCT examination. Vojnosanit
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85 Burnside N. Blunt thoracic trauma. Surg 2014;32(5):254-60.
86 Dwivedi S, Gharde P, Bhatt M, Johrapurkar SR. Treating traumatic injuries of the diaphragm. J Emerg Trauma Shock 2010;3(2):173-6.
87 Fontaine EJ. Pneumothorax and insertion of a chest drain. Complications of chest drains. Surgery 2011;29(5):244-6.
88 Boersma WG SJ, Smit HJM. Treatment of haemothorax. Respir Med 2010;104(11):1583-7.
89 Bock JS BR. Blunt cardiac injury. Cardiol Clin 2012;30(4):545-55.
90 Nishijima DK, Simel DL, Wisner DH, Holmes JF. Does this adult patient have a blunt intra-abdominal injury? JAMA 2012;307(14):1517-27.
91 Groven S, Eken T, Skaga NO, Roise O, Naess PA, Gaarder C. Abdominal injuries in a major Scandinavian trauma center: performance
assessment over an 8 year period. J Trauma Manag Outcomes 2014;8:9.
92 Prachalias AA. Isolated abdominal trauma: diagnosis and clinical management considerations. Curr Opin Crit Care 2014;20(2):218-25.
93 O’Dowd V, Lowery A, Khan W, Barry K. Seatbelt injury causing small bowel devascularization: case series and review of the literature. Emerg
Med Int 2011;2011:675341.
94 Alsayali M, Winnett J, Rahi R, Niggemeyer LE, Kossmann T. Management of blunt bowel and mesenteric injuries: experience at the Alfred
Hospital. Eur J Trauma Emerg Surg 2009;35(5):482-8.
95 Bansal V, Tominaga G, Coimbra R. The utility of seat belt signs to predict intra-abdominal injury following motor vehicle crashes. Traffic Injury
Preven 2009;10(6):567-72.
96 American College of Surgeons. Abdominal compartment syndrome: a decade of progress. J Am Coll Surg 2013;216(1):135-46.
97 Kirkpatrick AW, De Waele J, Jaeschke R, Malbrain ML, De Keulenaer B, Duchesne J et al. Intra-abdominal hypertension and the abdominal
compartment syndrome: updated consensus definitions and clinical practice guidelines from the World Society of the Abdominal Compartment
Syndrome. Intensive Care Med 2013;39:1190-206.
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98 Gabbe BJ, Simpson PM, Sutherland AM, Wolfe R, Fitzgerald MC, Judson R et al. Improved functional outcomes for major trauma patients in
a regionalized, inclusive trauma system. Ann Surg 2012;255(6):1009-15.
99 Rhodes CM, Smith HL, Sidwell RA. Utility and relevance of diagnostic peritoneal lavage in trauma education. J Surg Educ 2011;68(4):313-7.
100 Whitehouse JS, Weigelt JA. Diagnostic peritoneal lavage: a review of indications, technique, and interpretation. Scand J Trauma Resusc
Emerg Med 2009;17:13.
101 Castrillon GA, Soto JA. Multidetector computed tomography of penetrating abdominal trauma. Sem Roentgenol 2012;47(4):371-6.
102 O’Malley E, O’Callaghan A, Coffey JC, Walsh SR. Role of laparoscopy in penetrating abdominal trauma: a systematic review. World J Surg
2012;37(1):113-22.
103 Wallis A, Kelly MD, Jones L. Angiography and embolisation for solid abdominal organ injury in adults: a current perspective. World J Emerg
Surg 2010;5:18.
104 Demetriades D. Total management of the open abdomen. Int Wound J 2012;9(Supp 1):17-24.
105 Burlew CC. The open abdomen: practical implications for the practicing surgeon. Am J Surg 2012;204(6):826-35.
106 Langley JM, Dodds L, Fell D, Langley GR. Pneumococcal and influenza immunization in asplenic persons: a retrospective population based
cohort study 1990–2002. BMC Infect Dis 2010;10:219.
107 Pasternack MS. Patient information: preventing severe infection after splenectomy (Beyond the Basics), < http://www.uptodate.com/contents/
preventing-severe-infection-after-splenectomy-beyond-the-basics>; 2014.
108 Duchesne JC, Kimonis K, Marr AB, Rennie KV, Wahl G et al. Damage control resuscitation in combination with damage control laparotomy:
a survival advantage. J Trauma 2010;69(1):46-52.
109 Bezuhly M, Fish JS. Acute burn care. Plast Reconstr Surg 2012;130(2):349e-58e. doi: 10.1097/PRS.0b013e318258d530.
110 Rex S. Burn injuries. Curr Opin Crit Care 2012;18(6):671-6. doi: 10.1097/MCC.0b013e328359fd6e.
111 Australian and New Zealand Burns Association. Early management of severe burns (EMSB). Albany Creek: Australian and New Zealand Burns
Association; 2013.
112 Singh S, Handy J. The respiratory insult in burns injury. Curr Anaesth Crit Care 2008;19(5–6):264-8.
113 Asmussen S, Maybauer DM, Fraser JF, Jennings K, George S, Keiralla A et al. Extracorporeal membrane oxygenation in burn and smoke
inhalation injury. Burns 2013;39(3):429-35.
114 Cancio LC. Airway management and smoke inhalation injury in the burn patient. Clin Plast Surg 2009;36(4):555-67.
115 Hassan Z, Wong JK, Bush J, Bayat A, Dunn KW. Assessing the severity of inhalation injuries in adults. Burns 2010;36(2):212-6.
116 Edgar D (ed). Burn survivor rehabilitation: principles and guidelines for the allied health professional. Australian and New Zealand Burn
Association, <http://www.aci.health.nsw.gov.au/__data/assets/pdf_file/0003/154083/anzba_ahp_guidelines_october_2007.pdf>; 2007
[accessed 04.15].
117 Hawkins A, MacLennan PAP, McGwin GJ, Cross JM, Rue L. The impact of combined trauma and burns on patient mortality. J Trauma-Injury
Infect Crit Care 2005;58(2):284-8.
118 Hyllienmark P, Brattstr ÖM, Larsson E, Martling CR, Petersson J, Oldner A. High incidence of post-injury pneumonia in intensive care-treated
trauma patients. Acta Anaesthes Scand 2013;57(7):848-54.
119 Yokoe DS, Mermel LA, Anderson DJ, Arias KM, Burstin H, Calfee DP et al. Compendium of strategies to prevent healthcare associated
infections. Infect Control Epidemio. 2008;29(Suppl 1):S12-21.
120 Michelet P, Brégeon F, Perrin G, D’Journo XB, Pequignot V, Vig V et al. Early onset pneumonia in severe chest trauma: a risk factor analysis.
J Trauma 2010;68(2):395-400.
121 Cavalcanti M, Ferrer R, Morforte R, Garnacho A, Torres A. Risk and prognostic factors of ventilator-associated pneumonia in trauma patients.
Crit Care Med 2006;34:4.
122 Munro N, Ruggiero M. Ventilator-associated pneumonia bundle: reconstruction of best care. AACN Adv Crit Care 2014;25(2):163-75.
123 Howard PK, Steinmann RA, Sheehy SB. Sheehy’s emergency nursing: Principles and practice. St Louis: Mosby Elsevier; 2010.
124 Kobziff L. Traumatic pelvic fractures. Orthopaed Nurs 2006;25(4):235-41; quiz 42-3.
125 SAM Medical Products. Pelvic Sling II, <http://www.sammedical.com/products/sam-pelvic-sling-ii> [accessed 04.15].
126 Wiss DA, Ovid Technologies I. Fractures. Philadelphia: Lippincott Williams & Wilkins; 2006.
127 Stehan H, Peter D. ABC of burns. Br Med J 2004;328(7452):1366.
128 Sheehy SB, Newberry L. Sheehy’s emergency nursing: Principles and practice. St Louis: Mosby; 2003.
129 Richards CE, Mayberry JC. Inital management of the trauma patient. Crit Care Clin 2004;20(1):1-11.
130 Kohn MA, Hammel JM, Bretz SW, Stangby A. Trauma team activation criteria as predictors of patient disposition from the emergency
department. Acad Emerg Med 2004;11(1):1-9.
131 Eckert KL. Penetrating and blunt abdominal trauma. Crit Care Nurs Q 2005;28(1):41-59.
132 Olthof DC, van der Vlies CH, Scheerder MJ, de Haan RJ, Breenen LFM, Goslings JC, van Delden OM. Reliability of injury grading systems for
patients with blunt splenic trauma. Injury 2014;45(1):146-50.
133 Grunwald TB, Garner WL. Acute burns. Plast Reconstr Surg 2008;121(5): 311e-319e.
 Chapter 25

Resuscitation
Trudy Dwyer, Jennifer Dennett, Ian Jacobs

KEY WORDS Learning objectives

cardiac arrest After reading this chapter, you should be able to:
cardiopulmonary • identify the benefits of an international approach to resuscitation
resuscitation systems
sudden cardiac • discuss the importance of basic life support in the context of advanced
arrest life support
• describe the safety precautions of defibrillation
• discuss the principles of therapeutic hypothermia
• discuss indications, actions and routes of administration of medications
used in advanced life support
• outline the treatment algorithm for both shockable and non-shockable
rhythms
• outline the nurse’s role in facilitating family presence during an arrest.

Introduction
The continuum of critical illness for an individual can span the period before
and beyond hospital admission. Resuscitation is often required outside the
critical care environment. The ‘cardiac arrest’ team has evolved to use a more
proactive, early intervention approach, utilising a range of rapid response
systems and instruments to detect deterioration in patients’ clinical status (see
Chapter 3). It is well recognised that improved outcomes from cardiac arrest
are dependent on early recognition and initiation of the ‘chain of survival’.1
This chapter introduces the resuscitation systems and processes in both the pre-
hospital and the in-hospital settings.The chain of survival provides a framework
for the management of the person experiencing cardiac arrest and resuscita-
tion in specific circumstances. The chapter expands on the final link in the
chain, advanced life support, to outline advanced airway management, rhythm
recognition, administration of medications and post-resuscitation care. Resus-
citation involves many moral and ethical issues, such as family presence during
resuscitation, deciding when to cease or initiate resuscitation and near-death
experiences (see Chapter 5).
830 SECTION 3 SPECIALTY PRACTICE

Cardiac arrest Acute myocardial infarction is the most common

precursor to cardiac arrest. In victims of trauma, drug
Coronary heart disease (CHD) is the leading cause of overdose and drowning, the predominant cause of cardiac
death in most industrialised countries, with over half of arrest is asphyxia. Cardiac arrest in children is less common
these being due to sudden cardiac arrest (SCA).2,3 Despite and even more rarely sudden,14,15 with the common
advances in CHD management, survival outcome figures causes being trauma, congenital heart disease, long QT
from SCA remain poor with the survival rate reported to syndrome, drug overdose, hypoxia and hypothermia. The
be between 1% and 31% annually.4 Survival after SCA is most common arrhythmia in infants is bradycardia, and
dependent on the presenting rhythm, early defibrillation, the prognosis is especially poor if asystole is present.14,16
effective cardiopulmonary resuscitation, early advanced Chest compression should be started if the pulse is less
life support and post-resuscitation care.5,6 Because the than 60/minute with poor perfusion.16
presenting rhythm with the majority of witnessed SCAs
is ventricular fibrillation (VF), bystander cardiopul- Pathophysiology
monary resuscitation and early defibrillation are the major In sudden cardiac arrest with cardiac origin, it is believed
interventions influencing outcome after SCA.2,6,7 The that myocardial ischaemia leads to ventricular irritabil-
percentage of patients in out-of-hospital cardiac arrest ity and the progression from ventricular tachycardia (VT)
(OHCA) presenting with VF is decreasing with time, to VF and ultimately asystole.17 After the onset of VF (in
possibly secondary to the use of beta-blockers or increased animal studies), carotid arterial blood flow continues for
presence of implantable cardioverter-defibrillators.8 approximately 4 minutes even in the absence of cardiac
compressions, as coronary perfusion pressure (the pressure
Incidence/aetiology of cardiac arrests gradient between the aorta and the right atrium) falls over
The prevalence of CHD varies worldwide; thus estimates this period.17 This initial phase is characterised by minimal
of the incidence of SCA are difficult to obtain.9 In ischaemic injury, and it is during this time that defibrilla-
Australia, CHD is the leading cause of disease burden (9%) tion is most likely to result in the restoration of a perfusing
and accounts for 16.5% of all deaths.10 There are many rhythm, while initiation of effective cardiac compressions
factors that contribute to cardiac arrest. In adults, the will increase the coronary perfusion pressure.17
most common cause of cardiac arrest is a primary cardiac Progression of the cardiac arrest beyond 4 minutes
event,11 with coronary artery disease accounting for up results in accumulation of toxic metabolites, depletion
to 90% of all victims.12,13 CHD is the most likely cause of high-energy phosphate stores and the initiation of
of death in those over 35 years of age, compared to non- ischaemic cascades.17 Increasing probability of irreversible
cardiac causes such as drowning, acute airway obstruction cellular injury exists where a cardiac arrest extends for
or trauma for people less than 35 years of age.13 longer than 10 minutes, and the return of a spontaneous
While causes of cardiac arrest are numerous, most often circulation during this period may initiate a reperfusion
it is associated with ventricular fibrillation triggered by injury17 (see Chapter 11 for further discussion).
an acutely ischaemic or infarcted myocardium or primary
electrical disturbance.3 Causes of cardiac arrest may be Resuscitation systems and
separated into two categories, primary and secondary, as
displayed in Table 25.1. processes
Since the rediscovery of the effectiveness of closed-chest
TABLE 25.1 cardiopulmonary resuscitation (CPR) in 1960 and its
Causes of cardiac arrest subsequent widespread adoption, CPR has saved the lives
of many, potentially ensuring years of productive life.18 As
P R I M A RY C A U S E S S E C O N D A RY C A U S E S CPR quickly became one of the most widely-used and
Acute myocardial infarction Cessation of breathing researched procedures, voluntary coordinating bodies
Cardiomyopathy Airway obstruction developed throughout the world.13 Organisations such as
Electrical shock (low- and Severe bleeding the European Resuscitation Council (ERC), the American
high-voltage) Hypothermia Heart Association (AHA), the New Zealand Resuscitation
Congenital heart disease Hypoglycemia Council (NZRC), the Heart and Stroke Foundation of
(e.g. prolonged Q-T) Drug-induced proarrhythmia Canada, the Resuscitation Council of Southern Africa and
Drugs Metabolic disturbance
the Australian Resuscitation Council (ARC) established
Electrical disturbance
practice guidelines to improve standards in resuscitation,
Trauma
and coordinated resuscitation activities on a national basis.19
Neuromuscular disease
However, as standardised recording of outcome data did
Adapted with permission from Konstantopoulou A, Tsikrikas S, not exist, resuscitation endeavours could not be compared
Asvestas D, Korantzopoulos P, Letsas KP. Mechanisms of meaningfully between countries.19 Consequently, the Inter-
drug-induced proarrhythmia in clinical practice. World J
Cardiol 2013;5(6):175.
national Liaison Committee on Resuscitation (ILCOR)
was formed in 1992 to promote global discussion and
 CHAPTER 25 RESUSCITATION 831

consistency of guidelines between these international are not monitored and the predominant presenting rhythms
resuscitation councils.19 The AHA, ARC, NZRC, ERC are VF/VT (16.9%) and asystole/pulseless electrical
and ILCOR guidelines are subject to constant review and activity (PEA) (72.3%).23 Many factors such as age, time
modification based on emerging scientific data. Guidelines of day, presence or absence of morbidity before or during
and recommendations are classified according to scientific the hospital admission, absence of ‘not-for-resuscitation’
evidence. The most recent substantive guidelines from orders, quality of the CPR, asystole and non-ICU location
ILCOR were published in October 201020 and further contribute to the low in-hospital survival rates.25,26
revision will be published in 2015 but were not available at
the time of publication. Chain of survival
To optimise a person’s chance of survival, the ‘chain of
Survival of arrests survival’ strategy has been developed,27 which represents
Despite recent advances in resuscitation and technology, a sequence of four events that must occur as quickly as
the survival rate for OHCA to hospital discharge remains possible: early recognition, early CPR, early defibrilla-
low at about 6.7–8.4%.2,3 Factors associated with higher tion and post-resuscitation care (see Figure 25.1). These
rates of mortality for adults are: age over 80 years, unwit- time-sensitive, sequential actions must occur to optimise
nessed arrest, delays before commencing CPR, delayed a cardiac arrest victim’s chances of survival. Communities
defibrillation (pre-shock pauses) and delays prior to with integrated links along this chain have demonstrated
resumption of CPR (post-shock pauses) and non- higher survival rates after OHCA than those with deficien-
ventricular tachycardia/fibrillation rhythm.21 The outcome cies in these links.2,26
statistics for children after OHCA are similarly poor.14
Marked differences in the inclusion criteria and outcome Early recognition of cardiac arrest
definitions may, however, also explain the wide variations The chain of survival begins with early recognition of a
in survival rates from cardiac arrests. In recognition of medical emergency and the activation of a rapid response
these variations, the Utstein guidelines were developed system.2,28 However, the chain of survival has not always
and implemented to consistently document, monitor and been adequate when a cardiac arrest occurs in the hospital,
compare out-of-hospital cardiac arrests.These guidelines: from the point of view of early recognition, timeliness
• establish uniform terms and definitions for or availability of equipment or staff.25,29 Two-thirds of
out-of-hospital resuscitation in-hospital cardiac arrests are potentially avoidable, with
• establish a reporting template for resuscitation studies up to 84% of all in-hospital cardiac arrests demonstrating
to ensure comparability evidence of deterioration in the 6–8 hours preceding the
arrest.30,31 In recent years early warning systems, based on
• define time points and time intervals relating to abnormal vital signs, have been implemented to facilitate
cardiac resuscitation
the early recognition of the deteriorating patient (see
• define clinical items and outcomes that emergency Table 25.2)32–36 (see Chapter 3 for further discussion).
medical systems should gather While the best early warning scoring system continues
• develop methods for describing resuscitation systems. to be debated, in the United Kingdom the National
In-hospital resuscitation has survival to hospital Early Warning Score (NEWS) shows promise with the
discharge rates of around 18–25%.22–24 The majority of early identification of patients at risk of unexpected
cardiac arrests occur on the general wards where patients ICU admission or cardiac arrest.37 To further facilitate

FIGURE 25.1 Chain of survival.

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832 SECTION 3 SPECIALTY PRACTICE

TABLE 25.2
Early calling criteria

CHILDREN
AREA A D U LT S 0–12 MONTHS 1–8 YEARS

Airway Threatened Threatened Threatened

Breathing All respiratory arrests All respiratory arrests All respiratory arrests
RR <8 RR <20 RR <15
RR >27 RR >50 RR >35
SpO2 <90% Grunting respirations SpO2 <90%
SpO2 <90%
Circulation All cardiac arrests All cardiac arrests All cardiac arrests
PR <50 PR <100 PR <90
PR >130 PR >180 PR >160
Systolic BP <90 Systolic BP <50 Systolic BP <80
Capillary return >4 seconds
Marked pallor
Neurology Sudden fall in the level of Floppy Floppy
consciousness (fall in the Glasgow Unresponsive Unresponsive
Coma Scale score of ≥2 points) Depressed conscious level Depressed conscious level
Repeated or prolonged seizures Prolonged seizures Prolonged seizures
Other Any patient you are seriously worried about who does not fit the above criteria
Note: these values are a guide and vary with different organisations.
BP = blood pressure; PR = pulse rate; RR = respiratory rate.
Adapted from:
Prytherch DR, Smith GB, Schmidt PE, Featherstone PI. ViEWS – Towards a national early warning score for detecting adult inpatient
deterioration. Resuscitation 2010;81(8):932–7
Smith GB, Prytherch DR, Meredith P, Schmidt PE, Featherstone PI. The ability of the National Early Warning Score (NEWS)
to discriminate patients at risk of early cardiac arrest, unanticipated intensive care unit admission, and death. Resuscitation
2013;84(4):465–70.

earlier activation of the rapid response teams, family and Continue CPR until responsiveness and normal
patients have been provided with a means to activate the breathing return. Ideally, these interventions are performed
team on a patient’s behalf.38 simultaneously or in rapid sequence and will take no
longer than 60–90 seconds to complete. This systematic
Basic life support approach correlates closely with the principles of basic life
When a patient is identified as in potential or actual arrest, support (BLS) in that, where a life-threatening abnormal-
a primary and secondary survey should be conducted in ity is detected, immediate intervention is required before
the DRSABCD sequence:39 further assessment (see Figure 25.2).
• Danger – check for danger (hazards or risks to safety).
Airway
• Responsive – check for response (if responsive/
unconscious). Recognition of airway obstruction includes listening for
inspiratory (stridor), expiratory or grunting noises. The
• Send – send for help. work of breathing can be assessed by the respiratory rate,
• Airway – open the airway. Airway assessment is intercostals, subcostal or sternal recession, use of accessory
undertaken to establish a patent airway while
muscles, tracheal tug or flaring of the alae nasi. Nasal
maintaining cervical spine support (if injury is
flaring is especially evident in infants with respiratory
suspected).
distress. Noisy breathing is obstructed breathing, but the
• Breathing – check breathing. Breathing includes the volume of the noise is not an indicator of the severity
assessment and establishment of breathing, noting rate, of respiratory failure. Should obstruction to air flow be
pattern, chest movement and tissue oxygenation. detected, then the airway should be opened using three
• CPR – start CPR. Give 30 chest compressions (almost manoeuvres: the head-tilt, chin-lift and jaw thrust. Assess a
2 compressions/second) followed by 2 breaths. person’s airway without turning them onto the side unless
• Defibrillation – attach an automated external the airway is obstructed with fluid (vomit or blood) or
defibrillator as soon as available and follow its prompts. submersion injuries.39
 CHAPTER 25 RESUSCITATION 833

FIGURE 25.2 Basic life support flow chart.1

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834 SECTION 3 SPECIALTY PRACTICE

The airway of the infant differs from that of the older Cardiopulmonary resuscitation
child or adult in that the infant has a large head and tongue Individuals should commence cardiac compressions if
and small mouth, and the larynx is narrower, shorter, more the victim is unconscious, unresponsive, not moving
anterior and acutely angled.17 The airway of an infant is and not breathing normally. Where possible, change the
also more cartilaginous and can be easily occluded when person delivering the compressions every 2 minutes.
the neck is hyperextended; in addition, the large tongue Pulse check by lay rescuers and health professionals in
can easily fall back to obstruct the pharynx.40 Hence, the BLS is not recommended. Assessment of effective chest
head of an infant should be maintained in the neutral compression by healthcare professionals may be made
position, whereas a child aged 1–8 years will require the by continuous end tidal CO2 (ETCO2) monitoring. For
‘sniffing position’, with varying degrees according to age. CPR to be effective the patient should be flat, supine
The chin-lift and head-tilt manoeuvres may be used in and on a firm surface. The chest should be compressed
children to obtain the appropriate positioning for age. in the midline over the lower half of the sternum, which
Jaw thrust may be used if head-tilt/chin-lift is contra- equates to the ‘centre of the chest’, at a depth of 5–6 cm
indicated.40 Do not use the finger sweep to clear the airway (in adults) and at a rate of 100–120 compressions per
of an infant, as this may result in damage to the delicate minute for adults, infants and children, with the rate rising
palatal tissues and cause bleeding, which can worsen the to 120/min for the newborn.27 CPR should be initiated
situation. Use of finger sweep can force foreign bodies when the heart rate is 60 beats/min for the neonate,
further down into the airway.40 Suction is more useful for infant and the small child and 40 beats/min for the large
removing vomitus and secretions. child. Performed correctly, external cardiac compressions
(ECC) can produce a systolic blood pressure peak of
Practice tip 60–80 mmHg (in adults) and a cardiac output of 20–30%
of normal.27,41 With external chest compressions it takes
An infant will only require 5 to 8 cc/kg with each time to reach optimal levels of coronary perfusion pressure
ventilation.126 and, ultimately, blood flow. Any interruption to chest
Reproduced with permission from Yost CC, Bloom R. compressions therefore decreases the coronary perfusion
Neonatal resuscitation. Crit Care Obstetr 2010:108. pressure and resultant blood flow, ultimately reducing
survival.42 After 30 compressions open the airway and give
two breaths.43
Breathing Survival potentially improves when an individual
To assess for the presence of breathing, look, listen and receives a higher number of chest compressions during
feel for breath sounds for no more than 10 seconds. If the CPR, even if the person receives fewer ventilations.
person is unresponsive with absent or abnormal breathing, Because of this, it is recommended that a 30:2 compres-
call for help and compressions should be commenced sion-to-ventilation ratio is used in adults, children and
immediately. Agonal gasps are not to be considered as infants regardless of the number of rescuers, and 3:1 for
normal breathing. Typically, the arterial blood will remain neonates. Having noted this, in the advanced life support
saturated with oxygen for several minutes following the paediatric setting, the compression ratio changes to 15:2
cardiac arrest and, as cerebral and myocardial cell oxygen- and a ratio of 3:1 for the newborn with any number of
ation is limited more by the absence of cardiac output as rescuers (see Table 25.3). The average person may not
opposed to the reduced PaO2, effective compressions are only be reluctant to initiate mouth-to-mouth resus-
more important than rescue breaths.27 citation,44 but will also take 8 seconds to deliver one

TABLE 25.3
CPR for adults, children and infants

AGE A I R W AY COMPRESSION (CPR) 1 OR 2 PERSON

Infants <1 year Jaw support or chin-lift Two fingers or two overlying thumbs on the lower 30 : 2
(no head-tilt) end of the sternum with hands encircling the chest PALS 15 : 2 (2 rescuers)
(preferred), 100 beats/min
Younger child: Head-tilt more than infants Heel of one hand, 100 beats/min 30 : 2
1–8 years but less than adults PALS 15 : 2 (2 rescuers)
Older child: Head-tilt Two hands, 100 beats/min 30 : 2
9–14 years PALS 15 : 2 (2 rescuers)
Adult Head-tilt Two hands, 100–120 beats/min 30 : 2

PALS = paediatric advanced life support.

Adapted with permission from Australian Resuscitation Council and New Zealand Resuscitation Council (ARC and NZRC). Australian
Resuscitation Council Guidelines. Victoria, Australia: Australian Resuscitation Council, <http://www.resus.org.au>; 2014.
 CHAPTER 25 RESUSCITATION 835

breath.45 When a rescuer is reluctant to perform rescue Devices to augment compression

breaths, external cardiac compression (ECC) without As external cardiac compression supplies only 30% of
expired air resuscitation (EAR) should be encouraged, as normal cardiac output52 and 15% of normal cerebral blood
the generally held belief is that ECC alone is better than flow, there is a great need to find ways to improve cardiac
no CPR at all.46,47 compression. While no circulatory adjunct is currently
Evaluation during resuscitation recommended, several are being routinely used in the
pre- and in-hospital settings.53 A few of the devices are
Maintenance of an effective cardiac output during
outlined in Table 25.4.
CPR is evaluated by palpating the carotid or femoral
Given the limited available information on the
pulse in adults (brachial in children); this was once the
outcomes associated with use of any of these devices and
‘gold standard’ for assessing circulation. However, neither
the absence of evidence to demonstrate these devices
lay-persons nor professionals can rapidly (in less than
are superior to conventional manual CPR, no device is
10 s) and accurately perform this step. Pulse checks are
currently recommended as a routine substitute for manual
not recommended for evaluation after defibrillation until
CPR.20,54,55 There is, however, a growing incidence of the
2 minutes of CPR have been performed, regardless of the
use of some of these devices in the pre-hospital envi-
rhythm post defibrillation.
ronment and in situations where it is difficult to provide
The use of capnometry as a non-invasive technique
high-quality compressions such as during transport,
for monitoring the effectiveness of CPR is recom-
prolonged cardiac arrests and cardiac catheter laborites.55
mended.12 As the partial pressure of the ETCO2
concentration correlates with pulmonary blood flow These devices should be used in a properly supervised
during CPR, the adequacy of resuscitation efforts is program and the users should be well trained.39,53
evaluated by measuring this parameter. ETCO2 also
Practice tip
correlates with cardiac output, return of spontaneous
circulation (ROSC) and outcomes in cardiac arrest.48,49 A CPR should commence if the patient is unconscious,
mean ETCO2 of 20 mmHg or above has been associated unresponsive, not moving and not breathing, even if the
with survival from cardiac arrest, while a mean ETCO2 patient is taking the occasional gasp.
<10 mmHg is associated with poor outcomes.49 A rise
in ETCO2 during CPR may indicate the return of Reproduced with permission from Australian Resuscitation
spontaneous circulation.50 Having noted this, hyper- Council and New Zealand Resuscitation Council (ARC and
NZRC). Australian Resuscitation Council Guidelines. Victoria,
ventilation during CPR is not recommended and may
Australia: Australian Resuscitation Council; 2014. Available
be harmful. Near infrared spectroscopy can be used to from: http://www.resus.org.au/.
measure regional cerebral oxygen saturation. A higher
mean somatic tissue oxygenation (sSO2) is associated
with higher ROSC.49 Similarly, animal studies indicate Defibrillation
that hyperventilation is associated with raised thoracic While CPR has been associated with improved survival
pressure, decreased coronary and cerebral perfusion to discharge from hospital, it cannot be substituted for the
and reduced return of spontaneous circulation. Clinical definitive treatment of early defibrillation. It is thought
studies show that rescuers consistently hyperventilate that CPR will supply sufficient oxygen to the brain and
patients during a cardiac arrest.51 heart until defibrillation is available. Ultimately, despite

TABLE 25.4
Augment compression devices54,127,128

DEVICE DESCRIPTION

Active compression– • Utilises a small portable device to compress and decompress the chest (‘plunger method’)
decompression (ACD-CPR) • Enhances ventilation and venous return by raising the negative intrathoracic pressure,
which facilitates venous return, thus priming the heart for subsequent compressions127
Interposed abdominal • Least technical device
compression (IAC) combined • The abdomen is compressed (midway between the xiphisternum and the umbilicus)
with CPR (IAC-CPR) alternately with the rhythm of chest compression
• Rarely utilised method
• Results in increased resistance in the descending aorta, thus raising the coronary perfusion
pressure128
Non-invasive automated • Utilises a load-distributing band (LDB) to compress the anterior chest
chest compression device • The device is built around a backboard that contains a motor54
(e.g. AutoPulse) • The motor tightens or loosens LDB around the patient’s chest
836 SECTION 3 SPECIALTY PRACTICE

the most effective CPR, the single-most important cause recognition may reduce the ‘hands-off ’ period using a
of decreased prognosis in pulseless VT/VF cardiac arrests manual defibrillator.59,60 The combined pre-shock and the
is a delay in electrical defibrillation.3 post-shock pause ideally should be less than 5 seconds.12
This can be achieved by continuing compressions while
Precordial thump the defibrillator is charging and resuming chest compres-
A precordial thump is a single, sharp blow delivered with sions immediately after the delivery of the shock. Fully
a clenched fist to the mid-sternum of a victim’s chest automatic defibrillators are programmed to assess the
from a height of 25–30 cm above the sternum.7 The rhythm, charge the defibrillator and deliver shocks without
mechanical energy generated by the precordial thump user intervention.
may generate a few joules, and therefore is applied within To facilitate early defibrillation, ILCOR endorses the
the first few seconds of onset of a shockable rhythm, but concept of non-medical individuals being authorised,
it has a very low success rate at converting VF/VT to a educated and encouraged to use defibrillators.12 This
perfusing rhythm.56,57 Because of the very low success rate public access to early defibrillation has seen the placement
and the brief period for application, delivery of the thump of defibrillators on aircraft, in casinos and cricket
must not delay accessing help or a defibrillator. Only in grounds, with non-medical personnel such as police,
situations where the VF arrest is witnessed and monitored flight attendants, security guards, family members and
and a defibrillator is not immediately on hand (i.e. critical even children successfully initiating early defibrillation.60
care environments) would the delivery of the precordial The effectiveness of training non-traditional out-of-
thump be appropriate.20 hospital first responders to use the AED has improved
survival to discharge rates.20 Similarly, in-hospital cardiac
Electrical defibrillation arrests also occur in any area, and all healthcare workers
Defibrillation is the passage of a current of electricity should be capable of initiating early defibrillation.12 The
through a fibrillating heart to simultaneously depolarise ARC notes that, while BLS does not have to include
the mass of myocardial cells and allow them to repolarise the use of adjunctive equipment, the use of AEDs by
uniformly to an organised electrical activity.12 persons with education in their use is supported and
should be taught. Figure 25.3 outlines the integration of
Practice tip defibrillation with BLS.
Effective BLS can slow the loss of amplitude and
Practice tip
waveform of VF. Interruptions to effective CPR should
be kept to a minimum. When using the defibrillator in manual mode, limiting
the pre-shock analysis pause to 5 seconds should
Reproduced with permission from Deakin CD, Nolan JP, Soar J,
Sunde K, Koster RW, Smith GB et al. European Resuscitation improve survival.
Council Guidelines for Resuscitation 2010 Section 4. Adult
advanced life support. Resuscitation 2010;81(10):1305–52. For 90% of people in VF, return of a perfusing rhythm
will occur after a single shock.
There are two types of external defibrillators: the However, it is rare that a pulse will be palpable with
manual external defibrillator and the automatic external the perfusing rhythm; hence the immediate resumption
defibrillator (AED). The AED can be either fully of chest compressions in the post-shock period is
automatic or semiautomatic. The manual defibrillator supported.12 Failure to successfully convert VF after the
requires the user to be able to immediately and accurately single-shock strategy may indicate the need for a period
recognise arrhythmias and make the decision whether of effective CPR (30:2) for 2 minutes and rhythm re-
to initiate defibrillation or not. In comparison, the AED analysis, followed by shock if indicated.12 A single-shock
automatically detects and interprets the rhythm without strategy is now recommended for all patients in cardiac
relying on the user’s recognition of arrhythmias. AEDs arrest requiring defibrillation for VF or pulseless VT.39
can be operated in both manual and semiautomatic mode. Not all of the electrical energy delivered during defibril-
When using an AED, the user determines whether the lation will traverse the myocardium. Table 25.5 outlines
person is unresponsive, not breathing and pulseless.58 some of the common factors contributing to the success
After checking for a pulse, the AED requires only four or failure of defibrillation. Studies have demonstrated that
steps to operate: 1) turn power on; 2) place self-adhesive lower-energy biphasic defibrillators are associated with
electrodes on a victim’s chest; 3) rhythm analysis follows greater first-shock efficacy, require lower joules, cause less
(hands-off period); 4) then (if advised by the machine) myocardial dysfunction and increase return of sponta-
press the shock button. The AED will automatically neous circulation when compared with the monophasic
interpret the cardiac rhythm and, if VF/VT is present, will defibrillator.61,62 The optimum defibrillation energy level
advise the operator to provide a shock. This ‘hands-off ’ is that which sufficiently abolishes the arrhythmia to
period using the AED may result in significant interrup- enable the return of an organised rhythm, with minimal
tions to chest compressions and adversely impact patient myocardial damage.12,61 Other biphasic energy levels
survival. Health professionals with expertise in rhythm may be used providing there is relevant clinical data for
 CHAPTER 25 RESUSCITATION 837

FIGURE 25.3 Advanced life support flow chart.1

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TABLE 25.5
Factors contributing to the success or failure of defibrillation129-132

SUCCESS FA I L U R E PRECAUTIONS

• VF duration • Inadequate contact with the chest (excessive chest • Place defibrillation electrodes at least 8 cm away
• Early defibrillation hair) from ECG electrodes, or implantable medical
(if VF <3 min) • Faulty positioning of the paddles devices, pacemakers, vascular access devices
• Initial CPR (if VF • Synchronise button in the ‘on’ position, flat battery • Remove medication patches, wipe the area before
>3 min) or fractured lead applying defibrillation electrodes
• Presenting rhythm • Positioning over bone/fat or breast tissue, chest size • Do not defibrillate unless all clear of the bed/patient
(VT/VF) • Drying out of gel conduction pads • Do not charge/discharge paddles in the air
• Paddle/pad size • Patient factors: acidosis, hypoxia, electrolyte • Do not have the patient in contact with metal
and placement imbalance, drug toxicity, hypothermia • Do not allow oxygen to flow onto the patient
• Use of self- • Time of respiration (best delivered at end-expiration) during delivery of the shock (at least 1 m from the
adhesive pads • PEEP and auto-PEEP (air-trapping) should be patient)
minimised • Ensure the chest is dry
• Paddles/electrodes too small (8–12 cm electrodes • Do not use electrode gels and pastes as these can
for adults) spread between the paddles and potentially spark
ECG = electrocardiogram; PEEP = peak end-expiratory pressure; VF = ventricular fibrillation; VT = ventricular tachycardia.
Developed from:
Ristagno G, Li Y, Gullo A, Bisera J. Amplitude spectrum area as a predictor of successful defibrillation. In: Anaesthesia and
Pharmacology of Intensive Care Emergency Medicine APICE: Springer; 2011, pp 141–60
Monteleone PP, Borek HA, Althoff SO. Electrical therapies in cardiac arrest. Emerg Med Clin North Am 2012;30(1):51–63
Link MS, Atkins DL, Passman RS, Halperin HR, Samson RA, White RD et al. Part 6: Electrical therapies automated external
defibrillators, defibrillation, cardioversion, and pacing: 2010 American Heart Association Guidelines for Cardiopulmonary
Resuscitation and Emergency Cardiovascular Care. Circulation 2010;122(18 suppl 3):S706–19
Morley P. Cardiopulmonary resuscitation. In: Harley I, Hore P, eds. Anaesthesia: An introduction. 5th ed. East Hawthorn, Victoria:
IP Communications; 2012, pp 174–89.
838 SECTION 3 SPECIALTY PRACTICE

a specific defibrillator that suggests that an alternative 0.1–0.16. Consequently, a significant number of patients
energy level provides adequate shock success.1,63 If the rely on the provision of advanced life support (ALS) for
initial shock is unsuccessful, subsequent shocks should be survival. ALS extends BLS to provide the knowledge
delivered at the initial dose or higher energy levels may and skills essential for the initiation of early treatment
be selected.12,62 In children, it is recommended 4 J/kg for and stabilisation of people post-cardiac arrest. Advanced
the initial and subsequent shocks for both biphasic and skills traditionally include defibrillation, advanced airway
monophasic defibrillators.12 Standard adult AEDs and pads management and the administration of resuscitation drugs.
are suitable for use in children older than 8 years. Ideally, While BLS is generally initiated prior to ALS, where a
for children between 1 and 8 years, paediatric pads and an defibrillator and a person trained in its use are available,
AED with paediatric capability should be used.1,64 These defibrillation takes precedence over BLS and ALS. The
pads are placed as per the adult methodology. If the AED ARC and NZRC algorithm for management of cardio-
does not have a paediatric mode or paediatric pads, the pulmonary arrest (see Figures 25.3 and 25.4) outlines the
standard adult AED and pads can be used.25 Defibrillation two decision paths of therapy in ALS: 1) defibrillation
of infants less than 1 year of age is not recommended.12 and CPR for pulseless VT/VF (shockable) and 2) identi-
The importance of early, uninterrupted chest compres- fying and treating the underlying cause for non-VT/VF
sions and early defibrillation are well promulgated in the (non-shockable).
ILCOR guidelines.12 As the length of time from collapse
is difficult to accurately estimate, it is imperative rescuers Advanced airway management
perform chest compressions until the defibrillator is both A person with signs of acute respiratory distress should
available and charged.65,66 be administered oxygen at the highest possible concen-
tration, including initially during CPR.43 Oxygen should
Advanced life support never be withheld for fear of adverse effects, as rescue
Basic life support provides about 20–30% of normal breaths provide an inspired oxygen concentration of
cardiac output and a fraction of inspired oxygen (FiO2) of only 15–18%. The administration of oxygen alone does

FIGURE 25.4 Advanced life support for infants and children flow chart.1

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 CHAPTER 25 RESUSCITATION 839

not result in adequate ventilation and, as such, the estab- • laryngeal mask airway
lishment of an effective airway is paramount. Airway • oesophageal–tracheal combitube laryngeal tube (King
management is essential in the performance of CPR, airway)
and may be administered using a variety of techniques.
These may include: compression-only CPR with high- • endotracheal intubation
flow oxygen by face-mask, bag-mask ventilation, insertion • tracheostomy.
of a supraglottic airway (SGA) device that does not require While the endotracheal tube (ETT) is considered the
laryngoscopy or tracheal intubation.67 ‘gold standard’ for airway management in a cardiac arrest,
The choice of advanced airway adjunct is deter- as it protects the airway, assists effective ventilation, ensures
mined by the availability of equipment and experienced delivery of high concentrations of oxygen and eases
personnel67 (see Table 25.6 and Chapter 15): suctioning, no studies have found that ETT use during
• oropharyngeal (Guedel’s) airway a cardiac arrest increases survival. It is vital that CPR not
• nasopharyngeal airway be interrupted for more than 10 seconds during attempts

TABLE 25.6
Adjuncts used during resuscitation1,12,133–135

A I R W AY T Y P E DESCRIPTION P R A C T I C E C O N S I D E R AT I O N S

Oropharyngeal Conforms to the curve of the Incorrect size or placement may contribute to airway obstruction by pushing
(Guedel’s) airway palate, moving the tongue the tongue back into the pharynx. Unlike adult insertion, the insertion of the
forward away from the oropharyngeal airway in infants and young children is inserted right-way-up;
posterior pharyngeal wall a tongue depressor or laryngoscope should be used to aid insertion
Sizes from 000–5
Nasopharyngeal Soft tube inserted into the Use with caution in patients with head injuries
airway nasopharynx With the exception of infant’s head-tilt, jaw support or jaw thrust is still
necessary when using either the oropharyngeal or the nasopharyngeal
airway
Bag–valve–mask A self-inflating bag that may BVMs are often inappropriately used and offer no protection to the airway
(BVM) systems be connected to a face mask, Two-person technique is preferable
laryngeal mask airway or Single-person BVM ventilation may result in a poor seal around the patient’s
endotracheal tube (ETT) mouth and the delivery of less than optimal tidal volumes12
When using a BVM it is best performed using two rescuers, although not
always possible
As the airway is not protected, smaller tidal volumes with supplementary
oxygen can provide adequate oxygenation and reduce the risk of gastric
inflation, regurgitation and aspiration
The mask should be used right-way-up with children and upside-down with
infants
The soft circular mask is preferred for infants, as it provides an excellent seal
with low dead space
Laryngeal mask Consists of a tube with an The LMA is used as a first-line adjunct when endotracheal intubation is not
airway (LMA) elliptical cuff fitted at the available
distal end that inflates in the The LMA is easier to insert than a Combitube, more rapidly inserted and
hypopharynx around the requires less equipment than the ETT
posterior perimeter of the When used as a first-line airway device, the LMA provides a clear airway
larynx with a significantly lower risk of gastric overinflation and regurgitation than
The LMA is inserted orally the BVM12
using a blind technique so As with adults, the LMA can be used safely and effectively in infants133
that the distal end of the LMA: size 1 for <5 kg; size 1.5, 5–10 kg; size 2, 10–20 kg; size 2.5, 20–30 kg;
mask abuts against the base size 4, 50–70 kg; size 5, 70–100 kg; size 6, >100 kg
of the hypopharynx, behind Use in newborns over 34 weeks gestation and weighing more than 2 kg133
the cricoid cartilage, and the Complications of LMA include gastric aspiration, partial airway obstruction,
cuff is inflated to form an coughing or gastric insufflation
airtight seal around the larynx Contraindications include patients unable to open their mouths adequately;
pharyngeal pathology; airway obstruction at or below level of the larynx;
low pulmonary compliance or high airway resistance; or increased risk of
aspiration
840 SECTION 3 SPECIALTY PRACTICE

TABLE 25.6 continued

A I R W AY T Y P E DESCRIPTION P R A C T I C E C O N S I D E R AT I O N S

Oesophageal– The ETC is a double-lumen It is effective in maintaining an airway when performed by unskilled
tracheal airway with proximal and personnel and is a suitable alternative to tracheal intubation
Combitube (ETC) distal cuffs that is passed into The ETC enables ventilation, whether it is positioned in the oesophagus or
the oesophagus the trachea
Only one size needed for most adults
Laryngeal tube (LT) Airway tube with a small Use is comparable to classic LMA and ProSeal LMA134
oesophageal cuff and a larger
pharyngeal cuff. The distal
tip is positioned in the upper
oesophagus
I-gel The cuff of the I-gel is made Very easy to insert with minimal training.12
of gel and does not require Enables continuous chest compression without interruption for ventilation135
inflation
Endotracheal tube During intubation, direct Endotracheal intubation is a difficult skill to acquire and maintain
(ETT) application of firm pressure In addition to routine clinical methods, ETT placement can be confirmed by
to the cricoid cartilage either measurement of ETCO2 or use of an oesophageal detector; the latter
is required to compress is more reliable in a non-perfusing rhythm (Class IIb)
the oesophagus between Immediate complications associated with intubation include oesophageal
the trachea and vertebral intubation; right main bronchi intubation; or ETT occlusion (kinking, sputum,
column and minimise/prevent cuff, blood)
regurgitation of gastric
contents

Developed from:
Australian Resuscitation Council and New Zealand Resuscitation Council (ARC and NZRC). Australian Resuscitation Council
Guidelines. Victoria, Australia: Australian Resuscitation Council, <http://www.resus.org.au>; 2014.
Deakin CD, Nolan JP, Soar J, Sunde K, Koster RW, Smith GB et al. European Resuscitation Council Guidelines for Resuscitation
2010 Section 4. Adult advanced life support. Resuscitation 2010;81(10):1305–52
Zhu X-Y, Lin B-C, Zhang Q-S, Ye H-M, Yu R-J. A prospective evaluation of the efficacy of the laryngeal mask airway during neonatal
resuscitation. Resuscitation 2011;82(11):1405–9.
Yamaga S, Une K, Kyo M, Suzuki K, Kobayashi Y, Nakagawa I et al. Gas insufflation in the stomach during cardiopulmonary
resuscitation using laryngeal tube ventilation in comparison with bag-valve-mask ventilation. Circulation 2012;126(21
Supplement):A295.
Soar J. Which airway for cardiac arrest? Do supraglottic airways devices have a role? Resuscitation 2013;84(9):1163–4.

at endotracheal intubation. Waveform capnography or an Once an airway has been established, continue chest
oesophageal detector device should be applied to confirm compressions without interruption for ventilation.Ventilate
the ETT placement.12,67 the lungs at a rate of approximately 10 breaths a minute
ETCO2 may also be used to monitor the quality of and an inspiratory time of 1 second with sufficient volume
the CPR. Given the limitations noted in Table 25.6, to produce a normal chest rise. Ventilation adjuncts may
a variety of adjunct airway/ventilation management include:
devices are available, such as: bag–mask ventilation (BMV); • a simple face mask with filter and oxygen connector
supraglottic airways devices such as the laryngeal mask (pre-intubation)
airway (LMA) and the classic laryngeal mask airway; the • bag–valve–mask systems
oesophageal-tracheal airway (Combitube); and the I-gel.
The benefit of the supraglottic airways devices is that • ventilators.
they are easily inserted without interruption to chest If available, automated ventilators can be used. These
compressions. Currently, there is no evidence to support may be set to deliver a tidal volume of 6–7 mL/kg at a rate
the routine use of any particular advanced adjunct airway of 10 breaths/min. The automated ventilator may be used
devices.67 Healthcare professionals trained to use supraglot- with either the face mask or other adjunct airway devices.16
tic airway devices (e.g. LMA) may consider their use for Having noted this, there is currently no evidence to suggest
airway management during cardiac arrest and as a backup that the use of automated ventilators during cardiac arrest is
or rescue airway in a difficult or failed tracheal intubation. more beneficial than bag–valve–mask devices.16
 CHAPTER 25 RESUSCITATION 841

Rhythms Non-VF/VT
There is an association between the initial cardiac arrhyth- Non-VF/VT arrhythmias include pulseless electrical
mias and survival to discharge after SCA. Cardiac arrest activity and asystole. PEA or electromechanical dissociation
rhythms can be divided into two subsets: (EMD) reflects dissociation between the heart’s electrical
1 ventricular fibrillation and pulseless ventricular and mechanical activities, and the two terms are used inter-
tachycardia changeably. It is important to note that PEA/EMD may
2 non-VF/VT incorporating asystole and pulseless
present as any rhythm normally compatible with a pulse (e.g.
electrical activity. sinus rhythm, sinus tachycardia/bradycardia). PEA is charac-
terised by a stroke volume insufficient to produce a palpable
The most common arrhythmias observed in SCA
pulse, despite adequate electrical activity.70 Management of
are pulseless VT and VF, with 60–85% of all patients
PEA includes identifying and correcting reversible causes,
initially presenting with these lethal arrhythmias.6
In-hospital PEA occurs as the initial rhythm in approxi- summarised as the 4 Hs and 4 Ts in Table 25.7.
mately 30–37% of cases68,69 and the overall neurologically
intact survival rate is 10%.68 Asystole is the most common
arrest arrhythmia in children (40% versus 35% in TABLE 25.7
adults)68 because their hearts respond to prolonged severe Causes of pulseless electrical activity
hypoxia and acidosis by progressive bradycardia leading THE FOUR Hs T H E F O U R Ts
to asystole.12
• Hypoxia • Tamponade
Ventricular fibrillation and pulseless ventricular • Hypovolaemia • Tension pneumothorax
tachycardia • Hypo/hyperthermia • Toxins/poisons/drugs
• Hypo/hyperkalaemia • Thrombosis: pulmonary/
As previously noted, the only intervention shown to and metabolic disorders coronary
unequivocally improve long-term survival after a VF or
pulseless VT arrest is prompt and effective BLS, uninter- Adapted with permission from: Australian Resuscitation
Council and New Zealand Resuscitation Council (ARC and
rupted chest compressions and early defibrillation.12 VT
NZRC). Australian Resuscitation Council Guidelines. Victoria,
and VF rhythms are displayed in Figures 25.5 and 25.6. Australia: Australian Resuscitation Council, <http://www.
Energy levels and subsequent shocks are equivalent for resus.org.au>; 2014.
both VF and pulseless VT.

FIGURE 25.5 Ventricular tachycardia.

FIGURE 25.6 Ventricular fibrillation.

M3536A 26 Apr 2006 12 : 32: 01: Delayed Alarms Paused Adult HR 133 bpm
Monitor Mode

II 10 mm/mV 25 mm/sec .05-150Hz Diagnostic

842 SECTION 3 SPECIALTY PRACTICE

FIGURE 25.7 Asystole.

Careful confirmation of asystole (see Figure 25.7) on Vasopressors such as adrenaline and vasopressin have
two leads and the absence of a palpable pulse are essential been used as adjuncts in cardiac arrests to improve the
when making the decision to manage asystole. When an success of CPR.While there is no evidence that shows that
in-hospital arrest has an initial rhythm of asystole, survival the routine use of any vasopressor during a cardiac arrest
to discharge has been reported as 10.66%.68 will increase survival to discharge from hospital, adrenaline
is still recommended.12A randomised controlled trial has
Medications administered during shown that, although patients in cardiac arrest that receive
cardiac arrest adrenaline demonstrate significant improved likelihood
Resuscitation drugs can be administered during a cardiac of ROSC, significant improvement in their survival to
arrest using a variety of routes including peripheral and discharge from hospital is not seen.72
central veins or intraosseously. Administration by the The optimal dose of adrenaline in the pre-hospi-
central venous route remains the optimal method, but the tal and in-hospital settings remains unclear. Current
decision to access peripheral versus central cannulation recommendations propose that adrenaline 1 mg should
will depend on the skill of the operator. Peripheral venous be administered for VT/VF following the second shock
cannulation is the quickest and easiest method; however, the and then every second loop thereafter. For asystole and
patient in cardiac arrest may have inaccessible peripheral EMD administer 1 mg of adrenaline in the initial loop,
veins.23 Should a decision be made to insert a central line then every second loop (see Table 25.8).1 Research on
during a cardiac arrest, this must not take precedence the use of vasopressin continues, with a meta-analysis
over defibrillation attempts, CPR or airway maintenance. reporting that using the drug during the resuscitation of
Medications inserted into a peripheral line should be cardiac arrest patients offers neither overall benefit nor
flushed with at least 20 mL (adults) of an isotonic solution disadvantage for the patient.73 While there are reports that
followed by at least 1 minute of continuous external vasopressin produces no overall change in survival after
cardiac compressions. Where there is difficulty accessing cardiac arrest when compared with adrenaline, there is no
a peripheral vein, selected medications may be adminis- evidence to support or refute the use of vasopressin as an
tered via an intraosseous route.23 Tracheal administration of alternative to or in combination with adrenaline.74,75 The
medication is no longer recommended as the dose delivered American Heart Association guidelines propose that vaso-
is unpredictable and the optimal dose is unknown.23 pressin may replace the first or second dose of epinephrine
Intraosseous infusion involves the insertion of a metal during cardiopulmonary resuscitation.76
needle with trocar (usually utilising a drill) into the bone The optimal role and exact benefit of antiarrhyth-
marrow and provides a rapid, safe and reliable access to mic medications in cardiac resuscitation is yet to be
the circulation. The marrow sinusoids of long bones are fully elucidated, but they have very little, if any, role to
a non-collapsible venous system in direct connection play in the treatment of cardiac arrests.12 The common
with the systemic circulation, allowing drugs to reach the antiarrhythmic drugs include amiodarone, magnesium,
central circulation as quickly as medications injected into atropine and calcium (see Table 25.8). Lignocaine is
central veins. Intraosseal access is safe and effective for use no longer recommended as first-line management in
in patients of all age groups.71 General blood specimens cardiac arrest. Amiodarone is the leading antiarrhyth-
such as biochemistry values, blood cultures, haemoglobin mic medication because its safety and efficacy have been
and cross-match studies can also be taken from the marrow demonstrated.77 If, after the third shock, the VT/VF has
at cannulation.17 not reverted, a bolus injection of 300 mg of amiodarone
is recommended and 150 mg for recurrent or refractory
Practice tip VT/VF. There is no evidence of improved survival with
Attempts at peripheral cannulation in children should
the use of atropine in a cardiac arrest with asystole or
be aborted after 1 minute and an intraosseous needle
PEA.23 Calcium chloride has little use in the management
inserted.
of arrhythmias unless caused by hyperkalaemia, hypocal-
caemia or hypermagnesaemia, or an overdose of calcium
 CHAPTER 25 RESUSCITATION 843

TABLE 25.8
Medications used during resuscitation

DOSE
ACTION I N D I C AT I O N S A D U LT S PA E D I AT R I C ADVERSE EVENTS

Adrenaline is a catecholamine VF and pulseless VT VF and pulseless VT: VF and pulseless VT: Tachyarrhythmias;
that increases aortic diastolic resistant to the three 1 mg after the 2nd 10 mcg/kg after the hypertension;
pressure and coronary artery initial counter shocks shock then after every 2nd shock then after coronary
perfusion by producing PEA and asystole second cycle every second cycle vasoconstriction;
arteriolar vasoconstriction. It PEA and asystole: PEA and asystole: increased myocardial
may facilitate defibrillation by 1 mg in the initial 10 mcg/kg oxygen consumption
improving myocardial blood cycle, then every immediately, then
flow during CPR. Traditionally second cycle every second cycle
the first-line medication for
the treatment of VF and
refractory VT, adrenaline has
not demonstrated improved
outcomes after cardiac arrest
and has been associated with
post-resuscitation myocardial
dysfunction
Amiodarone directly affects VT/VF refractory to Initial bolus dose: Initial dose: Vasodilation and
smooth muscle and blocks three shocks 300 mg in 20 mL 5 mg/kg bolus over hypotension,
calcium channels and alpha- Polymorphic VT dextrose. A further 2 minutes, which bradycardia, heart
adrenergic receptors, resulting and wide complex 150 mg could be may be repeated to a block
in coronary and peripheral tachycardia of considered for maximum of 300 mg May have negative
arterial vasodilation and a uncertain origin refractory cases Periarrest: IV infusion inotropic effects
reduction in afterload and Control of Periarrest: An infusion 5–15 mcg/kg/min as Use with caution in
systemic blood pressure haemodynamically of 15 mg/kg over continuous infusion renal failure
stable VT when 24 hours may be (max of 1.2 g in 24 h) Avoid use in torsades
cardioversion commenced de pointes and other
unsuccessful (in causes of prolonged
the presence of LV Q-T
dysfunction)
Adjunct to electrical
cardioversion of SVT
Prophylaxis of
recurrent VF/VT
Magnesium is a major Torsades de pointes Bolus dose: 5 mmol IV or IO bolus: Hypotension with
intracellular cation resulting in with or without a Periarrest: May be 0.1–0.2 mmol/kg rapid administration
smooth muscle relaxation and pulse; cardiac arrest followed by infusion May be followed Use with caution if
membrane stabilisation associated with of 20 mmol infused by an infusion of renal failure present
digoxin toxicity over 4 hours 0.3 mmol/kg over Muscle weakness,
Failure of defibrillation 4 hours paralysis and
and adrenaline to respiratory failure
reverse VF and Tachycardia and
pulseless VT excitement
Documented
hypokalaemia or
hypomagnesaemia
Calcium is essential to nerve Hypocalcaemia, Bolus dose: 5–10 mL 0.2 mL/kg 10% Calcium is
and muscle impulse formation hyperkalaemia, 10% calcium chloride calcium chloride, incompatible with a
and excitation overdose of calcium (6.8 mmol) or 0.7 mL/kg 10% range of medications
blockers calcium gluconate and may precipitate in
via IV IV lines
Tissue necrosis with
extravasation may
occur
844 SECTION 3 SPECIALTY PRACTICE

TABLE 25.8 continued

DOSE
ACTION I N D I C AT I O N S A D U LT S PA E D I AT R I C ADVERSE EVENTS
Sodium bicarbonate Correcting a Bolus dose: 1 mmol/ 0.5–1 mmol/kg via IV Should not be
(NaHCO3) is an alkaline agent metabolic acidosis kg administered over or IO administered routinely administered
that may be used to correct an (pH <7.1), or base 2–3 min. As NaHCO3 over 2–3 min Alkalosis,
acidosis. Routine administration deficit of ≤10 or after is incompatable with hypernatraemia,
of sodium bicarbonate for 15 min; pre-existing many medications, hyperosmolality,
treatment of in-hospital and hyperkalaemia; it should be paradoxical cerebral
out-of-hospital cardiac arrest is tricyclic administered by acidosis, depressed
not recommended antidepressant a separate line or cardiac contractility
overdose and urinary flushed before and and metabolic
alkalinisation in after administration acidosis
overdose; or hypoxic
lactic acidosis
Potassium is an electrolyte Persistent Slow bolus: 5 mmol 0.03–0.07 mmol/ Hyperkalaemia
essential for cell membrane documented kg via slow with bradycardia,
stabilisation that is occasionally VF, suspected administration IV or IO hypotension with
used in ALS hypokalaemia or Periarrest: 0.2 mmol/ possible asystole and
hypomagnesaemia, kg/h as a continuous extravasation may
and cardiac arrest infusion; dilute with lead to tissue necrosis
associated with at least 50 times its
digoxin toxicity volume and mix well,
as can be fatal
0.2–0.5 mmol/kg/h to
a max of 1 mmol/kg
if hypokalaemia
severe but not
immediately
life-threatening
ECC = external cardiac compression; IO = intraosseous; LV = left ventricular; PEA = pulseless electrical activity; SI = sinoatrial;
SVT = supraventricular tachycardia; VF = ventricular fibrillation; VT = ventricular tachycardia.
Adapted with permission from: Australian Resuscitation Council and New Zealand Resuscitation Council (ARC and NZRC). Australian
Resuscitation Council Guidelines. Victoria, Australia: Australian Resuscitation Council, <http://www.resus.org.au>; 2014.

channel-blocking drugs. Sodium bicarbonate is no longer determining the precise rhythm and appropriate medical
administered routinely,76 as it may cause hypernatraemia, interventions.16 The presence or absence of adverse signs
hyperosmolality and intracellular acidosis from the rapid and symptoms will dictate interventions. Adverse factors
ingress of CO2 generated from its dissociation. However, may include clinical evidence of:
it is recommended if the cardiac arrest is associated with
hyperkalaemia or tricyclic antidepressant overdose.12 • low cardiac output (unconscious, unresponsive, systolic
BP <90 mmHg, increased sympathetic activity)
There are insufficient data to support the routine
use of magnesium in cardiac arrests,78 except if torsades • reduced diastolic filling time (excessive tachycardia,
de pointes is suspected.12,76 Thrombolytics should not be e.g. heart rates of >150/min, wide complex
routinely administered in a cardiac arrest, but they may tachycardia and supraventricular tachycardia)
be considered in adults with proven or suspected • excessive bradycardia (heart rates of <40/min)
pulmonary embolism or acute thrombotic aetiology.12
Effective CPR should be continued for at least 60–90 • raised end-diastolic filling pressure (presence of
pulmonary oedema or raised jugular venous pressures)
minutes following the administration of the fibrinolytic
medication as there is evidence in these situations of good • reduced coronary blood flow (chest pain).
neurological outcome and survival following extended Interventions can broadly be divided into three options
periods of CPR.50 for immediate treatment:
During the arrest, strategies should be initiated to 1 antiarrhythmics (refer to periarrest in Table 25.8)
prevent the development of serious periarrest arrhythmias.
Whenever possible, arterial blood gases, serum electro- 2 electrical cardioversion
lytes and a 12-lead ECG should be obtained to assist with 3 cardiac pacing.
 CHAPTER 25 RESUSCITATION 845

Common periarrest arrhythmias and interventions caesarean section in the setting of maternal cardiac arrest
are covered in Chapter 11. Antiarrhythmic interventions may save both infant and mother.
such as medications, physical manoeuvres and electrical The principles of airway, breathing and circula-
therapies may be proarrhythmic.16 These proarrhyth- tion remain the same, but modifications must be made
mic interventions alter the cardiac depolarisation and/ because of the physiological changes that occur with
or repolarisation, lengthening or shortening the QT and normal pregnancy.82 A number of factors may need to be
predisposing to fatal arrhythmias.79 considered when resuscitating a pregnant woman. Any
situation that affects haemodynamic status will be exacer-
Fluid resuscitation bated in a supine position, as autocaval compression may
Fluid resuscitation may be considered if hypovolaemia is result in a fall in cardiac output of up to 25%.83 During
suspected as a possible cause of the cardiac arrest. Sodium CPR, the mother may be placed in the left lateral tilt
chloride (0.9%) or Hartmann’s solution are recommended (15–25°) or supine with a pillow under the right buttock,
as a rapid infusion in the initial stages of resuscitation to displace the uterus from the inferior vena cava, facil-
(at least 20 mL/kg). There is no evidence to support the itating venous return and cardiac output.83–85 Often, the
routine administration of fluids during a cardiac arrest in angle of the tilt is overestimated, potentially reducing the
the absence of hypovolaemia. quality of the chest compressions.84 The uterus may also
be manually and gently displaced to the left to remove
Temporary cardiac pacing caval compression.83–85 While ventilation-to-compression
During a cardiac arrest, temporary cardiac pacing may ratios remain the same for a pregnant woman, chest
be required for sustained symptomatic bradycardia compression may be complicated by flaring of the ribs,
unresponsive to medical intervention. Two types of raised diaphragm, obesity and breast hypertrophy.82
temporary cardiac pacing are utilised during a cardiac The superior displacement of stomach contents
arrest: transvenous (invasive) and transcutaneous (external, by the gravid uterus and a relaxed cardiac sphincter
non-invasive) pacemakers. As most current defibrillators contribute to an increased risk of gastric aspiration in
have the capacity to pace, transcutaneous pacemakers are the pregnant woman.82,86 Because of this increased risk,
generally used in an arrest situation. cricoid pressure should be applied until after the airway is
protected by a cuffed tracheal tube.85 Tracheal intubation
Ultrasound imaging should be attended to early, using a short-handled laryn-
Ultrasound imaging has been shown to have some goscope86 or with a blade mounted at more than 90°,85
benefit in the detection and diagnosis of reversible as airway anatomy is altered with the larynx more
causes of arrest including cardiac tamponade, pulmonary anterior and superior, while the pharyngeal mucosa is
embolism, pneumothorax, aortic dissection or hypo- slightly oedematous and friable.85 A tracheal tube a size
volaemia. Placement of the probe at the sub-xiphoid smaller than one normally chosen for a similar size non-
position prior to stopping for planned rhythm assessment pregnant woman may be used because of potential
will facilitate views within 10 seconds and minimise chest narrower airways secondary to oedema or swelling.82
compression interruptions.20 While the use of imaging Defibrillation energy, drug doses and administration are in
has not been shown to improve outcome, absence of accordance with ALS guidelines.85
heart motion on sonography during resuscitation is If maternal cardiac arrest occurs in the labour ward,
highly predictive of death.20 operating room or emergency department and BLS and
ALS measures are unsuccessful, the uterus should be
Special conditions emptied by surgical (scalpel) intervention within 4–5
Although not common, there are some clinical presenta- minutes.85 Maternal resuscitation may not be possible
tions that require special considerations in a cardiac arrest until the fetus is removed. Successful resuscitations have
scenario; these include pregnancy, electrical injuries and occurred after prompt surgical intervention.85 Refer
drowning. The principles of airway, breathing and circu- to Chapter 28 for additional information about critical
lation remain the same, but modifications must be made illness and pregnancy.
because of the physiological changes that occur.
Electrical injuries
Pregnancy Electrical burn injuries and lightning injuries are similar in
Researchers report that maternal mortality rates in that they occur infrequently, commonly cause widespread
the USA have either remained unchanged or increased acute and delayed tissue damage and can arrest the heart
in recent decades.80 Precipitants included pulmonary and respiratory centre. Burn injuries are discussed in
embolism, trauma, peripartum haemorrhage, amniotic Chapter 24. This section focuses on the cardiac arrest
fluid embolism, eclamptic seizure, congenital and acquired situation. High-voltage electrocution is associated with
cardiac disease, myocardial infarction, subarachnoid a high incidence of cardiac abnormalities, including
haemorrhage and cerebral aneurysm.81 Regardless of the arrhythmias, prolongation of the QT interval, ST and
aetiology, resuscitation following cardiac arrest in late T wave changes and myocardial infarction.82 The most
pregnancy is often unsuccessful. Hence, timely delivery by common cause of death with lightning injury is cardiac
846 SECTION 3 SPECIALTY PRACTICE

arrest due to VF or asystole or respiratory arrest.87 Because and efficiently.89 The exact composition of the resuscita-
of the potential for cardiac injuries, all patients should be tion team will vary between organisations, but generally
admitted for cardiac monitoring. the team should possess the following skills:89
A lightning strike may result in asystole followed by • advanced airway management and intubation skills
spontaneous return of circulation. If ventilation is initiated
early and severe hypoxia does not ensue, a patient’s chance • intravenous access skills including central venous access
of recovery should be better.87 Initial response of BLS • defibrillation and external pacing abilities
should always begin with D (danger), that is, avoidance of • medication administration skills
injury to the rescuer. Ensure that the environment is safe
for rescuers by disconnecting the electrical supply, where
• post-resuscitation skills.
As members of a resuscitation team in the hospital
possible, without touching the patient. Where high-
voltage lines (power lines) are in contact with the person generally do not work together but come from all areas
or the vehicle, no attempt should be made to extricate the of the hospital, the team should have a designated leader.
person from the vehicle until the situation is deemed safe The team leader gives direction and guidance, assigns tasks
by an authorised electricity supply person. Once the envi- and makes clinical decisions without directly performing
ronment is safe, commence BLS resuscitation. The neck specific procedures.16,89 The leader should engender the
and spine should be protected, as there may be trauma. team’s trust. Where leaders initiate structure within the
In lightning victims, emphasis is on the immediate arrest team, members not only work together better, they
resuscitation of those who appear unresponsive. Respi- also perform the tasks of resuscitation more quickly and
ratory arrest may be prolonged due to paralysis of the more effectively.89 The leader nominates the roles of arrest
medullary respiratory centre; if not corrected, cardiac team members. Roles of team members include airway
arrest secondary to hypoxia ensues. Fixed, dilated pupils management, chest compression, medication adminis-
should not be used as a poor prognosis of outcome, as tration (including IV access), documentation of events
victims can benefit from prolonged resuscitation without and care of family members. The team leader should be
major sequelae.87 responsible for post-resuscitation transfer, documenta-
tion, communicating with family members and healthcare
Drowning professionals and debriefing of the team.89
General issues in managing drowning presentations are The resuscitation scenario is both complex and
discussed in Chapter 23. This section focuses on resuscita- stressful for all participants. Often, participants express
tion of a cardiorespiratory arrest. Hypoxia and acute lung feelings that too many people are involved, with no one
injury from drowning result in respiratory arrest that, if person in control. Unfortunately, the concept of the multi-
not corrected, may proceed to a cardiac arrest.88 A patient’s disciplinary team, where all members’ contributions are
emotional state, associated diseases, previous hypoxia and equally respected, is often not evident in the literature.90
water temperature all influence this progression.82 In addition, while nurses already present at a cardiac arrest
The primary goal of initial intervention is the relief of in the hospital setting may be willing and competent to
hypoxaemia82 and restoration of cardiovascular stability.88 perform CPR, they may be prevented from doing so
Resuscitation of drowning victims follows BLS guidelines, because of the arrival of the cardiac arrest team.91,92
with commencement as soon as practical. Rescue
breathing may commence while the victim is still in the Post-resuscitation phase
water, provided it is safe for the rescuer.82 As drowning
victims may have swallowed considerable amounts of The aim of post-resuscitation care is the maintenance
water, vomiting and aspiration of gastric contents can be of cerebral and myocardial perfusion and the return of
a major problem during resuscitation. To minimise the a patient to a state of best possible health. Resuscita-
risks of inhalation, abdominal compression, the Heimlich tion does not cease with the return of spontaneous
manoeuvre and attempts to drain water from the lungs are circulation. However, ROSC after cardiac arrest does
not recommended. Instead, the victim should be placed on not always equate to a positive outcome for the patient.
the side for the initial assessment of airway and breathing.64 Mortality rates following in-hospital cardiac arrests vary
Cardiac arrest in these victims is secondary to hypoxia, so between 67% and 71%.93 This high mortality rate has
compression-only CPR is likely to be less effective and been attributed to multiple organs that are involved
should be avoided.82 Once experienced personnel arrive, with whole of body ischaemia during cardiac arrest. The
ALS and administration of oxygen should be initiated. reperfusion responses that occur following successful
The principles of respiratory support and ventilation are resuscitation are termed post-cardiac arrest syndrome.93
discussed in Chapter 15, and treatment of the sequelae of Coordinated care and specific interventions initiated in
a drowning victim is discussed in Chapter 23. the post-arrest phase can influence outcomes.94 Control
of body temperature, identification and treatment of acute
Resuscitation teams coronary syndromes and optimisation of mechanical
Resuscitation teams should be organised to ensure that ventilation are a few of the targeted objectives of care
the individual skills of each member are used effectively (ARC and NZRC Guideline 11.8).1
 CHAPTER 25 RESUSCITATION 847

Role of hypothermia in adults after outcome. Monitoring of blood sugar levels and treatment
of hyperglycaemia (>10 mmol/L) with insulin is recom-
cardiac arrest mended in the post-cardiac arrest period.1
During cardiac arrest, prolonged global ischaemia coupled
with inadequate reperfusion during the immediate Near-death experiences
post-resuscitation period can lead to severe cerebral With the rise in survival rates after a critical illness, there
hypoxic injury.95 Mild therapeutic hypothermia as part of are increasing numbers of documented near-death expe-
the post-cardiac arrest management provides significant riences and out-of-body experiences.99,100 Near death
survival benefit as well as improved cardiac and neurolog- has been described as unusual experiences during a
ical function.95–97 Several cooling techniques are described close brush with death.99,100 Experiences have typically
in Box 25.1. included memories of bright tunnels of light, deceased
Therapeutic cooling consists of the induction, main- relatives, out-of-body sensations, feelings of the presence
tenance and rewarming phases.98 ILCOR recommends of a deity and peace.101,102 These experiences may vary
that unconscious adult patients with spontaneous circu- between cultures: Euro-Americans may report a golden
lation after OHCA should be cooled to 32–34°C for colour light whereas people from Tibet may report a clear
12–24 hours if the initial rhythm was VF. Optimal targeted light.103 People report the experiences as pleasant, and they
temperature management continues to be examined with have resulted in positive life changes for the individual.
a recent randomised controlled trial reporting no statisti- After-effects of a near-death experience include absence
cally significant difference when comparing the survival of fear of death, a more spiritual view of life, less regard
and neurological outcomes of patients that were cooled to for material wealth and/or a heightened chemical sensi-
33°C compared to those that were cooled to 36°C.96 It is tivity.104 The incidence of near-death experiences after
important to note that shivering post-hyperthermia fever cardiac arrest is reported at 6–18%,99 with the frequency
must be avoided.1 Persistent hyperglycaemia following generally being higher in people under 60 years of age.104
cardiac arrest has been associated with poor neurological Hence, an awareness of the incidence of near-death expe-
riences and of the cultural differences and needs of the
BOX 25.1 person with a reported near-death experience is essential
post-cardiac arrest.103 Chapter 8 provides more informa-
Cooling techniques post-cardiac arrest
tion about family and cultural care.
External:
• Cooling blankets/pads, ice packs, wet towels, Special considerations
fanning, tents and cooling helmets
Internal:
The chapter to this point primarily has focused on the
physiological considerations of resuscitation to achieve
• Transnasal evaporating cooling the goal of preservation of cellular function. However,
• IV administration of cold saline or Hartmann’s this outcome is only achieved in a minority of cases.22–24
solution (15–30 mL/kg at 4°C over 30 minutes to Decision making around the initiation of CPR and resus-
achieve a 1.5°C fall in core temperature) citation interventions and the progression and termination
• IV heat exchange device of resuscitation involves a multitude of factors.
• Peritoneal and pleural lavage (not generally used) Family presence during an arrest
The practice of family members witnessing resuscitation
Adapted with permission from:
has become more evident over time. This shift in practice
Nolan JP, Morley PT, Hoek TV, Hickey RW, Kloeck W, Billi J
has been attributed to increasing patient autonomy and the
et al. Therapeutic hypothermia after cardiac arrest: an advisory
statement by the Advanced Life Support Task Force of the
presence of family at a cardiac arrest in popular television
International Liaison Committee on Resuscitation. Circulation shows. This has contributed to public support, and family
2003;108(1):118–21. members requesting – and expecting – to be present.105,106
Nielsen N, Wetterslev J, Cronberg T, Erlinge D, Gasche However, the issue of whether the family should be present
Y, Hassager C et al. Targeted temperature management during a cardiac arrest remains controversial. Proponents
at 33 C versus 36 C after cardiac arrest. N Engl J Med argue the importance of family being with loved ones
2013;369(23):2197–206. during their last moments, as this shortens the period of
Bernard SA, Gray TW, Buist MD, Jones BM, Silvester W, grieving and provides closure. Indeed, professional resus-
Gutteridge G et al. Treatment of comatose survivors of out- citation bodies recommend that family should be afforded
of-hospital cardiac arrest with induced hypothermia. N Engl J
the opportunity to be present. However, translating these
Med 2002;346(8):557–63.
recommendations into practice varies among healthcare
Polderman KH, Herold I. Therapeutic hypothermia and
controlled normothermia in the intensive care unit: practical
personnel. Commonly cited is a concern that the family
considerations, side effects, and cooling methods. Crit Care may interrupt the work of the resuscitation team, the
Med 2009;37(3):1101–20. ethical and medico-legal implications or concern about
offending the family.107,108 Contrary to these beliefs, there
848 SECTION 3 SPECIALTY PRACTICE

is limited evidence that family interfere with the perfor- • the arrest is not witnessed by emergency
mance of the resuscitation team.107–109 medical-services personnel.
Conflicting evidence exists as to the psychologi- Otherwise, the rule recommends transportation to the
cal effects of such an event on the family. Effects have hospital, in accordance with routine practice.114
been documented as ranging from no adverse effects108
through to expressions of distress, haunting conse- Legal and ethical considerations
quences and trauma.108 Indeed, families with experience Burgeoning technology in the 1960s enabled the support
recommend and support family presence as they believe of oxygenation and circulation for people whose illnesses
it was beneficial for their loved one and helped them to would have been lethal just a few years before. Enthusiasm
adjust to the family member’s death.110 Where families for restoration of life led healthcare workers to routinely
are provided the option of being present, a staff member initiate CPR for all patients who died in hospital.115 Unfor-
should be identified to have sole responsibility of tunately, this led to inappropriate resuscitation attempts
supporting the family. Chapter 8 is dedicated to family and the realisation of the economic, medical and ethical
and cultural care, providing additional information about
burden to society when survivors had a resultant poor
family support.
quality of life.116,117 In the 1970s, growing concern about
Ceasing CPR inappropriate application of CPR and patient’s rights led
The decision to cease CPR is often difficult; continuing authors to suggest means of forgoing resuscitation and
CPR beyond 30 minutes without ROSC is usually futile involving patients in decision making.118 Traditionally,
unless the arrest was compounded by hypothermia, the decision to initiate or withhold CPR was often made
submersion in cold water, lightning strike, drug overdose by the treating medical team in the absence of the patient
or other identified and treatable conditions such as inter- or family.119
mittent VF/VT.16 Prolonging resuscitation for more than Hospitals responded by developing procedures for
60 minutes may be beneficial for a severely hypothermic, withholding CPR through the documentation of ‘do not
child victim of near-drowning. Pupillary signs should not attempt to resuscitate’ (DNAR) orders, doctor’s orders
be used as a predictor of outcome in infants and children, for life-sustaining treatment, advance directives or living
as 11–33% of children with non-reactive pupils have wills119,120 (see Chapter 5). For patients or their surrogates
survived long-term after CPR.17 It is important to have to meaningfully participate in decision making about
eliminated all causes as far as possible. CPR and limitation-of-treatment orders, they must have
Termination of resuscitation is a multifactorial process, some understanding of survival rates and adverse effects
influenced by provider comfort and experience, patient associated with such interventions.117 Consequently, much
prognosis and the patient’s desires, wishes and values. debate has ensued over the right of a person to forgo
Organisational issues such as the local culture, protocols, treatment.
resources and guidelines will all impact termination Research proposes that, while patients want to be
decisions. With scientific advances such as extracorporeal involved in CPR decision making and want some form
membrane oxygenation (ECMO) as a bridge for refractory of advance directive, their knowledge is limited and
ventricular fibrillation and evidence-based protocols often derived from television dramas.119,121 Understand-
becoming more widely implemented, current impressions ing of quality of life, morbidity and outcomes after CPR
of termination decisions will change over time.111,112 It is strongly influences their preferences.122,123 Most patients,
appropriate to invite suggestions from team members, to and indeed healthcare workers, commonly hold unrealis-
ensure that all members are comfortable with a decision tic expectations of CPR success,121 and will often reverse
to stop the resuscitation attempt.16 Ultimately, terminating their preference for commencing CPR once they are
CPR is equivalent to a determination of death, and must be informed of the true probability of survival, functional
made by a doctor. In some out-of-hospital circumstances status and quality of life after resuscitation.124 When
it may be the paramedical staff who make this decision to compared to the general public, survivors following
stop CPR, essentially terminating resuscitation.113 Because cardiac arrest generally assess their quality of life as good
of this need, termination of resuscitation guidelines have 12 months post-arrest.123 Regardless of this, healthcare
been developed for use in the out-of-hospital setting. workers continue to demonstrate a reluctance to discuss
One prospectively validated termination of resuscitation CPR options with patients.125 Despite open discussion,
guideline is the ‘basic life support termination of resuscita- variations in the timing of the orders, poor documen-
tion rule’ which may be adopted to guide the termination tation and communication can result in CPR being
of pre-hospital CPR in adults.25 One such validated rule inappropriately commenced.120 Conversely, and contrary
is described below. to medical and nursing opinions, some people choose
In the pre-hospital setting stop CPR if: CPR even when they have a terminal illness, coma or
• no return of spontaneous circulation serious disability.122
and Standardised orders for limitations on life-sustaining
• no shocks are administered treatments (e.g. DNAR) should be considered to decrease
and the incidence of futile resuscitation attempts and to ensure
 CHAPTER 25 RESUSCITATION 849

that adult patients’ wishes are honoured. These orders consensus on DNAR decision-making practices or the
should be specific, detailed, transferable across healthcare termination of resuscitation. While researchers have
settings and easily understood. Processes, protocols and attempted to develop prognostic indicators for cardiac
systems should be developed that fit within local cultural arrest outcome, moralists would argue that the use of
norms and legal limitations to allow providers to honour such prognostic tools alone reflects utilitarianism, and that
patients’ wishes about resuscitation efforts.25 With the they should never be used in isolation of the input of the
exception of a zero survival rate there remains no formal patient and healthcare team.

Summary
Outcomes for patients after in-hospital sudden cardiac arrest remain poor. Successful management of a patient following
SCA depends largely on the timely implementation of the chain of survival. Nurses should understand the role of the
chain of survival in the resuscitation of the person following cardiac arrest.The chain emphasises the importance of early
recognition and intervention, continuous uninterrupted compressions and the early use of the defibrillator as a BLS skill.
Understanding when to start, when to continue and when to stop are equally important and are influenced by multiple
factors. Including the patient’s wishes in decision making is of utmost importance to ensure futile resuscitation attempts
are avoided. Despite the plethora of research on the topic of resuscitation, there is much we still do not know.

Case study
Matt, a fit, healthy 31-year-old, was playing football in a suburb of a major city on a Saturday afternoon
when he suddenly collapsed on the field. Two other footballers on the scene knelt down to render aid.
When Matt did not move they signalled for help, and an official first aid person at the scene ran onto the
field to assess Matt. Matt was unconscious, unresponsive and not moving. Cardiopulmonary resuscitation
was commenced by the first aid person utilising compression-only resuscitation at a rate of approximately
100 compressions per minute. The sports club at the field owned an AED; therefore another bystander
ran into the club and brought the AED onto the field and attached the pads onto Matt’s chest, while
compressions continued. During this time the coach of Matt’s team called triple zero (000).
The AED was turned on and instructed the first aid responders to ‘stand clear’. The rhythm was analysed
and a shock was advised and delivered as per the verbal cues, followed by immediate compressions. After
one more minute of CPR the second first aid person took over compressions and gave the first responder a
rest; after the second minute the AED once again advised a ‘stand clear’ message and analysed the rhythm,
and a second shock was advised and delivered, with compressions again immediately recommenced.
An ambulance responded and arrived at the scene 14 minutes post-collapse. They assessed the situation
and provided advanced life support measures as per the ARC guidelines. Compressions continued at a
rate of 100 per minute and, on arrival of an intensive care paramedic, Matt was intubated with a size 8
endotracheal tube and ventilation via bag and valve with supplemental oxygen was continued. The
ventilation rate was approximately 8–10 per minute. At 20 minutes after Matt collapsed, his cardiac rhythm
was noted to be VF and he had been given four shocks from the AED and then a further two shocks by the
paramedics. Matt had an intravenous cannula inserted and the first dose of adrenaline 1 mg was given,
and then repeated every 3 minutes (after every second loop of the shockable side of the ALS flow chart).
Amiodarone 300 mg IV was given after the third shock.
The ambulance was equipped with a mechanical automated chest compression device, which utilises a
load distributing band that squeezes the entire chest and hence delivers high-quality cardiac compressions.
Matt was rolled onto the device and the band was attached around his chest; the device was switched on
and took over the compressions at a rate of 100 per minute.
A call was made to the closest tertiary hospital to alert the centre that the patient was in refractory
ventricular fibrillation and request the possibility of rescue extracorporeal membrane oxygenation (ECMO).
ECMO is indicated for potentially reversible, life-threatening forms of respiratory and/or cardiac failure
that are unresponsive to conventional therapy. At no time during these procedures was there any sign of
ROSC. Matt was transferred to the ambulance and transported to the major hospital with compressions
and ventilations continuing.
850 SECTION 3 SPECIALTY PRACTICE

Upon arrival in the emergency department the ECMO response team was waiting and Matt’s femoral vein
and artery were percutaneously cannulated with size 15 and 17 French gauge catheters, respectively. He
was connected to venous-arterial ECMO and cooled to 32–34°C with the intravenous administration of
2 litres of cold saline as per hospital protocol for therapeutic hypothermia. Once connected to ECMO the
mechanical chest compression device was removed; however ventilation continued and Matt was taken to
the cardiac interventional catheter laboratory for urgent percutaneous interventional therapy. At this time
Matt had been in an arrested state for 1 hour and 20 minutes. During this time repeated shocks were given
in an attempt to revert his refractory ventricular fibrillation.
Percutaneous interventional therapy demonstrated a 98% occlusion in the left anterior descending artery
that was successfully stented. A further two shocks post-stent were given and Matt reverted to a sinus
rhythm after the second shock. Matt was transferred to the intensive care unit and over the following
2 days was slowly weaned from ECMO. Post-resuscitation care included reducing the fraction of inspired
oxygen as soon as possible with a targeted oxygen saturation of 90–95%, maintaining a normal PaCO2,
ensuring blood pressure was adequate (systolic pressure between 100 and 120 mmHg) and maintenance
of therapeutic hypothermia for the first 24 hours. Matt was extubated on day 3 and was discharged home
on day 8 with full neurological function to a very relieved family.

CASE STUDY QUESTIONS

1 Discuss the advantages and disadvantages of compression-only CPR.
2 What is the rationale for switching personnel during cardiac compressions?
3 Discuss the stage in the ALS flow chart that amiodarone is given.
4 Identify two common types of mechanical devices for cardiac compressions and how they augment
blood flow.

RESEARCH VIGNETTE

Nielsen N, Wetterslev J, Cronberg T, Erlinge D, Gasche Y, Hassager C et al. Targeted temperature management at
33°C versus 36°C after cardiac arrest. N Engl J Med 2013;369(23):2197–206

Background: Unconscious survivors of out-of-hospital cardiac arrest have a high risk of death or poor neurologic
function. Therapeutic hypothermia is recommended by international guidelines, but the supporting evidence is
limited, and the target temperature associated with the best outcome is unknown. Our objective was to compare two
target temperatures, both intended to prevent fever.
Methods: In an international trial, we randomly assigned 950 unconscious adults after out-of-hospital cardiac arrest
of presumed cardiac cause to targeted temperature management at either 33 degrees C or 36 degrees C. The primary
outcome was all-cause mortality through the end of the trial. Secondary outcomes included a composite of poor
neurologic function or death at 180 days, as evaluated with the Cerebral Performance Category (CPC) scale and the
modified Rankin scale.
Results: In total, 939 patients were included in the primary analysis. At the end of the trial, 50% of the patients in the
33 degrees C group (235 of 473 patients) had died, as compared with 48% of the patients in the 36 degrees C group
(225 of 466 patients) (hazard ratio with a temperature of 33 degrees C, 1.06; 95% confidence interval [CI], 0.89 to 1.28;
P=0.51). At the 180-day follow-up, 54% of the patients in the 33 degrees C group had died or had poor neurologic
function according to the CPC, as compared with 52% of patients in the 36 degrees C group (risk ratio, 1.02; 95% CI,
0.88 to 1.16; P=0.78). In the analysis using the modified Rankin scale, the comparable rate was 52% in both groups (risk
ratio, 1.01; 95% CI, 0.89 to 1.14; P=0.87). The results of analyses adjusted for known prognostic factors were similar.
Conclusions: In unconscious survivors of out-of-hospital cardiac arrest of presumed cardiac cause, hypothermia at a
targeted temperature of 33 degrees C did not confer a benefit as compared with a targeted temperature of 36 degrees C.
(Funded by the Swedish Heart-Lung Foundation and others; TTM ClinicalTrials.gov number, NCT01020916.)
 CHAPTER 25 RESUSCITATION 851

CRITIQUE
In this study Nielsen aimed to determine whether cooling patients to 33°C provided any advantage compared to
cooling patients to 36°C post cardiac arrest as part of a targeted temperature management strategy.96 Randomisation
of the 939 patients was undertaken using a computer generated sequence and permuted blocks of varying size
were used to account for potential biases between study sites. Those who assessed patient outcomes were blinded
to treatment allocation. In addition to the researchers who implemented a standardised protocol, a doctor who
was blinded to treatment allocation performed a neurological evaluation 72 hours following completion of the trial
interventions. The primary end point was survival at 180 days, with secondary outcomes being neurological outcome
as assessed by the Cerebral Performance Category (CPC) and Modified Rankin scores. The study was powered to
detect a 20% reduction in baseline mortality of 44% in the 33°C group compared with 55% in the 36°C group.
In assessing this study one should adopt a systematic approach of determining the study characteristics, understanding
the results and assessing the applicability of the findings to the patients you manage. With regard to the study
characteristics, Table 1 in the journal article provides the baseline characteristics of the patients and known prognostic
factors (e.g. bystander CPR, age, sex, initial rhythm etc) in each of the treatment arms. Both groups appear to be very
similar. It is interesting to note that both groups were initially quite hypothermic (35°C), time to commencement of basic
life support was a median of 1 minute and approximately 80% of patients had an initial shockable rhythm. Figure 1 in
the journal article demonstrates good temperature separation with each intervention reaching target temperature within
8 hours of randomisation and that temperature being maintained for the next 20 hours as per study protocol.
In understanding the findings of the study, the authors found no difference in either primary or secondary outcomes
between the two interventions. Death at 180 days occurred in 48% and 47% of patients allocated to 33°C and 36°C,
respectively (HR 1.01; 95% CI 0.87 to 1.15). Further, there was no difference observed in neurological outcome. The
authors conclude that their study did not provide evidence that targeting a temperature of 33°C following out-of-
hospital cardiac arrest offers any advantage over a target temperature of 36°C. The authors appropriately identified
the limitations of their study.
So what does this mean for current practice? Firstly, it should be understood that this study was designed to detect
a difference in outcome between the two treatment temperatures. It failed to detect any such difference. This is not
the same as concluding the two temperatures were equivalent and the study was not designed as an equivalence
trial. Equivalence trials are designed to test the hypothesis that the two interventions are not too different within
predetermined values of what would be considered (often clinically) as equivalent. Secondly, as previously noted the
proportion of patients with initial shockable rhythm and 50% of the study patients receiving basic life support within
1 minute are quite different to the mainstream population of out-of-hospital cardiac arrests. As such, the findings of this
study may lack some generalisability in this regard. Further, it remains unknown if similar findings would be observed in
patients presenting with pulseless electrical activity or asystole. Conversely, the implementation of a target temperature
of 36°C may be logistically easier in the ICU and potential for complications related to therapeutic hypothermia.
This study does not provide any support to justify not initiating therapeutic hypothermia. The authors clearly state that
the prevention of fever is important in this patient cohort and this is consistent with the current evidence. Accordingly,
one should interpret the findings of this study as in support of a targeted temperature control strategy where a
temperature range of 33°C to 36°C is maintained.

Lear ning a c t iv it ie s
1 Does the study recommend a target body temperature of 33°C for unconscious patients admitted to hospital
following out-of-hospital cardiac arrest?
2 What limitations did the commentary highlight in the above recommendation?
3 What, in research outcome terms, is the importance of the doctor who performed the neurological evaluations
being blinded to treatment allocation?
4 What would be the practical advantage of a protocol change from therapeutic hypothermia to a targeted
temperature of 36°C?
852 SECTION 3 SPECIALTY PRACTICE

Online resources
American Heart Association (AHA), www.americanheart.org
Australian Resuscitation Council (ARC), www.resus.org.au
Center for Pediatric Emergency Medicine (CPEM), http://cpem.med.nyu.edu
European Resuscitation Council (ERC), www.erc.edu
International Liaison Committee on Resuscitation (ILCOR), www.ilcor.org/en/home
New Zealand Resuscitation Council (NZRC), www.nzrc.org.nz
The Regional Emergency Medical Services Council of New York City, www.nycremsco.org/default.asp

Further reading
Luo X, Zhang H, Chen G, Ding W, Huang L. Active compression–decompression cardiopulmonary resuscitation (CPR) versus
standard CPR for cardiac arrest patients: a meta-analysis. World J Emerg Med 2013;4(4):266–72.

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 CHAPTER 25 RESUSCITATION 855

81 Lewis G, ed. Saving mothers’ lives: The continuing benefits for maternal health from the United Kingdom (UK) Confidential Enquires into
Maternal Deaths. Seminars in Perinatology. Elsevier; 2012.
82 Soar J, Perkins GD, Abbas G, Alfonzo A, Barelli A, Bierens JJ et al. European Resuscitation Council guidelines for resuscitation 2010: Section
8. Cardiac arrest in special circumstances: electrolyte abnormalities, poisoning, drowning, accidental hypothermia, hyperthermia, asthma,
anaphylaxis, cardiac surgery, trauma, pregnancy, electrocution. Resuscitation 2010;81(10):1400-33.
83 Lipman S, Cohen S, Einav S, Jeejeebhoy F, Mhyre JM, Morrison LJ et al. The Society for Obstetric Anesthesia and Perinatology consensus
statement on the management of cardiac arrest in pregnancy. Anesth Analg. 2014;118(5):1003-16.
84 Jeejeebhoy FM, Zelop CM, Windrim R, Carvalho JC, Dorian P, Morrison LJ. Management of cardiac arrest in pregnancy: a systematic review.
Resuscitation 2011;82(7):801-9.
85 Hoek TLV, Morrison LJ, Shuster M, Donnino M, Sinz E, Lavonas EJ et al. Part 12: Cardiac arrest in special situations 2010: American Heart
Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular eare. Circulation 2010;122(18 suppl 3):S829-S61.
86 Gupta S. Maternal cardiac arrest and resuscitation: some burning issues! J Obstet Anaesth Crit Care 2013;3(1):1.
87 Zafren K, Durrer B, Herry J-P, Brugger H. Lightning injuries: prevention and on-site treatment in mountains and remote areas: official guidelines
of the International Commission for Mountain Emergency Medicine and the Medical Commission of the International Mountaineering and
Climbing Federation (ICAR and UIAA MEDCOM). Resuscitation 2005;65(3):369-72.
88 Layon AJ, Modell JH. Drowning: update 2009. Anesthesiology 2009;110(6):1390-401.
89 Yeung JHY, Ong GJ, Davies RP, Gao F, Perkins GD. Factors affecting team leadership skills and their relationship with quality of
cardiopulmonary resuscitation. Crit Care Med 2012;40(9):2617-21.
90 Hunziker S, Johansson AC, Tschan F, Semmer NK, Rock L, Howell MD et al. Teamwork and leadership in cardiopulmonary resuscitation.
J Am CollCardiol 2011;57(24):2381-8.
91 Jones L, King L, Wilson C. A literature review: factors that impact on nurses’ effective use of the medical rmergency yeam (MET). J Clin Nurs
2009;18(24):3379-90.
92 Dwyer T, Mosel Williams L, Mummery K. Defibrillation beliefs of rural nurses: focus group discussions guided by the theory of planned
behaviour. Rural Remote Health 2005;5:322.
93 Nolan JP, Neumar RW, Adrie C, Aibiki M, Berg RA, Böttiger BW et al. Post-cardiac arrest syndrome: epidemiology, pathophysiology, treatment,
and prognostication: a scientific statement from the International Liaison Committee on Resuscitation; the American Heart Association
Emergency Cardiovascular Care Committee; the Council on Cardiovascular Surgery and Anesthesia; the Council on Cardiopulmonary,
Perioperative, and Critical Care; the Council on Clinical Cardiology; the Council on Stroke. Resuscitation 2008;79(3):350-79.
94 Binks A, Nolan J. Post-cardiac arrest syndrome. Minerva Anestesiol 2010;76(5):362-8.
95 Nolan JP, Morley PT, Hoek TV, Hickey RW, Kloeck W, Billi J et al. Therapeutic hypothermia after cardiac arrest: an advisory statement by the
Advanced Life Support Task Force of the International Liaison Committee on Resuscitation. Circulation 2003;108(1):118-21.
96 Nielsen N, Wetterslev J, Cronberg T, Erlinge D, Gasche Y, Hassager C et al. Targeted temperature management at 33 C versus 36 C after
cardiac arrest. N Engl J Med 2013;369(23):2197-206.
97 Bernard SA, Gray TW, Buist MD, Jones BM, Silvester W, Gutteridge G et al. Treatment of comatose survivors of out-of-hospital cardiac arrest
with induced hypothermia. N Engl J Med 2002;346(8):557-63.
98 Polderman KH, Herold I. Therapeutic hypothermia and controlled normothermia in the intensive care unit: practical considerations, side
effects, and cooling methods. Crit Care Med 2009;37(3):1101-20.
99 Greyson B. Incidence and correlates of near-death experiences in a cardiac care unit. General Hospital Psychiatry 2003;25(4):269-76.
100 Greyson B. Getting comfortable with near death experiences. Missouri Med 2013;110(6):471.
101 James D. What emergency department staff need to know about near-death experiences. Adv Emerg Nurs J 2004;26(1):29-34.
102 Parnia S, Fenwick P. Near death experiences in cardiac arrest: visions of a dying brain or visions of a new science of consciousness.
Resuscitation 2002;52(1):5-11.
103 Belanti J, Perera M, Jagadheesan K. Phenomenology of near-death experiences: a cross-cultural perspective. Transcultural Psychiatry
2008;45(1):121-33.
104 Cant R, Cooper S, Chung C, O’Connor M. The divided self: near death experiences of resuscitated patients – a review of literature. Int Emerg
Nurs 2012;20(2):88-93.
105 Mazer MA, Cox LA, Capon JA. The public’s attitude and perception concerning witnessed cardiopulmonary resuscitation. Crit Care Med
2006;34(12):2925-8.
106 Ong MEH, Chung WL, Mei JSE. Comparing attitudes of the public and medical staff towards witnessed resuscitation in an Asian population.
Resuscitation 2007;73(1):103-8.
107 Hung MS, Pang S. Family presence preference when patients are receiving resuscitation in an accident and emergency department.
J Adv Nurs 2011;67(1):56-67.
108 Jabre P, Belpomme V, Azoulay E, Jacob L, Bertrand L, Lapostolle F et al. Family presence during cardiopulmonary resuscitation.
N Engl J Med 2013;368(11):1008-18.
109 Schmidt B. Review of three qualitative studies of family presence during resuscitation. The Qualitative Report 2010;15(3):731-6.
110 Dwyer TA. Predictors of public support for family presence during cardiopulmonary resuscitation: a population based study. Int J Nurs Stud
2015; in press, <http://dx.doi.org/10.1016/j.ijnurstu.2015.03.004>.
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111 Stub D, Bernard S, Pellegrino V, Smith K, Walker T, Stephenson M et al. Issues in establishing the refractory out-of-hospital cardiac arrest
treated with mechanical CPR, hypothermia, ECMO and early reperfusion (CHEER) study. Heart, Lung and Circulation 2012;21:S163.
112 Chen Y-S, Lin J-W, Yu H-Y, Ko W-J, Jerng J-S, Chang W-T et al. Cardiopulmonary resuscitation with assisted extracorporeal life-support
versus conventional cardiopulmonary resuscitation in adults with in-hospital cardiac arrest: an observational study and propensity analysis.
Lancet 2008;372(9638):554-61.
113 Adams BD, Benger J. Should we take patients to hospital in cardiac arrest? BMJ 2014;349:5659.
114 Morrison LJ, Eby D, Veigas PV, Zhan C, Kiss A, Arcieri V et al. Implementation trial of the basic life support termination of resuscitation rule:
reducing the transport of futile out-of-hospital cardiac arrests. Resuscitation. 2014;85(4):486-91.
115 Lynn J, Gregory CO. Regulating hearts and minds: the mismatch of law, custom and resuscitation decisions. J Am Geriatr Soc 2003;
51(10):1502-3.
116 European Resuscitation Council. Part 2: ethical aspects of CPR and ECC. Resuscitation 2000;46:17-27.
117 Salins NS, Pai SG, Vidyasagar M, Sobhana M. Ethics and medico legal aspects of “not for resuscitation”. Indian J Palliat Care 2010;16(2):66.
118 Rabkin M, Gillerman G, Rice N. Orders not to resuscitate. NEngl J Med 1976;295:364-72.
119 Kerridge I, Pearson S, Rolfe I, Lowe M. Decision making in CPR: attitudes of hospital patients and health care professionals. Med J Aust
1998;169:128-31.
120 Mockford C, Clarke B, Field R, Fritz Z, Grove A, Waugh N et al. A systematic review of do-not-attempt-cardiopulmonary-resuscitation
(DNACPR) orders: summarising the evidence around decision making and implementation. Resuscitation 2014;85:S85.
121 Harris D, Willoughby H. Resuscitation on television: realistic or ridiculous? A quantitative observational analysis of the portrayal of
cardiopulmonary resuscitation in television medical drama. Resuscitation 2009;80(11):1275-9.
122 Yuen JK, Reid MC, Fetters MD. Hospital do-not-resuscitate orders: why they have failed and how to fix them. J Gen Intern Med
2011;26(7):791-7.
123 Smith K, Andrew E, Lijovic M, Nehme Z, Bernard S. Quality of life and functional outcomes 12 months after out-of-hospital cardiac arrest.
Circulation 2015;131(2):174-81.
124 Heyland D, Frank C, Groll D. Understanding cardiopulmonary resuscitation decision making: perspectives of seriously ill hospitalised patients
and family members. Chest 2006;130:419-28.
125 Sharma RK, Jain N, Peswani N, Szmuilowicz E, Wayne DB, Cameron KA. Unpacking resident-led code status discussions: results from a
mixed methods study. J Gen Int Med 2014;29(5):750-7.
126 Yost CC, Bloom R. Neonatal resuscitation. Crit Care Obstetr 2010:108.
127 Luo X, Zhang H, Chen G, Ding W, Huang L. Active compression-decompression cardiopulmonary resuscitation (CPR) versus standard CPR for
cardiac arrest patients: a meta-analysis. World J Emerg Med 2013;4(4):266-72.
128 Babbs CF. The case for interposed abdominal compression CPR in hospital settings. Analg Resusc: Curr Res 2013;3:1. of. 2014;6:2.
129 Ristagno G, Li Y, Gullo A, Bisera J. Amplitude spectrum area as a predictor of successful defibrillation. In: Anaesthesia and Pharmacology of
Intensive Care Emergency Medicine APICE: Springer; 2011, pp 141-60.
130 Monteleone PP, Borek HA, Althoff SO. Electrical therapies in cardiac arrest. Emerg Med Clin North Am 2012;30(1):51-63.
131 Link MS, Atkins DL, Passman RS, Halperin HR, Samson RA, White RD et al. Part 6: Electrical therapies automated external defibrillators,
defibrillation, cardioversion, and pacing: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency
Cardiovascular Care. Circulation 2010;122(18 suppl 3):S706-S19.
132 Morley P. Cardiopulmonary resuscitation. In: Harley I, Hore P, eds. Anaesthesia: An introduction. 5th ed. East Hawthorn, Victoria: IP
Communications; 2012, pp 174–89.
133 Zhu X-Y, Lin B-C, Zhang Q-S, Ye H-M, Yu R-J. A prospective evaluation of the efficacy of the laryngeal mask airway during neonatal
resuscitation. Resuscitation 2011;82(11):1405-9.
134 Yamaga S, Une K, Kyo M, Suzuki K, Kobayashi Y, Nakagawa I et al. Gas insufflation in the stomach during cardiopulmonary resuscitation
using laryngeal tube ventilation in comparison with bag-valve-mask ventilation. Circulation 2012;126(21 Supplement):A295.
135 Soar J. Which airway for cardiac arrest? Do supraglottic airways devices have a role? Resuscitation 2013;84(9):1163-4.
 Chapter 26

Postanaesthesia recovery
Paula Foran, Andrea Marshall

KEY WORDS Learning objectives

anaesthesia After reading this chapter, you should be able to:
neuromuscular • describe the principles of immediate postoperative care with regard to
blockade respiratory and cardiovascular management
postanaesthesia care • discuss the assessment and management of complications following
surgery and general anaesthesia
postoperative
complications • discuss the principles and possible complications of central neural
blockade
• discuss the signs, symptoms and treatment for anaesthetic complications
such as malignant hyperthermia, inadvertent hypothermia and awareness
under anaesthesia.

Introduction
In 1751, realising that postoperative patients were vulnerable, the first Post Anaes-
thetic Care Unit was created.1 By the 1940s the importance of recovering from
anaesthesia was recognised. Areas close to the operating theatre were created
allowing patients leaving the operating theatre to be closely monitored for signs
of respiratory failure so that appropriate management could be instituted.1 Today,
perianaesthesia nursing is recognised as a specialty in its own right and post-
graduate education opportunities exist to support nurses to develop expertise
in this area.
While surgical techniques and anaesthetic medications have changed expo-
nentially, the primary purpose of immediate postanaesthesia/postoperative care,
whether provided in the postanaesthesia care unit (PACU) or intensive care
unit (ICU), has altered little in the last 70 years. The focus remains on critical
evaluation and stabilisation of patients after surgery, with an emphasis on anti-
cipation and prevention of complications arising from either the anaesthetic or
the surgical procedure.2 While this chapter is titled ‘Postanaesthesia recovery’, it
is worth noting that patients are also recovering from their own specific surgical
procedure, which may require specific assessment and management.
Timely, appropriate surgery and high quality pre- and postoperative care may
be key in preventing deaths in the first 48 hours after surgical procedures.3 The
Australian National Consensus Statement on essential elements for recognising
and responding to clinical deterioration4 reports that measurable physiological
858 SECTION 3 SPECIALTY PRACTICE

abnormalities occur prior to adverse events such as cardiac some evidence of skeletal muscle relaxation. In stage III
arrest and death and suggests that early recognition of anaesthesia swallowing, retching and vomiting reflexes
changes in a patient’s condition, followed by prompt and disappear sequentially during induction and reappear in
effective treatment, can minimise poor outcomes. Surgical the same order during emergence from anaesthesia.6
complications are estimated to account for approxi- During recovery from anaesthesia, if the patient is
mately 40% of all adverse events,5 making surgical patients breathing using diaphragmatic muscles but does not have
prime candidates for clinical deterioration. This increased intercostal muscle involvement, they are likely still in
risk might require some patients to be admitted to the stage III of anaesthesia. Lack of muscle tone, particularly
intensive care unit following surgery, especially if they in the jaw and abdomen, also suggests that the patient is in
require ongoing high level assessment and management. stage III anaesthesia. As the anaesthesia lightens, respiration
Postoperative patients who are not critically ill may also will have a normal rate and rhythm.
be recovered in ICU after hours, and it is this group of Stage IV of anaesthesia lasts from when respiration stops
patients to which this chapter is directed. In this chapter to failure of the circulatory system, hence is referred to as
a brief overview of nursing the patient in the period the stage of overdose. Determining the stage of anaesthesia
following surgery and anaesthesia is provided with the cannot be done by assessing any single parameter. Rather,
focus being on the recovery of non-critically ill patients. all clinical signs should be considered in relation to the
In this chapter we will review anaesthesia and commonly patient’s clinical condition and the particular anaesthetic
used anaesthetic agents, postanaesthesia nursing care and agent used.
assessment and management of specific postoperative
complications. We acknowledge that postanaesthesia care
nursing is a specialty in its own right and that this chapter
Anaesthetic agents
will provide an overview. We encourage readers to refer to Once referred to as the ‘art of anaesthesia’, modern anaes-
the end of this chapter for further reading about this specialty. thesia now rests firmly on scientific foundations; however,
the practice still remains a mixture of science and art.7
Introduction to anaesthesia The aim of good anaesthesia is to provide the safest anaes-
thetic, in the lightest plane possible, which allows a given
There are five components to anaesthesia. These include procedure to be performed while the patient is pain free.
hypnosis, analgesia, muscle relaxation, sympatholysis This is why other medications, such as muscle relaxants,
and amnesia. As a result of improvements in pharmaco- will be given in conjunction with anaesthetic agents so that
logical agents used in anaesthesia we now see patients muscle relaxation can occur at a lighter stage of anaesthesia.
emerging from anaesthesia in minutes rather than hours
and, consequently, patients can be discharged from peri- Non-opioid agents
anaesthesia care more quickly. Critical care nurses, whether Non-opioid intravenous agents include non-barbiturates,
they specialise in postanaesthesia recovery or not, need a barbiturates and sedatives. Non-opioid drugs interact
thorough understanding of the pharmacology related with gamma-aminobutyric acid (GABA), an inhibitory
to anaesthesia as this underpins patient assessment and neurotransmitter in the brain, with the specific actions
management. being drug dependent.
Phases of anaesthesia Non-barbiturates
There are four stages to anaesthesia that a critical care Propofol is likely the most common non-barbiturate used
nurse should recognise and consider when undertaking clinically. Its unique pharmacological characteristics include
patient assessment. The initiation of analgesia through to quick onset, relatively short emergence time and minimal
the loss of consciousness constitutes stage I, or the stage side effects, making propofol (2,6-diisopropylphenol)
of analgesia. This is the lightest level of anaesthesia and, one of the most widely used short-acting intravenously
although there is sensory and mental depression, patients administered anaesthetic/hypnotic drugs.8 Propofol as a 1%
can often obey commands, breathe normally and maintain solution is administered intravenously at a dose of 1.5 to
protective reflexes.6 Stage II begins with loss of conscious- 2.5 mg/kg for induction,9 although lower doses are used
ness and ends when a regular breathing pattern starts and for elderly patients and those with hypovolaemia or cardiac
the eyelid reflex is lost. Also called the stage of delirium, disease.10 As a single agent propofol is usually administered
stage II is characterised by excitement. Responses such as quickly (over 15 seconds) with unconsciousness occurring
vomiting and laryngospasm can also occur in this stage, in about 30 seconds. With a half-life of 2–9 minutes,
although with newer anaesthetic agents most patients emergence from this drug is rapid and there are usually few
move through this stage quite quickly. effects on the central nervous system. If continuous infusion
Stage III, the stage of surgical anaesthesia, lasts from the of propofol has been used for more than 12 hours, a longer
time of onset of regular breathing to breathing cessation. recovery period can be expected.10
Patients in stage III anaesthesia will not respond when a When administered, propofol can decrease cerebral
surgical incision is made. In stage III patients will have blood flow, cerebral perfusion pressure and intracra-
sensory depression, loss of recall, depressed reflexes and nial pressure. Blood pressure and cardiac output are also
 CHAPTER 26 POSTANAESTHESIA RECOVERY 859

reduced and this can be more pronounced in those Barbiturates

patients with compromised left ventricular function and Barbiturates as an intravenous anaesthetic agent have a
hypovolaemia. The depressant effect of propofol on the long history, and thiopental sodium was used frequently
respiratory system may result in airway and ventilatory
until the 1990s but is used less frequently since the intro-
support being required for those patients who are not
duction of non-barbiturates such as propofol.15 Previously,
already intubated and ventilated. There is some suggestion
in the literature that propofol may have some short- thiopental sodium was used in conjunction with other
acting analgesic properties,11 although this effect is not well anaesthetics because it had poor analgesic properties. The
established and conflicting results exist in the literature.12 disadvantages of thiopental sodium also include adverse
effect on respiratory function, coughing, laryngospasm and
Practice tip bronchospasm. The highly alkaline pH of the drug could
also contribute to tissue necrosis if extravenous adminis-
Propofol administered to elderly patients can result in a tration occurred. Thiopental sodium also has antianalgesic
significant drop in blood pressure. Therefore, this group properties at low doses, so patients recovering from surgery
of patients should be carefully monitored. may have more pain and therefore be irritable and restless
in the initial recovery phase.10
Etomidate is a short-acting hypnotic agent without any
analgesic effects. Although not available in all countries, and Practice tip
not licensed for use in Australia, etomidate is used in many
countries, especially for intubation of critically ill patients, Obese patients administered thiopental sodium may have
mainly because of the minimal cardiovascular effects of delayed wakening because the drug is highly fat soluble.
the drug.13 Etomidate causes only a slight increase in heart
rate and slight decrease in blood pressure. Cardiac index
and peripheral vascular resistance are not significantly Inhalation anaesthesia
influenced and the drug does not seem to be arrhythmo- Assessing emergence from inhalation anaesthesia requires
genic. Controversy does exist around the use of etomidate an understanding of the pharmacological effects of these
because it inhibits steroid synthesis with adrenal suppression agents, and an overview of their characteristics. A brief
lasing for 5–8 hours following a single dose.14 Consequently summary of these agents is provided in Table 26.1. These
etomidate should only be administered to select patients. agents are essentially depressant drugs and some are more

TABLE 26.1
Common inhalation anaesthetic agents6

AGENT CHARACTERISTICS

Isoflurane • Reduces systemic arterial blood pressure and systemic vascular resistance
• Heart rate increased during recovery
• Produces respiratory depression
• Produces skeletal muscle relaxation in a dose-related fashion
• Does not sensitise the myocardium to catecholamines compared to halothane so fewer arrhythmias are observed
• Patient awakens 15–30 minutes following termination of anaesthetic gas but may be longer if surgery
exceeds 45–60 minutes
Sevoflurane • Emergence from anaesthesia occurs in minutes
• Decreases blood pressure and systemic vascular resistance
• A respiratory depressant
• Does not increase risk of arrhythmias
• Can increase intracranial pressure in a dose-related manner
Desflurane • Extremely rapid emergence
• Dose-related decrease in blood pressure
• Low rate of cardiac arrhythmias
• Irritates respiratory tract and induces coughing
• May induce laryngospasm
• Almost totally eliminated by the respiratory system
Nitrous oxide • No side effects unless hypoxia is present
• Non-toxic and non-irritating
• Can be administered alone or in combination with other agents
• Diffusion hypoxia can occur when not enough nitrous oxide is removed from the lungs at the end of the
surgical procedure
860 SECTION 3 SPECIALTY PRACTICE

likely to affect myocardial and respiratory function than The most common opioid drugs used for pain relief in
others. Because of respiratory depression, during recovery the postoperative period include morphine and fentanyl
it is essential that patients are encouraged to continue (Table 26.2) with morphine the most widely used and
taking deep breaths. The increased rate and depth of the standard against which other pain-relieving agents are
breathing can also assist with eliminating the agents into compared.17 Pethidine is no longer commonly used for
the atmosphere. long-term pain relief due to the accumulation of norme-
peridine over time, which can result in central nervous
Practice tip system toxicity.18
Encouraging deep breathing during the recovery period
Practice tip
is essential to promote removal of inhalation gases.
Morphine is metabolised by the liver and the metabolites
Opioids are excreted by the kidneys so the analgesic and
sedating effects can be prolonged and potentially
Opioids are an important agent in the anaesthetic process
and the postoperative period, with their main purpose dangerous for patients with renal failure.
being to provide analgesia. Opioids also enhance the
effectiveness of inhaled anaesthetics allowing lower doses Practice tip
to be provided. In the postoperative period, opioids are
commonly administered to alleviate pain associated with Pethidine (meperidine) is metabolised in the liver to
the surgical process. normeperidine. Elderly patients have less tolerance to
Opioids, whether they are natural or synthetic substances, the central depressant effects of pethidine so this drug
bind to receptors producing a morphine-like or opioid should be avoided or the dose limited to 25 mg.
agonist effect.16 Opioid receptors include the mu (μ), delta
(δ) and kappa (κ) receptors located in the central nervous
Spinal and epidural opioid
system, mostly in the brain stem and spinal cord. The mu
receptors, specifically the mu-1 receptors, are responsible administration
for supraspinal analgesia effects when stimulated. When Opioids can be administered as part of either spinal
mu-2 receptors are stimulated hypoventilation, bradycardia, or epidural anaesthesia. In spinal anaesthesia, drugs are
physical dependence, euphoria and ileus can occur. administered into the cerebral spinal fluid that surrounds

TABLE 26.2
Opioid analgesics used for postoperative pain relief16

DRUG DOSEa A D VA N TA G E S D I S A D VA N TA G E S

Morphine IV: 4–10 mg Minimal effect on heart rate/rhythm Depresses respiratory rate and
Peak analgesic effect within and blood pressure tidal volume
20 minutes; duration 2 hours Can cause orthostatic hypotension
IM: 10 mg and syncope
Onset of action approximately Can cause nausea and vomiting
20 minutes with peak effect in Causes histamine release
45–90 minutes; duration of action
4 hours
Fentanyl IV: 1–2 mcg/kg OR 25–100 mcg Has little or no hypotensive effect Delayed onset respiratory
PRN for analgesia Usually does not cause nausea depression because of
Onset of action 4–6 minutes; and vomiting a secondary peak in the
peak effect within 5–15 minutes; concentration of the drug occurs
duration 20–40 minutes 45 minutes after apparent recovery
IM: Onset of action 7–15 minutes; Rapid IV administration can
duration 1 to 2 hours provoke bronchial constriction
Pethidine IV: 25–50 mg every 3–4 hours Minimal cardiovascular effects May slow rate of respiration but
hydrochloride IM: 25–100 mg every 3–4 hours although a transient increase this usually returns to normal within
(meperidine IM: Onset of action 10 minutes; in heart rate may occur with 15 minutes of IV injection
hydrochloride) duration of action 2 to 4 hours IV administration Can cause histamine release
Causes orthostatic hypotension

a
Average recommended doses for adults.
IM = intramuscular; IV = intravenous.
 CHAPTER 26 POSTANAESTHESIA RECOVERY 861

the spinal cord, and puncture of the dura is required for it should be used with caution in patients with known
this administration. In contrast with epidural admin- myocardial ischaemia. In small doses midazolam is used as
istration, the drugs are delivered outside the dura.19 an anti-emetic.25
Administration of morphine (0.1 to 0.2 mg) directly into
the spinal fluid results in a maximal concentration within Practice tip
5–10 minutes; the duration of action is 80–200 minutes.
In contrast, a higher dose of morphine is required when Midazolam does not affect intracranial pressure and,
administered into the epidural space (5 mg) with pain therefore, can safely be used in patients with intracranial
pathology or who are undergoing neurosurgery.
relief in effect within 30–60 minutes that can last up
to 24 hours. Additional morphine can be adminis- Although not commonly used, diazepam and
tered via the epidural route if required to a maximum lorazepam are longer acting benzodiazepines that may
of 10 mg in 24 hours. Fentanyl and sufentanil can also be used for induction and as an adjunct to intravenous
be administered epidurally and are more suited for anaesthesia. Both diazepam and lorazepam have a longer
continuous infusion. half-life and delayed onset of effect compared to that of
Opioid antagonists midazolam.10 Diazepam has few cardiovascular depressant
effects but is known to cause slight respiratory depression,
Should opioid-induced respiratory depression occur in an effect that is enhanced when it is administered at the
the postanaesthesia period an opioid antagonist might be same time as opiates.
needed. Naloxone is a pure opioid antagonist that reverses If required, the pharmacological effects of benzo-
the depressant effects of the drug and is usually admin- diazepines can be reversed. Flumazenil is a benzodiazepine
istered in a titrated fashion, assessing patient response. A agonist that should be administered intravenously in
dose of 0.1 mg to 0.2 mg is usually sufficient.The onset of 0.1-mg increments to avoid rapid reawakening. The usual
action is quick and occurs within 1–2 minutes of adminis- dose is 0.4 mg and the maximum amount administered
tration; the half-life is 30–80 minutes.20 After 3–5 minutes, should be no more than 1.0 mg.10 The drug takes effect
if reversal is still not achieved, additional doses of naloxone within 5 minutes of administration and has a duration of
can be administered.21 action between 1 and 2 hours.
When intrathecal or epidural opioids are administered
close observation of the patient, particularly respiratory Practice tip
and conscious state, is essential as there may be delayed
respiratory depression. Caution should also be taken with Flumazenil has a shorter duration of action than most
additional opioid administration during the first 24 hours benzodiazepines so patients should be carefully assessed
as the half-life of opioids administered via these routes is for resedation after the initial dose is administered. If
increased. signs of resedation are evident, additional flumazenil can
be administered every 20 minutes to a maximum dose of
Benzodiazepines and benzodiazepine 3.0 mg in a 1-hour period.
antagonists
Non-specific effects of benzodiazepines can be reversed
Benzodiazepines are sedatives that depress the limbic with the administration of physostigmine, an anticholin-
system and may cause some cortical depression.22 They esterase that crosses the blood–brain barrier. Physostigmine
interact with GABA, the inhibitory neurotransmitter, inhibits acetylcholinesterase making increased amounts
causing decreased orientation through a hypnotic of acetylcholine available at the central nervous system
effect, retrograde amnesia, anxiolysis and skeletal muscle receptors that are affected by benzodiazepines. Doses of
relaxation.10 The hypnotic action of benzodiazepines is 0.5 mg to 1.0 mg should be slowly administered in order
enhanced by the effects of opiates and barbiturates. to avoid cholinergic side effects.10
Midazolam is the most popular benzodiazepine used
in anaesthesia and critical care and has a wide variety of Butyrophenones
uses including procedural sedation and induction of anaes- As sedative agents, butyrophenones such as haloperidol
thesia. While routine premedications are no longer given, and droperidol produce a state of profound calm and
midazolam can be used for some patients to allay anxiety23 immobility where the patient appears to be pain free
and is also an intraoperative adjunct to both inhalation and and dissociated from their surroundings. Butyrophenone
regional anaesthesia. Midazolam affects the benzodiazepine use in anaesthesia is, however, uncommon. Haloperidol
receptors in the central nervous system causing reduced is rarely used because of its long duration of action and
anxiety and profound anterograde amnesia. Midazolam high incidence of extrapyramidal side effects. Droperidol
has a rapid onset of action – less than 60 seconds – with can be used on its own or in conjunction with fentanyl
a peak effect seen within 2–5 minutes.24 The duration of as part of a neurolept analgesic technique. Droperidol is
action is between 1 and 3 hours. Cardiovascular effects also administered in small doses (0.625–1.25 mg intra-
of midazolam include decreased blood pressure, increased venously) in the postoperative period to manage nausea
heart rate and reduced systemic vascular resistance; thus and vomiting.25
862 SECTION 3 SPECIALTY PRACTICE

Acetylcholine (ACh), a neurotransmitter that is deacti-

Practice tip vated by the cholinesterase family of enzymes, is stored
Some patients who have received droperidol report and released from the presynaptic terminal and is the only
feeling terrified and unable to express how they feel neurotransmitter used in the somatic nervous system.26
while also having an outward appearance of being ACh receptors are located on the motor end-plate and,
very calm. It is important that in the postanaesthesia when bound to ACh, membrane channels open and this
period support is provided to patients even if they results in an influx of sodium ions causing depolarisation
appear calm. of the motor end-plate membrane. Potassium ions exit
causing repolarisation, allowing the membrane potential
In the postanaesthesia period, regular stimulation of the to again become negative. These sequences allow muscle
patient and encouragement of deep breathing is necessary contraction to occur. ACh is broken down by acetyl-
as patients can drift back to sleep and have slow and/or cholinesterase, which is present in the synaptic cleft, and
shallow respirations. In some instances patients who have is metabolised before the excited muscle returns to its
received droperidol have become apnoeic.10 resting state. The broken down ACh elements are then
used for the manufacture of new ACh molecules in the
Neuromuscular blocking agents nerve terminal ending.
Since the 1940s neuromuscular blocking agents have been
Non-depolarising neuromuscular
used as pharmacological agents in anaesthesia. Although
not all patients will require neuromuscular blockade blocking agents
during anaesthesia, these agents may be given to facilitate Non-depolarising neuromuscular blocking agents block
endotracheal intubation. Muscle relaxation is also indicated the action of ACh at the postsynaptic receptor sites in the
to facilitate some surgical procedures such as abdominal neuromuscular junction (Figure 26.2) by competing with
surgery, in ophthalmic surgery to relax extraocular muscles ACh at these binding sites and blocking neuromuscular
and to facilitate mechanical ventilation. Nurses who are transmission.28 There are many different types of non-
responsible for the assessment and management of the depolarising neuromuscular blocking agents, and their
postoperative patient should understand the physiology of availability and use varies internationally.29 Although the
neuromuscular transmission and mechanism of action of end effect of these agents is similar, their pharmacologi-
the various neuromuscular blocking agents that may be cal effects differ in relation to onset of action, duration of
used in anaesthesia. effect and excretion (Table 26.3).
The neuromuscular junction has three components: Residual neuromuscular block is a complication that
the motor nerve fibre, the synaptic cleft and the can occur following use of neuromuscular blockade32
motor end-plate of striated muscle (see Figure 26.1). and can result in adverse respiratory complications.33

FIGURE 26.1 Neuromuscular junction.27

Adapted from Patton KT, Thibodeau GA. Anatomy and physiology. 7th ed. St Louis: Mosby; 2010, with permission.
 CHAPTER 26 POSTANAESTHESIA RECOVERY 863

TABLE 26.3
Pharmacological overview of commonly used non-depolarising neuromuscular blocking agents30

VECURONIUM AT R A C U R I U M CISATRACURIUM ROCURONIUM

PA N C U R O N I U M BROMIDE B E S Y L AT E BESYLATE BROMIDE

Dose for intubation 0.06–0.1 0.08–0.1 0.4–0.5 0.1–0.2 0.1

(mg/kg)
Intubation to 4.0 2.5–3.0 2.0–2.5 2.8–3.4 1.0–2.0
relaxation time (min)
Dose for muscle 0.04–0.08 0.05–0.06 0.2–0.5 2.5 0.6–1.0
relaxation (mg/kg)
Recovery time (min) 84–114 30–60 30–45 55–75 30–90
Reversible Yes Yes Yes Yes Yes
Time to reversal 40–60 25–80 (dose 20–35 10–15 5–10
(after initial dose, dependent)
in min)
Cumulative effects Yes Slight No No No
Fasciculations and No None No No No
muscle soreness
Risk of histamine Slight to none None Minimal No No
release
Cardiovascular Slight increase None Few None None
effects in pulse and
increase in blood
pressure

Adapted with permission from Drain CB. Neuromuscular blocking agents. In: Odom-Forren J, ed. Perianesthesia nursing: A critical
care approach. 6th ed. St Louis: Elsevier; 2013.

FIGURE 26.2 A, Normal muscle contraction. B, Neuromuscular blockade.31

Adapted from Siedlecki SL. Pain and sedation. In: Carlson K, ed. Advanced critical care nursing. St Louis: Saunders; 2009,
Figure 4-13, p 79, with permission.
864 SECTION 3 SPECIALTY PRACTICE

Pharmacological reversal of neuromuscular block can be A typical dose of suxamethonium is 0.5–1.5 mg/kg
used when the effects of the neuromuscular blocking agent administered intravenously. The onset of action is rapid,
remain present at the end of the surgery. Conventional usually within 30–60 seconds of administration. The
reversal of neuromuscular blockade involves administra- very rapid onset of paralysis when using suxamethonium
tion of an anticholinesterase. Anticholinesterase inhibits remains its true advantage as a patient can be intubated
the action of cholinesterases that inactivate ACh, thus almost immediately. Suxamethonium administration can
potentiating the effects of the neurotransmitter ACh, and induce hyperkalaemia so its use in patients with electro-
helps restore skeletal muscle activity.30 To avoid residual lyte disorders, such as those with severe burns or diabetic
neuromuscular blockade anticholinesterases should be ketoacidosis, is not recommended.36 The duration of
administered at least 20 minutes prior to extubation action of suxamethonium is relatively short as the drug
to help facilitate complete recovery of neuromuscular is hydrolysed rapidly by plasma pseudocholinesterase.
function.34 Anticholinesterases stimulate the muscarinic Paralysis associated with administration of suxameth-
receptors and elicit side effects including bradycardia, onium usually only lasts 5–10 minutes. Some patients may
arrhythmias, bronchospasm as well as nausea and vomiting. have reduced pseudocholinesterase activity. This can be
For this reason antimuscarinic agents such as atropine or an acquired deficiency that might be associated with liver
glycopyrrolate must be administered at the same time as disease, severe anaemia, malnutrition, prolonged pyrexia,
the reversal agent.26 pregnancy and renal dialysis. Congenital deficiencies in
Sugammadex is also used to reverse the effect of neuro- pseudocholinesterase are relatively uncommon.
muscular blockade, specifically when the agents rocuronium
and vecuronium are used. Sugammadex is the first selective Practice tip
neuromuscular drug binding agent and reverses the effect of
the neuromuscular blocking drugs through encapsulation. Patients with either acquired or congenital pseudo-
Hypersensitivity to sugammadex can occur within the first cholinesterase deficiency may remain paralysed for
5 minutes following administration and, as such, patients prolonged periods of time and may require mechanical
receiving this drug should be closely monitored for signs of ventilation for up to 48 hours.
drug-induced hypersensitivity.35
Factors influencing neuromuscular
Practice tip blocking agents
When patients return from surgery, review their anae-
There are a number of factors that can influence neuro-
sthetic record to see whether a neuromuscular blocking
muscular blocking agents. Many of these include drug
agent has been used and, if it was, whether a reversal
interactions and alterations in electrolyte balance (Table
agent was given.
26.4). Dehydration can also increase the sensitivity to
skeletal muscle relaxants because of increased neuro-
muscular excitability, slowed renal function and drug
Practice tip excretion and increased plasma concentration of the
relaxant. Acid–base balance can also influence neuro-
When dyspnoea occurs there is sometimes initial muscular blockade where acidosis and increased carbon
confusion between narcosis and residual muscle dioxide levels result in a stronger effect of the neuromus-
relaxants. Patients with narcosis may have a normal tidal cular blocking agent pancuronium.30 Hypothermia can
volume but the rate is slow; residual muscle relaxant antagonise the effect of neuromuscular blocking agents,
patients breathe very poorly due to a mechanical as with pancuronium, or can potentiate the effect as seen
problem with their muscles of respiration but their with suxamethonium.
respiratory effort is not impaired.
Non-steroidal anti-inflammatory drugs
Non-steroidal anti-inflammatory drugs such as ketorolac
Depolarising neuromuscular blocking and indomethacin can be used as analgesics in the post-
agents operative period, although indomethacin is used much less
Suxamethonium, also known as succinylcholine, is the frequently. Ketorolac has analgesic, anti-inflammatory
only depolarising neuromuscular blocking agent used and anti-pyretic actions and works by inhibiting the
in anaesthesia. Suxamethonium is most often used in cyclooxygenase enzyme system, thereby decreasing
rapid sequence induction for the purpose of endotra- prostaglandin synthesis. Ketorolac is administered by
cheal intubation. Suxamethonium works at the site of intramuscular or intravenous injection or given orally.
the acetylcholine receptor and causes persistent depo- An intramuscular dose of 30 mg as a loading dose can
larisation at the motor end-plate.30 Patients administered be followed by a further 15 mg after 6 hours. Ketorolac
suxamethonium demonstrate muscle fasciculations can also be used in conjunction with opioids for effective
because of the sudden increase in acetylcholine at the postoperative pain relief. The peak effect of ketorolac
motor end-plate. occurs in approximately 45–60 minutes so it can be
 CHAPTER 26 POSTANAESTHESIA RECOVERY 865

administered approximately 1 hour before the end of the

BOX 26.1
surgical procedure so that maximal pain relief occurs at
emergence from anaesthesia. Monoamine oxidase inhibitors
The interaction of this class of drug with common
Practice tip anaesthetic agents is important to recognise. Although
The recommended dose range of ketorolac is 15–60 mg. monoamine oxidase inhibitors (MAOI) are not as
Lower doses of ketorolac should be administered to the commonly used as in the past, many patients may still
elderly. be prescribed these for management of depression.
MAOIs inhibit N-demethylase and thus decrease the
breakdown of pethidine/meperidine. A type I response
Dissociative anaesthetics to this drug interaction includes seizures, agitation,
Ketamine is a dissociative drug that selectively blocks pain rigidity and hyperpyrexia. A Type II response includes
conduction and perception yet does not depress those parts hypotension, respiratory depression and coma.
of the central nervous system not involved in pain trans-
mission and perception.10 When patients are administered Adapted from Rasool F, Ghafoor R, Lambert DG.
ketamine they experience profound analgesia and uncon- Antidepressants and antipsychotics: anaesthetic implications.
sciousness but respiratory function is usually unimpaired. Anaesth Intensive Care Med 2014;15(7):314–17.
Ketamine can induce bronchodilation and some published
case reports suggest that this drug might be useful in asthma,
although adequately powered randomised controlled trials Local and regional anaesthesia
are required before definitive recommendations can be Local anaesthesia works by blocking nerve conduction so
made about this treatment.37 Ketamine also causes increased that the patient does not feel painful stimuli. Local anaes-
cerebral blood flow so should be avoided in those patients thetics work by binding to sodium channels, keeping them
at risk of developing increased intracranial pressure. open and inactive thus preventing depolarisation and
Of particular importance to the nurse managing a transmission of the neuronal action potential. A second
postoperative patient who has received ketamine is an mechanism may also cause disruption of the ion channel
understanding that psychic aberrations can occur on when local anaesthetic molecules are incorporated into
emergence from anaesthesia. Patients can experience vivid the cell membrane (Figure 26.3). The sensitivity to local
dreaming with or without psychomotor activity. They can anaesthetics depends on the nerve fibres, with sensitivity
appear confused, irrational and have hallucinations. These increased for the smaller nerve fibres. Myelinated fibres
effects can be managed by avoiding early verbal or tactile are also blocked before non-myelinated fibres, if they are
stimulation. If the patient does have augmented psychomo- of the same diameter.
tor responses and irrational behavior, medications such as
dexmedetomidine or a benzodiazepine can be administered. Practice tip

Practice tip Administration of local anaesthetics results in loss of

nerve function, and consequently pain, temperature,
Ketamine can be used as a sole anaesthetic agent for touch and proprioception are affected. Skeletal muscle
paediatric patients who appear to be less prone to tone is the last to be affected. This explains why patients
psychic disturbances. may be able to feel touch but not pain after receiving
local anaesthesia.
Drug interactions Assessment and management of the patient receiving
Many patients undergoing anaesthesia will be taking local or regional anaesthesia is provided later in this
medications in addition to those required for surgery and chapter.
anaesthesia. Whenever two or more drugs are given to a
patient there is a potential for drug interactions to occur.
Such interactions can have a potentially negative effect on
Assessment and management
the patient and knowledge of these interactions will help in the postoperative period
guide nursing assessment. Table 26.4 provides a summary
When caring for a patient immediately after surgery, it
of common medications and how these can interact with
is essential that the nurse has a full understanding of the
pharmacological agents used in surgery and anaesthesia.38
possible complications of each individual procedure that
has been performed. If a nurse is allocated a patient and
Practice tip they do not understand the surgical procedure they must
Some antibiotics such as gentamycin can potentiate ask, possibly at the time of anaesthetic handover, to gain
non-depolarising muscle relaxants and make reversal an understanding of what complications might occur in
of these agents more difficult their patient. It is beyond the scope of this text to discuss
all possible procedural complications. However, some
866 SECTION 3 SPECIALTY PRACTICE

TABLE 26.4
Drug–drug interactions38

DRUG INTERACTION R E S U LT MECHANISM

ANTIHYPERTENSIVE DRUGS
Propranolol Inhalation anaesthetics Bradycardia, hypotension Additive effect

Lignocaine Enhanced negative inotropic Propranolol reduces liver blood

effect flow and lignocaine clearance
Heparin Myocardial depression Heparin increases free
fatty acids, which displace
propranolol from plasma
protein binding sites, leading to
increased free propranolol
Lignocaine Non-depolarising muscle Increased duration of Synergistic effect
relaxants neuromuscular blockade
Digitalis Suxamethonium /succinylcholine Arrhythmias Direct effect or caused by
hyperkalaemia that can be
induced by succinylcholine
Thiazide diuretics Increased potassium excreted Combined effect of two drugs
by kidneys on kidneys promotes potassium
excretion
Quinidine Digitalis Can produce digitalis Decreased digitalis clearance
intoxication and increased concentration of
digitalis
Myasthenia gravis plus skeletal Postoperative respiratory Blockade of acetylcholine
muscle relaxants depression receptors at neuromuscular
postsynaptic membrane
ANTIBIOTICS

Neomycin Non-depolarising skeletal muscle Potentiate non-depolarising Neuromuscular blockade

Streptomycin relaxants muscle relaxants, respiratory caused by reduction in
Dihydrostreptomycin depression amplitude of end-plate potential
Polymyxin A
Polymxyin B
Colistin
Viomycin
Paromomycin
Kanamycin
Lincomycin
Gentamicin
Tetracycline
OPIOIDS

Morphine Inhalation anaesthetics Potentiation, respiratory and Depressant effects of inhalation

Fentanyl cardiovascular depression anaesthetics and opioids are
Sufentanil additive
Remifentanil
Pethidine/meperidine Inhalation anaesthetics Potentiation, respiratory and Depressant effects of inhalation
cardiovascular depression anaesthetics and opioids are
additive
Enovid Birth control pill potentiates Excess female sex hormones
Norinyl pethidine/meperidine with oral contraceptive therapy,
which may slow metabolism of
pethidine/meperidine
MAOI MAOI interacts with pethidine/ Type I: seizures
meperidine metabolite Type II: hypotension
 CHAPTER 26 POSTANAESTHESIA RECOVERY 867

DRUG INTERACTION R E S U LT MECHANISM

S Y M PAT H O M I M E T I C A M I N E S

Adrenaline Inhalation anaesthetics Cardiac arrhythmias Anaesthetic agents may

sensitise myocardium to
endogenous and exogenous
catecholamines
E L E C T R O LY T E S

Increased extracellular Skeletal muscle relaxants Increased resistance to Acute increase in extracellular
potassium depolarisation and greater potassium increases
sensitivity to non-depolarising end-plate transmembrane
muscle relaxants potential, thus causing
hyperpolarisation
Decreased Skeletal muscle relaxants Increased effects of Acute decrease in extracellular
extracellular depolarising muscle relaxants potassium lowers resting end-
potassium and increased resistance to plate transmembrane potential
non-depolarising muscle
relaxants
Increased calcium Non-depolarising skeletal muscle Decreased response Calcium increases release of
levels relaxants acetylcholine and enhances
excitation–contraction coupling
mechanism
Magnesium ions Muscle relaxants Potentiation Magnesium ions cause partial
muscle relaxation by blocking
release of acetylcholine
Calcium chloride Digitalis Additive effect on heart High concentrations of calcium
inhibit positive inotropic actions
of digitalis and potentiate
digitalis toxicity
MISCELLANEOUS

Furosemide Non-depolarising skeletal muscle Intensified neuromuscular block Electrolyte imbalance

Thiazide relaxants (hypokalaemia)
Ethacrynic acid
Procaine Non-depolarising and Enhanced neuromuscular Decreased end-plate potential
Lignocaine depolarising skeletal muscle blockade
relaxants
Lithium Non-depolarising and Potentiated neuromuscular Lithium ions are substituted for
depolarising skeletal muscle blockade sodium ions at presynaptic level
relaxants
Chlorpromazine Non-depolarising skeletal muscle Enhanced neuromuscular Potentiation of neuromuscular
relaxants blockade blockade
All inhalation Non-depolarising skeletal muscle Augment block in dose- Central nervous system
anaesthetics relaxants dependent manner depression or presynaptic
inhibition of acetylcholine
Insulin Corticosteroids, oral Reduction in effects Insulin antagonises effects
contraceptives, loop and thiazide
diuretics
Hydrocortisone Phenobarbital Decreased effect of the steroids Increased metabolism
Dexamethasone
Prednisone

Adapted from Nagelhout JJ. Basic principles of pharmacology. In: Odom-Forren J, ed. Perianesthesia nursing: A critical care
approach. 6th ed. St Louis: Elsevier; 2013, with permission.
868 SECTION 3 SPECIALTY PRACTICE

FIGURE 26.3 Mechanism of action for local anaesthesia.39

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Adapted from Friel CJ, Eliadi C, Pesaturo KA. Local anesthetic use in perioperative areas. Perioperative Nurs Clin 2010;5:203–14,
with permission.

examples of specific complications include: water intox- who will be caring for the patient at the time of transfer of
ication and/or sodium depletion in surgery that flushes care.The quality of the handover must be such that it allows
large amounts of saline solution or water under pressure the nurse to safely assume responsibility for the patient. It
(e.g. trans-urethral resection of the prostate [TURP], is important for nurses to understand this process, knowing
endometrial ablation); upper airway obstruction following what information needs to be gleaned from the handover
surgery under the muscle layer of the neck (thyroidec- as they accept responsibility for the patient’s care. In some
tomy, parotid cyst); postpartum haemorrhage (post lower hospitals there is also a nursing handover from the perioper-
uterine segment caesarean section) requiring assessment ative nurse that may provide information about the surgical
with fundal height measurements; specific vascular obser- procedure, dressing, drain tubes and any notable intraoper-
vations for patients following free flap surgery (deep ative events. There are a variety of different handover tools
inferior epigastric perforators [DIEP] or transverse rectus available internationally, many of which incorporate similar
abdominis myocutaneous [TRAM]), not just observing elements. For example, the SBAR mnemonic is used to
for arterial vascularity but also venous engorgement; and guide handover through discussion of the:
cervical shock in gynaecological patients that causes both Situation
a fall in blood pressure and heart rate. Background
Anaesthetic handover Assessment
Handover is an important component that will help guide Recommendation.
postoperative assessment and management. However, The Australian and New Zealand College of Anaesthetists
research suggests that postoperative patient handovers can recommended the ISOBAR acronym, which represents:
be fraught with technical and communication errors and,
Identification to ensure that the patient is correctly
if not done properly, may have potentially negative impacts
identified
for patient safety.40 There is no standardised and agreed
approach to handover; however, it is recognised that some Situation, including current clinical status and patient-
form of standard process is required.40 A formal handover centred care requirements
will be provided by the treating anaesthetist to the nurse Observations – latest observations
 CHAPTER 26 POSTANAESTHESIA RECOVERY 869

Background and history spasm with no air entry.44 Any of these problems can cause
Assessment and actions to establish an agreed life-threatening hypoxia if not rectified immediately.
management plan Some patients may leave the operating theatre with a
laryngeal mask or endotracheal tube in situ that can be
Responsibility and risk management.41 removed once they are awake and able to maintain their
Consistency in the handover method will help enhance own airway. In an intubated patient a systematic approach
its quality so it is important to know which approach is to determining whether the patient is ready to be extubated
used in your hospital. can help avoid extubation failure.45 This approach should
include assessing whether the patient is awake, cooperative
Respiratory assessment and and able to follow commands. Reversal of non-depolaris-
ing muscle relaxants should be noted and the train-of-four
management assessed if there is concern about the patient’s neuro-
Immediately after surgery patients are susceptible to events muscular function. The patient should be normothermic
that can compromise adequacy of ventilation and oxygen- and, if airway oedema is suspected, an endotracheal tube
ation, thus airway and respiratory management skills leak test should be performed where the cuff is deflated
are fundamental for nursing staff caring for this group.42 and breathing assessed prior to tube removal.
What differentiates non-critically ill postoperative patients
from other ICU patients is the residual effects of anaes- Assessment and management of
thesia medications that may include, but are not limited ventilatory capacity and oxygenation
to, narcotics, sedatives, hypnotics, inhalational gases,
muscle relaxants, intravenous fluids and blood products.42 The altered respiratory rate and depth that may occur
These medications can cause decreased rate and depth as a result of anaesthesia require focused assessment and
of breathing, which contributes to alveolar hypoventila- understanding of the ways in which anaesthetic agents can
tion and consequently results in increased levels of carbon influence both ventilator capacity and oxygenation in the
dioxide and decreased levels of oxygen in the blood.Anaes- postoperative period. For accurate assessment of respira-
thetic agents can also contribute to blunted responses to tory rate, measurement will need to be taken by observing
carbon dioxide and an overall decrease in minute venti- respirations over a 1-minute period; this process makes
lation.43 It is important to have a detailed knowledge it the vital sign that is most often neglected in clinical
and understanding of the respiratory system and how to practice.46 Recent research suggests that respiratory rate
assess the respiratory function of postanaesthesia patients. is considered an inferior vital sign to blood pressure,
For a detailed discussion of respiratory assessment and heart rate and temperature measurement.47 Inaccurate
monitoring, please refer to Chapter 13. assessment of respiratory rate continues despite recogni-
tion that it is considered to be the single most important
Assessment and management of vital sign in detecting patient deterioration.46 Assessment
of respiratory rate in the period following general anaes-
the airway thesia is of particular importance as patients may have
One of the most common complications seen in the received several pharmacological agents, including neuro-
immediate postanaesthesia period is airway obstruction.44 muscular blockade, narcotics and sedative agents, that
The depressant effects of anaesthesia can mean that the could directly influence respiratory function. Respiratory
postoperative patient is not able to protect or maintain a rate and depth directly influence minute ventilation and
patent airway. Signs that the patient might have an airway gas exchange. Capnography can be used to assess end-tidal
obstruction include increased respiratory effort, respira- carbon dioxide measurements48 and pulse oximetry can
tory muscle retraction, abnormal breath sounds and signs be used to assess oxygen saturation. More accurate and
of altered gas exchange. In many cases opening the airway detailed assessment of gas exchange requires arterial blood
by tilting the head backward and extending the neck gas analysis. Depending on the nature of the surgical
(if not contraindicated) can help restore airway patency. intervention, some patients may require a more detailed
Artificial airways may be used to prevent obstruction that respiratory assessment that incorporates inspection,
occurs when the patient’s tongue and epiglottis fall back palpation, percussion and auscultation (see Chapter 13).
on the posterior pharyngeal wall.
All airway complications are serious as they all, in
Practice tip
some way or another, obstruct the airway to varying
degrees and put the patient at risk of decreased oxygen- Following a pneumonectomy, the post-pneumonectomy
ation and possible hypoxia. These complications can space fills with air and on chest X-ray the trachea
be from an upper airway obstruction such as laryngeal should be midline. A chest tube is inserted and specific
spasm, subglottic oedema or lower airway obstruction orders on clamping and releasing the drain are given
such as bronchospasm and non-cardiogenic pulmonary by the surgeon. Unexpectedly rapid accumulation of
oedema. They may result from a simple problem, such fluid in the post-pneumonectomy space might indicate
as poor mandibular positioning where the tongue falls haemorrhage.
back obstructing the airway, to a complete laryngeal
870 SECTION 3 SPECIALTY PRACTICE

Because respiratory effort can be compromised, almost Specific assessment and management strategies for the
all postoperative patients will receive supplemental oxygen, patient with shock are provided in Chapter 21.
and with all patients the amount of oxygen received
should be guided by the patient’s clinical condition and Practice tip
assessment of arterial oxygen saturation. Oxygen therapy
helps to wash out residual anaesthetic gases and provides a Inadvertent hypothermia will cause vasoconstriction
higher concentration of inspired oxygen for patients who that may mask a low circulating blood volume.
may have residual effects of sedative and neuromuscular
blocking agents causing hypoventilation. Patients who Fluid and electrolyte balance
have had central neural blockade (epidural or spinal) or Postoperative patients are also particularly vulnerable to
regional blocks will be assessed individually for oxygen fluid and electrolyte imbalances due to the restrictions
requirements (see Chapter 13). Some patients may require on fluid and electrolytes preoperatively, fluid loss during
respiratory support in the postoperative period and will surgery, the patient’s physical status and the associated
remain intubated and ventilated for a period of time after stressors of surgery.2 The normal bodily response to the
surgery. If patients require ongoing mechanical ventilation stress of a surgical procedure is for the renal system to
they may require admission to ICU. For a detailed under- retain water and sodium.2 For these reasons, the patient
standing of patients requiring mechanical ventilation and requires a full body assessment of their fluid and electro-
ongoing respiratory support please refer to Chapter 15. lyte status.2 The primary goals of fluid management in the
Cardiovascular assessment and immediate postoperative phase are to maintain adequate
intravascular volumes, left ventricular filling pressures,
management cardiac output, blood pressure and the delivery of oxygen
When making an assessment of cardiovascular function, to the tissues.50 Normal concentrations of electrolytes and
it is worth remembering and evaluating the three vital body fluids are vital to maintain the physiological function
components of the circulatory system: the heart as a pump, of all bodily systems.50 The goals and strategies for volume
circulating blood volume and the arteriovenous system.2 replacement are patient dependent and should take into
All these factors come together to ensure adequate tissue consideration the preoperative condition of the patient,
perfusion, which is reliant on a satisfactory cardiac output.2 cardiovascular status and intraoperative fluid losses.51
In the postanaesthesia period assessment of cardiovascular
function will be frequently undertaken with monitoring Pain assessment and management
of blood pressure and heart rate. Detailed description of Experiencing postoperative pain has been found to be
cardiovascular assessment is provided in Chapter 9. the most common fear of surgical patients.52 Effective
Postoperative patients are at risk of developing cardio- pain management is considered to be both a right and
vascular complications as they will have generally had an expectation of care for all patients following surgery.53
some degree of blood loss, will have been administered Despite this, the practice of providing adequate post-
anaesthetic medications or have temperature changes that operative pain relief continues to be inadequate.52,54 Pain
may have altered vascularity. For example, central neural was once thought to be simply an unfortunate side effect
blockage will cause vascular vasodilation and interference of surgery with no detrimental effects; however, current
to the body’s sympathetic responses, which can lead to research does not support this contention.52
hypotension. Conversely, hypertension can be present Inadequate pain relief has been shown to alter the body’s
when patients experience pain. metabolic responses, which can delay recovery, extend
Hypotension can be transient or more sustained. hospital length of stay, increase morbidity rates and poten-
Transient hypotension can occur in relation to drug tially lead to the development of a chronic pain state.52
administration. Conversely, more sustained hypotension Conversely, effective pain control reduces postoperative
and the development of shock can occur in relation to complications, facilitates rehabilitation and provides a more
blood loss or from an altered distribution of flow that rapid recovery from surgery.52 For a detailed discussion
occurs secondary to sympathetic blockade and vaso- on pain assessment and pain management please refer to
dilation that can occur in regional anaesthesia. Decreased Chapter 7. More information on pain medications is also
cardiac output might be seen in some patients and could provided in Chapter 7 and earlier in this chapter in the
be related to decreased preload that occurs in hypovolae- discussion on anaesthetic drugs. Specifically, a summary of
mia or decreased cardiac output secondary to myocardial opioid analgesics is provided in Table 26.2.
injury contractility as a result of either myocardial injury It is firmly believed that adequate pain relief requires
or cardiac output and vasodilatory states.49 Shock is more than one analgesic, and this approach is referred to
characterised by a decrease in blood pressure (20–30% as ‘multimodal analgesia’.55 Specific pain management
decrease from the patient’s baseline) and an increase in techniques relevant to the postoperative period also
heart rate, and is not an uncommon occurrence in post- include a mix of narcotic and non-narcotic analgesics,
operative patients.44 Cardiovascular compromise that results patient-controlled analgesia, central neural blockade and
from blood and fluid loss can lead to hypovolaemic shock. peripheral nerve blocks.
 CHAPTER 26 POSTANAESTHESIA RECOVERY 871

A number of randomised controlled trials have been the postoperative period, with local anaesthetic agents
conducted to examine the effectiveness of intravenous having differing durations of action. Local anaesthetic
paracetamol (acetaminophen) in relieving postoperative agents with adrenaline may be given if a longer duration
pain and data suggest that it may be effective in a range of action is required.62
of inpatient and ambulatory procedures such as total
abdominal hysterectomy, tonsillectomy, caesarean section, Practice tip
joint replacement and laparoscopic cholecystectomy.56
Intravenous paracetamol may also help reduce nausea in Patients who have received a spinal blockade will have
postoperative patients.57 a greater motor block than those with an epidural. This
Tramadol is also an effective agent for pain relief. is because the local anaesthetic is injected into the
Tramadol binds to mu-opioid receptor and also inhibits the subarachnoid space with the cerebrospinal fluid where
reuptake of serotonin and noradrenaline.58 Tramadol can the spinal nerves are not myelinated, providing a denser
be administered intravenously and is also available in oral motor block.
and rectal preparations. The primary advantage of tramadol
is the relative lack of respiratory depression, an important Care of the patient following epidural or spinal
consideration in the immediate postoperative period.55 anaesthesia requires an understanding of the possible
Two categories of non-steroidal anti-inflammatory complications associated with this type of anaesthesia.
drugs (NSAIDs) are available: non-selective, which inhibit A wide range of complications can occur from minor
both COX-1 and COX-2 pathways (ibuprofen, naproxen, irritations to possibly life-threatening conditions63 and
ketorolac, diclofenac); and selective, which only inhibit include high spinal block, hypotension, bradycardia, spinal
COX-2 (celecoxib).55 All of these analgesics add to the and epidural haematoma, post-dural puncture headache,
repertoire of multimodal pain relief. nausea and vomiting, urinary retention and transient
neurological symptoms.62 In addition to normal post-
Patient-controlled analgesia operative observations, continual assessment for possible
Patient-controlled analgesia (PCA) can be effective for complications should be maintained including: observa-
many patients requiring ongoing pain relief following tion of the epidural catheter site for bleeding, catheter
surgery. The goal of PCA is to avoid the peaks and valleys migration, swelling or redness; discussion with the patient
of analgesia because the patient is able to control when regarding the onset of pain or tenderness at the catheter
pain relief is administered.59 The patient is also able to site; and protective care and observation of anaesthetised
anticipate activities such as rolling or coughing that limbs.62,63
are associated with increases in pain and is able to self- High spinal block
administer a narcotic bolus prior to the activity to manage
Assessing dermatomes after spinal and epidural anaesthesia
any pain that might occur. Following a loading dose of
is important to identify exaggerated dermatome spread that
analgesia the PCA pump is programmed based on the
can occur (Figure 26.4).64 Reduced doses of medications
patient’s needs and the pharmacokinetics of the drug
are necessary for select patients in whom a normal dose
being administered. The parameters programmed into the
might be excessive. Some patients may also experience an
PCA pump include the bolus dose and a lockout interval.
unusual sensitivity or spread of local anaesthetic, which
This allows the patient to attain immediate analgesia with
can lead to high spinal block.64 Signs and symptoms may
the lockout interval preventing acute increases in the
include dyspnoea, numbness or weakness in the upper
amount of drug delivered.60 Occasionally, patients will
extremities, nausea that often precedes hypotension and
require low-dose continuous administration through the
bradycardia.64 Blocking of the cardiac sympathetic fibres
PCA to maintain effective pain relief.59
from T1–T4 may cause loss of chronotropic and inotropic
Regional anaesthesia drive and a fall in cardiac output, which results in hypo-
Regional anaesthesia is a broad term to describe nerve tension and bradycardia.
blocks that block a region, for example arm blocks or
Practice tip
femoral blocks. Regional anaesthesia involves injecting
a local anaesthetic near major nerve bundles. To improve Elderly, pregnant, obese or very short patients may
accuracy of drug delivery selected nerves can be located have excessive dermatome spread if administered
using ultrasound guidance or a nerve stimulator.61 normal doses of spinal or epidural anaesthesia.
Central neural blockade – epidural/ Careful assessment of dermatome levels must be
spinal performed. Ice is often used to assess sensory block as
Central neural blockade or neuraxial anaesthesia is a hot and cold pass on the same pathway as pain. Central
generic term for epidural, spinal, epidural–spinal or neural blockade not only blocks sensory fibres but also
caudal anaesthesia,62 which blocks pain during a surgical motor function and sympathetic outflow. The level of
procedure. Many of the medications used in epidural or muscle block can be assessed using the Bromage score66
spinal anaesthesia can continue to provide pain relief in (Table 26.5).
872 SECTION 3 SPECIALTY PRACTICE

FIGURE 26.4 Dermatomes.65 TABLE 26.5

Modified Bromage score66
7ULIDFLDOQHUYH
SCORE CRITERIA
ILIWKFUDQLDOQHUYH &
1 Complete block (unable to move feet or knees)

&
2 Almost complete block (able to move feet only)
&
&
&
7
3 Partial block (just able to move knees)
7 7
7
7 7 4 Detectable weakness of hip flexion while supine
7 7
7
7
7 7 7
7
7
(full flexion of knees)
7
& 7 &
& 7 &
7 7 5 No detectable weakness of hip flexion while
7 7
7 7 supine
& 7 & & 7 &
7 7 7 / 7
7
/
6 Able to perform partial knee bend
/
/ /

& &
&
6
&
Note: This modified Bromage score differs from the
6
/ / 6 6 original score by including two additional criteria. The other
substantial difference is that the original Bromage score98
& & & &
6 6 began with grade I, which was free movement of legs and
/ /
feet, whereas in this modified Bromage scale score 1 is
/ /
complete block.
Adapted from Breen TW, Shapiro T, Glass B, Foster-Payne
/ /
/ / / /
D, Oriol NE. Epidural anesthesia for labor in an ambulatory
/ /
patient. Anesth Analg 1993;77(5):919–24, with permission.

6 6

6 6
These effects seem to be more pronounced in men and
urinary bladder catheterisation should be used for all but
the shortest acting blocks.64 If a patient with a central neural
Adapted from Nagelhout J, Plaus K. Nurse anesthesia.
4th ed. St Louis: Saunders; 2010, with permission.
block does not have a catheter postoperatively, close obser-
vation for urinary retention will be necessary as persistent
bladder dysfunction can also be a manifestation of serious
The level of differential blockade is judged by finding neural injury.64 The patient may not experience the
the level of sensory block with temperature sensitiv- sensation of a full bladder and, where suspected, performing
ity and recognising that the sympathetic block may be a bladder scan would be indicated. If the bladder is full and
two or more segments higher. Motor blockade will the patient is unable to void, a catheter may need to be
be approximately two segments lower.64 Sympathetic inserted until bladder muscle function returns.
cardiac accelerator fibres arise from T1–T4 (at and above
Transient neurological symptoms
mid-nipple level). Close monitoring of heart rate and
blood pressure should be initiated when the sensory In administering a spinal or epidural anaesthetic a needle
block is sitting around T6 because of the potential for passes through the skin, subcutaneous tissues, muscle and
sympathetic outflow to be blocked.64 A block at T1–T4 ligaments. It is therefore not surprising that this procedure
may produce profound bradycardia and hypotension may cause varying degrees of tissue trauma such as bruising
from arterial dilation and venous pooling.64 Conse- and localised inflammatory responses, with or without
quently, a significant fall in cardiac output may occur reflex muscle spasm. These muscle spasms may be respon-
without the body being able to compensate through sible for postoperative backache,64 which is usually mild
the usual sympathetic responses. This change in patient and self-limiting. Backache can be treated with warm/cold
condition should be treated as a medical emergency and packs or mild analgesics. Pain must be monitored carefully
treatment for shock implemented. Bradycardia can be per the chance it may be an important clinical sign of
treated with atropine and hypotension with fluid resusci- more serious complications, such as epidural haematoma
tation therapy and/or vasopressors.64 High spinal blocks and abscess.64
can affect respiratory muscles so ongoing assessment
of respiratory function should be initiated and airway
Spinal or epidural haematoma
support provided as required. Spinal and epidural haematomas are rare but devastating
complications that can occur following regional anaesthe-
Urinary retention sia. The incidence of epidural haematoma associated with
A block at the level of S2–S4 root fibres decreases urinary neuraxial anaesthesia is reported to be less than 1:150,000
bladder tone and may inhibit a patient’s ability to void, and and one in 2.2 million patients receiving spinal anaes-
epidural opioids can also interfere with normal voiding.64 thesia.67 Both epidural and spinal haematomas are more
 CHAPTER 26 POSTANAESTHESIA RECOVERY 873

likely to occur in patients who have abnormal coagulation Management of nausea and vomiting
levels, either disease-related or as a result of pharmacologi-
Postoperative nausea and vomiting (PONV) is a concern
cal therapies.64 Consequently, coagulation studies must be
for patients and clinicians alike and affects as many as
performed prior to neuraxial anaesthesia being considered
one-third of patients receiving anaesthesia. As the most
as changes in clotting profiles are an absolute contraindi-
undesirable postoperative complication, PONV also can
cation to insertion of these blocks. Clotting status must
contribute to complications such as wound dehiscence,
also be performed prior to removal of the catheter and
aspiration, increased intracranial pressure and increased
strict guidelines exist for removal in patients who are
cardiovascular demand. For some patients deep breathing,
receiving prophylactic anticoagulants,63 with recommen-
a cool cloth on the forehead and reassurance can help
dations specific to the anticoagulation medication used.
assist with nausea; however, for most postoperative
Epidural haematoma can lead to compression of
patients pharmacological interventions will be necessary.
the spinal nerves causing various degrees of irrevers-
Common pharmacological agents for the management of
ible damage. The symptoms of haematoma include
nausea and vomiting are listed in Table 26.6.
sharp back and leg pain with a motor weakness and/or
sphincter dysfunction.64 Recognition of these symptoms Thermoregulation
can be delayed until after the effect of the anaesthesia has
dissipated. In the event of such symptoms it is vital to The body has a highly sensitive system that provides a
call for immediate medical assistance. Rapid neurologi- balance between heat production and heat loss. This
cal imaging such as a computed tomography or magnetic consists of a complex feedback system that senses afferent
resonance imaging scan should be performed to assess the messages, compares them to a central integrated set-point
location, size and extent of the haematoma as neurologi- and sends reflex efferent messages to either cause vasocon-
cal outcomes are vastly improved if decompression occurs striction when the patient is cold or vasodilation when the
within 8–12 hours.64 patient is hot. Anaesthesia and the operating suite envi-
ronment provide the perfect storm for the development
Practice tip of inadvertent hypothermia with the cold environ-
ment, exposure, opened body cavities, suppression of the
Care must be taken when removing the epidural thermoregulation centre and medications that cause vaso-
catheter as up to half of reported incidents of epidural dilation. Inadvertent or unplanned hypothermia is defined
haematoma are associated with catheter removal. as a core temperature below 36°C70 and is divided into
Monitoring sensory observations after epidural removal three categories, mild (34–36°C), moderate (30–34°C)
is important to assess for complications, especially in and severe (≤30°C).71 Unlike the exposure hypothermia
those patients with abnormal clotting. discussed in Chapter 23, inadvertent or unplanned hypo-
thermia generally falls within the mild range but still has
Post-dural puncture headache devastating consequences and is associated with increased
mortality rates in postoperative patients.72 Sequelae of this
Post-dural puncture headache is not an uncommon condition may include infection, impaired wound healing,
complication of interventional neuraxial blockade68 and adverse cardiac events, altered drug metabolism, impaired
is the most common complication of spinal anaesthesia coagulation and increased postoperative discomfort.44
in the obstetric population.69 If either a spinal or epidural The pathophysiological effects of hypothermia include
needle accidentally tears the dura enough to cause a left oxyhaemoglobin shift, increased oxygen requirements
cerebrospinal fluid to leak out, this may cause a post-dural and the ability of vasoconstriction to mask a low circulat-
puncture headache. Cerebrospinal fluid is regenerated ing blood volume. Recognising these effects, nursing care
about 3 to 5 times over each day at a rate of approximately should include rewarming the patient, providing supple-
0.3 mL per minute.68 Although the exact mechanism mental oxygen and close monitoring of blood pressure
of the headache is theoretical, experts believe that there during rewarming because of the potential for the patient to
appears to be a definitive relationship between the loss of decrease their systolic blood pressure as vasoconstriction is
cerebrospinal fluid from the dural tear and the manifesta- reversed. Accurate temperature measurements reflecting the
tion of symptoms and, put very simply, fluid loss disrupts patient’s core temperature are required and rewarming with
the buoyancy of the brain.68 external warming devices can be used (see Chapter 23).
Conservative management of this condition includes
assisting the patient with full bed rest, maintaining
Practice tip
adequate hydration and assisting administering prescribed
medications such as analgesics and caffeine. An epidural During rewarming, patients with inadvertent hypo-
blood patch can be used to manage post-dural puncture thermia may initially decrease their body temperature
headaches. This is done by taking approximately 10 mL of before it starts to rise. This does not mean that the
autologous blood and injecting it into the epidural space first temperature reading was inaccurate; rather, it is
where the tear has occurred. The blood covers the area of an indication of a phenomenon called ‘after fall’ that
dural puncture and prevents further leakage of cerebro- occurs when rewarming hypothermic patients.
spinal fluid.69
874 SECTION 3 SPECIALTY PRACTICE

TABLE 26.6
Pharmacological interventions for postoperative nausea and vomiting44

DRUG (RECEPTOR D U R AT I O N COMMENTS AND

SITE AFFINITY) DOSEa OF ACTION ADVERSE EFFECTS RECOMMENDATIONS FOR USE
Droperidol Adult: 0.625–1.25 mg IV 12–24 hours Sedation, hypotension, Higher doses and doses that are
(dopamine) Paediatric: 20–50 mcg/kg EPS repeated too soon can cause
IV (children ≥2 years) sedation, EPS and QT prolongation
Prochlorperazine Adult: 5–10 mg IM or IV; 2–6 hours IV, Sedation, hypotension, Effective first-line agent
(dopamine) 25 mg PR IM, PO; EPS
Paediatric:b 0.13 mg/kg IM; 12 hours PR
0.2 mg/kg PO 2–3 times
daily; 0.1 mg/kg 3–4 times
daily PR
Promethazine Adult: 6.25–25 mg IM, IV 4 hours Sedation, hypotension, Good for patients with motion
(dopamine, or PR EPS sickness or undergoing surgery
histamine, Paediatric (≥2 years of age): affecting vestibular apparatus
acetylcholine) 0.25–0.5 mg/kg IV, IM, PRc
Diphenhydramine Adult: 12.5–50 mg IM, IV 4–6 hours Sedation, dry mouth, Good for patients with motion
(histamine, Paediatric (≥2 years of blurred vision, urinary sickness or undergoing surgery
acetylcholine) age): 1 mg/kg IV or PO retention affecting vestibular apparatus
(maximum, 25 mg for
<6 years of age)
Metoclopramide Adult: 10–20 mg IV 6–8 hours Sedation, hypotension, Increases gastric motility; good
(dopamine) Paediatric: 0.15–0.25 mg/kg EPS if nausea or vomiting is from gastric
stasis; reduce dose to
5 mg in renal impairment; consider
diphenhydramine to prevent EPS
in children
Ondansetron Adult: 4 mg IV; 4, 8 mg Up to Headache, Much more effective for vomiting
(serotonin) ODT or wafer 24 hours lightheadedness, than nausea; 2 mg may be
Paediatric: 0.05–0.1 mg/kg constipation sufficient to treat PONV in PACU
Granisetron Adult: 1 mg IV over Up to Headache, Much more effective for vomiting
(serotonin) 30 seconds 24 hours lightheadedness than nausea
Paediatric: N/A
Palonosetron Adult: 0.075 mg IV 24 hours Headache, constipation Prolonged duration of action; given
(serotonin) immediately before induction of
anaesthesia
Scopolamine Adult: 1.5 mg transdermal 72 hoursd Sedation, dry mouth, visual Good for patients with motion
(acetylcholine) patch disturbances, dysphoria, sickness or undergoing surgery
Paediatric: N/A confusion, disorientation, affecting vestibular apparatus;
hallucinations apply 4 hours before exposure
Dexamethasone Adult: 4–10 mg IV Up to Watch blood sugar in Generally well tolerated in healthy
Paediatric: 0.5–1 mg/kg 24 hours patients with diabetes; patients; may take time (hours) to
watch for fluid retention, work – administer before induction
especially in cardiac of anaesthesia
patients
Apretitant Adult: 40 mg PO 1–3 hours Up to Generally well tolerated Oral prophylaxis only; caution
before anaesthesia 24 hours with patients taking warfarin;
can reduce effectiveness of oral
contraceptives
a
Unless otherwise indicated, paediatric doses should not exceed the adult dose for each antiemetic agent.
b
Children weighing more than 10 kg or older than 2 years of age only. Change from IM to PO as soon as possible.
With administration PR, dosing interval varies from 8–24 hours depending on child’s weight.
c
Maximum of 12.5 mg in children younger than 12 years.
d
Remove after 24 hours when used to prevent or treat PONV. Instruct patient to wash the patch site and hands thoroughly.
ECG = electrocardiogram; EPS = extrapyramidal symptoms, such as motor restlessness or acute dystonia; IM = intramuscular;
IV = intravenous; ODT = orally disintegrating tablets; PACU = postanaesthesia care unit; PO = orally; PONV = postoperative nausea
and vomiting; PR = per rectum.
Adapted from: O’Brien D. Postanesthesia care complications. In: Odom-Forren J, ed. Perianaesthesia nursing: A critical care
approach. St Louis: Elsevier; 2013, with permission.
 CHAPTER 26 POSTANAESTHESIA RECOVERY 875

The postoperative bariatric patient the alveoli will collapse and desaturation will occur. By
73 sitting the patient up, the weight of the chest wall is lessened
The prevalence of obesity is increasing and therefore
allowing greater tidal volume. If the patient is hypotensive,
management of the bariatric or obese patient in the post-
a discussion with medical staff would be required to assess
operative period warrants detailed discussion. Bariatric
which problem is worse; however, the ‘banana’ position
patients undergoing anaesthesia will have particular needs
(head up and feet up) may be required. It is essential to
in the postanaesthesia period, irrespective of the surgical
provide support for positioning to ensure upright sitting
procedure. For example, the higher incidence of cardio-
position is maintained. If edentulous replace the teeth as
vascular disease means that careful electrocardiographic
these will assist in upper airway support.
monitoring should be implemented during recovery
from anaesthesia. Assessment of haemodynamic status
is important, as it is with any postoperative patient, and Assessment and management
accurate measurement of blood pressure is contingent on
the use of appropriately sized blood pressure cuffs.
of specific postoperative
Bariatric patients are also at increased risk for complications
resedation because many anaesthetic drugs are lipophilic
and metabolised more slowly by obese patients. Because of Laryngospasm
increased respiratory compromise, opioid should be used Laryngospasm is an involuntary forceful spasm of the
with caution and other pain management strategies, such laryngeal musculature that is caused by stimulation of the
as the use of non-steroidal anti-inflammatory agents, local superior laryngeal nerve.77 It is more common in young
anaesthesia or oral analgesia, should be considered.74 paediatric patients than in adults, and is most common in
Specific assessment and management relative to the infants 1–3 months old.77 Laryngeal spasm can result in
bariatric patient includes consideration for the prevention an incomplete or complete airway obstruction,78 with the
of venothromboembolism and pressure injuries. Proper latter being more uncommon. Prevention of this condition
fitting of compression stockings should be monitored includes extubating patients either deeply asleep or fully
so that a tourniquet effect of the stockings is avoided. awake (but not in between) and causes include fluid or
Knowledge of the surgical procedure and intraoperative secretions on the vocal cords.
positioning will help guide assessment of the patient for Treatment of laryngospasm includes gentle positive-
signs of intraoperative pressure injury. Intravenous access pressure ventilation, forward jaw thrust and intravenous
should be monitored closely as initiating intravenous lignocaine (1–1.5 mg/kg).79 If hypoxia develops, paralysis
access can be challenging in this patient group. with intravenous suxamethonium (0.5–1 mg/kg) or
The most important consideration in the postoperative rocuronium (0.4 mg/kg) and controlled ventilation may
period is the assessment of respiratory function. There is a be required.77
direct correlation between the degree of obesity a patient Signs and symptoms of laryngeal spasm include inspi-
suffers and the risk and rate of pulmonary complications.75 ratory stridor, dyspnoea, a distressed/sweating patient
Airway management may be difficult and hazardous due and on auscultation an upper airway noise can be heard.
to anatomical features such as a large tongue and excessive As postoperative patients generally have supplemen-
pharyngeal and palatal soft tissue impairing vision and tal oxygen, these symptoms may or may not include a
making mask ventilation awkward. decrease in oxygen saturations in mild laryngeal spasm.
The dynamics of respiration are also altered in bariatric Treatment of this condition will include sitting the patient
patients. There is a profound effect on the mechanics of up to facilitate ventilation, supplemental oxygen, gentle
the respiratory system with increased oxygen consump- suctioning of the upper airway and providing airway
tion and carbon dioxide production. Normocarbia is support as required.78 It is important to reassure the patient
maintained by an increase in minute ventilation to expel as anxiety can exacerbate the condition.
increased carbon dioxide produced through metabolic
activity of fat and the increased expenditure required Non-cardiogenic pulmonary oedema
for mobility and breathing.76 Reduction in chest wall Pulmonary oedema may be defined simply as increased
compliance also contributes to the increased work of total lung water. Non-cardiogenic pulmonary oedema
breathing. Functional residual capacity may also decline is where increased lung water occurs in the absence of
particularly if the weight of the chest wall exceeds alveolar a cardiac aetiology. In the post-anaesthesia period non-
closing capacity, which results in small airway closure, cardiogenic pulmonary oedema can occur because of
ventilation perfusion mismatch and subsequent hypoxia.76 upper airway obstruction such as laryngospasm,80
Postoperatively, decreased lung function and capacity bolus dosing with naloxone, reversal of neuromuscu-
is expected for approximately 5 days and acute airway lar blockade81 or significant hypoxia.44 In young athletic
obstruction is more likely during this period.76 males, non-cardiogenic pulmonary oedema may occur
Provided cardiovascular stability is established it may be in relation to the generation of negative intrathoracic
best to position obese patients sitting up. If the weight of pressure during an upper airway obstruction82 as the
the chest wall exceeds the closing capacity of the alveoli, diaphragm contracts against a closed or semi-closed
876 SECTION 3 SPECIALTY PRACTICE

glottis.77 The severity of pulmonary oedema corre- depend on the cause, specific symptoms and severity of
sponds to the degree to which high negative inspiratory the bronchospasm. This may include humidified oxygen,
pressures are generated.82 Symptoms usually occur within administration of a beta-2-adrenergic agonist, intubation
1 hour of the upper airway obstruction, but may present and intermittent positive pressure ventilation and perhaps
as much as 6 hours later.44 The patient may then develop antibiotics. Antihistamines and steroids may also be
sudden respiratory distress, tachypnoea, cough, shortness required.44
of breath, sudden decrease in oxygen saturation and the
classic sign of pink frothy sputum.44 Vital signs may or Aspiration pneumonitis
may not change. Mendelson syndrome, aspiration of gastric content
Rapid diagnosis and treatment are essential to alleviate that results in a severe pulmonary complication, was
this respiratory complication. Treatment of this condition first reported in 1946.83 Preoperative patient prepa-
includes providing supplemental oxygenation. Continuous ration, including fasting, is aimed at minimising the
positive airway pressure can be used and, if the patient risk of aspiration. Pregnant women, those with gastro-
requires airway management, they may be intubated and oesophageal reflux disease, obese and non-fasting patients
mechanically ventilated with positive end-expiratory are all at increased risk of aspiration pneumonitis.83
pressure.44 For further information on oxygenation and Clinical progression after aspiration varies widely,
caring for an intubated patient, please see Chapter 15. from no and very mild symptoms to bronchopneumo-
nia and possible development of acute respiratory distress
Subglottic oedema/post-intubation syndrome.83 The severity of progression is increased by
croup several factors including the aspirate pH, quantity of
Subglottic oedema or post-intubation croup is a compli- aspirate and the presence of solid particles.83 Symptoms
cation that occurs later than laryngospasm, but will almost include tachypnoea, tachycardia, cough and possible
always appear within 3 hours following extubation.77 bronchospasm.44 While this condition may be dramatic on
Although this condition can occur in adults, it is most onset it can also be insidious in nature. Bronchospasm that
commonly seen in the 1–4 year age group.44 The risk of occurs in a healthy patient should be investigated further.
developing subglottic oedema can be lessened in children
by allowing a slight gas leak around the endotracheal tube.77
Awareness under anaesthesia
Signs and symptoms of subglottic oedema include Awareness under anaesthesia results from an imbalance
inspiratory stridor, retractions, hoarseness, crowing respi- between anaesthetic need and delivery and is an uncommon
ration and a croup-like cough and a patient who is complication of anaesthesia, affecting only 0.1–0.2% of all
apprehensive and restless. Humidified oxygen may help surgical patients. Patients who have experienced awareness
reduce airway swelling and nebulised racemic adrenaline under anaesthesia report a perception of paralysis, being
can also help reduce subglottic oedema. If additional aware of conversations and surgical manipulations alongside
treatment is required, a helium–oxygen mixture can be feelings of helplessness, fear and pain. Depth of anaesthe-
used or dexamethasone administered.44 sia is assessed through monitoring of vital signs; however,
in some patients this is unreliable.84 There is growing
Bronchospasm evidence suggesting the awareness can lead to the devel-
Bronchospasm is a lower airway obstruction, character- opment of post-traumatic stress disorder,85,86 so appropriate
ised by spasmodic smooth muscle contraction that causes management of patients with this condition is essential.
narrowing of the bronchi and bronchioles.44 Generally, If a patient awakes from anaesthesia and tells you that
bronchospasm will occur in patients with a pre-existing they have suffered awareness under anaesthesia, comfort and
pulmonary illness such as asthma or chronic obstruc- support should be provided to the patient. Explain that the
tive pulmonary disease, but it may also develop in operation is over and that they are safe. The treating anaes-
healthy patients in the presence of allergy, anaphylaxis or thetist should be contacted immediately. It is important
pulmonary aspiration. For this reason, if a patient without not to dismiss the patient’s comments or contradict them
pulmonary pathology develops bronchospasm, a high in any way. Their report should be taken seriously and
degree of suspicion should be employed by the nurse to documented accurately in the patient’s notes and through
ensure that the underlying cause is not allergic or due established hospital incident reporting systems.
to pulmonary aspiration.
Signs and symptoms of bronchospasm include Emergence delirium
coughing, distinct wheeze upon auscultation, noisy Emergence delirium is a well-known phenomenon that
shallow respiration, chest retractions, use of accessory may occur in the postoperative period.87 In its milder
muscles, prolonged expiratory phase of respiration, hyper- form an awake patient may exhibit restlessness, disorienta-
tension and tachycardia. The nurse should sit the patient tion, irrational conversations and inappropriate behaviour,
up, provide assisted oxygen, call for medical assistance and and this may be referred to as emergence excitement.44
reassure the patient. Emergence delirium can also include symptoms such
Initial management of this patient will include removal as hallucinations, hypersensitivity to external stimuli
of the identified cause if possible,44 and treatment will and hyperactivity, with the patient often screaming and
 CHAPTER 26 POSTANAESTHESIA RECOVERY 877

thrashing.44,87 On assessment the patient’s eyes can appear in the time of onset and the presentation of clinical signs
glazed and they do not respond to verbal dialogue. Raised and symptoms.93
voices tend to worsen the situation so calm, confident Although most cases of malignant hyperthermia occur
reassurance is advised. within 30 minutes of anaesthesia and therefore will be seen
Children have a higher incidence, along with adults and treated in the operating suite, some patients may have
who have suffered a recent tragedy or bereavement, severe delayed symptoms up to 12 hours postoperatively.92 In some
preoperative anxiety, a history of drug dependency or circumstances the delayed onset has hindered timely recog-
psychiatric illness or who have had certain medications nition and treatment.93 Patients presenting with febrile
including ketamine, droperidol, opioids, benzodiazepines, illness after surgery should be assessed for malignant hyper-
scopolamine, atropine or large doses of metoclopramide.44 thermia. This is a particularly important consideration for
Clinical management of emergence delirium includes those patients who are discharged home after surgery but
protecting the patient from self-injury, ensuring your own re-present to the hospital emergency department.90
safety and calling for assistance. Patients should be assessed In malignant hyperthermia an intracellular skeletal
for hypoxia as a possible cause of the behaviour. If the muscle biochemical defect and exposure to trigger agents
cause of emergence delirium is known the cause should results in excessive amounts of calcium in the myoplasm
be treated. Sedation may be required.44 Clinical evidence released by the sarcoplasmic reticulum. The resultant high
also suggests that emergence delirium is increasingly seen level of calcium causes intense skeletal muscle contraction,
among military personnel who have seen active service.88 which in turn causes heat production, increased oxygen
If you have prior knowledge that a patient is prone to consumption and increased carbon dioxide production.91
emergence delirium, preparations can be made for their safe Malignant hyperthermia is a cyclic process that liberates
recovery by obtaining protective cot or bed sides to prevent heat and produces lactic acid.94 Cell membrane disruptions
injury, and ensuring appropriate human resources are lead to potassium, phosphate, magnesium and myoglobin
available to help physically manage the patient if necessary. leakage into the extracellular fluid, which results in
increased serum levels.95 Early symptoms of malignant
Practice tip hyperthermia include tachycardia, tachypnoea, sweating,
rise in end-tidal carbon dioxide levels, hyperthermia and
Postoperative delirium often lasts about 20 minutes possibly master muscle spasm.96 Treatment of malignant
with the patient eventually falling back to sleep before hyperthermia is detailed in Box 26. 2.
waking with no recollections of the incident.
BOX 26.2
Delayed emergence Management of malignant hyperthermia
Time to emerge from anaesthesia is variable between
• Stop trigger agents immediately.
patients, and may depend on a multitude of factors including
the type of anaesthesia and length of surgery.89 Occasion- • Administer 100% oxygen and hyperventilate.
ally, the time for a patient to awake may be slower than • Call for help – press emergency bell.
expected44 and this could be due to a plethora of factors.89 • Contact the operating theatre to get specialised
Delayed emergence may occur in a patient who was help from an anaesthetist.
recovering in the ICU, or may be the reason for an admission • Obtain sodium dantrolene, the treating agent, and
to ICU. The most common cause of delayed awakening is administer 2.5 mg/kg up to 10 mg/kg.
prolonged effect from anaesthesia and associated medica-
tions, but it could also be due to metabolic complications • Notify pharmacy department to replenish stores of
sodium dantrolene.
including hypoglycaemia, hyponatraemia, hypocalcaemia,
hypomagnesaemia, hypercarbia, hypoxia, hypothermia, • Use aggressive cooling to prevent the patient
hypovolaemia or neurological injury.44 The primary reaching the thermal critical level of >40.6°C.
management is always in support of airway, breathing and • Assist in associated management of arrhythmias
circulation, while the cause is sought.89 and electrolyte imbalance.

Malignant hyperthermia • Assess cardiac function, urine output and colour

(urinary catheterisation may be required).
Malignant hyperthermia is a rare, catastrophic, often fatal
syndrome that is triggered by volatile anaesthetic agents Adapted with permission from:
and suxamethonium.90 It is an autosomal dominant
Hooper VD. Care of the patient with thermal imbalance. In:
disorder of the skeletal muscle that occurs only in geneti- Odom-Forren J, ed. Perianesthesia nursing: A critical care
cally predisposed humans.90 The incidence of this disorder approach. 6th ed. St Louis: Elsevier; 2013
is thought to be somewhere between 1:3000 and 1:50,000 Hirshey Dirksen S, Van Wicklin S, Ledrut Mashman D, Neiderer
anaesthetics.91 Case fatality rate has fallen from 70% in the P, Merritt D. Developing effective drills in preparation for a
1970s to less than 10% in 2006.92 Although its pathogen- malignant hyperthermia crisis. AORN 2013;97(3):330–52.
esis is relatively well understood, there is wide variability
878 SECTION 3 SPECIALTY PRACTICE

The treating medication, dantrolene sodium, is a skeletal Transferring care of the

muscle relaxant that decreases the amount of calcium
released by the sarcoplasmic reticulum, thus reversing the postoperative patient:
pathophysiology of malignant hyperthermia. The dose of
dantrolene sodium in malignant hyperthermia is 2.5 mg/kg discharge to an inpatient ward
given intravenously, regardless of age with no upper dose Without question, the immediate postoperative period
limit.97 Dantrolene sodium when given intravenously has will require high quality, safe nursing care to detect and/
a half-life of 5 hours; some patients may require up to or prevent serious complications.101 Many factors affect
30 mg/kg over 24 hours.98 Because symptoms reoccur in the patient’s response to anaesthesia and surgery, thus the
25% of patients subsequent doses of dantrolene sodium length of stay for each patient will vary.101
are required, usually as 1 mg/kg over 6 hours for the first For this reason most PACUs have discharge criteria
24–48 hours.99, 100 that involve a thorough assessment of the patient’s vital
signs, pain, conscious state, nausea and vomiting and
Practice tip escalation of care plan prior to patient discharge from the
PACU.101 These criteria are used to determine when a
Sodium dantrolene must be reconstituted with sterile
patient is ready to be discharged to the ward and can be
water because of compatibility issues. Reconstituted
used in the ICU when non-critically ill patients are in
sodium dantrolene is very alkalotic (pH 9.5) so care must
ICU recovering from anaesthesia (Table 26.7). Critically
be taken to prevent extravasation. Patients receiving
ill postoperative patients will have their discharge managed
this drug should be monitored for thrombophlebitis.
by the ICU clinician team.

TABLE 26.7
Discharge criteria for the postoperative patient

Conscious state • Conscious and able to respond appropriately to verbal stimuli

Respiratory function • Able to protect his or her own airway
• Has a cough reflex
• Respiratory rate must be greater than 12 breaths per minute
• Oxygen saturation should be >95% on room air and assessed at least 10 minutes after
oxygen discontinued
• Need for supplemental oxygen should be determined by medical team for those patients
who do not have an oxygen saturation >95% on room air
Cardiovascular function • Vital signs need to be within normal limits and considered in relation to the patient’s
preoperative vital signs. Heart rate and blood pressure should be within 20% of
preoperative
Temperature • Patient’s core temperature should be between 36°C and 37°C
Pain • The patient should be pain free or have pain at a manageable level
Nausea and vomiting • The patient should be free from nausea and vomiting
• Patients with persistent nausea may return to the ward after liaison with medical staff and
appropriate ongoing management in place
Wound care • Dressings should be dry and intact
• Drains should be labelled with amount, date and time. Drainage should be assessed to
ensure excessive drainage is not present
• Women who have had a lower caesarean section will have their fundal height assessed.
The fundal height should be equal to or less than the level of the umbilicus
Neurological and neurovascular • Should be within normal limits
observations
Documentation • Nursing documentation completed legibly in ink
• Ensure medical staff have written up appropriate notes and orders
 CHAPTER 26 POSTANAESTHESIA RECOVERY 879

Summary
In conclusion, patients who have received anaesthesia and undergone surgical procedures are vulnerable to a multitude
of different complications. Although they may not be critically ill, patients who are transferred to the ICU immediately
following surgery require close monitoring and observation. Respect for, and knowledge and understanding of, such
complications will allow the nurse to provide a safer postoperative journey.

Case study
Mr Jones is a 62-year-old man who presented with a compound fracture of his left tibia and fibula
following a workplace fall. He has had one past anaesthetic with no untoward events and no family
history of anaesthetic complications. Due to his past history of unstable Prinzmetal angina and
COPD he is sent to