Cardiac Arrest

Cardiac Arrest
Preface
William J. Brady,
MD
Nathan P. Charlton,
Benjamin J. Lawner,
MD
DO, EMT-P
Guest Editors
Sara F. Sutherland,
MD
Medical resuscitation has been around for many thousands of years. The physician has
performed resuscitation on a multitude of patients, using many methods, in a range of
settings. Over these many millennia, the science of resuscitation has guided the clinician in the art of medical care. We have progressed from early methods, such as
hanging an inverted patient from a tree limb and using a bellows inserted into the
rectum, to more refined (and effective) contemporary interventions and strategies.
Undoubtedly, clinicians of the future will look back at us with similar disbeliefcan
you believe it.they were actually pushing on the patients chest.and shocking the
heart! Nonetheless, the science of resuscitation has progressed to the point that
we are now beginning to apply therapies, provide interventions, and offer management
strategies in an evidence-based methodstarting on the street and continuing in the
hospital. Over the past 3 decades, resuscitation science and the resultant recommendations have changed markedly, from the early use of cardioactive medications and
invasive airways to continuous chest compressions and early defibrillation.
Contemporary evidence suggests that the basic interventionsincluding appropriate
cardiopulmonary resuscitation with activation of the emergency response system,
adequate chest compressions, and early electrical defibrillationthat are provided early,
correctly, and consistently, likely impact the cardiac arrest patient most favorably.as
compared to the more advanced therapies. In fact, of the five goals noted in the American Heart Associations Guidelines 2010, three focus on such basic interventions1:

Immediate recognition and activation of the emergency response team;

Early CPR with emphasis on chest compressions;
Rapid defibrillation;
Effective advanced life support; and
Integrated postcardiac arrest care.
Interestingly, only one of these goals is listed as effective advanced life support.
And the new actor on the resuscitation stage is focused postarrest care, ranging
from the basics of optimization of oxygen, ventilation, and systemic perfusion to the
more complex therapeutic hypothermia and emergent coronary reperfusion.
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Preface
We are all involved in cardiac arrest resuscitation at a truly exciting time. We must
focus on the basics of resuscitation. These interventions are likely the most beneficial,
particularly at the early stage of arrest. The science is guiding us in that direction. We
must strive to bring this science consistently and reliably to the patients side in each
and every resuscitation. This edition of the Emergency Medicine Clinics of North
America is intended to provide a concise review of sudden cardiac arrest in all its facets of presentation and management. We hope that you, the clinician, will use it to care
for our mutual patients.
DEDICATIONS
William J. Brady: This text is written for the clinicians who stand ready 24/7/365 to
manage patients in extremis; these clinicians include law enforcement officers, fire
rescue personnel, nurses, therapists, and physicians, among many others, who
rush to the aid of others on a daily basis, often with no advanced warning and with
minimal patient information. I am honored to work with such clinicians at the University
of Virginia Medical Center and in the Thomas Jefferson EMS Region of Central Virginiamy thanks to all of you for your hard work, selfless efforts, and dedication to the
patient, oftentimes in the most extreme circumstances. I must also give thanks to
my wonderful, patient, and understanding wife, King, and my awesome children,
Lauren, Anne, Chip, and Katherineyou guys are my love and inspiration, forever
and always..the best thing that has ever happened to me.
Nathan Charlton: To Jennifer, Will, and Ben, whose patience and understanding
are truly amazing. To the residents who make work worthwhile and to my colleagues
who allow me to grow every day.
Benjamin Lawner: I would like to thank my colleagues at the University of Maryland Department of Emergency Medicine for their guidance and support, in particular,
Dr Amal Mattu. Also, any expression of gratitude would be incomplete without
mentioning my familyspecial thanks to April, Evan, and Eliot for their unconditional
patience and support.
Sara Sutherland: I would like to dedicate my work on this book to all the
bystanders and volunteer and professional EMTs who get to these patients in the first
seconds or minutes of cardiac arrest and, by doing so, allow the advanced management of these patients to result in successful outcomes. Thank You.
William J. Brady, MD
Departments of Emergency Medicine and Medicine
University of Virginia School of Medicine
Charlottesville, VA 22908, USA
Nathan P. Charlton, MD
Department of Emergency Medicine
Benjamin J. Lawner, DO, EMT-P
University of Maryland School of Medicine
110 South Paca Street, 6th Floor, Suite 200
Baltimore, MD 21201, USA
Preface
Sara F. Sutherland, MD
E-mail addresses:
WB4Z@hscmail.mcc.virginia.edu (W.J. Brady)
NPC8A@hscmail.mcc.virginia.edu (N.P. Charlton)
blawn001@umaryland.edu (B.J. Lawner)
SAO4R@hscmail.mcc.virginia.edu (S.F. Sutherland)
REFERENCE
1. Field JM, Hazinski MF, Sayre MR, et al. 2010 American Heart Association Guidelines for cardiopulmonary resuscitation and emergency cardiovascular care
science. Circulation 2010;122:S6406.
xvii
Cardiac Arrest
Introduction
In April 2011, a 51-year-old man boards a plane with his wife for a well-deserved vacation. One hour into the flight, the mans wife is yelling for a doctor. The man is slumped
over in his seat, unresponsive. Miraculously, another passenger comes to the rescue,
performs CPR, and uses the planes defibrillator to resuscitate the man to the cheers of
passengers. Approximately 22 minutes later, the flight crew safely lands the plane, and
the patient is able to thank his rescuer as he is taken to the hospital, where he fully
recovers.
Someone suffers sudden cardiac arrest in the United States, on average, once
every 90 seconds. This story is important because it shows what is possible if someone
stops to help. It so happens that the rescuer works as an RN, but it could have been
anyone.
This edition of Emergency Medicine Clinics of North America is devoted to CPR and
other adjuncts used to link the Chain of Survival and enhance survival. Readers who
have saved a life using CPR know the profound sense of awe when the power of resuscitation is witnessed and a victim survives. It is miraculous that a person, who was as
good as dead when they collapsed, rises to resume their life and experience the
second chance shared by all survivors of sudden cardiac arrest. Celebration of survival
is often fleeting, as the majority of victims of sudden cardiac arrest do not survive, even
though recent advances in the science of resuscitation have led to bold innovation that
has dramatically improved survival. Training programs in CPR were first developed in
1960 by the American Heart Association. While the 50th Anniversary of CPR was officially recognized in 2010, its origins can be traced to early recorded history.
An early recorded reference to artificial breathing appears in the book of Kings in the
Old Testament, where the prophet Elisha restored the life of a boy through a technique
that included placing his mouth on the mouth of the child, and is the earliest account of
mouth-to-mouth ventilation.1
And when Elisha was come into the house, behold, the child was dead, and laid
upon his bed. He went in therefore, and shut the door upon them twain, and
prayed unto the LORD. And he went up, and lay upon the child, and put his mouth
upon his mouth, and his eyes upon his eyes, and his hands upon his hands: and he
stretched himself upon the child; and the flesh of the child waxed warm. Then he
returned, and walked in the house to and fro; and went up, and stretched himself
upon him: and the child sneezed seven times, and the child opened his eyes.
Despite this early case report, mouth-to-mouth breathing was not officially recognized until 1740, when the Paris Academy of Sciences boldly recommended mouth-tomouth resuscitation for drowning victims, followed in 1767 when the Society for the
Recovery of Drowned Persons formed and became the first organized effort to deal
with sudden and unexpected death. In 1768, the Dutch Humane Society was founded,
in which physicians and laypersons collaborated to aid victims of drowning in the waterways. Mouth-to-mouth ventilation was systematically studied in the late 1950s and
published in several leading medical journals, leading to its widespread acceptance
and a means of ventilation support.26 In 1957, the United States military adopted the
mouth-to-mouth resuscitation method to revive unresponsive victims.
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Introduction
Devices for ventilation were developed in the early 20th century and led to the
development of negative pressure ventilators (iron lung) housed in areas of the
hospital that eventually became intensive care units. In 1952, an epidemic of poliomyelitis struck Copenhagen, which overwhelmed the supply of negative pressure ventilators. Positive pressure ventilation was developed as a substitute, and hundreds of
volunteers were able to perform manual ventilation using an airway tube with an air
reservoir. Endotracheal positive pressure ventilation eventually supplanted negative
pressure ventilation and became the standard during the 1960s.
Palpation of pulses and heartbeat as a means to assess cardiovascular status has
been used by health care providers for over 3000 years; however, descriptions of
(open chest) cardiac massage did not appear until the 19th century. In 1891, Dr Friedrich Maass described the performance of chest compressions in humans; in 1903, Dr
George Crile reported the first successful use of external chest compressions in
human resuscitation, and in 1904, the first American case of closed-chest cardiac
massage was performed by Dr George Crile. Several decades went by and in the
late 1950s, Knickerbocker, Jude, and Kouwenhoven described external cardiac
massage, or chest compressions, as a useful resuscitation technique that, in contrast
to open cardiac massage, required little technical expertise.7
In 1955, Zoll described the first successful closed-chest human defibrillation. In
1979, the first portable automatic external defibrillator (AED) was developed, followed
by the implantable defibrillator in 1981.8 The combination of airway, breathing, circulation, and defibrillation (and the telephone) led to the American Heart Association
description of the chain of survival with the four links of early access, early CPR,
early defibrillation, and early advanced cardiac life support (ACLS).
How were each of these concepts integrated into a cogent set of resuscitation
guidelines and then disseminated? By 1960, the key elements for modern day CPR
were in place, namely airway, breathing, and circulation. Lay rescuers were first
trained in 1961 in Cleveland. The first CPR guidelines were published in 1966, followed
by large-scale training sessions in Seattle in the 1970s where upwards of 100,000
people were taught to perform CPR during a single session.9 These efforts have
paid off and Seattle has enjoyed the highest survival rates following out-of-hospital
cardiac arrest in the nation.10
In 2000, the Cardiac Arrest Survival Act was passed, requiring AED programs to be
instituted in all federal buildings. In addition, the use of AEDs was added to the list of
protections under Good Samaritan laws, which were previously enacted in all 50
states to protect the lay public from liability if first aid or CPR was performed in an
emergency. Getting back to our story, the FAA required that AEDs must be carried
on commercial flights as minimum equipment, and that all members of the flight
crew be trained in their use.
Chest compression rate and depth with minimal pauses in compressions are key
determinants of return of spontaneous circulation and survival. In 2005, the benefits
of bystander CPR with minimal interruptions to chest compressions were recognized
and translated into modifications to the AHA emergency cardiovascular care (ECC)
CPR Guidelines, which has resulted in widespread improvements in survival. The
modern day success rates for survival from out-of-hospital cardiac arrest with intact
neurologic function remains highly variable with ranges from 3% to 16.3% at sites
participating in the Resuscitation Outcomes Consortium.10 The great difference in
survival rates are due to differences in incidence and risk, as well as how the community and health care system respond to cardiac arrest.
The 2010 AHA Guidelines for CPR and ECC recommend a change in the basic life
support (BLS) sequence of steps from A-B-C (Airway, Breathing, Chest compressions)
Introduction
to C-A-B (Chest compressions, Airway, Breathing) for adults, children, and infants
(excluding the newly born; see Neonatal Resuscitation section). This revolutionary
change is intended to promote bystander CPR, even by untrained lay rescuers, and
emphasizes that high-quality chest compressions alone, without intubation or supplemental ventilations, is the preferred approach to cardiac arrest resuscitation, even by
trained rescuers.
There is increasing recognition that systematic postcardiac arrest care after return
of spontaneous circulation can improve the likelihood of patient survival with good
quality of life. This recognition led to a fundamental change to the 2010 guidelines
with the addition of a fifth link to the chain of survivalcomprehensive and integrated
postarrest care. Postcardiac arrest care has significant potential to reduce early
mortality caused by hemodynamic instability and later morbidity and mortality from
multiorgan failure and brain injury.
Sudden cardiac arrest continues to be a leading cause of death in the United
States, claiming the lives of more than 300,000 people each year, with half of those
cases occurring out of hospital. While you were reading this, several people suffered
sudden cardiac arrest in the United States. In this issue of Emergency Medicine Clinics
of North America, leading experts in the field of resuscitation science share their
knowledge with the readers to improve the care provided to victims of cardiac arrest.
This comprehensive overview should prove of enormous benefit to clinicians who care
for these patients by expanding our clinical armamentarium to combat the loss of life
due to sudden cardiac arrest. It is incumbent on each of us to provide the level of
community leadership that allows for prompt action to assist those who have suffered
cardiac arrest. At least one airline passenger and his family are thankful for bystander
assistance today.
Robert E. OConnor, MD, MPH
PO Box 800699
E-mail address:
REO4X@hscmail.mcc.virginia.edu
REFERENCES
1. Scherman N, editor. 2 Kings 4:32-35. Brooklyn, NY: Mesorah Publications Ltd;

2001. p. 8867.
2. Safar P, McMahon M. Mouth-to-airway emergency artificial respiration. JAMA
1958;166:145960.
3. Safar P, Escarraga LA, Elam JO. A comparison of the mouth-to-mouth and mouthto-airway methods of artificial respiration with the chest-pressure arm-lift
methods. N Engl J Med 1958;258:6717.
4. Gordon AS, Frye CW, Gittelson L, et al. Mouth-to-mouth versus manual artificial
respiration for children and adults. JAMA 1958;167:3208.
5. Elam JO, Greene DG, Brown ES, et al. Oxygen and carbon dioxide exchange
and energy cost of expired air resuscitation. JAMA 1958;167:32834.
6. Safar P. Ventilatory efficacy of mouth-to-mouth artificial respiration. JAMA 1958;
167:33541.
7. Kouwenhoven WB, Jude JR, Knickerbocker GG. Closed-chest cardiac massage.
JAMA 1960;173:10647.
xxi
xxii
Introduction
8. Zoll PM, Linenthal AJ, Gibson W, et al. Termination of ventricular fibrillation in man
by externally applied electric countershock. N Engl J Med 1956;254:727.
9. Cobb LA, Alvarez H, Kopass MK. A rapid response system for out-of-hospital
cardiac emergencies. Med Clin North Am 1976;60:28390.
10. Nichol G, Thomas E, Callaway CW, et al. Resuscitation Outcomes Consortium
Investigators. Regional variation in out-of-hospital cardiac arrest incidence and
outcome. JAMA 2008;300(12):142331.
FURTHER READINGS
Safar P. History of cardiopulmonary cerebral resuscitation. In: Kaye W, Bircher N,

editors. Cardiopulmonary resuscitation. New York: Churchill Livingstone; 1989.
p. 153.
West JB. The physiological challenges of the 1952 Copenhagen poliomyelitis
epidemic and a renaissance in clinical respiratory physiology. J Appl Physiol
2005;99:42432.
C a rd i a c A r re s t :
A Pu b l i c H e a l t h
Perspective
Dawn Taniguchi, MDa, Amy Baernstein,
Graham Nichol, MD, MPHc,*
MD
KEYWORDS
Cardiac arrest Emergency medical services Resuscitation
Cardiac arrest describes the loss of mechanical activity of the heart as confirmed by
the absence of signs of circulation.1 Sudden cardiac death is further described as
a death from a cardiac cause within 1 hour from the onset of symptoms in a person
without any prior condition that would appear fatal.2 The World Health Organization
proposed an alternate definition based on the recognition that many cardiac arrests
are not witnessed: an unexpected, unexplained death within 1 hour of symptom onset
for witnessed events, or within 24 hours of last observed alive and symptom-free, for
unwitnessed events.3 Sudden cardiac arrest is a term commonly applied to such an
event when the patient survives.4
Episodes of cardiac arrest have multiple causes. In addition to primary cardiac
events, respiratory arrest, pulmonary embolism, trauma, cerebral events, and many
other conditions can lead to sudden unexpected death. For the purposes of surveillance, research, and treatment, it would be ideal to reserve sudden cardiac arrest
for only primary cardiac events. However, this goal is elusive. Even with a full narrative
of the death, experts often disagree on appropriate classification.5 In survivors of outof-hospital cardiac arrest, 12-lead electrocardiogram and history are poor predictors
of which patients have significant cardiac lesions at the time of emergency catheterization.6 Among victims of cardiac arrest who had high-grade coronary stenosis at
autopsy, only a small minority were previously known to have coronary heart disease.7
Classification of causes of arrest based on information acquired in-hospital is conditioned on survival to hospital, making it susceptible to selection bias. There is significant and important variation in the proportion of patients with cardiac arrest who are
treated or transported by emergency medical services (EMS) providers,8 so relying on
data from this source does not distinguish reliably among causes of cardiac arrest.
a
Department of Internal Medicine, University of Washington, 1959 NE Pacific Street, Box

356421, Seattle, WA 98195, USA
b
Department of Medicine, University of Washington, 325 Ninth Avenue, Seattle, WA 98104, USA
c
Department of Medicine, University of Washington-Harborview Center for Prehospital Emergency Care, University of Washington, Box 359727, 325 Ninth Avenue, Seattle, WA 98104, USA
* Corresponding author. Box 359727, 325 Ninth Avenue, Seattle, WA 98104.
E-mail address: nichol@uw.edu
Emerg Med Clin N Am 30 (2012) 112
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Taniguchi et al
These observations suggest that the cause of arrest can accurately be determined
only by conducting a postmortem examination.
Because it would be impractical to perform an autopsy on every fatal arrest, classification must rely on information available to paramedics in the out-of-hospital setting. For
the purpose of evaluation of prehospital emergency care of cardiac arrest, a pragmatic
alternative definition of sudden cardiac arrest9,10 includes patients with nontraumatic,
out-of-hospital cardiac arrest, who are assessed by EMS personnel and (1) receive
attempts at external defibrillation (by lay responders or emergency personnel), or receive
chest compressions by organized EMS personnel; or (2) are pulseless but do not receive
attempts to defibrillate or CPR by EMS personnel. The latter includes patients with (1)
a do not attempt resuscitation directive signed and dated by a physician, (2) extensive
history of terminal illness or intractable disease, or (3) request from the patients family.
Each of these definitions has inherent limitations. The suddenness (ie, time course)
and cause are difficult to assess because only about two-thirds of cases are witnessed and, in most cases, an autopsy is not performed. Consequently, information
from other sources is used to assess timeline and cause, including death certificates,
EMS reports, medical records, and medical examiner reports. These sources are used
independently or in combinations with each other. Information from death certificates
tends to exclude patients who are successfully resuscitated and have been found to
overestimate death by cardiac cause.11 Studies limited to patients with cardiac arrest
who are treated by EMS take into account patients who are assessed but not treated
because of futility (ie, those with late recognition of death), resulting in an underestimation of incidence and overestimation of survival relative to those that include all
patients with cardiac arrest who are assessed or treated by EMS. Surveillance using
multiple sources is needed to capture all appropriate cases of cardiac arrest.12
INCIDENCE
Incidence of disease is defined as the occurrence rate per year for the condition within
a population at risk. It is calculated by taking a ratio of the number of persons developing a disease each year divided by the population at risk. Given some of the complications with data collection described above, it is difficult to establish an accurate
incidence. The incidence of cardiac arrest treated by EMS is greater than 55 per
100,000 person-years in the United States.11 Combining information from death certificates, EMS reports and hospital record review suggests that the incidence of cardiac
arrest is 95 per 100,000 person years,10 or 8.04 per 100,000 person-years among children and 126.52 per 100,000 person-years among persons older than 20.13 Another
factor that affects incidence rates is that the number of individuals within a given
area may fluctuate by time of day and day of week. Large cities that have more people
during the working week may seem, falsely, to have a higher rate of cardiac arrest than
would be expected based on the corresponding census population.
There is virtually no data available on incidence of cardiac arrest in the developing
world.4
The incidence of cardiac arrest has markedly declined during the last 30 years
(Fig. 1).1416 This decline is correlated with a decrease in overall cardiovascular
mortality.17 The reasons for this decline are likely multifactorial, but are mostly attributed to improvements in primary and secondary prevention of coronary heart disease.
SURVIVAL
Survival is defined as the number of survivors divided by the number of individuals who
experienced the event of interest. Survival after cardiac arrest depends, in part, on the
Cardiac Arrest: A Public Health Perspective
Fig. 1. Incidence of cardiac arrest over time. (From Adabag AS, Luepker RV, Roger VL, et al.
Sudden cardiac death: epidemiology and risk factors. Nat Rev Cardiol 2010;7(4):21625; with
permission.)
population considered.18 Among 39 sites worldwide that published their outcomes

over time, median survival for all rhythm groups to hospital discharge was 6.4% (interquartile range [IQR], 3.7%10.3%).19 Among 10 sites in North American that collated
data describing patients with cardiac arrest using similar definitions contemporaneously with each other, survival for all rhythm groups to hospital discharge was median
of 8.4% (IQR, 5.4%10.4%).10 Experts have attempted to standardize reporting and
comparison of outcomes by disseminating the Utstein template for cardiac arrest.1
Despite this standardization, there is a greater than fivefold regional variation in
survival among patients with any initial rhythm, as well as among patients with ventricular fibrillation.10 This large variation reemphasizes that cardiac arrest is a treatable
condition. However, regional variation in outcome after cardiac arrest is not fully
explained by the Utstein factors, which include patient factors, such as age, gender,
and initial rhythm; and EMS factors, such as time to arrival and time to first defibrillation.20 Moreover, despite the marked decline in coronary artery disease mortality
during the last 30 years,21 few communities have been able to achieve sustained
improvements in survival after cardiac arrest.17,2224
NET BURDEN
Out-of-hospital cardiac arrest affects approximately 490,000 individuals in Europe

each year25 and approximately 350,000 individuals in the United States.10 It is the third
leading cause of death in the United States (Fig. 2; extrapolated from10 and http://
www.cdc.gov/nchs/fastats/deaths.htm, accessed March 11, 2011). The related
condition of in-hospital cardiac arrest affects approximately 200,000 individuals in
the United States (R Merchant, personal communication, March 10, 2011). Thus,
reduction of the burden of illness associated with cardiac arrest is a critical public
health issue.
NEED FOR PUBLIC HEALTH SURVEILLANCE OF CARDIAC ARREST
The true incidence of out-of-hospital cardiac arrest and survival from cardiac arrest
are unknown. Current health surveillance systems cannot accurately determine the
burden of out-of-hospital cardiac arrest, nor measure progress toward reducing this
Taniguchi et al
Fig. 2. Leading causes of death in United States.
burden. The Cardiac Arrest Registry to Enhance Survival (CARES) collates cases of
out-of-hospital cardiac arrest from participating agencies in the United States, but
includes only cases of presumed cardiac origin.26 The National EMS Information
System (NEMSIS) is an ongoing effort to create a national EMS database.27 Because
NEMSIS relies on self-report, events submitted by states do not necessarily represent
all EMS events occurring within a state and states vary in criteria used to determine the
types of EMS events submitted to the NEMSIS dataset.28 Moreover, NEMESIS has
a high rate of missing the vital data on functional status at discharge, limiting its ability
to assess the comparative effectiveness of resuscitation interventions. The International Resuscitation Network demonstrated that data related to out-of-hospital
cardiac arrest can be collated from five different countries, but does not collect
data on an ongoing basis.29 Other registries have focused on assessment of specific
resuscitation interventions (eg, European Resuscitation Council Hypothermia
Network).30 Get With the Guidelines-Resuscitation (formerly known as American Heart
Association National Registry for Cardiopulmonary Resuscitation) collates cases of inhospital cardiac or respiratory arrest from institutions that are primarily in the United
States,3134 but excludes cases of out-of-hospital cardiac arrest. Thus, although there
are several prior and existing multicenter electronic clinical databases, none comprehensively assesses the benefits and harms of emergency cardiovascular care interventions in real-world settings on an ongoing basis through the continuum of care
from EMS to hospital discharge by using a scalable, sustainable method.
Clinicians and policy makers need improved estimates of incidence to determine
the absolute clinical and public health burden of cardiac arrest. Preventive and treatment measures aimed at reducing mortality from cardiac arrest can only derive from
a reliable and valid estimate of its incidence and outcome. However, several barriers to
effective surveillance of cardiac arrest exist. A common obstacle is that EMS and
hospital systems may be reluctant to share outcome data because of concerns about
how the data will be used and potential violation of regulations that protect personal
health information. Even before the advent of the Health Insurance Portability and
Accountability Act (HIPAA), EMS providers, quality assurance staff, and researchers
often had difficulty ascertaining the functional status at hospital discharge of patients
treated by EMS. However, under HIPAA, disclosure of information is permitted under
specific circumstances, including public health disease reporting (http://www.hhs.
gov/ocr/privacy/, accessed February 24, 2011). This is a strong argument for making
cardiac arrest a reportable event.
PATIENT-LEVEL RISK FACTORS
Our understanding of why some individuals experience sudden cardiac arrest while
other clinically comparable persons do not is incomplete and contributes to the
ongoing public health challenge posed by cardiac arrest. Patient-level risk factors
include fixed and modifiable factors. Overall, about 80% of people who suffer cardiac
arrest have coronary artery disease (often undiagnosed), 10% to 15% have cardiomyopathy, and 5% to 10% have another problem, such as congenital heart disease or
primary arrhythmogenic problem (eg, long QT syndrome or Brugada syndrome).35
Fixed
The risk of cardiac arrest increases with age, peaking in people aged 75 to 84 years.
Females have a lower incidence of cardiac arrest than males.11 Genetic risk factors for
cardiac arrest include polygenetic factors that contribute to atherosclerosis, in addition to relatively rare genetic syndromes that directly cause arrhythmia such as
congenital long QT syndrome and Brugada syndrome. However, the marked reduction in the incidence of ventricular fibrillation over the last few decades15 suggests
that genetics have a relatively small contribution to population-attributable risk. It
remains unclear how to incorporate increased understanding of genetic risk into
mass screening of individuals to cardiac arrest.
Modifiable
Health behaviors affect cardiac arrest risk. Given that 80% of sudden cardiac arrest is
attributable to coronary disease, modification of risk factors, such as hypertension, diabetes, hyperlipidemia, and smoking, logically reduces both sudden and non-sudden
cardiac deaths.17 Regular exercise lowers cardiac arrest risk and can decrease
mortality in people with established cardiac disease; however, risk is acutely increased
during the period of exertion.36 This relationship may reflect the balance between
sympathetic and parasympathetic tone.
Cigarette smoking is thought to be the single most important cause of preventable
death in the United States. An estimated 443,000 persons in the United States die
prematurely each year due to exposure to tobacco smoke.37 The deleterious effects
of smoking may be mediated through increased plasma catecholamines, heart rate,
and arterial blood pressure, resulting in coronary spasm and increases in myocardial
work and oxygen supply. Collectively these effects lower ventricular fibrillation (VF)
thresholds. In patients who successfully quit smoking, rates of cardiac arrest return
to near normal over time. Of great concern is the effect of passive smoking, which
has been associated with an increase in smoking-related disease, primarily heart
disease.
People who consume a moderate amount of alcohol (26 drinks per week) have
a lower risk of sudden cardiac arrest when compared with nondrinkers. However,
heavy consumption has been associated with increased risk. The interplay between
alcohol and cardiac arrest is unclear but its protective effects are thought to be mediated via increased levels of high-density lipoprotein.38,39
Taniguchi et al
A diet that includes fatty fish is rich in n-3 polyunsaturated fatty acids and has been
associated with a lower risk of VF.40 Research suggests that the acids stabilize action
potentials by altering sodium and calcium ion channels in cardiac myocytes.
Diabetes may be a risk factor for cardiac arrest, independent of its contribution to
coronary artery disease.41,42 A proposed mechanism is abnormal prolongation of
the QT interval due to diabetic autonomic dysfunction, although this has not been
proved.43 Moderate or vigorous, but not lesser, physical exertion is associated with
increased risk of cardiac arrest.44 Acute45 and chronic46 mental health conditions
are associated with increased risk of cardiac arrest. However, it is difficult to objectively measure characteristics such as anger, anxiety, hostility, and aggressiveness
because there are many confounding issues.
Structural
Dilated or hypertrophic cardiomyopathy accounts for about 10% to 15% of cases of

cardiac arrest.35 Decreased left ventricular function, regardless of ischemic or nonischemic cause, is a strong predictor of cardiac arrest.47 Despite that severe left
ventricular dysfunction is the best available risk predictor for sudden cardiac arrest,
it was observed in less than a third of all cases in one community.48 Other structural
abnormalities, such as congenital malformations, scar from prior myocardial infarction, infiltrative diseases, and myocarditis, also predispose to cardiac arrest.49
Coronary Ischemia
Up to 71% of patients with cardiac arrest have coronary atherosclerosis and nearly half
have an acute coronary occlusion.6,50,51 Moreover, there is a high incidence (97%) of
coronary artery disease in patients resuscitated from out-of-hospital cardiac arrest
who undergo immediate angiography.6 Among these, 50% have acute coronary occlusion. However, the absence of ST elevation on a surface 12-lead ECG after resuscitation from cardiac arrest is not strongly predictive of the absence of coronary occlusion
on acute angiography. A case series of patients with unsuccessful field resuscitation
suggested that in such patients VF is more likely to be associated with coronary atherosclerosis than was asystole or pulseless electric activity.52 An autopsy study compared
case subjects who died within 6 hours of symptom onset due to ischemic heart disease
and who were not seen by a physician within 3 weeks with control subjects who died
within 6 hours of symptom onset due to natural or unnatural noncardiac causes.
Control subjects were matched to case subjects by age, gender, and socioeconomic
status.53 Intraluminal thrombosis was observed in 93% of case subjects versus 4% of
control subjects. Collectively, these studies suggest that patients who are resuscitated
from out-of-hospital VF have a high likelihood of having an acute coronary occlusion.
Medications
Medications that reduce coronary disease would logically reduce the rate of cardiac
arrest. Indeed, statins decrease mortality due to cardiac arrest,54,55 most likely acting
via anti-ischemic rather than antiarrhythmic mechanisms.56 Beta-blockers, aldosterone
antagonists, angiotensin-converting enzyme inhibitors, angiotensin receptor-blockers,
and omega-3 fatty acids may also contribute to reduced risk of cardiac arrest.57
Medications also have the potential to promote cardiac arrest. Medications that
prolong the QT interval, including antiarrhythmics, antipsychotics, and many other
classes of medications, may cause ventricular arrhythmias and, therefore, cardiac
arrest. Hypokalemia and hypomagnesemia may have the same effect. However, it is
unknown how much medication-induced or electrolyte-induced arrhythmias
contribute to the overall incidence of cardiac arrest.58
Initial Rhythm
The exact mechanism of collapse in an individual patient is often difficult to establish

because more than 40% of all cases present without prior warning59 and are not
readily under close observation. Therefore, much of what we understand is hypothesized from information obtained or observed after the event has begun. In the vast
majority of cases, individuals who suffer cardiac arrest have evidence of structural
heart disease. In general, approximately 80% have coronary atherosclerosis, another
10% to 15% have nonischemic cardiomyopathy, and the remaining 5% to 10% have
a congenital disorder or no evidence of structural disease.51 Usually this underlying
structural abnormality predisposes an individual to a fatal or near fatal arrhythmia
that is precipitated by an acute trigger, such as an ischemic event or electrolyte imbalance. The rhythm that is first recorded after the onset of cardiac arrest classified into
three categories: (1) ventricular tachyarrhythmias, including pulseless ventricular
tachycardia and VF (VT/VF); or (2) pulseless electrical activity (PEA); or (3) asystole.
Initial rhythm has a large impact on survival: published rates of survival after treatment of any initial rhythm range from 0% to greater than 20% among those with
EMS-treated arrest and 0% to 45% for those with VF arrest.11,19,60 Consistently,
survival is greatest in patients with a first-recorded rhythm of VF.61
VF is characterized by rapid, ineffective, uncoordinated movement of the ventricles
that does not produce a pulse. The ECG of VF shows measurable electrical activity
with chaotic, irregular ventricular complexes. If untreated, the electrical organization
of the ventricular fibrillation signal deteriorates into asystole over minutes.62 Coronary
ischemia is thought to be the primary precipitant of VT/VF, a correlation confirmed in
recent studies.46 The cause of PEA is diverse and related to a variety of factors,
including hypoxia, hypovolemia, electrolyte imbalance, tamponade, pneumothorax,
and thromboembolism.46
Historically, most out-of-hospital cardiac arrest cases documented VT/VF as the
first recorded rhythm. The incidence of VF has declined steadily in regions that have
tracked EMS data over 10 to 21 years.16,63,64 The decline of VF may be attributed
to treatment of cardiac risk factors, increasing rates of ICD placement, and increasing
use of beta-blockers.6466 Another possibility is that multisystem organ failure is
becoming more common and presenting frequently as non-VF cardiac arrest. This
decline is of substantial importance for public health because survival rates are significantly less for PEA compared with VT/VF.60
COMMUNITY-LEVEL RISK FACTORS
Socioeconomic and Racial Differences
Disparities in the incidence of and survival from cardiac arrest are observed across
socioeconomic gradients and between races.33,67 In New York City, for example,
a prospective study found that age-adjusted incidence of cardiac arrest was 10.1
per 10,000 for blacks and 5.8 per 10,000 for whites; survival to discharge was 1.4%
for blacks and 3.4% for whites. However, after adjustment for socioeconomic factors,
prior functional status, initial rhythm, and characteristics of the event, no significant
racial differences were found.68
Environmental
There is temporal variability in cardiac arrest frequency, with cardiac arrest peaking in
the morning and in the winter.69 Underlying patient, EMS system, and environmental
factors need to be explored to offer further insight into these observed patterns.
Various physiologic processes have been proposed to explain the diurnal
Taniguchi et al
phenomenon, such as increased clotting or increased parasympathetic instability.

Some researchers have suggested that part of the morning peak in cardiac arrest
may be due to a reporting artifact (ie, when patients die during the night but are not
discovered until early morning). Potential interventions to reduce periodic variation
in unexpected cardiac death include resource allocation of EMS and hospital
resources to match anticipated need.
A PUBLIC HEALTH APPROACH TO CARDIAC ARREST
Survival from cardiac arrest varies tremendously across communities. As noted

above, this variation is associated with variation in prehospital emergency care. There
are many ways to improve the chain of survival after cardiac arrest, including improved
communications from citizens to EMS, delivery of care to the patient, delivery of the
patient to the hospital, and delivery of cardiac and critical care. Yet few communities
have been able to achieve sustained improvements in outcome.
There is only a twofold variation in outcome after care for the related disorder of
acute myocardial infarction, but correlates of such variation have been better elucidated. These include geographic region,7072 hospital volume,73,74 urban location,75
teaching status,72,76 and safety net status.77 Variation in outcome does not seem to
associate with large differences in protocols or processes of care, such as rapid
response teams, clinical guidelines, use of hospitalists, and medication checks.78
Instead, hospitals in the top or bottom tier of risk-standardized mortality after myocardial infarction differ substantially in terms of their organizational goals and values,
senior management involvement, staff presence and expertise in care for patients
with acute myocardial infarction, communication and coordination among relevant
groups, and problem solving and learning. It has been suggested that such cultural
differences are a major factor in regional variation in outcomes after cardiac arrest.79
SUMMARY
A cardiac resuscitation system is an interconnected community, EMS, and hospital

response to out-of-hospital cardiac arrest.80 A critical component of such a response
is ongoing measurement and improvement of the process and outcome of care. Such
regional systems of care have improved provider experience and patient outcome for
other time-sensitive conditions, including ST-elevation myocardial infarction and lifethreatening traumatic injury. The time has come for us to come together to implement
such resuscitation systems of care in our communities. Interested physicians, EMS
providers, and members of the lay public have begun this process in Arizona, Minnesota, North Carolina, Pennsylvania, and Washington (www.heartrescueproject.com,
accessed March 29, 2011). Ongoing efforts and evaluation are needed in these and
other communities to ensure that public health is improved by reducing death and
disability due to cardiac arrest.
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Circulation 2010;121(5):70929.
Out-of-Hospital
Card iac A rrest
Tanner S. Boyd,
MD
a,
*, Debra G. Perina,
MD
KEYWORDS
Prehospital Out-of-hospital Cardiac arrest Resuscitation
ACCESS AND PRESENTATION
Emergency medical services (EMS) medical care has changed significantly since its
inception. Initially, ambulances functioned merely as transport vehicles. Today, EMS
has matured into an integrated part of the health care system, with the ability to provide
advanced care en-route to a hospital. Regional dispatch centers now decide which
resources should respond to an emergency call. EMS dispatchers are trained in
emergency medical dispatch techniques and can provide prearrival instructions to
bystanders, thereby expediting initial first aid and cardiopulmonary resuscitation (CPR).
Historically, much of the medical care provided by EMS grew out of traditional practice with little scientific basis. Today, in mature EMS systems, rigorous research
studies are being completed and evidence-based medicine concepts used to determine proven benefit before introduction of new procedures, drugs, and adjuncts to
out-of-hospital care. A research base for EMS practice now exists, a large component
of which is related to out-of-hospital cardiac arrest (OHCA) techniques and therapies
to improve survival. Current research is ongoing to evaluate the best treatment options
for patients with OHCA.
Emphasis is placed on layperson education and all level of provider courses to
rapidly access the emergency system in cases of OHCA to receive appropriate treatment. The patient (before arrest) or a witness or bystander must first recognize the
problem and activate the EMS system. The more rapid this activation occurs, the
more rapidly definitive care can arrive to the OHCA situation. Delays in arrival affect
ultimate outcomes. Depending on the circumstances surrounding the presentation,
delays can frequently occur. Cardiac arrests witnessed by bystanders or that which
occur in a public area result in EMS being accessed more rapidly than in an unwitnessed event.1 A Swedish study found that a period of activation of less than 4 minutes
The authors have nothing to disclose.

a
Emergency Medicine Residency, Department of Emergency Medicine, University of Virginia
School of Medicine, University of Virginia, PO Box 800699, Charlottesville, VA 22908, USA
b
Division of Prehospital Care, Department of Emergency Medicine, University of Virginia
School of Medicine, University of Virginia, PO Box 800699, Charlottesville, VA 22908, USA
* Corresponding author.
E-mail address: tanner.boyd@gmail.com
doi:10.1016/j.emc.2011.09.004
emed.theclinics.com
14
Boyd & Perina
from time of cardiac arrest to EMS activation increased the 1-month survival rate from
2.8% to 6.9% (P<.0001).2 Likewise, more rapid EMS response times3 and shorter
times to CPR initiation increase overall survival. The same conditions can also be
extrapolated to traumatic cardiac arrests as well, although outcome in such settings
is less optimal.
Delays in accessing care can also occur in patients with chest pain who are at high
risk for OHCA or in a prearrest state. One of the largest randomized trials to date
addressing delays in treatment to patients experiencing chest pain is the European
Myocardial Infarction Project.4 Collecting data from 15 European countries and
Canada between 1988 and 1992, this study found the largest delays occurred in
female patients, those older than 65 years, those who had experienced chest pain
in the previous 24 hours, and those with pulmonary edema. Characteristics of patients
with the shortest delay to summoning an ambulance included those with a history of
previous myocardial infarction (MI), those in shock, and those experiencing ventricular
fibrillation.
These factors associated with delays to EMS activation were also noted again in
numerous smaller studies with the addition of other factors such as lower socioeconomic status, a family member being present at symptom onset, and the belief that
symptoms were not severe enough to summon EMS. Some studies suggest increased
frequency of atypical symptoms in women causing a larger time gap between onset of
symptoms and access of care,5 whereas others show no gender difference at all.6 A
large Swedish study reviewing demographics of patients with acute MI over 15 years
found that before the age of 65 years, there was no gender difference in hospital delay.
However, after 65 years of age, there was an increased time delay for women.7
Adding to delay in access to care, certain populations can present without chest
pain at all and suddenly experience OHCA. Elderly and diabetic patients may have
atypical presentations of acute MI with nonspecific symptoms such as dizziness,
syncope, malaise, nausea, vomiting, or abdominal pain. Patients experiencing a significant cardiac or prearrest event may also present with congestive heart failure, hypotension, or severe respiratory distress. These presentations not only can cause delays
in access of care but also may mislead health care personnel, causing a delay in
recognition of the prearrest setting that can degenerate into OHCA if not properly
recognized and treated promptly.
Ready access to automated external defibrillator (AED) devices that can rapidly
analyze and deliver electrical shocks if indicated should also be part of the overall
community strategy to decrease delays in access to care. Strategies for optimal
survival of patients with OHCA include minimizing delays in accessing care, proper
placement of AEDs in locations where patients with OHCA may be more likely encountered, and dispatch call centers staffed by trained emergency dispatchers who use
prearrival instructions to begin bystander care and CPR before EMS arrival. Public
awareness, lay provider education campaigns, CPR AED instruction, and encouragement to use the EMS system all play important roles in the ultimate reduction in the
access to care.
DEMOGRAPHICS
It is estimated that more than 166,000 patients experience OHCA each year.8 Several
historical risk factors have been associated with OHCA. A diagnosis of congestive
heart failure carried an OHCA incidence of 21.87 per 1000 subject years, whereas
a history of diabetes mellitus, previous MI, smoking, and hypertension resulted in incidences of 13.80, 13.69, 9.18, and 7.54, respectively.9 Cardiac arrests, along with MIs
Out-of-Hospital Cardiac Arrest
and unstable angina, seem to have a circadian variation, with a morning peak after the
initiation of daily activities.10 EMS response to patients with OHCA seems to be more
frequent during this period as well.
A well-defined body of resuscitation literature has reported that survivors of cardiac
arrest have a greater chance of successful resuscitation if the presenting rhythm is
shockable and the least likelihood if the presenting rhythm is asystole. Patients with
OHCA have been reported to have initial rhythms of ventricular tachycardia, ventricular fibrillation, or a shockable rhythm as determined by an AED 23% of the time.
Another 9% of patients with OHCA had nonshockable rhythms per AED, with 40%
showing asystole, 20% pulseless electrical activity (PEA), and the final 9% being
unknown or undetermined rhythms.11 OHCA research suffered from the lack of
a consistent definition of cardiac arrest and poor reporting across EMS services until
the creation and adoption of the uniform data collection and reporting criteria, Utstein
criteria, which now allow researchers to nationally pool data and perform comparisons
across services.12 OHCA rates show a wide variation with the overall incidence calculated, using the uniform criteria, to be 95 per 100,000 subject-years.
OHCA OUTCOMES
It is estimated that more than 166,000 patients experience OHCA each year. This
public health condition has defined a research agenda to identify effective treatments
and strategies that could result in increased survival rates. Despite efforts, OHCA
survival rates remain bleak. Before adoption of the Utstein criteria, outcomes in
patients with OHCA were difficult to measure secondary to the lack of standardization
of variables between EMS systems. Some of these variables included pulse presence
on arrival to the emergency department (ED), general return of circulation, and definition of what constitutes patient survival. This inconsistency led to the 1995 adoption of
uniform definitions, data collection sets, and reporting with the use of the Utstein
criteria that has allowed greater standardization and comparison between research
studies.12 Despite this, comparison of research data is still hampered by differences
in EMS systems, response times, patient downtimes, and bystander CPR and AED
availability.
Despite research limitations, several factors seem to be associated with an
increased chance of survival in OHCA. Bystander CPR, witnessed arrest, initial presenting rhythm of ventricular fibrillation, and short response times to defibrillation
are all associated with increased survival rates.13,14 Eisenburger and colleagues15
also showed that having a cardiac arrest in a public place was an independent
predictor of improved outcome. Immediate defibrillation of patients in ventricular fibrillation results in a pulse-generating rhythm and survival to hospital discharge in 56% of
patients. This decreases, with each successive defibrillation attempt eventually reaching 6% by the third attempt. Survival rates have been shown to be at their highest if
defibrillation occurs within the first 6 minutes of cardiac arrest, decreasing as the
interval increases up to 11 minutes, and leveling off after that time.15
There is a large degree of variability reported in OHCA survival ranges, with a low of
6% and a high of 46%. However, the largest cumulative meta-analysis study to date
documented a mean survival to hospital discharge for all rhythm groups of only 7.6%
and a hospital admission rate of only 23.8%.16 This outcome variability is attributable
to the factors previously mentioned in addition to local population characteristics and
other factors. Liu and colleagues17 reported that younger age, nonwhite race, and
male gender were associated with better outcomes. Time of EMS arrival is linked to
higher survival rates, with even a 1-minute decrease in mean response times showing
15
16
Boyd & Perina
an approximate 1% (0.7%2.1% range) absolute increase in survival. In addition to

response times, decreasing overall pauses in CPR is associated with better results.18
EMS-witnessed cardiac arrests seem to have the best outcomes followed by
bystander-witnessed arrests with bystander CPR, bystander-witnessed arrests
without bystander CPR, and unwitnessed arrests.19
The benefits of advanced life support (ALS) versus basic life support (BLS) on
cardiac arrest outcomes have been questioned by some. The largest study to date,
the Ontario Prehospital Advanced Life Support study, looked at the effects of multiple
EMS variables on OHCA outcomes as ALS was phased into their EMS system. In
phase 1 of this study, age, witnessed arrest, bystander CPR, CPR by fire or police,
and short EMS response times were independently associated with survival in multivariate analysis.20 In phase 2, a target of 8 minutes was set for the time from call
receipt to response on scene with a defibrillator. Of the 1641 patients with cardiac
arrest in the study, 90% of calls met this target with a 33% improvement in overall
survival to discharge in all rhythm groups. This response time was estimated to
save an additional 21 lives at a cost of $2400 per life.14 When all patients were
analyzed, there were a total of 1391 patients who were enrolled in the defibrillation
plus BLS phase of the study and another 4247 patients enrolled in the advanced
cardiac life support (ACLS) phase. The population with ACLS had greater return of
spontaneous circulation (ROSC) rates (12.9% vs 18.0%, P<.001) and survival to
hospital admission rates (10.9% vs 14.6%, P<.001), but hospital discharge rates
were unchanged (5.0% vs 5.1%; P 5 .83). This rate led to an odds ratio of 1.1 for
ACLS relative to BLS. This rate did not relate favorably to the odds ratios of 4.4,
3.7, and 3.4 for witnessed arrest, early CPR, and early defibrillation, respectively, in
achieving meaningful impact of OHSA survival rates.21
Another study comparing prehospital ACLS in OHCA with and without intravenous
(IV) medications found no difference in ROSC, survival to hospital admission, or
hospital discharge among shockable rhythm groups. However, if the initial rhythm
was PEA or asystole, the IV group had better rates of ROSC (29% vs 11%, P<.001)
and survival to hospital admission (31% vs 16%, P<.001) but not to hospital discharge
(2% vs 3%, P 5 .65).22 This finding of lack of ALS impact on hospital discharge rates
was not supported in a meta-analysis of 37 articles from 1999 describing 39 EMS
systems and 33,124 patients. This study reported the odds ratio of survival to hospital
discharge for BLS plus defibrillation systems to be 1.71 (95% confidence interval [CI],
1.092.70; P 5 .01) for ACLS, 1.47 (95% CI, 0.892.42; P 5 .07) for 2-tiered BLS and
ALS systems, and 2.31 (95% CI, 1.473.62; P<.01) for 2-tiered BLS with defibrillation
and ALS systems. This study was not sufficiently powered to demonstrate whether 1or 2-tiered systems had better survival rates but was able to show that ALS is more
effective than BLS plus defibrillation alone.13 Regardless of whether one believes
the data showing no benefit in hospital discharge with ACLS or favors the studies
showing some improvement, both studies reported that ACLS improves survival to
hospital admission and ROSC in the out-of-hospital setting.
Hospital destination for survivors of OHCA also seems to influence outcomes. Lui
and colleagues17 reported that hospital survival rates varied among hospitals from
29% to 42% despite identical EMS treatment. Another study also showed that
outcomes at designated critical care medical centers are better.23 Callaway and
colleagues24 found that hospitals with cardiac catheterization capability that come
across at least 40 cardiac arrests per year have better outcomes, regardless of how
many beds are in the hospital or whether it is considered a teaching hospital or not.
Patients with cardiac arrests caused by ST elevation MIs who arrive at the ED with
ROSC generally have better outcomes.25 Surprisingly, higher survival rates are not
limited to urban areas alone because rural locations have also documented neurologically intact survival to hospital discharge rates as high as 22%.
When to terminate out-of-hospital resuscitation efforts is still a topic of controversy
with the wish to not prolong efforts beyond potential benefit along with the possibility of
neurologic devastation weighed against the desire to not declare death prematurely.
Concern for the safety and well-being of both EMS providers and the public because
of the rate of ambulance accidents when running with lights and sirens, benched
against the lack of proved benefit of transport of patients with OHCA without ROSC,
has led to general acceptance of termination of resuscitation efforts in the field. Multiple
rules have been validated for the termination of prehospital CPR, with the most popular
one resulted from methodology that determined only 46% of cardiac arrests needed
transportation.26 This rule states that if there is no ROSC after 3 rounds of BLS with defibrillation pauses every 1 to 2 minutes, if no shock was delivered by an AED, and if the
cardiac arrest was unwitnessed by an emergency medical technician or firefighter, then
all resuscitation efforts may be terminated.26 When validated, this rule had a sensitivity
of 57.5% to 64.4%, a specificity of 90.2% to 100.0%, and a positive predictive value of
99.5% to 100.0%.26,27 When neurologic status was factored in, this rule correctly identified 100% of those discharged with good neurologic outcome and 36% of those with
poor neurologic outcome or who did not survive.28 Although some EMS systems have
enacted this, others prefer to make decisions on a per-case basis. Individual case
factors that may lead to transportation despite this validated termination rule are airway
difficulties, persistent ventricular dysrhythmias, excessively public location, family
members who are unable to accept field termination, lack of IV cannulation, and cultural or language barriers. In addition, many emergency physicians do not feel comfortable pronouncing a PEA code in the field. Regardless of the decision to transport or
terminate efforts at the scene, family members are generally accepting of termination
in cases of unsuccessful out-of-hospital resuscitation efforts.
OHCAs can also be traumatic in origin. Patients with this condition have an
extremely high mortality rate, with survivors having significant morbidity. However,
as with medical cardiac arrests, research suggests that a small subset of these
patients can potentially benefit from timely aggressive treatment. Studies looking at
the impact of EMS care concluded that any intervention that delays a patients hospital
arrival has a negative impact on survival in the trauma patient. Although resuscitative
thoracotomy is a possibility in the setting of traumatic cardiac arrests to allow for open
cardiac massage, pericardiotomy for tamponade release, cardiac/aortic penetration
occlusion, or descending aortic cross-clamping until definitive repair, this procedure
only applies to a small subset of patients. These patients include those in arrest
less than 4 minutes before ED arrival, those with signs of life on ED arrival, or those
with suspected pericardial tamponade leading to arrest. Prognosis is dismal in those
without signs of life on ED arrival and in patients with asystolic or bradyasystolic
rhythms; resuscitative thoracotomy is generally not recommended.
RESPONSE SYSTEMS AND PROCESS
To improve cardiac arrest outcomes, each link in the chain of survival must be optimized. In the prehospital world, this optimization includes the prompt identification
of a cardiac arrest, proper dispatch of care, rapid initiation of CPR, immediate defibrillation, high-quality CPR, and rapid transport to the most appropriate hospital. Public
education campaigns continue to improve awareness of cardiac arrest signs and
symptoms, but there is little that can be done to improve outcomes unless the emergency response system is activated.
17
18
Boyd & Perina
The first person a caller speaks with when calling 911 is a trained dispatcher.
Outcomes have been shown to be better when dispatchers receive more frequent
cardiac arrest calls.29 Unfortunately, any sign of breathing, including agonal breathing,
decreases the chances that a dispatcher will recognize a cardiac arrest.30 However,
teaching dispatchers to recognize agonal breathing increases not only the detection
of cardiac arrests31 but also the frequency with which CPR instructions are given.32
To help dispatchers, computer systems have been developed to assist in the detection of OHCA. The Medical Priority Dispatch System has been shown to have a sensitivity of 76.7% and a specificity of 99.2% at detecting a cardiac arrest.33 Likewise, the
Advanced Medical Priority Dispatch System increased the number of people accurately identified as being in cardiac arrest compared with dispatchers alone.34 Despite
these guides, it is clear that these computer systems continue to misidentify patients
with OHCA, and, thus, there is still room for improvement in dispatcher detection of
cardiac arrests.
Once a cardiac arrest is identified, dispatchers can then give CPR instructions to
a bystander over the phone until further help arrives. Telephone instructions have
been shown to increase the rates of bystander CPR35 and enhance outcomes.29 A
simulation study showed that a lay volunteer, without any training in CPR, can do
compressions just as well with phone instructions as a previously trained person
without directions. This finding is easily extrapolated into the real world because
some compressions are better than no compressions. Only 2% of witnesses to a
cardiac arrest refuse to do CPR.30 When receiving instructions, directions to put the
phone down during chest compressions do not improve CPR quality.36 With the
advent of widespread cell phones, there is ongoing research using video calls to
help dispatchers aid bystanders in CPR instructions.37
Studies have also shown that the time to initiation of chest compressions is more
rapid if the caller is given hands-only instructions (ie, no rescue breaths) rather than
standard CPR instructions.38 Given the possibility that hands-only CPR could improve
outcomes, 2 recent articles in the New England Journal of Medicine compared the
new technique to standard CPR with ventilations. In one study, there was a trend,
although not statistically significant, toward increased rates of survival to hospital
discharge with hands-only CPR in the subgroups with a cardiac cause of OHCA
(15.5% vs 12.3%, P 5 .09) and with a shockable rhythm (31.9% vs 25.7%, P 5 .09).39
Another study reported a slightly more positive trend to hospital discharge (19.1% vs
14.7%, P 5 .16) but no change in 30-day mortality (8.7% vs 7.0%, P 5 .26).40 With no
apparent harm and possible benefit in providing hands-only CPR instructions, recently
released American Heart Association guidelines call for compression-only CPR in the
initial management of cardiac arrest. This recommendation is particularly relevant to
dispatcher phone instructions because of the relative ease of remotely guiding someone
through compression-only CPR.
As time to first defibrillation has been shown to positively affect outcomes in OHCA,
a variety of methods have been developed to increase the speed with which someone
in a shockable rhythm is defibrillated. The development of AEDs has given the lay
public access to easy-to-use lifesaving interventions. AEDs have been widely placed
in strategic locations, including public locations to facilitate more rapid defibrillation
of the cardiac arrest patient. In addition, law enforcement officers, firefighters, and
other first responders in many communities carry AEDs. Approximately 80% of police
departments are used as first responders to medical events; of these law enforcement
first responders, 39% carry AEDs. In general, 31% of police departments carry AEDs.41
High-quality uninterrupted chest compressions have been correlated with increased survival rates. Various devices have been created to increase the quality of
compressions. Pressure-sensing devices placed between the chest and a providers

hands give real-time feedback to improve the quality of compressions. Mechanical
devices that replace EMS providers may give more consistent compressions and
free providers for other tasks in the resuscitation process.
Another innovation in methods of CPR is the concept of cardiocerebral resuscitation
(CCR). CCR aims to improve outcomes through refocusing certain interventions in
CPR to maximize myocardial and cerebral perfusion. In CCR, chest compressions
are started immediately and continued for 200 continuous compressions. During
this time, oxygen is given via a noninvasive airway (ie, no endotracheal intubation),
and defibrillator pads are placed on the patient. The rhythm is analyzed, and, when
appropriate, a shock is given followed immediately by another interval of 200 compressions without pulse check. Epinephrine is given early, and endotracheal intubation
is delayed until after 3 rounds of chest compressions are completed.42 Some have
modified CCR by intubating earlier if the initial rhythm is not shockable.43 Although
much research is still underway regarding CCR, the early data is favorable. One study
designed as a before-and-after intervention introducing CCR into an EMS system
while all other factors remained constant reported that the rate of those who survived
to discharge increased (47% vs 20%; P = not reported) and the total number of
patients neurologically intact (39% vs 15%; P 5 not reported) increased.44 Another
study reported that the overall adjusted odds ratio of survival for CCR was 3.1 (95%
CI, 1.964.76), with some age ranges improving more than others. All age ranges
except for 70 to 79 years reached significance in their confidence intervals.45 When
the first 3 years of this data was presented in percentages, CCR showed a survival
to hospital discharge increase of 5.4% versus 1.8% (P 5 not reported).42 Despite
much promise, this new method of CPR requires further ongoing study.
When ROSC occurs, it is vital to transport the patient to the most appropriate
hospital rapidly. However, transport provides its own pitfalls to a pulseless patient still
undergoing active resuscitation. Although compression quality en-route was equivalent in one study, hands-off time increased during transport when compared with
on-scene resuscitation.44 Another study showed that the efficiency of chest compressions, relative to being on scene, were 95% in a moving ambulance and 86% in a helicopter.46 The rate and quality of chest compressions have been shown to increase as
the speed of an ambulance increased.47 Use of lights and sirens en-route to a hospital
saved a mean of 2.62 minutes, yet only 4.5% of patients received time-critical interventions, none of which occurred during the specific time saved.48 Given the risk of
priority EMS transport to both providers and the public, consideration should be given
to mitigate the use of lights as sirens unless absolutely necessary because minimal
benefit has been shown by doing so. Longer transport times were not associated
with increased survival, thereby calling for more research into bypassing smaller
hospitals and taking patients directly to a regionally designated resuscitation
hospital49,50; this issue is being thoroughly reviewed at this time with conflicting
evidence noted for and against such transportation strategies. At present, patients
who have undergone resuscitation are often taken to the closest hospital, stabilized,
and then transferred to a larger more-specialized hospital. For these interfacility transports, specialized critical care ground or air transport units are often used that include
a combination of advanced EMS providers, critical care nurses, or physicians. These
services can provide specialized care options such as vasoactive drug administration,
blood product transfusions, intra-aortic balloon pumps, ventilator management, and
so forth. Despite the criticality of the patients transported, rearrest occurs while being
transported to a tertiary care facility in a minority of patients with cardiac arrest who
have undergone resuscitation.51
19
20
Boyd & Perina
For those patients with ROSC, studies using therapeutic hypothermia have been
promising. The definitive studies were conducted in Europe and Australia with therapeutic hypothermia showing benefit for those patients presenting with ventricular
fibrillation, who remained in a coma, and who did not have persistent hypotension
while being cooled to the target range within 4 hours of ROSC.52 The current American
Heart Association consensus guidelines call for such patients to be cooled as soon as
possible but within 4 hours of ROSC to a core body temperature between 32 C and
34 C. This cooling can be accomplished on-scene or en-route by cooling of the
patient with 2 L of ice-cold normal saline or lactated Ringer solution. No studies to
date have shown that initiation of cooling by EMS improves either hospital discharge
rates or neurologic function compared with cooling after arrival in the ED.53 Further
study is needed in this regard.
SUMMARY
Despite research and advances in cardiac arrest resuscitation, outcomes have not
changed appreciatively in nearly 3 decades, remaining dismal in most areas of the
United States.16 With a renewed focus on maximizing each link in the chain of survival,
short-term outcomes (eg, ROSC and survival to hospital admission) are slowly
increasing. Education is making the public more knowledgeable and able to recognize
and provide prompt attention to patients in whom OHCA occurs. Studies bear out that
improvements in EMS dispatch, response times, and more rapid defibrillation times
have had an impact, albeit small, producing better outcomes. Standardization and
use of the Utstein criteria have allowed higher-quality research to be conducted on
patients with OHCA. Continued advancement in ACLS care gives us the hope of further improving outcomes. Regardless, further study is needed in all aspects of OHCA
treatments if we are to meaningfully improve survival of such patients. There is still
opportunity to improve each link in the OHCA chain of survival.
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24. Callaway CW, Schmicker R, Kampmeyer M, et al. Receiving hospital characteristics associated with survival after out-of-hospital cardiac arrest. Resuscitation
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25. Pleskot M, Hazukova R, Stritecka H, et al. Long-term prognosis after out-ofhospital cardiac arrest with/without ST elevation myocardial infarction. Resuscitation 2009;80(7):795804.
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26. Morrison LJ, Verbeek PR, Zhan C, et al. Validation of a universal prehospital termination of resuscitation clinical prediction rule for advanced and basic life support
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27. Morrison LJ, Visentin LM, Kiss A, et al. Validation of a rule for termination of
resuscitation in out-of-hospital cardiac arrest. N Engl J Med 2006;355(5):47887.
28. Ruygrok ML, Byyny RL, Haukoos JS, et al. Validation of 3 termination of resuscitation criteria for good neurologic survival after out-of-hospital cardiac arrest. Ann
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29. Kuisma M, Boyd J, Vayrynen T, et al. Emergency call processing and survival
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30. Bohm K, Rosenqvist M, Hollenberg J, et al. Dispatcher-assisted telephoneguided cardiopulmonary resuscitation: an underused lifesaving system. Eur J
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31. Roppolo LP, Westfall A, Pepe PE, et al. Dispatcher assessments for agonal breathing improve detection of cardiac arrest. Resuscitation 2009;80(7):
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32. Bohm K, Stalhandske B, Rosenqvist M, et al. Tuition of emergency medical
dispatchers in the recognition of agonal respiration increases the use of telephone assisted CPR. Resuscitation 2009;80(9):10258.
33. Flynn J, Archer F, Morgans A. Sensitivity and specificity of the medical priority
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36. Brown TB, Saini D, Pepper T, et al. Instructions to put the phone down do not
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37. Johnsen E, Bolle SR. To see or not to seebetter dispatcher-assisted CPR with
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38. Dorph E, Wik L, Steen PA. Dispatcher-assisted cardiopulmonary resuscitation. An
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in out-of-hospital cardiac arrest. N Engl J Med 2010;363(5):43442.
41. Hawkins SC, Shapiro AH, Sever AE, et al. The role of law enforcement agencies in
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42. Bobrow BJ, Clark LL, Ewy GA, et al. Minimally interrupted cardiac resuscitation
by emergency medical services for out-of-hospital cardiac arrest. JAMA 2008;
299(10):115865.
43. Kellum MJ, Kennedy KW, Barney R, et al. Cardiocerebral resuscitation improves
neurologically intact survival of patients with out-of-hospital cardiac arrest. Ann
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44. Olasveengen TM, Wik L, Steen PA. Quality of cardiopulmonary resuscitation
before and during transport in out-of-hospital cardiac arrest. Resuscitation
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45. Mosier J, Itty A, Sanders A, et al. Cardiocerebral resuscitation is associated with

improved survival and neurologic outcome from out-of-hospital cardiac arrest in
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47. Chung TN, Kim SW, Cho YS, et al. Effect of vehicle speed on the quality of closedchest compression during ambulance transport. Resuscitation 2010;81(7):8417.
48. Marques-Baptista A, Ohman-Strickland P, Baldino KT, et al. Utilization of warning
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50. Spaite DW, Stiell IG, Bobrow BJ, et al. Effect of transport interval on out-ofhospital cardiac arrest survival in the OPALS study: implications for triaging
patients to specialized cardiac arrest centers. Ann Emerg Med 2009;54(2):
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51. Hartke A, Mumma BE, Rittenberger JC, et al. Incidence of re-arrest and critical
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23
I n - H o s p i t a l C a rd i a c
Arre st
Peter P. Monteleone,
MD
a,
*, Christine M. Lin,
MD
KEYWORDS
Sudden cardiac arrest Hospital
In-hospital sudden cardiac arrest
Cardiopulmonary resuscitation
Cardiopulmonary resuscitation (CPR) developed in different environments from the

inpatient setting; out-of-hospital medical and traumatic cardiac arrest victims are
different from patients hospitalized with cardiac arrests, but much of the early literature focused on these outpatients.15 Resuscitation was often targeted at select populations and implemented with only specific tools and interventions. As an often-cited
1985 JAMA editorial stated, In some ways we have wandered from treating sudden
expected death to practicing universal resuscitation.6 As resuscitation has grown and
developed over decades, the patients treated, and the processes used, have grown
more complex. This complexity is shown in in-hospital sudden cardiac arrest (IHSCA),
because revolutions in modern medical practice have provided more advanced
means of treating cardiopulmonary arrest and have led to the survival of more ill,
more complicated, and more rigorously analyzed patients.
DEMOGRAPHICS
Epidemiologic analysis of sudden cardiac death is challenging. In the out-of-hospital

arena, the challenges of data derived from death-certificates, lack of rescuer experience in diagnosis, and lack of access to pre-event and postevent data are obvious.
However, when cardiac arrest occurs in the hospital, periarrest monitoring makes
epidemiologic analysis more straightforward. However, the many distinct hospital
types, patient presentations, and types of periarrest care further complicate this analysis for the inpatient.
Consider also the variable definition of sudden cardiac arrest (SCA) itself. Is SCA
defined as pulselessness developed within 2 hours of development of symptoms
leading to arrest? Twenty-four hours? What of the patient in long-term intensive
care who requires increasing doses of vasoactive medications and who develops
Department of Medicine, University of Virginia, PO Box 800136, Charlottesville, VA

22908-0136, USA
b
Department of Medicine, University of Virginia, Charlottesville, VA 22908, USA
E-mail address: ppm4u@Virginia.EDU
doi:10.1016/j.emc.2011.09.005
0733-8627/12/$ see front matter 2012 Published by Elsevier Inc.
emed.theclinics.com
26
Monteleone & Lin
pulselessness requiring CPR; is this patient experiencing SCA? Different studies have
included many different definitions ranging from patients being pulseless and apneic
to patients for whom a cardiac arrest form was filled out.7 Thus, the hospital-based
definition of SCA has many variables.
A annual rate of 370,000 and 750,000 in-hospital resuscitation attempts performed
in the United States is often cited in the literature.8,9 Although quoted frequently, this
number appears first as a contractor estimate provided in 1987,10 which highlights the
paucity of reliable data in the epidemiology of IHSCA. In 2003, the National Registry of
Cardiopulmonary Resuscitation (NRCPR) was developed as an American Heart Associationsponsored, prospective, multisite observational study of in-hospital cardiac
arrest (IHCA).11 Analysis of this dataset in 2003 reported an incidence of 0.17
(0.09) cardiac arrest events per bed per year. This rate did not vary significantly
between teaching (0.17) and nonteaching hospitals.
As of most recent analysis, in March 2010, the NRCPR has documented 49,130
pulseless cardiac arrests in all patients, visitors, employees, and staff within 366 facilities (including ambulatory care areas).12 They included in their analyses all patients
developing pulseless events warranting CPR. Mean duration of hospitalization before
an event was 151.9 hours; 31.9% (15,675) of patients had the event within 24 hours of
admission; and 23% (11,440) of patients experienced the event greater than 1 week
after hospitalization.
In this dataset, most IHSCA were experienced in men (57.5%) who were white
(69%). Mean age was 66.7 years, which does not mean that white men are at highest
risk of cardiac arrest, but only that, in the study population, IHSCA was more common
in this population (potentially because these white male patients at higher risk of
cardiac arrest were more likely to be hospitalized at the time of arrest). Forty-seven
percent (23,337) of IHSCAs occurred in intensive care units (ICUs), 2.3% (1117) in
the postanesthetic care unit/operating room, 33.9% (16,636) in general inpatient areas,
10.7% (5254) in emergency departments, and 4% (1951) in diagnostic intervention
areas. Ninety-two percent (45,216) of arrest events occurred in patients who had experienced a prior arrest. Patients in this analysis were often heavily monitored at the time
of IHSCA. Seventy-seven percent (38,180) had telemetric monitoring in place at the
time of arrest, 58.1% (28,529) had pulse oximetry monitoring, 8.4% (4133) had intraarterial catheter monitoring, and 5.0% (2428) had a pulmonary artery catheter in place.
This analysis also shows the complexity of the IHSCA population. Thirty-one percent
(15,170) of patients in the analysis had an invasive airway in place at the time of arrest;
24.9% (12,221) of the patients were on vasoactive medications; 24% (11,904) of
patients carried a diagnosis of heart failure; 42.5% (20,854) of patients had respiratory
insufficiency requiring oxygen supplementation; 32% (15,963) of patients had renal
insufficiency; and 13.1% (6,429) of patients had documented evidence of infection.
Despite the algorithmic foundation of treatments of OOHSCA and IHSCA being the
same, the two populations are different and the phenomenon of IHSCA and the treatment of the in-hospital SCA patient must be approached accordingly.
PATHOPHYSIOLOGY
Patients admitted to a hospital often suffer from multiorgan injury or multiorgan failure,
so the pathophysiology of IHSCA in these patients can be extremely complicated. The
frequency of severe pulmonary disease in admitted patients frequently leads to
a primary pulmonary cause of SCA that is not frequently seen in OOHSCA. A large
British trial characterized 11% of IHSCA as primary respiratory, 56% primary cardiac,
and 18% combined.13 In these patients, hypoxia or hypercarbia secondary to
In-Hospital Cardiac Arrest
pulmonary failure precipitated cardiac arrest rather than it being a primary cardiac
event. This pathophysiology is important because, in addition to acute cardiac life
support being provided, urgent work must also be done to correct the underlying
pulmonary pathophysiology to address the underlying respiratory process. Short of
pulmonary embolism and drowning victims, this primary respiratory cause of SCA is
seen less frequently in the OOHSCA population.
Even when the cause of SCA is primarily cardiac, the pathophysiology of IHSCA can
be complex secondary to the multiorgan dysfunction of many inpatients. In OOHSCA,
approximately 70% of primary cardiac arrest is thought to be secondary to coronary
heart disease.14 This percentage is an imperfect statistic secondary to the inability to
perfectly characterize cause of death in this patient population. Nonetheless, it shows
that a large percentage of OOHSCA is secondary to myocardial ischemia. Trauma,
primary dysrhythmia, and pulmonary embolism make up a large portion of the other
causes of OOHSCA.
In IHSCA, the frequency of multiorgan dysfunction in the inpatient population raises
a multitude of other possible causes. The distinct pathophysiologies of cardiac arrest
includes the dysrhythmia of pulseless ventricular tachycardia (VT) and ventricular fibrillation (VF), the complete electrical failure of asystole, and the electromechanical dissociation of pulseless electrical activity. In IHSCA, ventricular ectopy can be precipitated
iatrogenically by medications or therapies, by renal dysfunction and electrolyte
disarray, by hypoxia or hypoglycemia and myocyte irritability, by the catecholaminergic
state of sepsis, and so forth. Asystole can represent the end state of any of these conditions or result from overwhelming insult to the cardiac conduction system. Electromechanical dissociation can be precipitated by pulmonary embolism, massive myocardial
infarction, progressive severe heart failure, metabolic disarray, and so forth.
These variable comorbid conditions in individuals experiencing IHSCA are extremely
common. Shown repeatedly in series analyzing IHSCA, including the NRCPR dataset
as well as recent work assessing IHSCA defibrillation, are rates of respiratory insufficiency approaching 36%, renal insufficiency approaching 33%, hepatic insufficiency
7%, metabolic derangement 17%, diabetes mellitus 33%, acute stroke 4%, sepsis
11%, and malignancy 10%. This high rate of comorbidity shows the complex population of IHSCA victims.4,12
PREDICTION
As discussed later, the mortality and morbidity of IHSCA is extremely high. In the IHSCA
population, the opportunity for intensive evaluation exists before an arrest occurs. A
major goal is thus to predict which admitted patients will experience IHSCA so therapy
can be designed to prevent it. As shown by data on inpatient telemetry use, physicians
are not good at predicting which inpatients will arrest. One large study in a 5-year period
at a tertiary care Toronto hospital showed that only 20 ISCHAs occurred in telemetrically
monitored patients of the 367 cardiac arrests that occurred in 357 patients.15 Although
this dataset is imperfect evidence that the 95% of nontelemetrically monitored
patients with IHSCA were not predicted to be at high risk of IHSCA, it nonetheless
shows that there is room for improvement for health care personnel in predicting which
patients are at highest risk of IHSCA. Furthermore, among certain populations (most
notably women), the classic predictors of risk for SCA (coronary disease, structural
heart disease, and so forth) may be even less reliable for prediction.16
Furthermore, improved prediction of mortality resulting from IHSCA would not only
allow for therapeutic efforts in prevention but also in death planning when limited therapeutic options exist. The therapeutic as well as social benefit of improved mortality
27
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Monteleone & Lin
prediction for both patients and patients families would thus be enormous. However,
IHSCA mortality predictions based on clinical gestalt are no better than chance
alone.17 Multiple attempts at using multivariate analysis to develop prediction models
for mortality resulting from IHSCA have thus been developed. Perhaps the most
robust grew from the NRCPR dataset.12 This work showed that advanced age, black
race, noncardiac/nonsurgical illness, preexisting malignancy, acute stroke, trauma,
septicemia, hepatic insufficiency, patient location on a general floor or in the
emergency department, and prearrest use of vasopressors or assisted/mechanical
ventilation were independently predictive of in-hospital mortality. It also showed that
cardiac monitoring and shockable initial pulseless rhythms were strongly associated
with survival.
In general, the duration of arrest, primary rhythm, time to CPR/resuscitation, and
primary mode of arrest (respiratory vs cardiac) are the key factors that have repeatedly
been shown to influence survival after inpatient hospital cardiac arrests.18 The van
Walraven criteria for predicting patients unlikely to be discharged from hospital after
cardiopulmonary arrest were unwitnessed arrest, initial rhythm other than VF/VT,
and duration of resuscitation of more than 10 minutes.19 This collection of clinical
features has been shown in smaller institutional studies as well.20,21 However, the
most commonly cited score for predicting survival is the prearrest morbidity index,22
which lists hypotension, renal insufficiency, and age as the greatest risk factors for
poor outcome.22 In contrast, a retrospective chart review by Dancui and colleagues23
showed that length of hospitalization before the arrest event as well as increased body
mass index (BMI) were significantly correlated with survival. For patients in that study,
renal insufficiency was associated with better outcome, which was thought to be
secondary to electrolyte abnormalities being recognized sooner with appropriate
interventions made in a timely manner; a rapidly identified and correctable cause.
However, clinicians are unable to reliably predict which individuals are likely to have
a favorable outcome in a postarrest situation.
PRESENTATION
With thorough evaluation and monitoring of inpatients, as well as with the performance
of frequent assessments by nurses, physicians, and medical assistants, the ways in
which IHSCA is discovered are variable. In the NRCPR dataset, the onset of the IHSCA
was witnessed in 79.2% of instances. Pulselessness at the time of the need for CPR
being established was present 90.7% of the time and thus almost 10% of the time
a pulse was being assessed at the time of development of pulselessness.12
Equally interesting is the time of cardiac arrest occurrence during hospitalization.
The NRCPR dataset shows that approximately 32% of events occurred within 24
hours of admission, 34% of events occurred within 1 week of admission, and 23%
occurred more than 1 week after admission.12 This distribution of arrest occurrence
shows how variable the presentation of IHSCA can be, from the acute arrest of the
newly admitted patient about whom little is known and to whom little intervention
has been performed, to the patient in long-term admission who has often undergone
a multitude of tests and interventions and has nonetheless suffered IHSCA. This fact
alone speaks to the wide variety of IHSCA.
With the use of inpatient telemetry, electrophysiologic change precipitating arrest
can cause an alert even if the patient is alone. However, the question often arises
about how useful telemetric monitoring is toward early identification, and thus
treatment, of IHSCA. Schull and Redelmeier15 assessed the impact of telemetric
monitoring on mortality. Of 8932 patients admitted to telemetrically monitored
inpatient beds over 5 years, 20 suffered cardiac arrest. Of those arrests, only 56% of
the patients monitored by electrocardiogram were recognized from abnormal
signaling by the monitor. Of arresting patients, 3 survived to discharge; only 2 of these
survivors had monitor-signaled events. Among all 8932 patients evaluated, approximately 1 in 5000 were survivors of monitor-noted cardiac arrests. This finding
suggests that physicians are not accurate at predicting who will arrest and thus
who should have telemetric monitoring. It also suggests that, despite the use of telemetry monitoring, such surveillance often does not rapidly identify IHSCA. In addition,
when telemetry does detect the onset of IHSCA, it does not seem to favorably affect
mortality. Thus, although inpatient telemetry may be useful for many elements of
medical care, it does not seem to play an important role in identification and treatment
of IHSCA, or affect its outcome.
Regarding the electrocardiographic rhythm in which IHSCA presents, in the NRCPR
dataset, the first documented rhythm in patients with IHCA was asystole in 36.2%
(17,772), pulseless electrical activity (PEA) in 33.4% (16,409), VF in 13.5% (6633), and
pulseless VT in 8.5% (4198); the rhythm was not documented in 8.4% (4110) of cases.12
Thus, in this broad analysis, 22% (10,831) of patients presented with pulseless VT or VF
(ie, a rhythm warranting defibrillation). This trend has also been shown in several smaller
studies.23,24 Recent analysis of OOHSCA initial rhythms found that 26% (3336 of 12,930
patients) were found to have an initial rhythm of VF or pulseless VT.25
RESPONSE SYSTEMS AND PROCESS
In any given institution, sudden and unexpected cardiopulmonary arrests are managed
by health care teams, rather than individual health care workers. Hospitals can be
thought of as contained emergency response systems, where the chain of survival
that is critical to out-of-hospital arrests can be applied to an inpatient setting. In hospitals, cardiac arrest is a common event, with some variation resulting from the various
institutions particular inpatient populations. In general, inpatient cardiac arrests seem
to be more associated with progressive respiratory failure, circulatory shock, or both,
rather than an acute coronary event or myocardial ischemia.26 In out-of-hospital arrests,
citizen CPR and early defibrillation have been consistently shown as the most effective
interventions to increase survival.27 However, as detailed later, arrests that take place in
the in-hospital setting have their own unique challenges to overcome. Despite modern
CPR having existed for more than 40 years, the overall survival rate from in-hospital
arrests remains poor. Although approximately 45% to 50% of those who suffer an arrest
have return of spontaneous circulation (ROSC),11 combined studies in more than 40,000
patients show a survival rate to discharge of only approximately 15%.11,23
Cardiac arrest teams (CATs) often comprise trained medical, nursing, and respiratory
therapy staff. Depending on the location (teaching vs urban or rural/community hospitals), both the physician and ancillary staff can be highly variable. Some institutions
require that the CAT comprise individuals trained and continually recertified in advance
cardiac life support (ACLS) at regular intervals; other institutions only require basic life
support (BLS) knowledge for team members. Even the physical structure of an institution
can affect the structure of the CAT; if an institution has multiple buildings, the CAT leader
may be the one who mainly practices in an outpatient setting.28 In addition, rural hospitals may not have equipment or medication readily available (eg, automated external
defibrillator/defibrillator) that may be needed in a cardiopulmonary arrest.20 In these situations, the arrest often more closely follows an out-of-hospital scenario than a true IHCA.
Because teaching hospitals comprise a large number of institutions and serve
a large patient population, trainees (resident physicians) with varying levels of medical
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Monteleone & Lin
or surgical knowledge often function as team leaders on CATs. Leadership, team

management, and resource allocation are key components when managing highrisk situations such as cardiopulmonary arrest.29 However, a recent survey of internal
medicine residents has shown that almost half (48%) thought that standard training
was inadequate to effectively lead a CAT.30 In addition, ACLS training focuses on algorithms, not team management. The same survey reported that postevent feedback
was rare; qualitative studies have shown that postevent debriefing allows residents
to focus and reflect on items that may have led to improved performance30,31 with
better rates of ROSC in patients. However, when teams incorporate real-time audiovisual feedback, quality of CPR and time to ROSC improved.32 In addition, during
a cardiac arrest, rhythm interpretation is often done by the physician leader; however,
the likelihood of an inappropriate shock is greater when performed manually and the
proportion of inappropriate manual shocks was higher for resident physicians in
IHCAs than for paramedics in out-of-hospital cardiac arrests.32
Even within nonteaching institutions, there is a wide variability in physician leadership.
A simulation study has shown that, comparing teams led by general practitioners versus
hospitalists, general practitioners showed a significant difference in the time to defibrillation and administration of the first dose of epinephrine, and had lower compression
rates than those who primarily worked in a hospital setting.33 Overall, it seems that experience is a key factor, as shown by a study that showed that inexperienced providers
(those who experienced <5 cardiac arrests events per year) who were CAT leaders
were less likely to have ROSC or have the patient survive until discharge.28
It is also recognized that, even if a dedicated CAT exists within an institution, such
teams are usually not immediately available and most medical emergencies must be
managed by ad-hoc teams. It has been postulated that survival after inpatient cardiac
arrests depends more on first responders (as in the community) than on CATs,34
which, in turn, affects outcomes because, compared with preformed teams (in which
members are familiar with and work with one another), ad-hoc teams had less handson CPR time in the first 3 minutes of an event and delayed their first defibrillation with
a shockable rhythm,33 which are the 2 variables that have been proved to improve
mortality in out-of-hospital arrest situations. In addition, after-hours cardiac arrests
(evening and weekends) are associated with twice the mortality of office-hour arrests,
which is thought to be a result of both the availability and the experience of staff.35
In recent years, several institutions have developed a precardiac arrest team, or
a rapid response team (RRT). An RRT is typically a multidisciplinary team of medical,
nursing, and respiratory staff charged with the prompt evaluation, triage, and treatment
of patients with signs of clinical deterioration who are not currently being treated in an
ICU. The development of RRTs (see the article by McCURDY and colleagues elsewhere
in this issue for further exploration of this topic) has grown and reflects an increasing
interest in hospital quality outcomes. Launched in 2006, the Institute for Healthcare
Improvements 100,000 Lives Campaign has recommended that hospitals implement
RRTs as a possible strategy to reduce preventable in-hospital deaths.36 However,
despite widespread adoption, the results of studies examining RRTs and their effect
on patient outcomes and mortality are contradictory. Some studies indicate that the
presence of RRTs decreases the activation of CATs, but not the incidence of cardiac
arrest events, unplanned ICU admissions, or unexpected deaths.37 A recent metaanalysis performed in 2010 looked at 18 studies that involved nearly 1.3 million hospital
admissions; implementation of an RRT was associated with a 33.8% reduction in the
rate of cardiopulmonary arrest outside the ICU but was not associated with a lower
mortality. In the past decade, the effect of RRT implementation on hospital mortality
has shifted toward the null,38 suggesting that there may have been early bias in the
literature toward the benefit of these teams. Also, although RRT intervention may
prevent cases of cardiopulmonary arrest, it may only represent a short-term impact
in these severely ill patients and not affect long-term mortality. However, respiratory
failure and hemodynamic instability (which are often triggers for RRTs) should be recognized by CAT team members as common antecedents to IHCAs.
OUTCOMES
Multiple studies have shown institutional variation in survival after inpatient cardiac
arrest.39,40 The literature has consistently shown a high mortality (60%70%)4143 of
IHCA, although it has been shown to be lower in urban, teaching, and large hospitals.41,44 This difference in outcome is thought to be secondary to postarrest ICU care.
Nonetheless, the low survival rate to discharge is offset by most patients tending to
have good neurologic recovery. In most studies of patients after arrest, the American
Heart Associations Cerebral Performance Score (CPC) is often used to assess
a patients neurologic status. A CPC score of 1 corresponds with a normal life in which
an individual is conscious and alert, but may have some minor psychological or neurologic deficits. A CPC score of 2 is also considered a good neurologic outcome, with
which people can function in a sheltered environment and are able to perform independent activities of daily living (IADL). NRCPR data from approximately 14,000
patients has shown that most (86%) patients with a CPC score of 1 at the time of
admission had a postarrest CPC score of 1 at the time of discharge.11
A later, prospective analysis of 36,902 patients showed that 73% had a good neurologic outcome with a CPC score of 1 or 2. In addition, a favorable neurologic outcome
was significantly associated with interventions in place before arrest, witnessed/monitored status, time to defibrillation, and duration of CPR.45 One small German study of
354 patients found that almost one-third of patients who had cardiac arrests and who
survived to ICU admission were still alive 5 years after discharge.46 Given the concerns
about the rapidly aging population, a study of 956 patients at a United States teaching
hospital showed that IHCAs in octogenarians had a similar discharge rate (11%),47
suggesting that survival after an IHCA tends to have a favorable and sustained
outcome in these patients.
SUMMARY
In 1960, in a landmark article published in the Journal of the American Medical Association, Kowenhoven and colleagues48 wrote, Cardiac resuscitation after cardiac arrest
or ventricular fibrillation has been limited by the need for open thoracotomy and direct
cardiac massage. As a result of exhaustive animal experimentation . immediate resuscitative measures can now be initiated to give . adequate cardiac massage without
thoracotomy. Anyone, anywhere, can now initiate cardiac resuscitative procedures.
All that is needed are two hands. Since that time, resuscitation, which was never originally recommended for all patients, has grown into a common medical treatment.
Resuscitation from IHSCA has grown increasingly complex as a result of medicines
ability to sustain very ill patients as well as the range of interventions available to the
practitioner.
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C a rd i o p u l m o n a r y
Resuscitation Update
Joshua C. Reynolds, MDa, Michael C. Bond,
Sanober Shaikh, MDa
MD
b,
*,
KEYWORDS
Cardiopulmonary resuscitation Cardiac arrest
Chest compression
Based on extensive research into means of lowering the morbidity and mortality associated with cardiac arrest, the American Heart Association (AHA) drastically revised its
guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiovascular
care in 2010. The AHA no longer recommends rescue breathing or pulse checks by
untrained laypeople or, for trained responders, the interruption of chest compressions
to check the victims pulse. Instead, emphasis is placed on the delivery of high-quality
chest compressions and early defibrillation. Even medications (eg, epinephrine and
atropine) are no longer emphasized, because they have not been shown to improve
outcomes. This article summarizes the AHA 2010 guidelines for CPR and emergency
cardiovascular care with a discussion of the science supporting these recommendations; in certain instances, additional recommendations beyond that of the AHA are
made (Table 1).
The old mantra of A-B-C (airway, breathing, and circulation) has been replaced by
C-A-B (circulation, airway, and breathing). Delay in the start of chest compressions
is minimized by placing circulation first. Individuals who are fearful of performing
rescue breathing are more likely to start the resuscitation process if they only have
to do chest compressions.1 The C in CAB is further delineated by the four Cs
of cardiac arrest care: (1) chest compressions; (2) cardioversion and defibrillation;
(3) cooling (ie, postarrest therapeutic hypothermia); and (4) catheterization (ie, early
catheterization for all patients who have had a cardiac arrest, regardless of whether
ST segment elevation is evident on their electrocardiogram).
CIRCULATION
Circulation, specifically, high-quality chest compressions, is the most critical portion of

CPR. Chest compressions augment the cardiocerebral circulation, and any interruption in them decreases the likelihood of favorable neurologic outcomes. Cardiocerebral
a
Department of Emergency Medicine, University of Maryland Medical Center, Baltimore, MD, USA
Department of Emergency Medicine, University of Maryland School of Medicine, Baltimore,
MD, USA
* Corresponding author. 110 South Paca Street, Suite 200, 6th Floor, Baltimore, MD 21201.
E-mail address: mbond@smail.umaryland.edu
b

doi:10.1016/j.emc.2011.09.006
emed.theclinics.com
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Reynolds et al
Table 1
Major changes of the 2010 AHA cardiopulmonary resuscitation guidelines
BLS
Change
Explanation
No pulse checks
If the patient is unresponsive and has no

breathing or abnormal breathing, chest
compressions should be performed.
ABC becomes CAB
Circulation is to be addressed first with the

initiation of chest compressions.
Compression:ventilation ratio of 30:2
should be maintained after the first round
of 30 chest compressions.
Push Hard, Push Fast

(high-quality CPR is emphasized)
100 compressions/min at a depth of at least

2 inches.
Hands-only CPR for the untrained lay rescuer
Hands-only CPR is easier to perform for those

with no training and eliminates the
reluctance that individuals may have with
rescue breathing.
ACLS
Should follow all of the BLS recommendations listed above.
Atropine removed from asystole/PEA
Atropine is no longer recommended for

routine use in the management of asystole
and PEA arrest.
End-tidal carbon dioxide monitoring

of all intubated patients
A new Class 1 recommendation for all adults

who are intubated is that they have
continuous quantitative waveform
capnography for confirmation and
monitoring of endotracheal tube
placement.
Cricoid pressure is no longer recommended

for routine use
The routine use of cricoid pressure during the

placement of an endotracheal tube is no
longer recommended. Instead, it should be
used only to improve visualization of the
vocal cords.
Routine use of chronotropic drugs

is recommended for bradycardia.
For symptomatic or unstable bradycardia,

intravenous infusion of chronotropic drugs
is now recommended as an equally
effective alternative to external pacing
when atropine is not effective.
Postresuscitation therapeutic hypothermia
Postcardiac arrest care in those who have not

returned to a normal mental status should
include the initiation of therapeutic
hypothermia to optimize neurologic
recovery.
Cardiac catheterization
Patients with return of spontaneous

circulation should be considered for
urgent cardiac catheterization regardless
of whether there is ST-segment elevation
on their postresuscitation
electrocardiogram. In the field, patients
suspected of having acute coronary
syndrome should be transported to
a facility with reperfusion capabilities.
Cardiopulmonary Resuscitation Update
resuscitation represents a comprehensive strategy to maximize circulation. It emphasizes chest compressions over ventilation in patients thought to have had an arrest
from a cardiac cause.25 In patients who have experienced a primary pulmonary arrest,
rescue breathing should commence as soon as possible, but this scenario is not
common in adults. Hyperventilation and pauses in compressions to administer rescue
breathing impair cardiocerebral blood flow and are associated with increased
morbidity and mortality rates (discussed later).6
Pulse Check
Assessment of circulation traditionally begins with a pulse check. For many years,
emergency care providers have been trained to check for a carotid or femoral pulse,
because those pulses are closest to the central circulation and should be palpable at
lower arterial blood pressures. Even seasoned healthcare providers have difficulty
reliably discerning the presence of a pulse,716 and the search can become a lengthy
process.5,9,12 Laypersons are now instructed not to check for a pulse but to focus
instead on evaluating the person for other signs of life. They should assume that
a person is in cardiac arrest if he or she is unresponsive and breathing abnormally.
Healthcare providers should spend a maximum of 10 seconds searching for a pulse;
if a definitive and reliable pulse is not detected, they should begin chest compressions
immediately.17,18
Compression Technique
Chest compressions restore partial circulation to the heart and brain by building up
and maintaining coronary and cerebral perfusion pressure.18,19 The perfusion of these
two organs is critical to short-term and meaningful long-term survival. Chest compressions are deceptively difficult to deliver correctly,5,20,21 but it is imperative that they be
performed with the highest degree of perfection possible. The ideal components of
effective chest compressions and alternative methods of delivering them are discussed next.
Proper positioning of the patient and rescuer is fundamental to proper compression
delivery. The recommended position in out-of-hospital scenarios is to kneel perpendicular beside the patients torso.22 For in-hospital cardiac arrest response, the rescuer should stand beside the bed at the level of the patients torso. Patients who
have an in-hospital cardiac arrest are usually on a bed or stretcher, and the mattress
absorbs a significant amount of the force delivered. Placing a firm backboard between
the patient and the mattress minimizes this loss.2326 If possible, air-filled mattresses
should be deflated before starting compressions.27,28
Place the heel of one hand on the lower half of the sternum, with the heel of the opposite hand over top of the first.2932 In adults, depress the sternum at least 2 inches3336
and allow proper recoil before the next compression. Compression time and recoil time
should be equal, and the chest should re-expand completely before the next compression.3741 During the upstroke of compressions, the hands should be slightly removed
from the chest wall. This technique helps ensure adequate recoil. Inadequate recoil
results in higher intrathoracic pressure and an impaired hemodynamic profile (ie,
decreased coronary perfusion pressure, cardiac index, myocardial blood flow, and
cerebral perfusion).39,42
The recommended raw rate for compression delivery is at least 100 compressions
per minute. Matlock demonstrated that singing, humming, or listening to the Bee
Gees song Stayin Alive improved compliance with the 100-compressions-perminute recommendation.43 The total number of compressions per minute is a predictor
of return of spontaneous circulation (ROSC) and neurologically intact survival.44,45
37
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Reynolds et al
The best outcomes have been achieved in patients who received 68 to 89 compressions per minute after out-of-hospital arrest and at least 80 compressions per minute
after in-hospital cardiac arrest.44
The recommended compression-to-ventilation ratio is based on expert consensus
and one case series.4650 The general guideline is a ratio of 30:2 (compressions:ventilations) in adults.5156 If an advanced airway management device is in place, then two
providers can perform a combination of uninterrupted compressions and intermittent
ventilations. However, an advanced airway device should be inserted and used to
provide ventilations only after the patient has received 2 to 3 minutes of chest compressions and attempted defibrillation, if appropriate.
Barriers to Delivering Effective Chest Compressions
Every effort should be made to minimize interruptions in chest compressions.2,5760

Interruptions are common and can consume 24% to 57% of the total resuscitation
time.5,20,21,44 Even a brief pause in compressions results in a dramatic drop-off in
coronary and cerebral perfusion pressures.61 Adequate coronary perfusion washes
out inflammatory mediators and renews myocardial energy substrates. Chest compressions restore adequate coronary perfusion pressure, but they must be truly
continuous if they are to reach a threshold for successful defibrillation and resuscitation.62,63 Maintaining perfusion pressure to cerebral tissue is also vital because of the
brains extreme sensitivity to ischemic injury.
Typical advanced cardiac life support (ACLS) interventions result in numerous
pauses in chest compressions. Advanced airway management accounts for almost
25% of all interruptions, with a median duration of almost 2 minutes.64 Pulse checks
should be limited to 10 seconds. Compressions should not be stopped to check the
patients pulse unless there is some other evidence of ROSC, such as an increase
in the patients oxygenation level, as measured by pulse oximetry or end tidal carbon
dioxide (EtCO2) measurement. Pokorna and colleagues65 showed that individuals with
ROSC had a mean increase of 10 mm Hg on EtCO2 readings compared with cardiac
arrest victims who did not survive (P<.001). Measuring EtCO2 is an easy, noninvasive
way to monitor for ROSC without the need to interrupt chest compressions.
Chest compressions should be continued through defibrillation or resumed
immediately afterward without a postshock pulse check, because ROSC is not instantaneous, even after successful defibrillation.2,5760 Even the interruption in compressions while preparing for defibrillation results in a drop-off of coronary perfusion
pressure, so every effort should be made to transition seamlessly into defibrillation.61
Edelson and colleagues66 reported that the traditional method of stopping compressions, analyzing the heart rhythm, charging the defibrillator, and then delivering the
shock to the patient resulted in an average hands-off time of 14.8 seconds. When
compressions were stopped only during the rhythm analysis and shock delivery, as
recommended by the current AHA guidelines, the average hands-off time was 11.5
seconds. In accordance with the AHA guidelines, compressions were continued while
the defibrillator was charging. However, if the defibrillator was charged in anticipation
of shocking the patient, and then compressions were held for rhythm analysis and
immediate shock delivery, the average hands-off time was only 3.9 seconds. This
time could be further reduced if the providers immediately resumed compressions
after rhythm analysis. Several studies have shown that it is completely safe for a
rescuer wearing standard examination gloves to continue chest compressions during
use of a biphasic defibrillator with self-adhesive pads.67,68 Lloyd and colleagues67
reported that the average and maximal current leakages were 280 and 900 mA,
respectively, which are far less than the occupational and medical electrical safety
standards for medical equipment. Yu and colleagues68 demonstrated that these

currents can be reduced further by the use of a resuscitation blanket. The fear of
rescuers being shocked dates back to the use of older monophasic defibrillators;
recent studies demonstrate that this risk is not present with the newer biphasic
defibrillators.
Rescuer fatigue is another pitfall in delivering high-quality, continuous chest
compressions. After just 1 minute of performing CPR, the depth of compressions is
compromised. Rescuers tend not to recognize their own fatigue until after approximately 5 minutes of CPR.69 A shallow depth not only fails to generate adequate coronary perfusion pressure but also leads to inadequate chest recoil. Incomplete recoil
further compromises coronary perfusion pressure and adversely increases intrathoracic pressure.40,70 Providers delivering chest compressions should rotate every
2 minutes to minimize the effects of rescuer fatigue, and the switch should take less
than 5 seconds. One technique to minimize the interruption is to position a rescuer
on either side of the patient for more seamless transitions.
Hands-only CPR
Minimizing interruptions in chest compressions is paramount to restoring circulation

to the heart and brain. Hands-only CPR removes many of the barriers to delivering
effective chest compressions.71 The performance of hands-only CPR allows the
rescuer to focus solely on compression technique. Ventilations are often not necessary during the first few minutes of resuscitation, because blood oxygen levels usually
remain adequate for several minutes after a cardiac arrest from a nonrespiratory
cause.1 The acceptable duration is not known. Agonal gasping and chest wall recoil
may provide some amount of passive ventilation and oxygenation during handsonly CPR.
This simplified version of conventional CPR is easier for laypersons, who are often
reluctant to perform mouth-to-mouth resuscitation for fear of acquiring a communicable disease.72,73 Hands-only CPR has better patient outcomes than no CPR and
outcomes similar to those achieved with conventional CPR.7478
Alternative CPR Techniques
Many alternative techniques of CPR have been documented in the literature, with
mixed evidence of effectiveness. High-frequency chest compressions are delivered
at a rate exceeding 120 per minute but are otherwise similar to conventional chest
compressions.79 Two clinical trials demonstrated improved hemodynamic profiles
generated by rapid compressions but not improved patient outcome.80,81 There is
insufficient evidence to recommend the routine use of this technique.
Open-chest CPR with direct cardiac massage is typically used after cardiac arrest
from a traumatic chest injury. Case series of open-chest CPR for nontraumatic cardiac
arrest in inpatients after cardiac surgery8284 and out-of-hospital cardiac arrest8386
revealed improved coronary perfusion pressure and ROSC compared with conventional (closed-chest) CPR. There is insufficient evidence to recommend routine use
of this technique, but it may be used if the chest is already open (ie, intraoperatively)
or cardiac arrest occurs soon after thoracotomy or laporatomy.
Interposed abdominal compression (IAC) is another strategy that has been proposed to increase cardiocerebral perfusion. IAC requires three providers and involves
alternating chest compressions with abdominal compressions.85 The first provider
performs conventional chest compressions, while the second compresses the
abdomen with similar hand position and depth midway between the xiphoid process
and umbilicus during chest wall recoil. The third provider delivers intermittent
39
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Reynolds et al
ventilation, typically via an advanced airway management device. IAC improves the
diastolic aortic pressure and venous return, which results in higher coronary perfusion
pressure. Two randomized controlled trials (by the same author) of in-hospital cardiac
arrest demonstrated improved survival compared with conventional CPR,86,87 but
a randomized controlled trial of out-of-hospital cardiac arrest patients showed no
benefit with this technique.88 The only published complication of IAC CPR is traumatic
pancreatitis in a child.89 This technique could be considered for victims of in-hospital
cardiac arrest if a sufficient number of trained providers are present. An external study
to validate the findings of the two original studies is needed before this technique can
be recommended for routine use.
A precordial thump is a forceful striking of the anterior chest wall, which is used to
mechanically stun the myocardium to convert a ventricular tachyarrhythmia into a perfusable rhythm.90 Case reports and case series demonstrate mixed effectiveness for
this maneuver.90100 It has been associated with sternum fracture, osteomyelitis,
stroke, and adverse arrhythmias.98100 The precordial thump technique is not recommended for unwitnessed cardiac arrests, but it may be considered for witnessed,
monitored, unstable ventricular tachycardia (VT) if a defibrillator is not immediately
available and if it does not delay conventional resuscitation.1
Percussion pacing, an extension of the precordial thump, is essentially rhythmic
percussion of the chest wall with a fist to pace the myocardium. Several case reports
and small case series have documented successful resuscitation with this technique,
but there is insufficient evidence to support its routine use.101107
DEFIBRILLATION
Early defibrillation is critical to survival after sudden cardiac arrest (SCA). The most
frequent initial rhythm in out-of-hospital witnessed SCA is ventricular fibrillation (VF),
and the chance of successful defibrillation diminishes rapidly over time.108110 ACLS
protocols continue to stress the importance of early defibrillation for the unstable
rhythms of VF and pulseless VT.111
CPR Before Defibrillation
The rate of survival-to-hospital discharge is higher among patients who experienced

an unwitnessed SCA and received 1.5 to 3 minutes of CPR followed by defibrillation.112,113 In witnessed SCA, early defibrillation is imperative; CPR should be performed while the defibrillator is being prepared. Chest compressions increase the
myocardial readiness for the defibrillation by delivering oxygen and metabolic
substrates.20 Patients who receive early defibrillation have a higher likelihood of
survival and of return to their prearrest quality of life.114 Every minute that a patient
remains in VF/pulseless VT arrest decreases the chance of survival by 10%.115
Hands-on Defibrillation
Minimizing interruptions during chest compressions improves the likelihood of ROSC.

In the past, hands-off time during defibrillation was thought to be unavoidable, given
the need to prevent electrocution of the rescuer during shock delivery. However,
studies have affirmed that it is extremely safe to continue compressions during defibrillation when a biphasic defibrillator is used with self-adhesive electrodes and the
rescuer wears standard examination gloves.67,68 The simulated rescuers in these
studies perceived no electrical charge, despite voltage delivery during the compressions. Therefore, uninterrupted manual chest compressions are feasible during shock
delivery, without risk of harm to the rescuer. The AHA did not adopt this practice in the
2010 guidelines, but future iterations might recommend interruption of chest compressions solely for the purpose of rhythm analysis.
Pulse Check After Defibrillation
Compressions should be resumed immediately after defibrillation. The patients rhythm

and pulse should not be checked after defibrillation. Even if the patient is successfully
converted out of VF/VT, the myocardium is probably stunned and unable to generate
adequate perfusion pressures. The pulse and rhythm can be checked at the next
2-minute interval. Ideally, compressions should be continued throughout the defibrillation and stopped only to relieve a tired rescuer or for a rhythm check before the next
defibrillation attempt. Compressions support and maintain adequate perfusion.
AIRWAY AND BREATHING
The current AHA basic life support and ACLS guidelines have repositioned airway and
breathing below circulation for individuals who have experienced SCA from a cardiac
cause. In this scenario, the oxygen reserve tends to be adequate, so giving priority to
ventilation lowers the survival rate. In the early stages of SCA, poor cardiocerebral
oxygenation is caused by decreased perfusion, not decreased ventilation or oxygenation. However, for patients who have experienced SCA from a pulmonary cause (eg,
drowning, choking, or respiratory failure), in whom oxygen reserve is likely depleted,
the airway and breathing should be restored as quickly as possible.
Details about airway management in the cardiac arrest patient are beyond the
scope of this article but are presented elsewhere in this issue. Relevant AHA recommendations are summarized next116:
1. It is unknown whether administration of 100% inspired oxygen is beneficial to
people who have sustained SCA; however, there is no evidence that it causes
harm in short-term resuscitation. Therefore, the use of 100% oxygen is reasonable
during initial resuscitative efforts.
2. Chest compressions cause air to be expelled during the compression phase and
oxygen to be passively drawn into the chest during the recoil phase. Therefore,
the passive inhalation of oxygen via a nonrebreather facemask is likely to be sufficient for several minutes after the onset of SCA in patients who have a patent
airway.
3. Bag-mask ventilation can be challenging to perform correctly and is best done by
two trained rescuers. If this technique is used, it is recommended that a tidal
volume of approximately 600 mL be delivered over 1 second at a rate of 8 to 10
times per minute.
4. The routine use of cricoid pressure is no longer recommended. The application of
this pressure does not decrease the risk of aspiration117119 and impedes ventilation.120123 Cricoid pressure should be reserved for helping to visualize the vocal
cords during endotracheal intubation.
5. If advanced airway placement interrupts chest compressions, insertion of the
airway can be delayed until the patient fails to respond to initial CPR or defibrillation
attempts or demonstrates ROSC.
6. Continuous waveform capnography, in addition to clinical assessment, is the most
reliable method of confirming and monitoring correct placement of an endotracheal
tube. Capnography also has the benefit of alerting the providers to ROSC, as evidenced by an increase of more than 10 mm Hg in the patients EtCO2 level.65
7. Ventilations should be provided every 6 to 8 seconds (810 breaths per minute).
Higher ventilations rates, which are common during resuscitation, can increase
41
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Reynolds et al
intrathoracic pressure, resulting in diminished venous return and reduced cardiac

output.6,124 High ventilation rates can also cause gastric inflation, which increases
the risk of aspiration and can impede ventilation further by elevating the diaphragm
and restricting lung expansion.
SUMMARY
The 2010 AHA guidelines for CPR and emergency cardiovascular care present a significant change from how most people have learned adult CPR. The mantra is no longer
A-B-C (airway, breathing, and circulation) but instead C-A-B (circulation, airway,
and breathing). High-quality chest compressions (100 per minute at a depth of at least
2 in) should be started as soon as possible and continued with minimal interruptions.
Interruptions should be limited to rhythm checks or the exchange of providers performing compressions. Defibrillation should be delayed until at least 30 chest compressions have been done. After a patient has been resuscitated, the focus of the
providers needs to shift to postresuscitation care, which emphases the maintenance
of cardiocerebral perfusion pressure, achieving therapeutic hypothermia, and considering the patient for early cardiac catheterization. The four Cs of CPR (compressions,
cardioversion, cooling, and catheterization) are the only interventions that have been
shown to improve long-term outcomes.
ACKNOWLEDGMENTS
The manuscript was copyedited by Linda J. Kesselring, MS, ELS, the technical
editor and writer in the Department of Emergency Medicine at the University of
Maryland School of Medicine.
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protocol significantly improves outcome in a porcine model of prolonged
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61. Mader TJ, Paquette AT, Salcido DD, et al. The effect of the preshock pause on
coronary perfusion pressure decay and rescue shock outcome in porcine
ventricular fibrillation. Prehosp Emerg Care 2009;13:48794.
62. Paradis NA, Martin GB, Rivers EP, et al. Coronary perfusion pressure and the
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63. Reynolds JC, Salcido DD, Menegazzi JJ. Coronary perfusion pressure and
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Care 2010;14:7884.
64. Wang HE, Simeone SJ, Weaver MD, et al. Interruptions in cardiopulmonary
resuscitation from paramedic endotracheal intubation. Ann Emerg Med 2009;
54:645.e152.e1.
65. Pokorna M, Necas E, Kratochvil J, et al. A sudden increase in partial pressure
end-tidal carbon dioxide (PEtCO2) at the moment of return of spontaneous
circulation. J Emerg Med 2010;38:61421.
66. Edelson DP, Robertson-Dick BJ, Yuen TC, et al. Safety and efficacy of defibrillator charging during ongoing chest compressions: a multi-center study. Resuscitation 2010;81:15216.
67. Lloyd MS, Heeke B, Walter PF, et al. Hands-on defibrillation: an analysis of electrical current flow through rescuers in direct contact with patients during
biphasic external defibrillation. Circulation 2008;117:25104.
68. Yu T, Ristagno G, Li Y, et al. The resuscitation blanket: a useful tool for handson defibrillation. Resuscitation 2010;81:2305.
69. Manders S, Geijsel FE. Alternating providers during continuous chest compressions for cardiac arrest: every minute or every two minutes? Resuscitation 2009;
80:10158.
70. Aufderheide TP, Pirrallo RG, Yannopoulos D, et al. Incomplete chest wall decompression: a clinical evaluation of CPR performance by EMS personnel and
assessment of alternative manual chest compression-decompression techniques. Resuscitation 2005;64:35362.
71. Olasveengen TM, Wik L, Steen PA. Standard basic life support vs. continuous
chest compressions only in out-of-hospital cardiac arrest. Acta Anaesthesiol
Scand Suppl 2008;52:9149.
72. Hew P, Brenner B, Kaufman J. Reluctance of paramedics and emergency
medical technicians to perform mouth-to-mouth resuscitation. J Emerg Med
1997;15:27984.
73. Sirbaugh PE, Pepe PE, Shook JE, et al. A prospective, population-based
study of the demographics, epidemiology, management, and outcome of
out-of-hospital pediatric cardiopulmonary arrest. Ann Emerg Med 1999;33:
17484.
74. SOS-KANTO study group. Cardiopulmonary resuscitation by bystanders with
chest compression only (SOS-KANTO): an observational study. Lancet 2007;
369:9206.
75. Bohm K, Rosenqvist M, Herlitz J, et al. Survival is similar after standard treatment and chest compression only in out-of-hospital bystander cardiopulmonary
resuscitation. Circulation 2007;116:290812.
76. Iwami T, Kawamura T, Hiraide A, et al. Effectiveness of bystander-initiated
cardiac-only resuscitation for patients with out-of-hospital cardiac arrest. Circulation 2007;116:29007.
77. Ong ME, Ng FS, Anushia P, et al. Comparison of chest compression only and
standard cardiopulmonary resuscitation for out-of-hospital cardiac arrest in Singapore. Resuscitation 2008;78:11926.
78. Sayre MR, Berg RA, Cave DM, et al. Hands-only (compression-only) cardiopulmonary resuscitation: a call to action for bystander response to adults who
experience out-of-hospital sudden cardiac arrest: a science advisory for the
public from the American Heart Association Emergency Cardiovascular Care
Committee. Circulation 2008;117:21627.
79. Ornato JP, Gonzalez ER, Garnett AR, et al. Effect of cardiopulmonary resuscitation compression rate on end-tidal carbon dioxide concentration and arterial
pressure in man. Crit Care Med 1988;16:2415.
80. Kern KB, Sanders AB, Raife J, et al. A study of chest compression rates during
cardiopulmonary resuscitation in humans. The importance of rate-directed
chest compressions. Arch Intern Med 1992;152:1459.
81. Swenson RD, Weaver WD, Niskanen RA, et al. Hemodynamics in humans
during conventional and experimental methods of cardiopulmonary resuscitation. Circulation 1988;78:6309.
82. Anthi A, Tzelepis GE, Alivizatos P, et al. Unexpected cardiac arrest after cardiac
surgery: incidence, predisposing causes, and outcome of open chest cardiopulmonary resuscitation. Chest 1998;113:159.
83. Pottle A, Bullock I, Thomas J, et al. Survival to discharge following open chest
cardiac compression (OCCC). A 4-year retrospective audit in a cardiothoracic
specialist centreRoyal Brompton and Harefield NHS Trust, United Kingdom.
84. Raman J, Saldanha RF, Branch JM, et al. Open cardiac compression in the
postoperative cardiac intensive care unit. Anaesth Intensive Care 1989;17:
12935.
85. Babbs CF. Interposed abdominal compression CPR: a comprehensive evidence
based review. Resuscitation 2003;59:7182.
86. Sack JB, Kesselbrenner MB, Bregman D. Survival from in-hospital cardiac arrest
with interposed abdominal counterpulsation during cardiopulmonary resuscitation. JAMA 1992;267:37985.
87. Sack JB, Kesselbrenner MB, Jarrad A. Interposed abdominal compressioncardiopulmonary resuscitation and resuscitation outcome during asystole and
electromechanical dissociation. Circulation 1992;86:1692700.
88. Mateer JR, Stueven HA, Thompson BM, et al. Pre-hospital IAC-CPR versus standard CPR: paramedic resuscitation of cardiac arrests. Am J Emerg Med 1985;3:
1436.
89. Waldman PJ, Walters BL, Grunau CF. Pancreatic injury associated with interposed abdominal compressions in pediatric cardiopulmonary resuscitation.
Am J Emerg Med 1984;2:5102.
90. Pellis T, Kette F, Lovisa D, et al. Utility of pre-cordial thump for treatment of
out of hospital cardiac arrest: a prospective study. Resuscitation 2009;80:
1723.
91. Amir O, Schliamser JE, Nemer S, et al. Ineffectiveness of precordial thump for
cardioversion of malignant ventricular tachyarrhythmias. Pacing Clin Electrophysiol 2007;30:1536.
92. De Maio VJ, Stiell IG, Spaite DW, et al. CPR-only survivors of out-of-hospital
cardiac arrest: implications for out-of-hospital care and cardiac arrest research
methodology. Ann Emerg Med 2001;37:6028.
93. Haman L, Parizek P, Vojacek J. Precordial thump efficacy in termination of
induced ventricular arrhythmias. Resuscitation 2009;80:146.
94. Dale KM, Lertsburapa K, Kluger J, et al. Moxifloxacin and torsade de pointes.
Ann Pharmacother 2007;41:33640.
95. Pennington JE, Taylor J, Lown B. Chest thump for reverting ventricular tachycardia. N Engl J Med 1970;283:11925.
96. Bornemann C, Scherf D. Electrocardiogram of the month. Paroxysmal ventricular tachycardia abolished by a blow to the precordium. Dis Chest 1969;56:
834.
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97. Rahner E, Zeh E. Regulation of ventricular tachycardia with precordial fist blow.
Med Welt 1978;29:165963.
98. Ahmar W, Morley P, Marasco S, et al. Sternal fracture and osteomyelitis: an
unusual complication of a precordial thump. Resuscitation 2007;75:5402.
99. Miller J, Tresch D, Horwitz L, et al. The precordial thump. Ann Emerg Med 1984;
13:7914.
100. Muller GI, Ulmer HE, Bauer JA. Complications of chest thump for termination of
supraventricular tachycardia in children. Eur J Pediatr 1992;151:124.
101. Chan L, Reid C, Taylor B. Effect of three emergency pacing modalities on
cardiac output in cardiac arrest due to ventricular asystole. Resuscitation
2002;52:1179.
102. Dowdle JR. Ventricular standstill and cardiac percussion. Resuscitation 1996;
32:312.
103. Eich C, Bleckmann A, Paul T. Percussion pacing in a three-year-old girl with
complete heart block during cardiac catheterization. Br J Anaesth 2005;95:
4657.
104. Eich C, Bleckmann A, Schwarz SK. Percussion pacing: an almost forgotten
procedure for haemodynamically unstable bradycardias? A report of three
case studies and review of the literature. Br J Anaesth 2007;98:42933.
105. Iseri LT, Allen BJ, Baron K, et al. Fist pacing, a forgotten procedure in bradyasystolic cardiac arrest. Am Heart J 1987;113:154550.
106. Tucker KJ, Shaburihvili TS, Gedevanishvili AT. Manual external (fist) pacing
during high-degree atrioventricular block: a lifesaving intervention. Am J Emerg
Med 1995;13:534.
107. Zeh E, Rahner E. The manual extrathoracal stimulation of the heart. Technique
and effect of the precordial thump (authors transl). Z Kardiol 1978;67:299304.
108. Holmberg M, Holmberg S, Herlitz J. Incidence, duration and survival of ventricular fibrillation in out-of-hospital cardiac arrest patients in Sweden. Resuscitation
2000;44:717.
109. Larsen MP, Eisenberg MS, Cummins RO, et al. Predicting survival from out-ofhospital cardiac arrest: a graphic model. Ann Emerg Med 1993;22:16528.
110. Valenzuela TD, Roe DJ, Cretin S, et al. Estimating effectiveness of cardiac arrest
interventions: a logistic regression survival model. Circulation 1997;96:330813.
111. Link MS, Atkins DL, Passman RS, 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:S70619.
112. Cobb LA, Fahrenbruch CE, Walsh TR, et al. Influence of cardiopulmonary resuscitation prior to defibrillation in patients with out-of-hospital ventricular fibrillation.
JAMA 1999;281:11828.
113. Wik L, Hansen TB, Fylling F, et al. Delaying defibrillation to give basic cardiopulmonary resuscitation to patients with out-of-hospital ventricular fibrillation:
a randomized trial. JAMA 2003;289:138995.
114. Bunch TJ, White RD, Gersh BJ, et al. Long-term outcomes of out-of-hospital
cardiac arrest after successful early defibrillation. N Engl J Med 2003;348:
262633.
115. Hayakawa M, Gando S, Okamoto H, et al. Shortening of cardiopulmonary resuscitation time before the defibrillation worsens the outcome in out-of-hospital VF
patients. Am J Emerg Med 2009;27:4704.
116. Neumar RW, Otto CW, Link MS, et al. Part 8: Adult advanced cardiovascular life
support: 2010 American Heart Association Guidelines for Cardiopulmonary
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S72967.
Lawes EG, Campbell I, Mercer D. Inflation pressure, gastric insufflation and
rapid sequence induction. Br J Anaesth 1987;59:3158.
Petito SP, Russell WJ. The prevention of gastric inflation: a neglected benefit of
cricoid pressure. Anaesth Intensive Care 1988;16:13943.
Salem MR, Wong AY, Mani M, et al. Efficacy of cricoid pressure in preventing
gastric inflation during bag-mask ventilation in pediatric patients. Anesthesiology 1974;40:968.
Asai T, Goy RW, Liu EH. Cricoid pressure prevents placement of the laryngeal
tube and laryngeal tube-suction II. Br J Anaesth 2007;99:2825.
Brimacombe J, White A, Berry A. Effect of cricoid pressure on ease of insertion
of the laryngeal mask airway. Br J Anaesth 1993;71:8002.
McNelis U, Syndercombe A, Harper I, et al. The effect of cricoid pressure on
intubation facilitated by the gum elastic bougie. Anaesthesia 2007;62:4569.
Turgeon AF, Nicole PC, Trepanier CA, et al. Cricoid pressure does not increase
the rate of failed intubation by direct laryngoscopy in adults. Anesthesiology
2005;102:3159.
ONeill JF, Deakin CD. Do we hyperventilate cardiac arrest patients? Resuscitation 2007;73:82.
49
Electrical Therapies
i n C a rdi a c A r re s t
Peter P. Monteleone,
Seth O. Althoff, MDc
MD
, Heather A. Borek,
MD
b,
*,
KEYWORDS
Cardiac arrest Automated external defibrillator
Cardiac pacing Defibrillation
With the clinical updates made in the 2010 American Heart Association (AHA)
Advanced Cardiac Life Support Guidelines, the focus of resuscitation from cardiac
arrest has returned to an emphasis on the basics.1 Although much importance is placed
on performance of high-quality, uninterrupted cardiopulmonary resuscitation (CPR),
many forget that emphasis should also be placed on early and appropriate use of defibrillation to treat ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT).
Electricity as a therapeutic modality is a science with a long history going all the way
back to the Leyden jar. Developed in 1745, this was the first glass capacitor capable of
storing electricity. Soon after its discovery, it was used to study electricitys clinical
effects.2 By 1775, there were descriptions of an apparent accidental cardiac defibrillation by Peter Abildgaard when having shocked a single chicken into lifelessness.
on repeating the shock, the bird took off and eluded further experimentation.35 As
early as 1788, Charles Kite described, in his Essay on the Recovery of the Apparently
Dead, what may have been the first successful intentional defibrillation, that of a
3-year-old girl who was successfully defibrillated after a fall.6,7
As knowledge of the dysrhythmias underlying sudden cardiac death grew, JeanLouis Prevost and Frederic Battelli noted in 1899 that after inducing VF with electricity,
a second larger shock delivered to an animal brought the animal back into sinus
rhythm.8 At the turn of the twentieth century, interest in the science skyrocketed
when the Consolidated Edison Electric Company of New York City made the transition
from direct to alternating current on their electric lines. While performing the switch,
multiple linemen working on the project died of electrocution. These deaths led

a
Department of Medicine, University of Virginia, PO Box 800136, Charlottesville, VA
22908-0136, USA
b
Department of Emergency Medicine, University of Virginia, PO Box 800774, Charlottesville,
VA 229080774, USA
c
Department of Emergency Medicine, Bridgeport Hospital, 267 Grant Street, Bridgeport, CT
06610, USA
E-mail address: hab2t@virginia.edu
doi:10.1016/j.emc.2011.09.007
emed.theclinics.com
52
Monteleone et al
to the companys funding of multiple research initiatives studying the lethality of electricity and how it could potentially be used therapeutically. The resulting work of William Kouwenhoven and Guy Knickerbocker at Johns Hopkins highlighted results
similar to those of Prevost and Battelli, that after a single shock induces VF, a second
counter-shock could restore sinus rhythm in dogs.9
It was with this foundation that Claude Beck, a cardiothoracic surgeon at Western
Reserve University/University Hospitals of Cleveland, made the decision to undertake
what became the first documented successful intentional defibrillation of an exposed
human heart after a 14-year-old patient developed cardiac arrest and documented VF.
The first shock failed to defibrillate the heart, the second shock succeeded, allowing
a sinus rhythm to recapture the myocardium and gaining dramatic support for
defibrillation as a treatment of cardiac arrest.2,10
The science of electrical therapy in cardiac arrest has considerably evolved to investigate multiple modes of cardiac defibrillation and cardiac pacing. Historic work done
around the globe has resulted in what currently is a fairly simple science, the termination of a dysrhythmia with an overwhelming current. Elegant and simple, it is a clinical
act fundamental to the modern treatment of sudden cardiac arrest. This article focuses on the use of electrical therapies, including defibrillation, cardiac pacing, and
automated external defibrillators in cardiac arrest.
DEFIBRILLATION
The first step to successful use of defibrillation is rapid and accurate identification of
the rhythms warranting defibrillation. With regards to current AHA Advanced Cardiac
Life Support algorithms, defibrillation is warranted to treat pulseless VT or VF. These
rhythms are incapable of sustaining a perfusing blood pressure and thus warrant defibrillation to break the dysrhythmia and allow a pulse-sustaining rhythm to resume.
The mechanism by which defibrillation breaks the dysrhythmia remains controversial. In general, it is thought that defibrillation alters the cardiac cellular transmembrane
electrical potentials making cardiac cells temporarily unexcitable by a wave of depolarization.11 The disorganized waves of VF and the organized wavefronts of VT are thus
left unable to excite the myocardium. The resultant absence of VT- or VF-induced
depolarization allows normal cardiac excitation pathways and resultant contraction
to resume.12 As new technology has developed, so too has understanding of the
varied and complex effects of defibrillation on the heart at the cellular, tissue, and
organ-specific levels. However, it is important to remember that although much is
known about clinical outcomes from different types of defibrillation, there is much to
learn about how these outcomes are mediated physiologically.
To understand the basics of defibrillation, it is important to review the basics of electrical energy. Voltage is a measure of electrical potential difference measured in volts.
In the defibrillation model, voltage is the stored electrical potential difference created
by the defibrillator device between the two defibrillator pads. Current is the flow of
electric charge through a medium and is what actually defibrillates the heart. Current
is expressed as voltage/impedance and is measured in amperes. Impedance is a
measure of resistance to the flow of current and is measured in ohms. In the defibrillator model, impedance is created by the electrical circuit itself and by the patients
body. Impedance is affected by patient body mass, temperature, skin moisture, types
of defibrillator pads, attachment of the pads to the patients body, and so forth. Energy
is the amount of work associated with the passage of one amp of current through one
ohm of resistance for one second. Energy is measured in Joules and is expressed in
the following equation: voltage current time. Although the current is what actually
Electrical Therapies in Cardiac Arrest
induces defibrillation, what is selected on the device by a clinician is the energy

(in Joules). Selecting an energy in Joules essentially alters what current is supplied
during defibrillation.
Monophasic Versus Biphasic Defibrillation
Although the terms monophasic and biphasic and the resultant discussion of waveform shape can often be daunting, the principle underlying the difference between
these types of defibrillation is actually quite straightforward. Essentially, monophasic
devices send current in a single direction across the defibrillation pads (from pad A
to pad B). Biphasic devices send a defibrillatory current initially in one direction for
a specified duration (from pad A to pad B) and then the current is reversed and flows
in the opposite direction (from pad B to pad A) for the remainder of the defibrillation.
There are many distinct types of biphasic waveforms used by the many varieties of
biphasic defibrillators. They use different energy settings and can distribute voltage
and current differently among these settings. Some can also vary the duration of
the shock and the voltage to adapt to high-impedance patients. As demonstrated in
the ORBIT and TIMBER trials, there do not seem to be major differences in clinical
outcomes, including rate of return of spontaneous circulation or survival to discharge
in patients treated with monophasic versus biphasic defibrillation.13,14 One exception
was the ORCA trial, which demonstrated an improvement in neurologic outcomes
after discharge with the use of biphasic current.15
Despite little data demonstrating a clinical outcome difference, biphasic waveforms
do seem to defibrillate more effectively and with lower energies compared with monophasic waveforms. This observation has been demonstrated in animal and human
studies.1317 Although the exact physiologic explanation remains unclear, it seems
likely that the nature of the biphasic current allows more myocardium to be effectively
depolarized, and thus defibrillated, with less energy. These features collectively avoid
the high energies sometimes required by monophasic current, which can result in
higher rates of damage to myocardial tissue and damage to surface tissue, including
burns.18
In summarizing these data, the 2010 AHA guidelines state .over the last decade,
biphasic waveforms have been shown to be more effective than monophasic waveforms in cardioversion and defibrillation.1 There are no recommendations against
the use of monophasic defibrillators in these guidelines and, indeed, recommendations targeted to monophasic devices (regarding how to escalate energy in these
devices) are provided in the same guidelines. However, in light of the general expert
consensus support of biphasic devices, the growing trend across institutions has
been transition from monophasic to biphasic devices.
Single Versus Stacked Shocks
As a general rule stacked shocks for refractory VF or VT have fallen out of favor.
Before the 2005 AHA guidelines, shocks stacked in groups of three before initiation
of CPR were deemed appropriate on the grounds that the efficacy of the first shock
to defibrillate a monomorphic dysrhythmia was low. The improving efficacy of immediately repeated, or stacked, shocks was thought to be caused by the theoretical
decrease in transthoracic impedance, or TTI, after each shock.19,20 Emerging data
show that this theoretical improvement of stacking shocks does not seem to improve
the success of defibrillation or clinical outcomes.19,21 Stacking shocks leads to
decreased quality and quantity of CPR, potentially worsening outcome. Also, as
stated in the 2010 AHA guidelines, after a single shock intervening chest compressions may improve oxygen and substrate delivery to the myocardium, making the
53
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Monteleone et al
subsequent shock more likely to result in defibrillation.1 As a result, stacked shocks in

true pulseless arrest are no longer recommended, although some debate continues
regarding the use of shock stacking in experienced hands, in certain situations.
Fixed Versus Escalating Energy
During defibrillation, a large amount of current is dissipated away from the heart to the
various structures of the chest, including the bony chest wall and the lungs. Work with
dogs calculating the ratio of transcardiac to transthoracic threshold currents determined that only approximately 4% of current applied by defibrillation actually reaches
the heart.22 With such a limited percentage of current reaching the muscle to be
defibrillated, the idea of increasing defibrillation energy to defibrillate myocardium is
an important consideration. This notion was particularly important when the use of
monophasic current was standard.
Monophasic defibrillators do not compensate for impedance and simply create
a monophasic energy waveform that is also degraded in the face of high impedance.
These two facts made a strong case for using escalating energies for defibrillation failure, which suggested that transthoracic impedance was likely too high for successful
defibrillation. However, newer biphasic defibrillators use a biphasic truncated exponential waveform, a technology originally developed for implantable cardioverterdefibrillators (ICDs). The benefit of the biphasic truncated exponential waveform is
that it does not degrade in the face of high impedance. Also, many of the new biphasic
defibrillators include technology capable of adjusting the biphasic waveform to
compensate for high impedance. Therefore, the importance of a routine algorithm of
energy dose escalation has become less important since the dawn of the biphasic
defibrillator. The notion that higher energy levels may succeed where lower energy
levels have failed, however, does remain, resulting in the following statement in the
2010 AHA Guidelines: if higher energy levels are available in the device at hand,
they may be considered if initial shocks are unsuccessful in terminating the
arrhythmia.1
Time to Defibrillation
The initial rhythm in prehospital witnessed cardiac arrest is not uncommonly VF.23 It
has been well documented that the time to both CPR and defibrillation are critically
important in cardiac arrest. Survival rates decrease by approximately 7% to 10%
for every minute that passes from the time of arrest to defibrillation if no CPR is
provided.2326 VF eventually deteriorates to asystole over time.27 CPR can prolong
the period of VF and increase the time when defibrillation may be successful.2730
Because delays to both CPR and defibrillation decrease survival in witnessed cardiac
arrest, the current AHA guidelines recommend that the rescuer immediately start CPR
and use the automatic electronic defibrillator (AED)/defibrillator as soon as possible.31
In cases where there is an unwitnessed arrest, it is unclear whether initiating CPR
before defibrillation or immediate defibrillation provides better outcomes. Several
studies have attempted to answer this question with varying results. Two studies
demonstrated improved outcomes in patients receiving delayed defibrillation after
CPR by emergency medical services (EMS) providers where EMS call-to-arrival intervals were 4 minutes or longer.32,33 However, several other randomized controlled trials
assessing delayed defibrillation did not demonstrate any improvement in return of
spontaneous circulation or survival to discharge regardless of EMS response
interval.34,35 Although these results are contradictory, it has been demonstrated that
CPR before defibrillation, in cases where VF has been present for more than a few
minutes, may increase oxygen delivery and important metabolic substrates required
for successful termination of VF.36 The current recommendation suggests that

clinicians determine, based on an analysis of their patient, the most appropriate
time to defibrillate the individual.
CARDIAC PACING
The estimated incidence of out-of-hospital, EMS-treated cardiac arrest in North

America is 52.1 per 100,000 people.37 For cardiac arrest in the pediatric population,
the presenting rhythm is generally asystole or idioventricular bradycardia. In adult
cardiac arrest victims, the true prevalence of bradyasystole is unknown, although
some studies suggest the incidence may be as high as 25% to 56%.38 Bradyasystole
is generally defined as a cardiac rhythm with a ventricular rate less than 60 beats per
minute (in adults), periods of asystole, or both. There may be an absence or presence
of a pulse, which may or may not be adequately perfusing.
In the setting of asystolic cardiac arrest, there have been attempts to return circulation by external pacing. Intuitively, it would be thought that capturing a heartbeat
with electrical energy would improve patient survival; however, the available studies
are unconvincing. Cardiac pacing can be performed either transcutaneously or transvenously. In the emergency setting, transcutaneous pacing is rapidly available to prehospital and in-hospital personnel. Studies evaluating the use of pacing in cardiac
arrest have primarily evaluated trancutaneous pacing. Studies have assessed both
prehospital and in-hospital use of pacing in cardiac arrest. In studies of prehospital
asystolic arrest, little benefit in survival to hospital admission or hospital discharge
has been found with transcutaneous pacing versus standard resuscitation alone.
In a study of prehospital asystolic cardiac arrest, Hedges and colleagues39 found no
benefit in overall admission to the hospital or to hospital discharge when transcutaneous pacing was used versus standard medical resuscitation alone. However, in
this study the mean estimated time to pacing was 21.8 minutes. Barthell and
colleagues40 conducted a study evaluating the efficacy of prehospital pacing in asystolic cardiac arrest and pulseless electrical activity arrest. This study investigated 226
pulseless patients and found no benefit in survival for paced patients. Similarly, in
a larger study by Cummins and colleagues,41 no benefit was found in survival to
hospital admission or survival to hospital discharge despite a mean time to pacing
in this study of only 9 minutes. In addition, analysis of those patients with a mean
collapse-to-pacing time of less than 9 minutes with those with a collapse-to-pacing
time of greater than 9 minutes found no difference in survival to hospital admission.41
Similarly, evaluation of pacing for in-hospital cardiac arrest offers little available
evidence. In an examination of in-hospital asystole and bradycardia, Knowlton and
Falk42 found no difference in survival between paced patients and those receiving
standard pharmacotherapy. A limitation of this study was the small sample size,
including only 58 patients. Dalsey and colleagues43 performed a small study in which
52 patients initially received transcutaneous pacing after aystolic cardiac arrest,
pulseless electrical activity arrest, or hemodynamically compromised bradycardia.
Pacing was initiated after failure of standard medical resuscitation. No patient in the
series survived to hospital discharge. In a more recent evaluation, a systematic review
of the literature by Sherbino and colleagues44 found no benefit from transcutaneous
pacing in either in-hospital or prehospital asystolic arrest. Although evidence is limited,
based on the few available studies it seems that emergency cardiac pacing in the
asystolic patient has little value; there is no evidence that pacing is more beneficial
than standard resuscitation alone. Accordingly, the 2010 AHA guidelines do not
support the use of pacing in asystolic cardiac arrest.45
55
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Monteleone et al
Emergent cardiac pacing has historically been recommended for symptomatic

bradydysrhythmias and is a consideration for patients who are unresponsive to pharmacologic therapy. For example, in one study of 170 patients with symptomatic
bradycardia 54 were refractory to pharmacologic management and received external
cardiac pacing.46 Unfortunately, as in asystolic cardiac arrest, there is limited evidence that cardiac pacing results in improved outcomes in the bradycardic, hemodynamically compromised patient.
In the prehospital setting, a study of symptomatic bradycardia by Hedges and
colleagues47 found a trend toward improved survival to hospital discharge for transcutaneously paced patients versus nonpaced patients. Survival to hospital discharge
was 15% in the paced group versus 0% in the nonpaced group. However, this study
had multiple limitations and only included 51 individuals with only 27 paced. The
P value missed significance at 0.07. A prospective, controlled study by Barthell and
colleagues40 showed a significant improvement in resuscitation and survival to
hospital discharge in the transcutaneously paced group compared with controls for
symptomatic bradycardia. However, again in this study the sample size was small
(total of 13 patients) and there were inequalities between control and treatment groups
in terms of isoproterenol administration. In an interhospital study (patients being
transferred from hospital to hospital) by Vukov and Johnson,48 23 patients in a series
of 297 required transcutaneous or transvenous pacing for symptomatic bradycardia
that was unresponsive to atropine; of these 23 patients, 12 survived. Sherbino and
coworkers44 reviewed the literature of transcutaneous pacing in the prehospital
setting in patients with symptomatic bradycardia or bradyasystolic arrest and found
only seven studies, all of which were rated as having poor methodology by reviewers.
For symptomatic bradycardia this review seems to show no benefit in the prehospital
setting, although there may be a benefit for transcutaneous pacing in the in-hospital
setting.44,48 Sherbino and coworkers44 suggested that prehospital transcutaneous
pacing for symptomatic bradycardia be given a class indeterminate recommendation.
Because the data for the use of pacing for symptomatic bradycardia in the in-hospital
setting are more robust the AHA recommends transcutaneous pacing as a secondline therapy, to be considered when pharmacologic (atropine) management fails.45,49
Transcutaneous pacing may also be considered in patients presenting with unstable
bradycardia who have no intravenous access.49
A final indication for emergent cardiac pacing is overdrive pacing for torsades de
pointes (TdP). TdP may be either congenital or acquired. Congenital forms are caused
by inherited gene mutations encoding ion channels (sodium or potassium) involved in
cardiac action potential repolarization.5053 Acquired QT prolongation occurs most
commonly because of medications and toxins and electrolyte imbalances.50,53,54
Medication-induced QT prolongation is most commonly generated by potassium
efflux channel blockade.55,56
Refractory TdP can be treated by cardiac pacing, either chemical or electrical.
Pacing can be used prophylactically to suppress frequent, self-limited runs of TdP
or to override refractory, persistent TdP with a pulse before degeneration to VF. Any
patient with pulseless VT or VF must be treated with direct current cardioversion
and standard advanced resuscitation protocols. Isoproterenol is a b-adrenergic receptor agonist that causes positive inotropic and chronotropic effects, and is a
chemical means of overdrive pacing. Isoproterenol, however, may increase the risk
of dysrhythmia in patients with congenital long QT syndrome and, therefore, should
be reserved for those patients with acquired long QT syndrome.53,57
There are few studies evaluating the efficacy of electrical overdrive pacing for the
treatment of TdP. Although limited, these studies seem to show effective termination
of TdP when appropriately paced.58,59 Current AHA guidelines list overdrive pacing as
an option for polymorphic VT associated with familial long QT syndrome. It may also
be considered for acquired long QT syndrome when it seems to be pause induced or
associated with bradycardia.60
AUTOMATED EXTERNAL DEFIBRILLATORS
AEDs were created to decrease the time between cardiac arrest and defibrillation in
the out-of-hospital setting, although in-hospital applications are now not uncommon.
AEDs execute two important functions: they perform a cardiac rhythm analysis and
provide a shock delivery system. Manual defibrillation requires extensive training
because the operator is required to analyze the rhythm and determine the appropriate
treatment. The operator must also determine the amount of energy they wish to use for
defibrillation. AEDs simplify this process by internally analyzing the rhythm and, if
required, administering a shock of a predetermined, device-specific amount of
energy.
AEDs are classified as automatic and semiautomatic. Fully automatic machines only
require the operator to turn on the machine and appropriately place the electrode
pads. The machine then analyzes the rhythm and automatically delivers a shock, if
required. Semiautomatic machines analyze the rhythm and charge, but require the
operator to discharge the machine. As an additional function, AEDs often prompt
rescuers to provide CPR; some of the newer devices even give feedback regarding
the adequacy of the chest compressions being given.
The amount of energy received by the heart during defibrillation depends on the
amount of transthoracic impedance, which can be affected by such things as hair,
body weight, chest size, and pad size. The higher the impedance, the lower the
amount of energy and current generated, which may be insufficient to achieve defibrillation. AED pads are nonpolarized so either pad can be placed in various positions
without complications. There are four acceptable and equally effective positions to
place the pads: (1) anteriolateral, (2) anteroposterior, (3) anterior-left infrascapular,
and (4) anterior-right infrascapular.6165 Pads come in different sizes, ranging from
pediatric sizes of 24 cm2 up to the adult sizes of 8 to 12 cm in length. The larger
12-cm pads decrease transthoracic impedance and may achieve higher defibrillation
success rates than smaller pads.21,66 Also, briefly shaving any excess body hair or
wiping off any perspiration or water more accurately guarantees that the desired
energy is received.
The first AEDs delivered a monophasic current during defibrillation. Almost all
modern AEDs generate a biphasic current that requires less energy to achieve a
successful defibrillation, which has led to the ability to produce smaller units. Commercially available AEDs can provide either a fixed or escalating amount of energy
for subsequent shocks. For AEDs, AHA guidelines do not give specific recommendations for the amount of biphasic energy for the first shock, but state each additional
shock should be at least as strong as the initial shock, and energy may be increased
for additional shocks.31
AEDs automatically perform rhythm analysis using complex algorithms; QRS rate,
amplitude, slope, and morphology are just a few aspects of the electrocardiogram
that are evaluated. There are various algorithms that AED manufacturers use for their
specific machines. For this reason, the AHA has specific recommendations regarding
the specificity and sensitivity for each of the various rhythms. Manufacturers are recommended to report the performance of their algorithms using a standard format to
the Food and Drug Administration.31
57
58
Monteleone et al
In rhythm analysis, the most difficult challenge is differentiating fine VF from asystole
or artifact. Amplitude settings have to be set low enough to adequately detect VF and
high enough to exclude unnecessary shocks for asystole or artifact. Artifacts can be
caused by CPR, agonal respirations, transport of the patient, seizures, pacemaker
spikes, tremor and other rhythmic body motions, and electrostatic fields. Ideally,
each AED should have 100% specificity for detecting asystole or artifact. However,
because there are differences in the data acquisition algorithms for each different
machine, compiling a common test bank is impractical. To ensure integrity, each
manufacturer should provide their performance report and explain how the testing
was completed.
There are a few unique circumstances to consider when using an AED. AED use is
not contraindicated in patients who have an ICD. Occasionally, there may be some
discrepancies in rhythm analysis between the ICD and AED. If the ICD has a pacing
function, this may also interfere with the ability of the AED to appropriately detect
VF.67 If the ICD is delivering shocks, it is recommended to wait up to 1 minute before
attaching the AED. When placing the electrode pads for those patients with ICDs, the
anteroposterior and anterolateral locations are acceptable positions. It is not recommended to place the pads directly over the device.31 Patients who have transdermal
medication patches should have those removed before pad placement. The patch
may impede the energy delivery of the shock or cause burns to the patients skin.68
Patients who are extremely diaphoretic or found lying in water should be removed
from the water source and have their chest wiped off before pad placement.31
Cardiac arrest in children also poses a unique situation. Unlike adults, VF is relatively
uncommon and only observed in 5% to 15% of pediatric and adolescent arrests.6973
In those circumstances, defibrillation may improve outcomes; however, the lowest
effective energy dose is unknown.73,74 Most AED devices come with pediatric-sized
pads and a pediatric dose-attenuator cord. In children 1 to 8 years, it is recommended
to use the dose-attenuator system. For children less than 1 years of age, manual defibrillation is preferred; if that is not available, however, the pediatric dose-attenuator
system should be implemented. In circumstances where neither manual defibrillation
nor the pediatric dose-attenuator system are available, an adult AED should be
used.31 Some form of early defibrillation in infants and children is preferable to either
delayed or no such intervention.
Since 1995, the AHA has been instrumental in the development of the lay rescuer
AED or public access defibrillation programs. The goal of these programs was to
shorten the time interval between cardiac arrest and the initiation of CPR and defibrillation. A large prospective trial demonstrated a twofold increase in the number of
survivors of out-of-hospital cardiac arrest when early AED use was compared with
early EMS call.75 These programs emphasize placing an AED in public locations;
however, roughly 60% to 80% of out-of-hospital arrests occur in private or residential
areas. When studies evaluated residential use of AEDs, there was no significant difference demonstrated comparing early AED use with CPR alone.76,77 Both AED use and
CPR are vital to the potential survival of patients who have cardiac arrest. The mere
presence of an AED does not ensure proper use. When evaluating areas with established AED programs, one study demonstrated that the AED was only used in 34% of
arrested patients.75 As these programs evolve, it is extremely important to have quality
improvement measures and continual training of those first-responders to achieve the
maximum benefits that are capable with AEDs.
Several studies have considered the use of AEDs in the hospital setting. Four
studies demonstrated improved survival rates to hospital discharge, whereas one
study did not demonstrate increased rates of survival or return of spontaneous
circulation.7882 These studies primarily evaluated the use of AEDs by nursing staff or
medical emergency teams on nonintensive care unit patients experiencing cardiac
arrest. In these instances AEDs may decrease length of time between VT or VF cardiac
arrest and defibrillation. Patients who may most benefit from in-hospital AEDs are
those in unmonitored or nonintensive care unit beds or those in outpatient and diagnostic facilities. Although limited data are available, as with other studies evaluating
early AED use, increased access to AEDs at outpatient healthcare facilities is expected to improve patient outcome. The goal of decreasing the time from cardiac
arrest to defibrillation is the same for both in-hospital and out-of-hospital settings.
SUMMARY
Recognition and appropriate treatment of VF or pulseless VT is an essential skill for

healthcare providers. Appropriate defibrillation can improve survival and benefit
patient outcome. Similarly, increased public access to AEDs has been shown to
improve out-of-hospital survival for cardiac arrest. When combined with high-quality
CPR, electrical therapies are an important aspect of resuscitation in the patient with
cardiac arrest.
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63
The Impact of
th e C o d e D r u g s:
C a rd i o a c t i v e
Medications in
Card iac A rrest
Resuscitation
Kelly Williamson, MDa, Meghan Breed, BA, EMT-Ib,c,
Kostas Alibertis, BA, CCEMT-Pd,e,f, William J. Brady, MDc,d,g,h,*
KEYWORDS
Cardiac arrest Anti-arrhythmic agent Vasopressor
Approximately 325,000 cardiac arrests occur each year in the United States; primary
cardiac events represent the precipitating cause in 75% of all episodes of sudden
death. Most of these cardiac arrests (250,000) occur outside of a hospital annually.
Despite innumerable advancements in medical treatments and technology, survival
of individuals after an out-of-hospital cardiac arrest remains low, averaging less
than 7%.1
The human circulatory system is a complex vascular network, and dysfunction
rapidly leads to impaired oxygen delivery, progressive cellular dysfunction, organ
failure, and ultimately patient death. Therefore, interventions for victims of cardiac
arrest must be performed rapidly and efficiently to maximize the chance of a favorable cardiac and neurologic outcome. In an attempt to address this dysfunction and
Department of Emergency Medicine, Northwestern University, Chicago, IL 60611, USA

Department of Emergency Medicine, University of Virginia, Charlottesville, VA 22908, USA
c
Charlottesville-Albemarle Rescue Squad, Charlottesville, VA 22901, USA
d
Center for Emergency Preparedness and Response, University of Virginia, Charlottesville,
VA 22908, USA
e
Western Albemarle Rescue Squad, Crozet, VA 22932, USA
f
American Heart Association, Committee for Emergency for Cardiovascular Care, Dallas,
TX 75231, USA
g
Departments of Emergency Medicine and Medicine, University of Virginia School of Medicine, Charlottesville, VA 22908, USA
h
Albemarle County Fire Rescue, Charlottesville, VA 22901, USA
* Corresponding author. Departments of Emergency Medicine and Medicine, University of
Virginia School of Medicine. Charlottesville, VA 22908.
E-mail address: WB4Z@hscmail.mcc.virginia.edu
b

doi:10.1016/j.emc.2011.09.008
emed.theclinics.com
66
Williamson et al
alter its natural history, the American Heart Association (AHA) has proposed a 4-step
chain of survival to improve the outcomes of patients who experience an out-ofhospital cardiac arrest. The survival benefit of the first 3 steps, which include early
access to medical care, early initiation of cardiopulmonary resuscitation (CPR), and
early defibrillation, have been established in the literature and are discussed elsewhere in this issue. The incremental benefit of the fourth step in the chain of survival,
which is early access to advanced care including airway management and the use of
cardioactive intravenous (IV) medications, has not yet been well established, and
there have been few advances in the pharmacologic component of the chain of
survival.
The impact of advanced care has been questioned. Stiell and colleagues2
concluded that the use of cardioactive medications during cardiac arrest does not
improve survival to hospital discharge or the resulting neurologic status despite an
increase in the return of spontaneous circulation (ROSC) and survival to hospital
admission. The OPALS (Ontario Prehospital Advanced Life Support) trial examined
the incremental effect on the rate of survival of individuals after cardiac arrest of adding advanced life support to an already present rapid defibrillation program. The multicenter, controlled, clinical trial reviewed the cases of 5638 patients. The investigators
concluded that although the addition of cardioactive medications increased survival to
hospital admission, it did not affect survival to hospital discharge. Further work by
Stiell and colleagues3 examined the relative importance of interventions in cardiac
arrest with the determination of the value added by these therapies; selected odds
ratios supporting survival from cardiac arrest include the following: witnessed arrest
(4.4), any form of bystander CPR (3.7), electrical defibrillation less than 8 minutes
into arrest (3.4), and advanced life support with cardioactive medications (1.1). This
data set does not suggest that the advanced interventions offer significant benefit
when compared with the basic therapies such as CPR and defibrillation. Furthermore,
medication administration should not interfere with other lifesaving interventions such
as chest compressions and defibrillation.
Despite this less-than-impressive database supporting their use, the various cardioactive medications, or code drugs, remain prominently placed in the AHAs
Advanced Cardiac Life Support (ACLS) Guidelines 2010 (G2010).4 There are several
categories of medications used during cardiac arrest: vasopressor medications
(epinephrine, vasopressin, and atropine), antiarrhythmic medications (amiodarone
and lidocaine), and adjunct medications (sodium bicarbonate, calcium, magnesium,
and fibrinolytics). This review discusses the evidence for their use and notes their
current position in the AHA G2010.4
VASOPRESSOR MEDICATIONS
Vasopressors, namely epinephrine and vasopressin, are routinely administered during

cardiac arrest, and there is evidence to suggest that this usage positively affects
ROSC. There are, however, no published placebo-controlled clinical trials demonstrating that the administration of any vasopressor medication at any stage in the
management of pulseless ventricular tachycardia (VT), ventricular fibrillation (VF),
pulseless electrical activity (PEA), or asystole increases the rate of neurologically intact
survival to hospital discharge.4
Epinephrine is one of the most widely used drugs in the ACLS regimen, indicated for
VF, pulseless VT, PEA, and asystolic arrests. Epinephrine is a sympathomimetic agent
that serves as a potent adrenergic agonist stimulating both a and b receptors. Stimulation of the a1 and a2 receptors causes arterial vasoconstriction, which is deemed
Cardioactive Medications in Cardiac Arrest Resuscitation
beneficial because such vasoconstriction promotes higher perfusion pressures of the

coronary and cerebral vascular beds and increases the aortic diastolic pressure during
CPR. Stimulation of b1 receptor increases heart rate and myocardial contractility,
which may be helpful in the immediate postresuscitation period, but these effects
are often considered detrimental because they lead to increased myocardial oxygen
consumption and may impair subendocardial perfusion. In addition, b2 receptor stimulation causes vascular and respiratory smooth muscle relaxation, thereby diminishing
coronary and cerebral perfusion pressures.
There has been much research surrounding the use of epinephrine for cardiac
arrests. In general, the prognosis of patients who require epinephrine, the so-called
shock-resistant patients, during cardiac arrest remains extremely poor. These patients
are candidates for vasopressor therapy in that they have not responded favorably to
electrical defibrillation, thus the shock resistance notation. For instance, a retrospective analysis by Herlitz and colleagues5 examined 1360 patients who experienced a VF
arrest. Epinephrine was given in 417 cases (35%), and those who received the medication experienced ROSC more frequently and had a statistically significant improvement for survival to hospital admission compared with those who did not receive this
therapy. The rate of hospital discharge, however, did not differ between the 2 groups.
The investigators concluded that although patients receiving epinephrine had a more
favorable initial outcome, the final outcome was not significantly affected.
Several studies have compared the standard dose of epinephrine with escalating
doses as well as a high-dose strategy. Callaham and colleagues6 published a randomized, prospective, clinical trial that compared standard-dose and high-dose epinephrine for the initial treatment of prehospital arrest. A total of 816 patients were enrolled.
In this study, 13% of patients receiving high-dose epinephrine (15 mg IV) had ROSC
compared with 8% receiving standard-dose epinephrine (1 mg IV); furthermore,
more patients in the high-dose group survived to hospital admission. However, there
was no statistically significant difference in the occurrence of either survival to hospital
discharge or neurologically intact survival. A second prospective randomized study
published by Gueugniaud and colleagues7 also compared repeated high doses of
epinephrine with repeated doses of standard-dose (ie, 1 mg) epinephrine for out-ofhospital cardiac arrest. Although patients in the high-dose group had higher rates of
ROSC and survival to hospital admission, no differences in survival to hospital
discharge or neurologic status in the treatment groups were observed. Brown and
colleagues8 conducted a prospective multicenter trial also comparing standarddose epinephrine with high-dose epinephrine and concluded that there were no differences in the overall rate of ROSC, survival to hospital admission, survival to hospital
discharge, or neurologic outcome between the 2 groups. As a result of these studies,
high-dose epinephrine is not currently recommended in the treatment of cardiac
arrest.
The other primary bolus-dose vasopressor, vasopressin, is a peptide hormone that
is normally released from the posterior pituitary gland in response to physiologic
demands related to either significant hypovolemia and/or systemic hypoperfusion.
Endogenous vasopressin levels have been found to be significantly higher when
measured in patients who survived a cardiac arrest compared with those who
died.9 Synthetic vasopressin serves as a nonadrenergic vasopressor with pronounced
peripheral vasoconstriction by actions on the V1 receptors of the endothelium.
Different from epinephrine, however, vasopressin has no direct effect on cardiac
contractility and thereby does not increase myocardial and cerebral oxygen demand.
Animal studies have suggested that vasopressin increases blood flow in vital organs,
enhances cerebral oxygen delivery, and improves short-term survival and favorable
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neurologic outcome. Lindner and colleagues9 also demonstrated such findings in the
cardiac arrest scenario; these investigators noted that vasopressin not only increased
arterial and coronary pressures but also enhanced myocardial and cerebral blood
flows compared with standard doses of epinephrine in animal models of cardiac
arrest.
Human studies demonstrate less-than-convincing results when compared with
animal studies using vasopressin as a 1-time alternative to epinephrine as the first
or second vasopressor administered during cardiac arrest. Stiell and colleagues10
studied 200 inpatients who had a cardiac arrest. In this study, the patients were
randomized to receive either 1 mg of epinephrine or 40 units of vasopressin IV as
the initial vasopressor following cardiac arrest, with additional doses of epinephrine
then used as a rescue medication at the discretion of the resuscitation team. The
investigators noted that there was no survival advantage for vasopressin over
epinephrine. Guyette and colleagues11 examined the outcomes of patients receiving
epinephrine only, a combination of vasopressin and epinephrine, or no vasopressor
medications in cardiac arrest management. They concluded that ROSC was associated with witnessed collapse, bystander CPR, and initial cardiac rhythm of VF or
pulseless VT. The subjects who received vasopressin and epinephrine were more
likely to have a ROSC during the resuscitation and survive to hospital arrival than those
treated with epinephrine alone, although they do not comment on survival rates to
hospital discharge. This study was not constructed to determine ultimate patient
outcome, which is unfortunate with regard to a meaningful contribution to the resuscitation literature.
In 2004, Wenzel and colleagues12 published a study that concluded administration
of vasopressin did not change VT, VF, or PEA outcomes, although there was a more
frequent ROSC at the time of the event as well as a trend toward a better, although still
dismal, initial outcome for patients in asystole. In this study of 1219 patients, vasopressin had outcomes similar to those of epinephrine for patients who had VF or VT
during cardiac arrest but was demonstrated to be superior in patients with asystole
because these patients were 40% more likely to reach the hospital alive. Once again,
the ultimate outcome was not altered. Additional investigation of this topic includes
a randomized clinical trial in which 1442 patients received epinephrine and vasopressin during the cardiac arrest and 1452 received epinephrine alone. There were
no significant differences in ROSC, survival to hospital admission, survival to hospital
discharge, 1-year survival, or neurologic recovery at hospital discharge.13
Although there is no demonstrated benefit of vasopressin over epinephrine, there is
no evidence of harm either. Although large populations of cardiac arrest patients do
not benefit significantly from either vasopressor, it is conceivable that certain individuals do experience an advantage as a consequence of the medication. Thus, the use
of these medications should be continued in patients with cardiac arrest. The AHA
recommends that vasopressin (40 units IV) can be used as an alternate vasopressor
therapy for cardiac arrest, indicated in the treatment of adult shock-refractory VF or
pulseless VT as a 1-time alternative to epinephrine.4
PARASYMPATHOLYTIC MEDICATION (ATROPINE)
During cardiac arrest, parasympathetic tone is increased as a result of vagal stimulation, which leads to decreases in heart rate, systemic vascular resistance, and blood
pressure. Atropine is a parasympatholytic drug that enhances both sinoatrial node
automaticity and atrioventricular conduction via direct vagolytic action and competitive antagonism of acetylcholine at the sinoatrial and atrioventricular nodes. Because
asystole can be precipitated or exacerbated by excess vagal tone, atropine provides

a theoretic physiologic advantage. However, the literature on the use of atropine in
cardiac arrest is limited. There are no prospective, randomized, controlled trials that
support the use of atropine in asystole or PEA arrest, nor is there literature to suggest
its harmful effects or dispute its use in cardiac arrest.
Brown and colleagues14 examined the notion that atropine can aid in cardiac arrest
via its parasympathetic blockade. They published a case series of 8 patients who had
return of a regular rhythm after administration of atropine, 3 of whom ultimately
survived to hospital discharge. The investigators results suggest the value of atropine
in the treatment of asystole. Stueven15 published a retrospective review of 170
patients with asystole, of whom 43 patients received atropine for refractory asystole
after the administration of epinephrine and sodium bicarbonate, whereas 41 patients
did not. The investigator found 14% survival to hospital admission in the atropine
group, with 0% in the nonatropine group, although there were no survivors to hospital
discharge in either group. Coon and colleagues16 evaluated the efficacy of atropine for
treating asystolic prehospital cardiac arrests in a controlled prospective study.
Twenty-one patients were divided into atropine-treated and nonatropine-treated
(control) groups. The atropine-treated patients received 1 mg of atropine IV with
a repeat dose at 1 minute if no rhythm change occurred, as well as the same additional
medication therapy as the control group. Only 2 patients in each group were successfully resuscitated in the emergency department, and only 1 patient in the control group
was discharged alive. The investigators therefore question the usefulness of atropine
for brady-asystolic arrests.
Because no prospective clinical trials have examined the use of atropine in asystole
or bradycardic PEA arrest combined with lower-level clinical studies providing conflicting evidence, in G2010 the AHA commented that atropine is unlikely to have a therapeutic benefit in cardiac arrest and was therefore removed from the ACLS algorithm.4
This action is the first time that a major medication has been removed from the AHA
ACLS guidelines. However, there is neither demonstrated benefit nor harm in such
settings. On the contrary, the aggressive and early use of atropine in the prearrest
setting (ie, patients with intact although compromised perfusion) has demonstrated
benefit.17,18
ANTIARRHYTHMIC MEDICATIONS (LIDOCAINE AND AMIODARONE)
Lidocaine and amiodarone are the 2 most commonly used antiarrhythmic medications
in cardiac arrest, although their benefit has not been clearly established in clinical
trials. Lidocaine, well known and widely used as both an amide local anesthetic and
an antiarrhythmic agent, increases the electrical stimulation threshold of the ventricle
during diastole, thereby decreasing ectopic electrical myocardial activity. Paradoxically, this action has the unfortunate consequence of also serving to increase the defibrillation threshold. Amiodarone is the other primary antiarrhythmic agent that is
indicated in VF and pulseless VT. The drugs primary effects are via sodium and
calcium channel blockade, potassium efflux antagonism, and adrenergic blocking
effects; thus, amiodarone acts via a multitude of mechanisms.
The use of lidocaine for ventricular arrhythmias was initially supported by animal
studies, and 1 prehospital study reported that lidocaine usage improved short-term
survival.19 However, 3 additional randomized trials examined the effects of lidocaine
during cardiac arrest and reported less-than-impressive end results. Weaver and
colleagues20 randomized 199 patients who suffered an out-of-hospital cardiac arrest
to receive either epinephrine or lidocaine. The investigators determined that the rates
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of asystole were higher in patients who received lidocaine. Two additional studies
directly compared the outcomes of patients who received lidocaine with those
receiving amiodarone. Dorian and colleagues21 demonstrated that the use of amiodarone leads to substantially higher rates of survival to hospital admission in patients with
shock-resistant VF compared with lidocaine. A German study by Kentsch22 also
concluded that the use of lidocaine led to lower rates of ROSC compared with amiodarone. Thus, the evidence does not support the use of lidocaine in the management
of shock-resistant VF or pulseless VT.
Although there are data to advocate the use of amiodarone rather than lidocaine for
antiarrhythmic therapy in cardiac arrest, there are still questions on whether the
administration of amiodarone improves long-term outcomes. In a study that enrolled
347 patients, Dorian and colleagues21 concluded that the use of amiodarone leads to
substantially higher rates of survival to hospital admission in patients with shockresistant VF compared with lidocaine, but final outcomes were not different. Kudenchuck and colleagues23 published a study comparing amiodarone with placebo for
out-of-hospital cardiac arrest in patients with pulseless VT and VF. The investigators
examined 504 patients and concluded that patients who received amiodarone had
higher rates of survival to hospital admission, with an adjusted odds ratio of 1.6.
The study, however, was not sufficiently powered to determine a difference to hospital
discharge; no difference in ultimate outcome was found.
As a result of these studies, the AHA recommends the use of amiodarone for VF or
pulseless VT that is unresponsive to CPR, shock, and a vasopressor (class IIb recommendation). Amiodarone is first given as a dose of 300 mg IV, which can be followed
with a second dose of 150 mg IV after 5 minutes.4 Furthermore, the AHA concludes
that lidocaine has no proven short-term or long-term efficacy in cardiac arrest.
However, given its widespread familiarity and few immediate side effects, lidocaine
may still be considered an alternative to amiodarone for VF and pulseless VT, with
a class indeterminate; the drug should be given at an initial dose of 1 to 1.5 mg/kg
IV, followed by 0.5- to 0.75-mg/kg IV push at 5- to 10-minute intervals (maximum
dose, 3 mg/kg) if VF or pulseless VT persists.4
OTHER MEDICATIONS
In addition to the vasopressor and antiarrhythmic medications, several other adjunctive therapies have been examined for use in cardiac arrest, including sodium bicarbonate, magnesium, calcium, and fibrinolytic agents. The common theme among
these 4 general classes of medication is summarized by the following statement:
the use of these agents in cardiac arrest management does not demonstrate benefit
in all such patients; these agents, however, do potentially benefit specific patients in
cardiac arrest, introducing the concept of niche application of these drugs in certain
cardiac arrest scenarios. Examples of these situations include the patient with severe
hyperkalemia, profound hypocalcemia, and diagnosed or highly suspected pulmonary
embolism.
Sodium Bicarbonate
Sodium bicarbonate is a potent alkaline agent and an essential component in the

maintenance of acid-base homeostasis in the human body. Because of its role as
a potent buffer and presence in the AHA algorithms, sodium bicarbonate is frequently
used in cardiac arrest; Bar-Joseph and colleagues24 noted that bicarbonate is used in
54.5% of all cardiac arrests. They reviewed the use of bicarbonate in cardiac arrest
therapy.24 The BRCT III database comprises 2915 patients who experienced an
out-of-hospital cardiac arrest. Although the initial objective of the study was to
compare high-dose with standard-dose epinephrine during resuscitation, the investigators also examined sodium bicarbonate usage and determined that prebasic life
support or pre-ACLS intervals did not influence the decision to use sodium bicarbonate or when to administer it. They suggest that future guidelines for sodium bicarbonate use during resuscitation should emphasize the importance of pre-ACLS
hypoxia time in contributing to acidosis and define more specifically the interval in
which bicarbonate administration may be helpful. The investigators noted that both
early and aggressive buffer use were associated with improved, although still poor,
outcome in cardiac arrest resuscitation.24
There is, however, limited evidence to support its widespread use in cardiac arrest
because it can adversely affect perfusion in certain vascular beds, thereby unfavorably
altering acid-base status at the tissue and cell levels and promoting hyperosmolarity
and hypernatremia. As a result of this information, the AHA currently gives sodium
bicarbonate a level III recommendation for use in all patients in cardiac arrest.4 There
are several niche applications for sodium bicarbonate use, including severe acidosis,
sodium channel blocking agent overdose, and significant hyperkalemia.
Magnesium
Magnesium is an electrolyte whose ions are essential to many enzymatic processes,

most importantly, serving as a cofactor in the formation and use of the energy
substrate adenosine triphosphate. Hypomagnesemia, an electrolyte disturbance in
which there is an abnormally low level of magnesium in the blood, can precipitate
sudden cardiac death. It has therefore been hypothesized that the use of magnesium
may be beneficial in cardiac arrest.
Two case reports were published in the early 1990s that led to further investigation
of the role of magnesium in cardiac arrest. Tobey and colleagues25 reported the case
of a 46-year-old man who suffered a VF arrest, received 62 minutes of ACLS care, and
was successfully resuscitated on arrival in the emergency department when he
received 4 g of IV magnesium sulfate (MgSO4). Craddock26 reports a similar case in
which a 41-year-old woman experienced an asystolic cardiac arrest postoperatively
and subsequent ROSC, which was temporally related to the administration of 8 g of
IV MgSO4.
Because of these 2 dramatic case reports, Fatovich and colleagues27 conducted
the MAGIC (Magnesium in Cardiac Arrest) trial to determine if high-dose magnesium
was associated with increased survival from out-of-hospital cardiac arrest. A total of
67 patients were randomized to receive either 5 g MgSO4 or placebo as first-line antiarrhythmic drug therapy, with the remainder of their management dictated by standard ACLS. In this small study, the investigators concluded that the use of
magnesium as first-line drug therapy for out-of-hospital cardiac arrest was not associated with significantly improved survival. Thel and colleagues28 examined the use of
magnesium during in-hospital cardiac arrest, finding results similar to those of the
Fatovich study,27 and concluding that empiric magnesium supplementation did not
improve the rate of successful resuscitation, survival to 24 hours, or survival to hospital
discharge.2
There are 2 specific instances where its utility has been demonstrated: long QTrelated polymorphic VT (torsades de pointes) and toxemia of pregnancy. Long QTrelated polymorphic VT, or torsades de pointes, is a less common variety of VT that
demonstrates the characteristic electrocardiographic findings of a twisting-aboutthe-points morphology of sequential QRS complexes around an isoelectric baseline.
In this situation, magnesium is a negative inotrope and works by slowing electrical
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signals in the atrioventricular node. Magnesium is also useful in toxemia of pregnancy

or eclampsia. Eclampsia affects the vasculature and leads to vasospasm and convulsions, which may become fatal. The vasodilatory properties of magnesium can modify
these effects, and its administration is considered the standard of care in these cases.
The AHA does not recommend the routine use of magnesium for cardiac arrest,
although it receives a level IIb recommendation for torsades de pointes and is considered standard of care for the treatment of toxemia.
Calcium
Calcium is essential for living organisms, particularly as related to cellular physiology,

when the movement of calcium ions into and out of the cytoplasm functions as a signal
for cellular processes. However, calcium abnormality as a cause of cardiac arrest is
very rare. Because cardiac muscle depends on extracellular calcium ions for contraction and calcium exerts a stabilizing effect on myocardial cells, researchers have
attempted to determine if the routine use of calcium during cardiac arrest alters
survival. Like the other agents discussed in this article, conclusive evidence of a beneficial effect of calcium in cardiac arrest management is lacking.
One study by Stueven and colleagues29 examined 179 patients who presented in
asystole and 116 patients with electromechanical dissociation (ie, PEA). Calcium
use was not significantly found in patients who were resuscitated; for both rhythms,
patients who did not receive calcium were more likely to undergo successful resuscitation than those who received calcium. Harrison and Amey30 examined 480 patients
who suffered an out-of-hospital cardiac arrest and received calcium chloride during
the course of the arrest. They determined that there was no positive effect on patient
outcomes in cardiac arrest. Furthermore, Donovan and Propp31 argue that the routine
administration of calcium during cardiac arrest may even be deleterious because
natural cellular accumulation of calcium within the myocardium occurs during cardiac
arrest. Therefore, the AHA does not recommend the routine use of calcium
during cardiac arrest.4 There are, however, several potential niche applications for
its use, including hyperkalemia, severe hypocalcemia, and calcium channel blocker
overdose.4,32
Fibrinolytic Agents
Because coronary thrombosis and pulmonary thromboembolism are common precipitants of cardiac arrest, one final adjunctive medication that has been suggested in
patients with persistent PEA arrest is the fibrinolytic agents. Fibrinolysis is the process
by which a fibrin clot, the product of coagulation, is degraded. Fibrinolytic agents,
such as tissue plasminogen activator (t-PA), convert plasminogen to active plasmin,
which works to break down the fibrin mesh. Adults have been successfully resuscitated after the administration of t-PA when the condition leading to the arrest was
acute pulmonary embolism or myocardial infarction.33
In one large clinical trial, Abu-Laban and colleagues34 assessed whether the administration of t-PA during resuscitation would benefit patients with PEA of unknown
cause. A total of 233 patients with cardiac arrest were enrolled and randomly assigned
to receive 100 mg of t-PA or placebo IV along with standard resuscitation measures.
One patient in the t-PA group survived to hospital discharge, compared with none in
the placebo group, although more patients in the placebo group achieved ROSC.
Neither of these outcomes reached statistical significance, and the investigators
concluded that they found no evidence of a beneficial effect of fibrinolysis in patients
with undifferentiated cardiac arrest and PEA. A second prospective, randomized,
double-blind, placebo-controlled, multicenter trial was conducted by Bottiger and
colleagues35 to determine whether fibrinolysis with tenecteplase improves survival in

adults with witnessed out-of-hospital arrest of presumed cardiac origin. After the
enrollment of the first 443 patients, patients who presented in asystole were no longer
enrolled because of low survival, and the trial was ultimately terminated by the Human
Safety Committee of the sponsoring institution after the enrollment of 1050 patients for
futility because there were no significant differences in 30-day survival, hospital
admission, ROSC, 24-hour survival, survival to hospital discharge, or neurologic
outcome. Furthermore, there were more intracranial hemorrhages in the tenecteplase
group. The investigators therefore concluded that there was no improvement in
outcome when tenecteplase was used for out-of-hospital cardiac arrest compared
with placebo.
The AHA states that there is insufficient evidence to advocate for the routine use of
fibrinolytic agents during cardiac arrest but that their use should be considered on
a case-by-case basis; they receive a level IIb recommendation for cardiac arrest
secondary to pulmonary embolism.4
SUMMARY
The goal of treating patients who present with cardiac arrest is to intervene as quickly
as possible to affect the best possible outcome. The mainstays of these interventions,
including early activation of the emergency response team, early initiation of CPR, and
early defibrillation, are essential components with demonstrated positive impact on
resuscitation outcomes. Conversely, the use of the code drugs as a component of
advanced life support has not benefited patients with cardiac arrest in general.
Although short-term outcomes are improved as a function of these medications, the
ultimate outcome has not been altered, whether one considers survival to hospital
discharge or neurologic status at discharge. Direct harm has not been conclusively
demonstrated as a result of the use of these drugs. Furthermore, it is conceivable
that selected individuals do benefit from such interventions. At present, no data exist
that allow for the rapid identification of such patients who will derive benefit. Thus, the
authors agree with the AHAs recommendations in the G2010 regarding the code
drugs. Clinicians must be aware of this modest, at best, impact on cardiac arrest
outcome of these agents and not allow their use to hinder, interrupt, or otherwise
adversely affect management, namely, the timely performance of high-quality chest
compressions and early electrical defibrillation.
REFERENCES
1. Out of hospital cardiac arrest: statistical guidelines. American Heart Association;

2007.
3. Stiell IG, Wells GA, DeMaio VJ, et al. Modifiable factors associated with improved
cardiac arrest survival in a multicenter basic life support/defibrillation system:
OPALS Study Phase I results. Ann Emerg Med 1999;33:4450.
4. Neumar RW, Otto CW, Link MS, et al. 2010 American Heart Association guidelines
for cardiopulmonary resuscitation and emergency cardiovascular care science.
Part 8: adult advanced cardiovascular life support. Circulation 2010;122:
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5. Herlitz J, Ekstrom L, Wennerblom B, et al. Adrenaline in out-of hospital ventricular
fibrillation. Does it make any difference? Resuscitation 1995;29:195201.
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6. Callaham M, Madsen CD, Barton CW, et al. A randomized clinical trial of highdose epinephrine and norepinephrine vs standard-dose epinephrine in prehospital cardiac arrest. JAMA 1992;268:266772.
7. Gueugniaud PY, Mols P, Goldstein P, et al. A comparison of repeated high doses
and repeated standard doses of epinephrine for cardiac arrest outside the
hospital. European Epinephrine Study Group. N Engl J Med 1998;339:1595601.
8. Brown CG, Martin DR, Pepe PE, et al. A comparison of standard-dose and highdose epinephrine in cardiac arrest outside the hospital. The Multicenter HighDose Epinephrine Study Group. N Engl J Med 1992;327:10515.
9. Lindner KH, Brinkmann A, Pfenninger EG, et al. Effect of vasopressin on hemodynamic variables, organ blood flow, and acid-base status in a pig model of
cardiopulmonary resuscitation. Anesth Analg 1993;77:42735.
10. Stiell IG, Hebert PC, Wells GA, et al. Vasopressin versus epinephrine for inhospital cardiac arrest: a randomized controlled trial. Lancet 2001;358:1059.
11. Guyette FX, Guimond GE, Hostler D, et al. Vasopressin administered with
epinephrine is associated with a return of a pulse in out-of-hospital cardiac arrest.
12. Wenzel V, Krismer AC, Arntz HR, et al. A comparison of vasopressin and epinephrine for out-of-hospital cardiopulmonary resuscitation. N Engl J Med 2004;350:
10513.
13. Gueugniaud PY, David JS, Canzy E, et al. Vasopressin and epinephrine vs
epinephrine alone in cardiopulmonary resuscitation. N Engl J Med 2008;359:
2130.
14. Brown DC, Lewis AJ, Criley JM. Asystole and its treatment: the possible role of
the parasympathetic nervous system in cardiac arrest. JACEP 1979;8:44852.
15. Stueven HA, Tonsfeldt DJ, Thompson BM, et al. Atropine in asystole: human
studies. Ann Emerg Med 1984;13:8157.
16. Coon GA, Clinton JE, Ruiz E. Use of atropine for bradyasystolic prehospital
cardiac arrest. Ann Emerg Med 1981;10:4627.
17. Brady WJ, Swart G, DeBehnke DJ, et al. The efficacy of atropine in the treatment
of hemodynamically unstable bradycardia and atrioventricular block: prehospital
and emergency department considerations. Resuscitation 1999;41:4755.
18. Swart G, Brady WJ, DeBehnke DJ, et al. Acute myocardial infarction complicated
by hemodynamically unstable bradyarrhythmia: prehospital and emergency
department treatment with atropine. Am J Emerg Med 1999;17:64752.
19. Herlitz J, Bang A, Holmberg M, et al. Rhythm changes during resuscitation from
ventricular fibrillation in relation to delay until defibrillation, number of shocks
delivered, and survival. Resuscitation 1997;34:1722.
20. Weaver WD, Fahrenbruch CD, Johnson DD, et al. Effect of epinephrine and lidocaine therapy on outcome after cardiac arrest due to ventricular fibrillation. Circulation 1990;82:202734.
21. Dorian P, Cass D, Schwartz B, et al. Amiodarone as compared with lidocaine for
shock-resistant ventricular fibrillation. N Engl J Med 2002;346:88490.
22. Kentsch M, Berkel H, Bleifeld W. Intravenose amiodaronapplikation bei therapierefraktarem kammerflimmern. Intesivmedizin 1998;25:704 [in German].
23. Kudenchuck PJ, Cobb LA, Copass MK, et al. Amiodarone for resuscitation after
out-of-hospital cardiac arrest due to ventricular fibrillation. N Engl J Med 1999;
341:8718.
24. Bar-Joseph G, Abramson NS, Jansen-McWilliams L, et al. Clinical use of sodium
bicarbonate during cardiopulmonary resuscitationis it used sensibly? Resuscitation 2002;54:4755.
25. Tobey RC, Birnbaum GA, Allegra JR, et al. Successful resuscitation and neurologic recovery from refractory ventricular fibrillation after magnesium sulfate
administration. Ann Emerg Med 1992;21:926.
26. Craddock L, Miller B, Clifton G, et al. Resuscitation from prolonged cardiac arrest
with high-dose intravenous magnesium sulfate. J Emerg Med 1991;9:46976.
27. Fatovich DM, Prentice DA, Dobb GJ. Magnesium in cardiac arrest (the magic
trial). Resuscitation 1997;35:23741.
28. Thel MC, Armstrong AL, McNulty SE, et al. Randomised trial of magnesium in inhospital cardiac arrest. Lancet 1997;350:12726.
29. Stueven H, Thompson BM, Aprahamian C, et al. Use of calcium in prehospital
cardiac arrest. Ann Emerg Med 1983;12:1369.
30. Harrison EE, Amey ED. The use of calcium in cardiac resuscitation. Am J Emerg
Med 1983;1:26773.
31. Donovan PJ, Propp DA. Calcium and its role in cardiac arrest: understanding the
controversy. J Emerg Med 1985;3:10516.
32. Parham WA, Mehdirad AA, Biermann KM, et al. Hyperkalemia revisited. Tex Heart
Inst J 2006;33:407.
33. Bottiger BW, Arntz HR, Chamberlain DA, et al. Thrombolysis during resuscitation
for out-of-hospital cardiac arrest. N Engl J Med 2008;359:265162.
34. Abu-Laban RB, Christenson JM, Innes GD, et al. Tissue plasminogen activator in
cardiac arrest with pulseless electrical activity. N Engl J Med 2002;346:15228.
35. Bottiger BW, Bode C, Kern S, et al. Efficacy and safety of thrombolytic therapy
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trial. Lancet 2001;357:15835.
75
Airway Management
i n C a rdi a c A r re s t
Jose V. Nable, MD, NREMT-Pa,*, Benjamin J. Lawner,
Christopher T. Stephens, MD, EMT-Pd
b,c
DO, EMT-P ,
KEYWORDS
Cardiac arrest Airway management
Cardiopulmonary resuscitation Assisted ventilation
Intubation Ventilator
The mantra of airway, breathing, circulation (ABC) is well known to practitioners of

emergency medicine. It positions airway management as a preeminent feature of
any resuscitation and engenders memories of Dr Peter Safar and his groundbreaking
work on artificial respiration. Recent discoveries surrounding the physiology of cardiac
arrest have turned the ABC mnemonic around. Although effective exchange of oxygen
is important to survival, it seems that maintenance of coronary and cerebral perfusion
eclipses airway management as an overriding goal of any cardiac arrest situation. The
last iteration of the American Heart Association (AHA) guidelines deemphasizes endotracheal intubation as the penultimate goal of airway intervention in cardiac arrest.
Instead, emergency practitioners should focus on the rapid delivery of uninterrupted
compressions and other basic life support interventions that have proved to increase
both survival and neurologic recovery. Important questions about airway management
persist. It is no longer a question of when a patient in cardiac arrest must be intubated.
The decision to perform endotracheal intubation results from a complex synthesis of
environmental and clinical factors. It may not be feasible for a system that lacks
veteran paramedics to mandate securing the airway with an endotracheal tube.
Recent advances in the understanding of cardiac arrest physiology suggest that
airway management, in the immediate phase following cardiac arrest, is subordinate
to interventions such as defibrillation and quality cardiac compressions. When intubation is performed, it should not interfere with the ongoing resuscitation and thereby

a
Department of Emergency Medicine, University of Maryland Medical Center, 110 South Paca
Street, 6th Floor, Suite 200, Baltimore, MD 21201, USA
b
Department of Emergency Medicine, University of Maryland School of Medicine, 110 South
Paca Street, 6th Floor, Suite 200, Baltimore, MD 21201, USA
c
Baltimore City Fire Department, Baltimore, MD, USA
d
Division of Trauma Anesthesiology, Department of Anesthesiology, R Adams Cowley Shock
Trauma Center, University of Maryland School of Medicine, 22 South Greene Street, Room
S11C00, Baltimore, MD 21201, USA
E-mail address: JVNABLE@gmail.com
doi:10.1016/j.emc.2011.09.009
emed.theclinics.com
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Nable et al
decrease the coronary perfusion that is so vital to survival. This article reviews the
state of the art as it applies to airway management in the patient with cardiac arrest.
Like any other medical intervention, the plan for airway management should proceed
from a thorough understanding of current evidence, provider capability, and emergency medical services (EMS) system resources.
PARADIGM SHIFTS IN AIRWAY MANAGEMENT
Physiology of Cardiac Arrest Ventilation
Ventilation is the exchange of gas that occurs as a result of air movement caused by
changes in pressure. During spontaneous respirations, contractions of respiratory
muscles cause an expansion of the chest cavity. A negative intrathoracic pressure
(ITP) is generated, resulting in air moving into the lungs.1 This negative-pressure ventilation is replaced with positive pressures when medical personnel attempt resuscitation of a patient during cardiac arrest. Although positive-pressure ventilation (PPV) has
been an essential component of resuscitating critically ill patients, understanding the
physiology of PPV and how it relates to patients in cardiac arrest is crucial to optimizing conditions favoring successful resuscitations.
The physiologic effect of PPV reducing coronary perfusion has long been studied.2
PPV forces air into the respiratory system, increasing ITP. This increased ITP impedes
blood flow returning to the heart and causes a marked decrease in left and right
ventricular end-diastolic volumes, thereby reducing preload.3 The Starling law reveals
that this reduction in preload results in a direct decrease in cardiac output during chest
compressions, thus reducing coronary perfusion. Therefore, PPV has the paradoxic
and potentially harmful effect of reducing cardiac output during the resuscitation of
a patient during cardiac arrest.
In addition to reducing coronary perfusion, PPV reduces the effectiveness of chest
compressions by preventing negative ITP from being generated during recoil of the
chest wall.4 This negative ITP during the recoil phase of chest compressions assists
with blood return to the chest cavity.5 Drawing blood back to the heart increases preload, which in turn increases cardiac output with the next chest compression.
However, while performing PPV, the generation of a negative ITP during chest wall
recoil is hindered. PPV can consequently make chest compressions less effective at
generating sufficient cardiac output.
Furthermore, PPV causes an increase in intracranial pressure.6 The excess intrathoracic pressure generated during PPV is transmitted to the intracranial space via the
venous vasculature. This process can result in a reduction in cerebral blood flow.
Even if the patient were to be successfully resuscitated, the potential for anoxic brain
injury or other profound complications from reduced cerebral blood flow is a possible
drawback of PPV. The reductions in coronary and cerebral perfusion during PPV have
profound implications for the management of patients in cardiac arrest.
De-emphasizing PPV
The deleterious effects of PPV mandate that it must be avoided, or at least reduced.
Despite AHA guidelines addressing concerns for hyperventilation, providers often
ventilate at rates exceeding 30 breaths per minute.7 So even when providers are
specifically trained not to overventilate, they often continue to do so. A deemphasis of PPV during training of providers, along with constant instruction by
EMS medical directors and other continuing medical educators must highlight the
potential harmfulness of PPV. Given the negative effects associated with ventilation,
as discussed earlier, it is imperative to reduce PPV during cardiac arrest. The ABC
Airway Management in Cardiac Arrest
mantra of resuscitation has been the standard teaching since at least the early 1960s,8
so the reduction of PPV represents a major paradigm shift in the management of
patients in cardiac arrest, for which the emphasis on early airway management
including intubation has long been emphasized.
Shifting the focus of resuscitations away from ventilations may improve other
aspects that have proved to be more beneficial, such as increasing the amount of
time compressing the chest. The cardiocerebral resuscitation (CCR) algorithm
reduces interruptions to compressions by specifically concentrating on continuous
chest compressions.9 CCR is composed of cycles of 200 continuous compressions,
each followed by defibrillation, if indicated. No PPV is given until at least the third
cycle, when intubation may be considered. Instead, rescuers use passive insufflations
with nonrebreather masks. Kellum and colleagues10 found that CCR greatly improved
outcomes, with 48% of patients being discharged from hospital with good neurologic
functions, versus 15% using standard cardiopulmonary resuscitation (CPR). CCR
represents a major shift in the standard resuscitative techniques because it inverts
ABC to CAB (circulation, airway, breathing).
The need to not interrupt chest compressions, at least during initial phases of resuscitation, cannot be overemphasized. Despite compression/ventilation ratios that
underscore the need for more time compressing the chest, less than half the time
spent resuscitating a patient by rescuers, particular EMS providers, includes performing chest compressions.11 Chest compressions are vital to achieving needed coronary
perfusion pressures (CPP). A study by Reynolds and colleagues12 found that higher
CPPs than previously thought were associated with return of spontaneous circulation
(ROSC) after cardiac arrest. Interrupting compressions to ventilate results in lower
CPP, thereby reducing ROSC. Continuous chest compression has been shown to
improve neurologic outcome following cardiac arrest.13 Given the importance of
perfusion during resuscitation, good chest compressions while minimizing PPV should
be emphasized. Resuscitation methods that reduce any interruptions to chest
compressions are highly desirable.
The concept of uninterrupted compressions is further supported by data from
compression-only resuscitation by bystanders. A large study in Japan convincingly
found that compression-only resuscitation resulted in more favorable neurologic
outcomes compared with traditional CPR in patients who were apneic, had a shockable rhythm, or whose resuscitations were begun within 4 minutes of cardiac arrest.14
Moreover, chest compressions may also provide some ventilation in the form of
passive chest recoil.15 In this respect, chest compressions may be a form of ventilation management. As such, uninterrupted chest compressions should be stressed and
prioritized rather than mechanical ventilation.
EMERGENCY MEDICINE AIRWAY MANAGEMENT: FROM PREHOSPITAL TO THE
EMERGENCY DEPARTMENT
Recent studies and the latest iteration of the AHA guidelines have challenged the idea
of endotracheal intubation as the gold standard for airway control in the arrested
patient.16 Prehospital providers, although capable of performing endotracheal intubation, are implementing less invasive strategies such as passive ventilation and supraglottic airways. The direct impact of endotracheal intubation to patient survival is
a matter of debate. The focus of cardiac arrest management has shifted toward the
delivery of excellent basic life support, uninterrupted compressions, and prompt
defibrillation. Prehospital providers, emergency clinicians, and other critical care
providers must have a thorough appreciation of the evidence base surrounding airway
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management of the patient in cardiac arrest. Definitive airway control in the form of
endotracheal intubation should not be achieved at the expense of other interventions
linked to increased survival and improved neurologic outcome.
Passive Airway Management
PPV, although long considered a staple of CPR, is being reevaluated. A retrospective

study by Bobrow and colleagues17 examined patients with out-of-hospital cardiac
arrest who underwent airway management via passive insufflation or bag-valvemask (BVM) ventilation. Responding paramedics were permitted, at their discretion,
to deliver oxygen via BVM or nonrebreather facemask. In the subset of patients with
witnessed arrest, passive ventilation was associated with increased neurologically
intact survival to discharge. Despite study limitations that included a retrospective
design and a lack of control for postarrest care, the association between neurologic
recovery and passive oxygenation deserves consideration. Oxygen delivery via face
mask does not require additional skills or equipment. It avoids the complications of
hyperventilation and may minimize gastric distention. Although 1 retrospective study
does not constitute a robust evidence base, it nevertheless reminds rescuers that
a single strategy of airway control has potential complications. However, the AHA
guidelines do not recommend removal of ventilation from CPR performed by
advanced cardiac life support providers.16
Noninvasive Airway Management
BVM ventilation is a cornerstone of emergency airway management. BVM strategies

are taught to all levels of EMS personnel, from basic to paramedic. AHA guidelines
affirm that all health care providers should be familiar with BVM techniques.16
Airway management of the patient in cardiac arrest requires considerable attention
to detail. First, rescuers must ensure avoidance of hyperventilation. Overzealous
inflation of the BVM is associated with negative patient outcomes and complications
such as hypotension.18 As previously discussed, hyperventilation increases intrathoracic pressure, diminishes venous return, and decreases coronary perfusion.7,19
Current AHA guidelines recommend low-volume (600 mL) ventilations for patients
in cardiac arrest. Rescuers should deliver 2 breaths during the brief pause that
follows every 30 chest compressions. When an advanced airway is not deployed,
rescuers should not synchronize ventilations with compressions. Other airway
adjuncts, such as nasopharyngeal airway (NPA) and oropharyngeal airway (OPA),
may assist with maintenance of a tight facemask seal. Use of the OPA and NPA
may also decrease airway resistance through displacement of the tongue. Cricoid
pressure is also addressed in the 2010 guidelines. Although long considered
customary in nearly all airway management scenarios, the application of cricoid
pressure is not grounded in evidence-based practice. Recent studies associate
cricoid pressure with impaired glottic visualization, airway obstruction, and even
esophageal perforation.20,21 The potential for complications and the lack of proven
patient benefit resulted in a recommendation to avoid the routine use of cricoid
pressure.16 Like any other skill, BVM ventilation requires ongoing training and skills
maintenance. It may be technically difficult for one rescuer to achieve an adequate
face mask seal and provide ventilation sufficient to achieve chest rise. AHA guidelines corroborate that the presence of 2 rescuers is key to the execution of excellent
BVM technique.16 Guiding principles of effective BVM ventilation include avoidance
of hyperventilation, the delivery of low volumes, and the maintenance of an
adequate mouth-to-mask seal.
Supraglottic Airway Device: Selection and Use
Providers are faced with many choices with respect to available airway management
devices. Although BVM ventilation is often sufficient for the first few minutes of CPR,
there is a perceived need to secure the patients airway. Endotracheal intubation, long
considered the optimum means of airway management for patients in arrest, has been
supplanted by simpler and more rapid techniques that may have less potential for
complication. Maintaining proficiency in endotracheal intubation is a significant barrier
for many prehospital providers, and the link between prehospital intubation and
survival in out-of-hospital cardiac arrest is not well established. Supraglottic airway
devices mitigate some of the concerns and difficulties surrounding endotracheal intubation. In general, less training is required to achieve a baseline level of proficiency.
Studies with supraglottic devices, including laryngeal mask airways (LMA) and laryngeal tube airways, indicate that basic-level emergency medical technicians (EMT) can
successfully use these devices. Furthermore, time to ventilation is reliably shorter
when a supraglottic device is chosen as the initial method for airway management.
In the first few minutes of resuscitation, the importance of minimizing interruptions
in CPR cannot be overstated. Even when performed by experienced providers, endotracheal intubation may result in unacceptable pauses in chest compressions.22 Wang
and colleagues22 reported an alarmingly high rate of intubation-associated pauses.
The investigators found that the median total duration (sum) of endotracheal
intubation-associated CPR interruptions was 109.5 seconds per patient. The AHA
guidelines therefore endorse the use of supraglottic airways as a reasonable alternative to bag-valve-mask ventilation and endotracheal intubation in the management of
cardiac arrest.16 A supraglottic airway may confer additional advantages in the more
austere out-of-hospital setting. Placement of these devices does not generally require
visualization of the glottic opening. Blind insertion methods, such as those used for
LMA insertion, obviate neck extension and airway manipulation.
The 2010 guidelines review 2 common types of supraglottic airway: the laryngeal
mask and the laryngeal tube.16 Insufficient exists to recommend one device rather
than another. Providers deciding to implement a supraglottic strategy for airway control
should be mindful of device-specific considerations. First, insertion of these airways
necessitates that the patient have sufficient mouth opening. Trismus, trauma, or supraglottic obstruction interferes with proper device placement. Supraglottic airways are
less effective in the ventilation of patients with a fixed decrease in airway compliance.
Severe underlying airway obstruction and high airway resistance found in conditions
such as cystic fibrosis and severe chronic obstructive pulmonary disease (COPD)
may impair ventilation.23 Gravid patients have decreased lower esophageal sphincter
tone and may be at increased risk for aspiration. These considerations should be
weighed against the ease of insertion when using a supraglottic device for a patient in
cardiac arrest. The relative contraindications for a laryngeal mask airway may not be
relevant for failed endotracheal intubation. The supraglottic airways feature prominently
in existing algorithms for difficult airway management.23,24 LMA use should complement other method for airway control. Certain patients may not be ventilated sufficiently
with a supraglottic device. Providers directly responsible for airway management
should therefore receive training in BVM ventilation and other strategies for airway
control such as endotracheal intubation or esophageal tracheal combitube insertion.
Tracheal Intubation: Revisiting the Gold Standard (Polishing the Touchstone?)
Endotracheal intubation is the gold standard in advanced airway management. Benefits traditionally associated with endotracheal intubation include effective ventilation
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and protection from aspiration. Despite its long-standing place in emergency airway
management, there is a paucity of data that link endotracheal intubation to improved
survival and neurologic recovery from cardiac arrest. Clinically significant patient
outcomes are consistently matched with the delivery of excellent basic life support
to include uninterrupted and effective compressions. The performance of endotracheal intubation requires a considerable amount of initial provider training in addition
to ongoing skills maintenance. The challenge of visualizing a glottic opening and
placing a tube through the cords has been shown to interrupt the delivery of potentially
life-saving cardiac compressions. As previously noted, these pauses are detrimental
to achieving needed CPP associated with successful ROSC. Current AHA guidelines
caution against interruption of CPR, and providers are encouraged to synchronize
their intubation efforts with ongoing resuscitation. Further complicating the performance of endotracheal intubation is its unacceptably high complication rate. Hypoxemia, oropharyngeal trauma, and misplacement can result from failed or prolonged
intubation attempts. The decision to tracheally intubate a patient in cardiac arrest is
therefore contingent on several factors including level of provider training and experience. Frequent experience or frequent retraining is recommended for health care
professionals authorized and trained to perform endotracheal intubation.16
Endotracheal intubation is also seldom performed compared with other procedures
undertaken by prehospital providers. In a large study involving more than 40 EMS
agencies, more than 30% of patients intubated in the prehospital setting required
more than 1 attempt.25 Multiple attempts at endotracheal intubation can be associated with airway trauma, aspiration, hypoxemia, and other serious complications.26,27
Endotracheal intubation is a difficult procedure that requires a significant amount of
time, and it is potentially associated with major complications, so it should be deemphasized in the management of patients in cardiac arrest.
The timing of endotracheal intubation may be critically important to the question of
survival. In the first few moments of cardiac arrest, patient survival is most clearly
linked to the preservation of coronary perfusion and minimally interrupted CPR.10
Endotracheal intubation cannot therefore supplant the delivery of excellent and effective basic life support. AHA guidelines do not articulate or recommend a specific time
interval for endotracheal intubation. No studies exist to directly address the relationship of advanced airway timing to improved survival. Immediate tracheal intubation
is deemphasized.16 In some cases, ventilation with a BVM or supraglottic airway
may function as definitive airway control. Certain clinical situations may mandate
endotracheal intubation. When protective airway reflexes are absent and frequent
suctioning is required to maintain patency, the introduction of an endotracheal tube
is key to ongoing airway management. Some patients cannot be ventilated with
a BVM or supraglottic airway; these individuals require tracheal intubation for definitive
control. For cardiac arrest, the AHA guidelines remind providers to limit intubation
attempts to less than 10 seconds.16
Providers should be meticulous in the confirmation and subsequent anchoring of the
endotracheal tube. Patient movement and transfer from ambulance stretcher to emergency department bed carry a risk of dislodgement.28 Confirmation of placement is at
once clinical and objective. Providers ideally should visualize the tube through the glottic opening, auscultate lung sounds, and use end-tidal carbon dioxide. A multimodal
approach is desirable because any single strategy fails to detect the potentially lethal
complication of tube misplacement or dislodgement: Improper placement of endotracheal tubes into the esophagus.can remain undetected despite physical examination,
chest radiography, and pulse oximetry methods.28 The setting of cardiac arrest is time
dependent. The imperative to rapidly secure the airway, coupled with a patient
presenting in extremis, poses many challenges to both prehospital and hospital-based

providers. An ideal strategy for tube confirmation should therefore require little time,
a minimum amount of training, and exhibit high reliability. Despite several readily available methods and devices to assist providers with confirmation of placement, the single
most reliable indicator of successful tracheal intubation remains detection of exhaled
carbon dioxide.29,30 Colorimetric detectors are simple devices that are easy to deploy.
The devices answer the question of correct placement within the space of several PPVs.
When managing the airway of a patient in full arrest, providers must pay meticulous
attention to tube confirmation because the decreased exchange of carbon dioxide
may lead to false-negative readings.28,29 Although the presence of end-tidal carbon
dioxide is specific for successful tube placement, no single confirmation modality
approaches perfect sensitivity or 100% reliability. Because resuscitation is a dynamic
event, it is prudent to continuously monitor carbon dioxide throughout treatment and
transport. Waveform capnometry might not be readily available in all settings of emergency health care. However, waveform capnometry permits real-time assessment of
tube position and permits early detection of tube dislodgement or ineffective air
exchange.30 As stated in the 2010 AHA guidelines, providers should always use
both clinical assessment and devices to confirm endotracheal tube location immediately after placement and throughout the resuscitation.16
VENTILATORY MANAGEMENT STRATEGIES
Avoidance of Hyperoxia
Successful resuscitation of the victim of cardiac arrest must rely on a team approach
to airway management, as well as meaningful and thoughtful goals of oxygenation and
ventilation. Much of the research has been focused on adequate perfusion techniques, showing the negative aspects of airway control regarding outcome. Oxygenation strategies must be considered during airway and ventilation management
throughout resuscitation and ROSC. Most, if not all, attempts at reviving victims of
cardiac arrest involve the use of oxygen delivery systems by health care providers.
Therefore, oxygen should be considered a resuscitation drug and used as such.
Most medical providers consider oxygen an important but benign aspect of emergency care. So how much oxygen is too much? Many experts think that oxygenation
strategies are less important during resuscitation attempts, but are they? Is too little
oxygen or too much oxygen deleterious to patient outcomes? Historically, oxygen
has been a mainstay of emergency skills teaching since the early studies of CPR.
The recommendation now is to assist ventilations during cardiac arrest with 100%
forced inspiratory oxygen (FiO2), 5 times that of room air. Could this aggressive
oxygenation with 100% FiO2 be causing further harm in an already compromised
circulation? This goal of treating patients using hyperoxia should be carefully examined. There has been extensive research into examining the effects of high levels of
oxygen during prolonged ventilation of patients in the intensive care unit. The theory
is that such supranormal levels of oxygen are likely resulting in the production of
oxygen free radicals (OFR). These OFRs are capable of interrupting cellular signaling
pathways in addition to causing direct damage to the cells. In a recent multicenter
cohort study, hyperoxic patients admitted to the intensive care unit (ICU) after being
successfully resuscitated from cardiac arrest showed increased in-hospital
mortality.31 In this study, patients who were deemed to have arterial hyperoxia
(defined as partial arterial oxygen tension [PaO2] 300 mm Hg) were associated with
a higher mortality than hypoxic patients (PaO2 <60 mm Hg).31 In support of these
observations, studies of cardiac arrest using hyperoxia have shown a worsened
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oxidative stress and, hence, impaired neurologic outcomes.3234 In addition to OFRmediated oxidative stress, studies suggest that hyperoxia may compromise coronary
perfusion and cardiac output through coronary and peripheral vasoconstriction, thus
leading to worsened ischemia-reperfusion injury as well as fueling the inflammatory
response.3537 Based on these results, the idea of oxygenating and ventilating cardiac
arrest patients with 100% FiO2 should perhaps be revisited. However, this issue is
complex. Many experts argue that there is a major difference between early resuscitation and late resuscitation and/or ROSC. So is it necessary to titrate oxygen therapy
throughout the phases of resuscitation? A study of experimental cardiopulmonary
arrest suggested salutary effects of titrating oxygen delivery to arterial oxygen saturation in the early postresuscitation period.32 In addition to oxygenation issues, ventilation after ROSC involves a careful and thoughtful plan to optimize patient outcomes.
Ventilation During Induced Hypothermia
In the past decade, there has been a renewed interest in hypothermic treatment of
patients suffering from traumatic brain injury, stroke, and cardiac arrest. However,
there has been a paucity of evidence to support the use of routine hypothermia in
patients suffering from head injury or stroke. In contrast, there has been a significant
amount of data to suggest that routine use of induced hypothermia in patients who
have been resuscitated from cardiac arrest may improve neurologic outcome. The
protective effects of induced hypothermia are thought to be secondary to decreased
cerebral carbon dioxide production, decreased oxygen consumption, immunomodulation, and overall diminished cerebral edema and epileptic foci.3840 Despite
a renewed interest in hypothermic techniques for cardiac arrest resuscitation and
recovery, little has been studied with respect to ventilator therapy and lung
mechanics. Clinical scientists have had to rely on ventilator outcome data from similar
populations such as critically ill septic patients, patients having cardiac bypass, and
patients with neurotrauma. The literature is lacking with respect to changes in lung
physiology and ventilator management when caring for the patient in the ICU after
arrest.
During the initial moments after ROSC, many tasks must be completed with respect
to airway management. A goal-directed strategy must be implemented to ensure
optimal oxygenation and ventilation. If a supraglottic airway device has been used
in the field, it must be replaced by an endotracheal tube so that mechanical ventilation
can be commenced. The patient will likely be cooled in the first minutes to hours after
ROSC. To achieve the goals of induced hypothermia and improved neurologic
outcome, the patient should be sedated if the neurologic and hemodynamic states
warrant this.
Before the induction of hypothermia, a baseline panel of respiratory blood gases
should be examined. Evidence shows that the hypothermic state slows metabolism
and therefore likely alters normal gas exchange and cellular use. Hence, goals for
mechanical ventilation include optimizing blood gas levels, preventing hemodynamic
instability, and resting the patient. It can be assumed that all patients that are resuscitated and in a reperfusion state are at risk for hemodynamic instability, acute lung
injury, acute respiratory distress syndrome (ARDS), and other lung-related disorders
such as pneumonia, atelectasis, and pulmonary edema. Patients after arrest are at
particularly high risk for acute lung injury and ARDS, especially those transported
from the field. Many of these patients have associated lung comorbidities such as
COPD and history of smoking in addition to their coronary disease. Furthermore,
a large percentage of patients managed in the field have aspirated various amounts
of gastric contents before the placement of a definitive secured airway. In addition
to these pulmonary embarrassments, all resuscitated patients have the secondary

insult of ischemia-reperfusion injury to tissue beds including the lung. As a result,
attention must be focused on preventing further lung injury in these cooled, mechanically ventilated patients.
There are data suggesting that mild hypothermia may alter lung mechanics as well
as respiratory gas production and use. Hypothermic reduction in carbon dioxide
production may be masked by simultaneous alterations in lung compliance, resistance, and gas exchange.41,42 To test this notion of altered lung mechanics during
induced hypothermia, Aslami and colleagues43 studied the effects of mild induced
hypothermia on lung parameters in patients admitted to the ICU after resuscitation
from cardiac arrest. Parameters included tidal volume, positive end-expiratory pressure (PEEP), plateau pressure, respiratory rate, end-tidal CO2 (ETCO2), and FiO2. In
addition, static compliance and dead-space ventilation were recorded. The study
cohort was mechanically ventilated in a pressure-controlled mode with an inspiratory/expiratory time of 1:2. PaCO2 was decreased during the hypothermic period
with unchanged minute ventilation, whereas PaO2/FiO2 ratio increased without altering
PEEP levels. During rewarming, PaCO2 was unchanged; however, ETCO2 increased
with the same minute ventilation. Dead-space ventilation was unchanged and
decreased during hypothermia and rewarming, respectively. Conversely, respiratory
static compliance was unaltered throughout both hypothermic and rewarming
phases. Based on the results of these studies, it is likely that hypothermia decreases
carbon dioxide production in the mechanically ventilated postarrest population.
Furthermore, lower tidal volume, as used in patients with acute lung injury (ALI),
may prove to be beneficial in this patient population by resting the ischemiareperfused lung tissue in hypocapnia. Results suggest that tidal volumes as low as
4 mL/kg may be beneficial in these hypocapneic, hypothermic patients to prevent
further lung injury. Although lung compliance has been shown to be altered in most
critically ill ventilator-dependent patients, this may not be the case during temporary
induction of hypothermia in postarrest ICU management. In addition to the potential
of unaltered lung compliance in most patients, the suspected decrease in oxygen
demand and use during induced hypothermia may allow reduction in FiO2 as well as
PEEP levels throughout the postarrest recovery phase. Based on the limited literature
and anecdotal experience, ventilator management in the postarrest hypothermic
patient should be targeted to resting the lungs, which can be accomplished through
either a volume or pressure mode of ventilation, targeting smaller tidal volumes and
plateau pressures. In addition, it may be prudent to use minimal to moderate PEEP
in this patient population depending on the individuals oxygenation status. All patients
undergoing a hypothermic postarrest protocol should be mechanically ventilated,
using sedation and muscle relaxation. Muscle relaxants allow for controlled respirations, maintaining a narrow window of targeted blood gas values, in addition to preventing the shivering response, which could potentially alter metabolic goals.
Optimal Ventilator Support
Ventilatory management in patients with ROSC is critical to ensure metabolic

recovery. During the initial stages of ROSC, there is considerable damage to the
internal milieu of tissue beds and cells. Reperfusion injury results in catastrophic alterations in cellular signaling cascades and metabolic machinery. OFRs, inflammatory
cytokines, and acids are an integral part of this process and clinical scientists must
do whatever is necessary to prevent further cellular injury. Goals are therefore directed
at maintaining the organisms physiology in the most homeostatic state possible, to
allow recovery of viable tissues and cells, although this is easier said than done.
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Studies have shown that optimal ventilatory support in critically ill patients should
target strategies that minimize ALI and the potential for ARDS, as stated earlier. Traditional approaches used tidal volumes of 10 to 12 mL/kg and excessively high PEEPs.
To minimize risks of barotrauma and volutrauma (risks for ALI and ARDS), tidal volume
(Vt) must be set to lower levels (68 mL/kg) and best PEEP must be targeted, which is
defined as the lowest PEEP possible to ensure optimal oxygenation and hemodynamic stability. High levels of PEEP result in several undesirable effects. High intrinsic
PEEP or auto-PEEP leads to increased intrathoracic pressures, interrupting venous
return, diminishing cardiac output, and ultimately compromising both coronary and
global perfusion. In addition, high intrathoracic pressures may cause an increase in
intracranial pressure (ICP), which can be deleterious in an already compromised
recovering cerebrum.
Once the patient is stabilized, mechanical ventilator settings optimized, and hypothermic targets reached, a chest radiograph should be ordered to determine correct
endotracheal tube placement and whether any lung disorder is present. Blood gas
measurements should be followed closely in the first few hours of mechanical ventilation to ensure optimal respiratory physiology. ALI is suggested if the PaO2/FiO2 is less
than or equal to 300 mm Hg. If PaO2/FiO2 is less than 200, this indicates ARDS. Strategies to improve pulmonary derangements during hypothermic protocol include
titrated FiO2 and PEEP levels based on dynamic lung physiology. Recommended
guidelines suggest titrating the minimum FiO2 to maintain arterial oxygen saturations
at greater than or equal to 94%, with the goal of ensuring adequate oxygen delivery
while preventing hyperoxia.44 Studies of animal models of ROSC have shown that
ventilating with FiO2 of 100% in the first 15 to 60 minutes after ROSC worsens brain
lipid peroxidation, metabolic dysfunction, neuron degeneration, and short-term functional outcome compared with ventilation with room air or titrating FiO2 to arterial saturations between 94% and 96%.33,34,4548
Hyperventilation was once thought to be the best method to aid in reversing
a combined respiratory and metabolic acidosis that ensued after cardiac arrest.
Although theoretically beneficial, we have determined this practice to be detrimental.
Hyperventilating the hypothermic patient after arrest can be problematic for several
reasons. Increased minute ventilation (respiratory rate and Vt) decreases PCO2, thus
shifting the oxyhemoglobin dissociation curve to the left, altering the delivery of
oxygen to the tissues. In addition, lowered PCO2 alters cerebral circulation. Hypocapnia causes cerebral vasoconstriction, thus diminishing cerebral blood flow and
oxygenation, exacerbating neurologic ischemic injury. Hence, it is recommended to
use conventional ventilator modes, aiming for normocapnia, best PEEP, carefully
titrated to lowest FiO2 possible to maintain arterial saturations greater than or equal
to 94%, and a relaxed sedated patient. There is no compelling evidence to show
that any special ventilation method should be used other than those described earlier.
Clinicians must be vigilant and prevent hyperventilation, hypoventilation, and associated hypoxemia and hypercarbia, as well as ALI and/or ARDS. In addition to these
lung-sparing guidelines, several monitoring techniques are equally important to help
guide the clinician caring for the hypothermic patient after arrest.
Once the patient with ROSC has been stabilized in the ICU and is on mechanical
ventilation, an arterial catheter should be placed to monitor hemodynamics as well
as intermittent arterial blood gas measurements to help guide ventilator management.
In addition, continuous arterial pulse oximetry should be used and targeted to 94% to
96%, which should correspond to a PaO2 of 80 to 100 mm Hg. FiO2 should be titrated
down to reach these oxygenation goals. Continuous waveform capnography is now
considered the gold standard for monitoring integrity of the intubated patient as
well as to measure ETCO2 and maintain a normocapneic state of approximately 35 to

40 mm Hg and PaCO2 of 4045 mm Hg. Again, chest radiographs should be used as
needed to determine correct endotracheal tube positioning and to follow any developing lung disorders.
Ventilatory management of the patient being resuscitated from cardiac arrest is
a delicate balance that must take into account the goals of needing to optimize blood
gas levels while resting the patient, maintaining hemodynamic stability. Because such
patients have lung mechanics that closely resemble ARDS, the lowest possible PEEP
must be used. Hyperventilation must also be avoided. Furthermore, careful titration of
FiO2 to achieve goal arterial saturations greater than or equal to 94% is recommended.
SUMMARY
Airway management of the patient in cardiac arrest is of prime importance. Paradigm

shifts in the understanding of cardiac arrest physiology have resulted in changes to
overall management strategies. Historically, the tracheal intubation was considered
central to any successful resuscitation. Tracheal intubation confers advantages
compared with noninvasive ventilation, but it can no longer be recommended without
reservation. Neurologic recovery and improved survival is closely associated with
uninterrupted compressions, high-quality CPR, and basic life support interventions.
As opposed to placement of a tube through the glottic opening, the initial goal of emergency airway management is the provision of effective ventilation. Chest rise, as
produced with a BVM or supraglottic airway, may be sufficient in the first few minutes
of resuscitation. AHA guidelines and current research support the idea that deployment of an advanced airway may be deferred until the completion of 2 compression
cycles.10,16 Although the optimum timing for endotracheal intubation remains unclear,
there are no data to support the idea that it must be performed immediately. Providers
should focus on minimizing interruptions in compressions and delivering high-quality
basic life support. Emergency providers capable of performing endotracheal intubation must do so with the goal of integrating intubation attempts into the resuscitation
as opposed to expecting a protracted pause. Endotracheal intubation has complications, and providers should be sufficiently trained and retrained to maintain proficiency. Ideally, advanced airway placement should be confirmed clinically and with
the presence of end-tidal carbon dioxide. The addition of continuous waveform capnometry capability permits early recognition of unsuccessful tube placement or
dislodgement. Further, the goals of ventilator support of the resuscitated patient
include the need to use the lowest possible PEEP while carefully titrating FiO2 to avoid
hyperoxia.
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1. Zin WA. Elastic and resistive properties of the respiratory system. In: Lucangelo U,
Pelosi P, Zin WA, et al, editors. Respiratory system and artificial ventilation. New
York: Springer; 2008. p. 21.
2. Cournand A, Motley HL, Werko L, et al. Physiologic studies of the effects of intermittent positive pressure breathing on cardiac output in man. Am J Physiol 1947;
152:16274.
3. Fewell JE, Abendschein DR, Carlson CJ, et al. Continuous positive-pressure
ventilation decreases right and left ventricular end-diastolic volumes in the dog.
Circ Res 1980;46:12532.
4. Aufderheide TP, Sigurdsson G, Pirrallo RG, et al. Hyperventilation-induced hypotension during cardiopulmonary resuscitation. Circulation 2004;109:19605.
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5. Lurie KG, Zielinski T, McNight S, et al. Use of an inspiratory impedance valve

improves neurologically intact survival in a porcine model of ventricular fibrillation. Circulation 2002;105:1249.
6. Guerci AD, Shi AY, Levin H, et al. Transmission of intrathoracic pressure to the
intracranial space during cardiopulmonary resuscitation in dogs. Circ Res
1985;56(1):2030.
7. Aufderheide TP, Lurie KG. Death by hyperventilation. Crit Care Med 2004;32(9):
S34551.
8. Safar P, Elam JO, Jude JR, et al. Resuscitative principles for sudden cardiopulmonary collapse. Dis Chest 1963;43:3449.
9. Ewy GA. Cardiocerebral resuscitation: the new cardiopulmonary resuscitation.
Circulation 2005;111:213442.
10. Kellum MJ, Kennedy KW, Ewy GA. Cardiocerebral resuscitation improves survival
of patients with out-of-hospital cardiac arrest. Am J Med 2006;119:33540.
during emergency medical systems resuscitation. Circulation 2005;112:125965.
12. Reynolds JC, Salcido DD, Menegazzi JJ. Coronary perfusion pressure and return
of spontaneous circulation after prolonged cardiac arrest. Prehosp Emerg Care
2010;14:7884.
13. Kern KB, Hilwig RW, Berg RA, et al. Importance of continuous chest compressions during cardiopulmonary resuscitation: improved outcome during a simulated single lay rescuer scenario. Circulation 2002;105:6459.
369:9206.
15. Noc M, Weil HM, Tang W, et al. Mechanical ventilation may not be essential for
initial cardiopulmonary resuscitation. Chest 1995;108:8217.
16. Neumar RW, Otto CW, Link MS, et al. Part 8: Adult advanced cardiac life support:
2010 American Heart Association guidelines for cardiopulmonary resuscitation
and emergency cardiac care. Circulation 2010;1222(183):S72767.
17. Bobrow BJ, Ewy GA, Clark L, et al. Passive oxygen insufflation is superior to bag
valve mask ventilation for witnessed fibrillation out of hospital cardiac arrest. Ann
Emerg Med 2009;54(5):65662.
18. Davis DP. The impact of hypoxia and hyperventilation on outcome after paramedic rapid sequence intubation of severely head-injured patients. J Trauma
2004;57(1):18.
19. Wang HE, Yealy DM. Out of hospital endotracheal intubation: where are we. Ann
Emerg Med 2006;47(6):53241.
20. Hocking G, Roberts FL, Thew ME. Airway obstruction with cricoid pressure and
lateral tilt. Anaesthesia 2001;56:8258.
21. Hartsilver EL, Vanner RG. Airway obstruction with cricoid pressure. Anaesthesia
2000;55:20811.
22. Wang HE, Simeone SJ, Weaver MD, et al. Interruptions in cardiopulmonary resuscitation from paramedic endotracheal intubation. Ann Emerg Med 2009;54:
64552.
23. Barata I. The laryngeal mask airway: prehospital and emergency department
use. Emerg Med Clin North Am 2008;26:106983.
24. Lavery GG, McCloskey BV. The difficult airway in adult critical care. Crit Care Med
2008;36(7):216373.
25. Wang HE, Yealy DM. How many attempts are required to accomplish out-ofhospital endotracheal intubation? Acad Emerg Med 2006;13:3727.
26. Jaeger K, Ruschulte H, Osthaus A, et al. Tracheal injury as a sequence of multiple

attempts of endotracheal intubation in the course of a preclinical cardiopulmonary resuscitation. Resuscitation 2000;43:14750.
27. Mort TC. Emergency tracheal intubation: complications associated with repeated
laryngoscopic attempts. Anesth Analg 2004;99:60713.
28. Burton JH, Huff JS, Lavonas EJ. Verification of endotracheal tube placement.
Dallas (TX): American College of Emergency Physicians; 2009.
29. Grmec S. Comparison of three different methods to confirm tracheal tube placement in emergency intubation. Intensive Care Med 2002;28:7014.
30. Silvestri S, Ralls GA, Krauss B, et al. The effectiveness of out of hospital use of
continuous end tidal carbon dioxide monitoring on the rate of unrecognized misplaced intubation within a regional emergency medical services system. Ann
Emerg Med 2005;45:497503.
31. Kilgannon JH, Jones AE, Shapiro NI, et al. Association between arterial hyperoxia
following resuscitation from cardiac arrest and in-hospital mortality. JAMA 2010;
303:216571.
32. Balan IS, Fiskum G, Hazelton J, et al. Oximetry-guided reoxygenation improves
neurological outcome after experimental cardiac arrest. Stroke 2006;37:300813.
33. Liu Y, Rosenthal RE, Haywood Y, et al. Normoxic ventilation after cardiac arrest
reduces oxidation of brain lipids and improves neurological outcome. Stroke
1998;29:167986.
34. Zwemer CF, Whitesall SE, DAlecy LG, et al. Cardiopulmonary-cerebral resuscitation with 100% oxygen exacerbates neurological dysfunction following nine
minutes of normothermic cardiac arrest in dogs. Resuscitation 1994;27:15970.
35. McNulty PH, Robertson BJ, Tulli MA, et al. Effect of hyperoxia and vitamin C on
coronary blood flow in patients with ischemic heart disease. J Appl Physiol
2007;102:20405.
36. Lu J, Dai G, Egi Y, et al. Characterization of cerebrovascular responses to hyperoxia and hypercapnia using MRI in rat. Neuroimage 2009;45:112634.
37. Dyson A, Stidwill R, Taylor V, et al. The impact of inspired oxygen concentration
on tissue oxygenation during progressive haemorrhage. Intensive Care Med
2009;35:178391.
38. Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survivors of out-ofhospital cardiac arrest with induced hypothermia. N Engl J Med 2002;346:55763.
39. Polderman KH. Mechanisms of action, physiological effects, and complications
of hypothermia. Crit Care Med 2009;37:S186202.
40. Nordmark J, Enblad P, Rubertsson S. Cerebral energy failure following experimental cardiac arrest hypothermia treatment reduces secondary lactate/
pyruvate-ratio increase. Resuscitation 2009;80:5739.
41. Sitzwohl C, Kettner SC, Reinprecht A, et al. The arterial to end-tidal carbon
dioxide gradient increases with uncorrected but not with temperature-corrected
PaCO2 determination during mild to moderate hypothermia. Anesth Analg
1998;86:11316.
42. Deal CW, Warden JC, Monk I. Effect of hypothermia on lung compliance. Thorax
1970;25:1059.
43. Aslami H, Binnekade JM, Horn J, et al. The effect of induced hypothermia on
respiratory parameters in mechanically ventilated patients. Resuscitation 2010;
81:17235.
44. Peberdy MA, Clifton W, Callaway RW, et al. Part 9: Post-cardiac arrest care: 2010
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45. Marsala J, Marsala M, Vanicky I, et al. Post cardiac arrest hyperoxic resuscitation
enhances neuronal vulnerability of the respiratory rhythm generator and some
brainstem and spinal cord neuronal pools in the dog. Neurosci Lett 1992;146:
1214.
46. Vereczki V, Martin E, Rosenthal RE, et al. Normoxic resuscitation after cardiac
arrest protects against hippocampal oxidative stress, metabolic dysfunction,
and neuronal death. J Cereb Blood Flow Metab 2006;26:82135.
47. Richards EM, Fiskum G, Rosenthal RE, et al. Hyperoxic reperfusion after global
ischemia decreases hippocampal energy metabolism. Stroke 2007;38:157884.
48. Richards EM, Rosenthal RE, Kristian T, et al. Postischemic hyperoxia reduces
hippocampal pyruvate dehydrogenase activity. Free Radic Biol Med 2006;40:
196070.
P ro g n o s i s i n C a rd i a c
Arre st
Joseph P. Martinez,
MD
KEYWORDS
Cardiac arrest Prognosis Cardiopulmonary resuscitation
Neurologic outcome
Cardiac arrest (CA) remains a worldwide challenge. Nearly 450,000 Americans suffer
from CA annually, with another 350,000 to 700,000 Europeans involved.1,2 Out-ofhospital CA is the third leading cause of death in the United States.3 Survival rates
remain low, averaging 2% to 5% in most studies, occasionally as high as 10%. Inhospital arrests fare slightly better, with survival rates still a dismal 15%.4 Several
prognostic factors have been identified. These factors may be broadly divided into
prearrest factors, intra-arrest factors, and postarrest factors. Of note, the great
majority of the research on this topic was conducted before the development of protocols for therapeutic hypothermia (TH) for comatose survivors of CA. It is unclear
whether widespread adoption of TH will alter the prognostic capabilities of some of
these factors.
PREARREST FACTORS
Several factors alter the prognosis of CA even before the initiation of advanced life
support (ALS) measures. Some of these factors are specific to out-of-hospital CA
(OHCA) whereas others relate to in-hospital CA (IHCA). Well-established factors in
OHCA that influence the survival from CA include initial rhythm, location, age, witnessed arrest or not, bystander cardiopulmonary resuscitation (CPR), mode of arrest
(respiratory vs cardiac), and delay to arrival of rescue team (Table 1). Other factors
include time of day, day of week, and gasping or other abnormal respiratory efforts.
Some factors more specific to IHCA include ward experience (more than 5 resuscitations per year), hospital location, use of automated external defibrillator (AED), and
again, time of day/day of week (Table 2).
OUT-OF-HOSPITAL CARDIAC ARREST
It is clear that victims of OHCA have better outcomes if they present to emergency
medical services (EMS) providers in a shockable rhythm such as ventricular fibrillation
Disclosures: None.
Department of Emergency Medicine, University of Maryland School of Medicine, 110 South
Paca Street, Sixth Floor, Suite 200, Baltimore, MD 21201, USA
E-mail address: jmartinez@som.umaryland.edu
doi:10.1016/j.emc.2011.09.010
emed.theclinics.com
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Martinez
Table 1
Prognostic factors in out-of-hospital cardiac arrest
Factor
Association
Initial rhythm
VF/VT survival 6 times as high
Location
Public arrest: survival 34 times more likely

Workplace arrest: survival 6 times more likely
Age
Older age associated with worsened survival

Young adults (1835) with marginally better outcomes
CPR
Any form of bystander CPR greatly increases chance of survival
Time to defibrillation
AED use before EMS arrival 1.75-fold more likely to survive
Time of day
Peak incidence 810
Gasping
Survival 28% vs 8%; with bystander CPR survival 39% vs 9.4% if not
gasping
AM;
lowest survival midnight to 6 AM
Abbreviations: AED, automated external defibrillator; CPR, cardiopulmonary resuscitation; EMS,

emergency medical services; VF/VT, ventricular fibrillation/ventricular tachycardia.
(VF) or pulseless ventricular tachycardia (VT). Survival when a patient presents in

a shockable rhythm is up to 6 times as high as when they have a nonshockable
rhythm.5 These rhythms occur early in the course of an arrest and deteriorate to
rhythms less amenable to intervention. Time to defibrillation is important. The use of
an AED prior to EMS arrival is associated with a 1.75-fold increase in survival to
hospital discharge.6 People that have witnessed arrests in public places have a better
outcome. Survival is 3 to 4 times more likely if a patient arrests in a public place and 6
times more likely if they arrest in the workplace.7 In general, arrests in public or in the
workplace tend to be younger, to be men, and to be in VF. Those that arrest at home
are more likely to be elderly, female, unwitnessed, and not VF.7 If the event is witnessed and a bystander performs CPR, outcomes from CA are improved. Delays to
arrival of the rescue team and advanced age lead to worse outcomes.5 It is interesting
that although advanced age portends a poor prognosis, young adults (age 1835) do
not always fare better. In one study, their 1-month survival was only 6.3%. This group
tended to suffer from noncardiac arrests (the majority were drug overdoses), were
Table 2
Prognostic factors in in-hospital cardiac arrest
Factor
Association
Rhythm
VF/VT still has a better outcome but occurs much less frequently than in
OHCA (fewer than 20% of all IHCAs)
Time to CPR and

defibrillation
Survival 33% if CPR started in less than 1 min (vs 14% if >1 min)
Survival 38% if VF/VT defibrillated in <3 min (vs 21% if >3 min)
Hospital location
ICUs have better survival rates

Wards with >5 arrests per year have better survival rates
Hemodialysis units have better survival rates
Time of day
Night shift arrests have half the survival of daytime arrests
AED use
Worse survival (10.4% vs 15.4%) when used for nonshockable arrests

No survival benefit in shockable arrests
Abbreviations: ICU, intensive care unit; IHCA, in-hospital cardiac arrest; OHCA, out-of-hospital
cardiac arrest.
Prognosis in Cardiac Arrest
less likely to be witnessed, and were less likely to be in VF. Of those young adults who
did present in VF, survival was nearly 21%.8
Several clinical prediction rules for the termination of resuscitation have been developed and validated. Separate criteria were developed for basic and ALS teams. The
ALS rule stated that termination of resuscitation could be considered in the prehospital
setting if there was no return of spontaneous circulation (ROSC) at any point during the
resuscitation, no shock was given, the arrest was not witnessed by EMS personnel or
bystanders, and no bystander CPR was delivered.9 The basic life support rule recommended termination of resuscitation of patients treated by defibrillation-only emergency medical technicians if the following criteria were met: no ROSC before
transport, no shock given, and the arrest not witnessed by EMS personnel.10 In an
effort to optimize consistency among EMS providers, the investigators performed
a secondary cohort analysis and determined that using the basic life support criteria
as a universal rule would result in a lower overall transport rate without missing
any potential survivors.11
Recent study of the chronobiology of OHCA has elucidated several interesting principles. A study of nearly 10,000 patients in the United States and Canada showed that
the frequency of OHCA varied significantly across time of day, day of week, and month
of year. Even more interesting was that survival to hospital discharge also varied
according to time of day and day of week. Dividing the day into 4 6-hour time blocks,
it was shown that there is a daytime excess to CA with a peak between 8 AM and 10 AM.
Significant variation across day of week was seen with the maximal number of CAs
occurring on Saturdays. Contrary to other studies, there was no excess of CA on
Mondays or workdays. The maximum number of CAs occurred in December without
evidence of seasonal variability across these geographically distinct study centers. In
terms of prognosis, survival to discharge was lowest in the midnight to 6 AM time block,
likely due to these events occurring in private residences and being unwitnessed.
Survival was highest for arrests occurring on Mondays, but overall survival was not
different between weekdays and weekends.12 Further research into this topic may
assist hospitals with determining staffing patterns and resource allocation.
In a study using TH, the most important prognostic factor was time to ROSC, even in
those patients with non-VF arrests. When time to ROSC was 25 minutes or less,
survival to hospital discharge was 65.7% with nearly 58% of these patients having
predominantly good neurologic outcome. Outcomes were dismal in the group where
ROSC took longer than 25 minutes, with no survivors with good neurologic outcome.13
Gasping or abnormal breathing after CA has been recognized as an important prognostic factor; it is common but decreases rapidly with time. Gasping was seen in 33%
of those patients who arrested after EMS arrival but only 7% of those in whom EMS
arrival took longer than 9 minutes. Those who gasped were significantly more likely
to survive (28% vs 8% in the nongasper group, P<.0001).14 Gaspers who received
bystander CPR had a survival of 39% whereas nongaspers who received CPR had
a survival of only 9.4%. Gasping appears to indicate marginally adequate cerebral
perfusion. In animal studies, gasping increased ventilation and cardiac output,
decreased intracranial pressure, and increased cerebral perfusion pressure.15,16
There are concerns that laypersons and even some health care professionals delay
performing CPR when the victim is gasping, mistakenly believing that they are not
in arrest. In an effort to ensure that the presence of gasping does not delay the institution of CPR, the 2010 American Heart Association Guidelines for Cardiopulmonary
Resuscitation and Emergency Cardiovascular Care (AHA Guidelines for CPR and
ECC) prompts lay rescuers to provide CPR if the victim is not breathing or only
gasping.17
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IN-HOSPITAL CARDIAC ARREST
Survival from IHCA has not significantly changed in the last 30 years and hovers around
15% to 20%. Similar to OHCA, VF arrests have better outcomes. Such arrests can be
treated promptly and seem to signify recent onset of CA. However, there is a lower
prevalence of VF arrests in IHCA than in OHCA. VF/pulseless VT arrests occur in fewer
than 20% of IHCA versus rates as high as 45% to 71% in some OHCA studies conducted in public locations.18 In-hospital CA is more often caused by hypoxia or hypotension,
which may contribute to lower survival rates. Time to CPR or defibrillation is one of the
more important prognostic factors in IHCA. When CPR is started within 1 minute of
arrest, survival is 33% versus 14%. In VF/VT arrests, defibrillation within 3 minutes
yields survival rates of 38% versus 21% if the time interval is greater than 3 minutes.19
Hospital location changes prognosis in IHCA. CAs in intensive care units (ICUs) fare
better, despite these units housing sicker patients. In ICUs all arrests are witnessed and
monitored; there is immediate ALS availability, and often younger median age populations. In addition, patients selected for resuscitation may be more appropriate, due to
better use of Do Not Attempt Resuscitation orders. Relative frequency of resuscitation events may contribute to survival rates. Wards that have more than 5 CAs per year
have better survival rates, even if all ward personnel receive basic life support and
advanced cardiac life support training.20 Prognosis of arrest on hemodialysis units is
better than on general wards, again more likely due to environmental factors (all witnessed arrests, vascular access in place, CPR equipment readily available) than underlying patient characteristics. Hemodialysis unit arrests are more common on Mondays
and Tuesdays than on other days, presumably because of the longer hemodialysis-free
interval of the weekend.21 Time of day affects survival as well. Arrests occurring at night
on general hospital wards have one-half the likelihood of survival.
A recent and disconcerting finding was that AED use during IHCA did not improve
survival. The use of AEDs was actually associated with lower survival rates (16.3% vs
19.3% if AED not used, P<.001). This finding was primarily due to significantly worse
survival in patients with nonshockable rhythms (10.4% vs 15.4%, P<.001). There was
no offsetting survival benefit in patients with shockable rhythms (38.4% vs 39.8%,
P 5 .99). These results were consistent across hospital wards and from monitored
to unmonitored units.22 As mentioned previously, the prevalence of VF arrests in
OHCA is much higher than that of IHCA, which may partially account for the improved
survival in OHCA after implementation of public AED programs. The investigators
hypothesize that the lower survival in nonshockable rhythms may be a result of the
time required for AEDs to assess these rhythms, thus leading to longer hands-off
intervals during CPR. It is increasingly clear that high-quality CPR is the most effective
intervention in resuscitations of nonshockable rhythms, and the use of an AED may
hinder compression delivery.
INTRA-ARREST FACTORS
Several prognostic factors have been identified during the provision of active resuscitation (Table 3). These factors include partial pressure of end-tidal CO2 (PETCO2) and
the use of cardiac sonography. The utility of ultrasound during resuscitation includes
both detection of cardiac standstill and exclusion of reversible causes.
END-TIDAL CO2 MONITORING
Circulating blood delivers the CO2 that is produced in the body to the lungs. In CA,
CO2 is produced but not delivered to the lungs. Thus, PETCO2 approaches zero. Initial
Table 3
Prognostic factors intra-arrest
Factor
Association
PETCO2
Values less than 10 mm Hg at 20 min are not compatible with survival

Abrupt and sustained increase indicates ROSC
Ultrasonography
Cardiac standstill on ultrasound is predictive of failed resuscitation

regardless of rhythm on monitor
Abbreviations: PETCO2, partial pressure of end-tidal CO2; ROSC, return of spontaneous circulation.
PETCO2 may be high in cases of respiratory arrest as the heart continues to deliver
CO2 to the lungs during the period of asphyxia (as opposed to the abrupt cessation
of cardiac output in an arrest due to VF). With high-quality CPR, the main determinant
of CO2 delivery to the lungs is cardiac output. PETCO2 therefore correlates with
cardiac output. Kalenda23 was the first to report a decrease in PETCO2 in patients
who could not be resuscitated and a significant increase in those in whom ROSC
could be accomplished. In 1989, Sanders and colleagues24 published data in the
Journal of the American Medical Association showing that ETCO2 levels were predictive of successful resuscitation in both IHCA and OHCA. A landmark study25 published
in the New England Journal of Medicine in 1997 showed that a 20-minute PETCO2
level was able to predict mortality and was more reliable than the initial PETCO2 level.
Values less than 10 mm Hg after 20 minutes of CPR were not compatible with survival
and were felt to be helpful with decisions about the termination of resuscitation.25
More recently, it was found that a PETCO2 of 1.9 kPa (14.3 mm Hg) at 20 minutes
was predictive of death with a sensitivity, specificity, positive predictive value, and
negative predictive value of 100%.26 In the same study, no patient with an initial,
average, maximum, or final PETCO2 of less than 1.33 kPa (10 mm Hg) was successfully resuscitated.
The partial pressure of end-tidal CO2 can be useful as a guide to optimize compression depth and rate and to predict fatigue in the provider performing compressions.
Furthermore, an abrupt and sustained increase in PETCO2 in an intubated patient indicates ROSC.2730 Pulse checks are often unreliable in arrest situations. Close monitoring of PETCO2 trends may help to limit the amount of hands-off time during
compressions for lengthy pulse checks. It should be noted that PETCO2 may transiently
increase after the administration of sodium bicarbonate (as the bicarbonate is converted to water and CO2). This transient increase should not be confused with ROSC.
ULTRASONOGRAPHY
More emergency physicians are incorporating ultrasound into their daily practice. The
indications for emergency ultrasonography are expanding greatly. Many emergency
physicians are comfortable using ultrasound to evaluate for the presence or absence
of pericardial effusions. Some emergency physicians possess sufficient expertise to
estimate ejection fraction, assess for right ventricular enlargement, and examine the
valves. Emergency ultrasound examination assesses for cardiac standstill and reversible causes such as cardiac tamponade. Clinicians who are more adept at ultrasound
use are also using it to guide therapy in some cases. For example, a patient in pulseless electrical activity (PEA) with a dilated right ventricle and septal bowing into the left
ventricle may receive thrombolytics to treat a presumed pulmonary embolism. A parasternal ultrasound view may reveal the presence of an acute thoracic aortic dissection
and therefore alter the course of the resuscitation.
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Several studies have been published on the use of ultrasonography during resuscitations. A 2005 study of 70 patients in CA found that of the 34 that were in PEA, only 23
of them truly had PEA; the other 11 had pseudo-PEA with detectable cardiac activity
on ultrasound. All 36 patients in asystole and all 23 in true PEA had cardiac standstill
on ultrasound and none had ROSC. Of the 11 in pseudo-PEA that had identifiable
cardiac activity on ultrasound, 8 had ROSC.31 Another study found survival to hospital
admission was 27% in all patients with sonographic cardiac activity versus 3% in
those without activity. The numbers were very similar in those thought to have PEA
(26% vs 4%).32 Clinicians who used ultrasonography thought that it provided clinically
useful information in 97% of cases. A study that looked at 169 patients in CA found
136 had cardiac standstill on ultrasound despite the presence of a rhythm on cardiac
monitoring in 71 cases. Of those with cardiac standstill, none survived to leave the
emergency department regardless of initial rhythm.33 The investigators hypothesized
that cardiac standstill likely implies exhausted myocardial reserve that makes
successful resuscitation impossible despite electrical activity on the monitor. On the
other hand, if cardiac activity is visualized in a patient thought to have PEA, he or
she may benefit from an infusion of volume or the initiation of inotropes. Of the 341
patients in these studies, 218 were found to have cardiac standstill on ultrasound.
Only 2 of these had ROSC. Neither survival to hospital discharge nor favorable neurologic outcomes was reported.
A more recent study in Resuscitation34 examined the use of transesophageal echocardiography (TEE) in CA. TEE is not part of the average emergency physicians
arsenal. However, as more emergency physicians become adept at ultrasonography
and the cost of these transducers becomes lower, it may become more commonplace. The advantages of TEE during resuscitation are that the images are not
degraded by such factors as obesity or hyperinflated lungs, such as in a patient
with chronic obstructive pulmonary disease. In addition, once the probe is in position
it can be left there throughout the resuscitation, and the information is available to all
members of the treatment team. This real-time monitoring provides information about
the effectiveness of compressions, allows for identification of rhythms that may be
amenable to shocking (such as fine VF), and shows ROSC without needing a lengthy
pause for a pulse check.34 Studies such as these led the American Heart Association
to include the following statement in the 2010 AHA Guidelines for CPR and ECC:
Transthoracic or transesophageal echocardiography may be considered to diagnose
treatable causes of CA and guide treatment decisions.35 The use of ultrasound in
resuscitation has the potential to dramatically alter its course.
POSTARREST FACTORS
The prognostic factors examined up to this point have all been prior to the point of
ROSC. Once there has been ROSC, it is helpful to identify factors that predict survival
to discharge. Even more important is the quality of survival, typically the patients
neurologic outcome. Some immediate predictors of survival after ROSC have included
postarrest rhythm, heart rate variability, and lactate clearance. Prognosticating neurologic outcome requires a more complex algorithm that takes into account clinical
factors, biochemical testing, and other complex neurologic testing.
IMMEDIATE POSTARREST FACTORS
One small study examined the immediate postarrest rhythms in patients after ROSC.
Tsai and colleagues36 found that in patients who had an accelerated idioventricular
rhythm (AIVR) after arrest, 38% required repeated CPR (vs 4% in the non-AIVR group)
and none survived at 7 days (vs 50% in the non-AIVR group). Typically regarded as
a benign rhythm, AIVR is even considered to be a marker of reperfusion after thrombolysis. This study suggests that AIVR after CA may not be as benign. Another factor
that has been studied to greater depth is that of heart rate variability (HRV). HRV refers
to the beat-to-beat fluctuations in heart rate during sinus rhythm, and reflects the level
of autonomic modulations to heart rhythm. After CA, patients with a more potent
stress response have a better outcome.37 This stress response may include immediate baroreceptor sensing, which initiates an autonomic nervous response. This
response is assessed by HRV. A decrease in HRV is associated with an increase in
mortality in patients with critical illness and in survivors of CA.3842 Typically a
24-hour measurement, more recently it was demonstrated that a mere 10-minute
electrocardiography recording performed 30 to 60 minutes after a successful resuscitation could be analyzed and used to identify patients at risk of 24-hour mortality.43
Another study of HRV in survivors treated with TH showed that patients treated with
TH had higher HRVs and improved outcomes.44
Elevated lactate levels after CA imply tissue hypoperfusion. Lactate clearance has
been shown to correlate with decreased mortality in patients with trauma, burns,
and sepsis.4548 It has been shown that an elevated lactate level 48 hours after CA
is an independent predictor of mortality and unfavorable neurologic outcome.49 Early,
effective lactate clearance is associated with decreased early mortality and decreased
overall hospital mortality in survivors of CA.50 High lactate clearance at 12 hours postarrest is predictive of 24-hour survival.
NEUROLOGIC PREDICTORS
The ultimate question faced by providers and asked by families regards the quality of
life that survivors of CA will have. While many studies of resuscitation will use ROSC or
survival to hospital discharge as end points, the true measure that should be reported
are those survivors with favorable neurologic outcomes. This topic has been one of
much research and is of renewed interest in this era of TH. Several different factors
have been evaluated, from clinical parameters, to biomarkers, to electrophysiological
signs and advanced neuroimaging (Table 4). This research has led the American
Academy of Neurology (AAN) to publish an algorithm for use in predicting the outcome
of comatose survivors of CA.51 This algorithm uses these different factors in a stepwise
Table 4
Prognostic factors regarding neurologic outcome
Factor
Association
Caveats
Brainstem reflexes
Absence at day 3 predicts

poor outcome
May be affected by clinical

situation (sedatives/paralytics)
Myoclonic status
epilepticus
Predictive of in-hospital death

or poor outcome
Even if brainstem reflexes are

intact
Somatosensory evoked
potentials
Bilateral absence of N20 peak

predicts poor outcome
May be present initially and lost

later
Neuron-specific enolase
Value >33 mg/L on day 3 is

universally associated with
poor outcome
May be falsely elevated by

hemolysis
S-100B
Elevated levels associated with

poor prognosis
Peaks earlier than neuron-specific

enolase
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fashion over several days. Though regarded as a valuable tool, the algorithm has
limited utility in the emergency department.
CLINICAL SIGNS
Studies of neurologic outcome frequently cite the false-positive rate (FPR) of the test.
FPR refers to an outcome better than poor despite positive a test result. In other
words, a high FPR means that despite the test predicting poor neurologic outcome,
there are survivors with meaningful recovery. An FPR of zero means that the test
correctly predicts absence of meaningful recovery. Absent pupillary reaction to light
seems to portend a poor prognosis for meaningful recovery. However, the FPR at
time of admission is unacceptably high. Of more utility is the absence of pupillary reaction to light at day 3 with an FPR of zero. Absence of other brainstem reflexes at
72 hours (corneal reflex, oculocephalic reflex) show similar FPRs.52 Likewise, motor
response to noxious stimuli that is no better than extensor posturing carries a poor
prognosis. However, in a study involving TH, just under 15% of the very small sample
developed recovery of awareness on day 6 after extensor posturing on day 3.53 Thus,
it is cautioned that in patients treated with TH, using the motor response alone should
be avoided on day 3 and repeated on day 6.
Myoclonus status epilepticus is defined as spontaneous, repetitive, unrelenting,
generalized multifocal myoclonus involving the face, limbs, and axial musculature in
comatose patients. The presence of myoclonus status epilepticus was uniformly associated with in-hospital death or poor outcome.54,55 This finding was true even in
patients with intact brainstem reflexes or some motor activity. This presentation at
24 hours is ominous and accurately predicts poor outcome.
ELECTROPHYSIOLOGICAL TESTING
Another accurate predictor of poor outcome is the measurement of somatosensory

evoked potentials (SSEPs). The principal measurement is the N20 response from
the primary somatosensory cortex. N20 refers to a negative polarity peak measured
by an electrode over this area of the cortex 20 milliseconds after electrical stimulation
of the median nerve at the wrist. Bilateral absence of this peak on days 1 to 3 or later
accurately predicts poor outcome. The N20 response may be preserved initially only
to disappear later.56 Also, the presence of the N20 response is not helpful in predicting
outcome, as a normal N20 is associated with arousal from coma in only 60% of
subjects.57 Thus, only its absence bilaterally is of any utility.
BIOCHEMICAL TESTING
Although clinical parameters are easily evaluated, are readily available, and of virtually
no cost, they are also often affected by the clinical situation, including the use of sedative agents or paralytics. Biochemical markers, especially the well-studied neuronspecific enolase (NSE) and S-100B, appear to have a predictive value superior to
clinical signs, though they are not readily available in a timely fashion at many centers.
NSE is the neuronal form of the intracytoplasmic glycolytic enzyme enolase. It is
found mainly in neurons and neuroendocrine cells. NSE peaks in the serum and cerebrospinal fluid at 72 hours after injury.58 It has been demonstrated that an NSE value of
greater than 33 mg/L at days 1 to 3 after CPR was universally associated with a poor
outcome with an FPR of zero.54 A caveat is that small amounts of NSE can be found in
platelets and red cells, so hemolysis (or traumatic lumbar punctures, if measured in
cerebrospinal fluid) can falsely elevate the levels. S-100B is a protein present in glial
cells and Schwann cells. It is a sensitive marker for glial damage and peaks at 24
hours, declining then over the next 48 hours. Despite many studies of S-100B, this
marker predicts poor outcome with lesser confidence than NSE.54,5962 Therefore,
the AAN guidelines recommend using NSE preferentially. However, given the earlier
peak of S-100B, it may be more clinically useful than NSE at predicting outcome
when measured early in the course (such as in the emergency department).63 Further
studies will need to be undertaken to delineate the utility of measuring this biomarker
in the emergency department.
NEUROIMAGING
Computed tomography (CT) is readily available in most emergency departments, and

is often used as a screening tool in patients with neurologic dysfunction. Cerebral
edema seen on a noncontrast head CT may be a sign of global brain ischemia. A study
using CT Hounsfield units to quantify cerebral edema found that a difference in gray
matter/white matter ratio of less than 1.18 at the basal ganglia level was 100% predictive of death.64 Advances in magnetic resonance (MR) imaging techniques have
dramatically altered the evaluation of acute ischemic strokes, and show promise as
an adjunct to assessing neurologic outcome after CA. However, its advantages are
offset by the inherent difficulties of obtaining an MR image of a critically ill patient.
Multivariate assessment of the post-CA patient is clearly of more utility than relying
on one modality. The use of clinical signs in combination with biochemical markers,
electrophysiological examinations, and even advanced neuroimaging is under investigation. The AAN guidelines use a combination of clinical signs including the absence
of brainstem reflexes or presence of myoclonic status epilepticus, combined with
SSEP testing and measurement of NSE, to develop an algorithm to help clinicians
predict the outcome of comatose survivors of CA. This algorithm may require further
validation or modification as more information is gained about neurologic outcomes in
this era of TH.
SUMMARY
CA remains a tremendous problem throughout the world, with rates of successful

resuscitation remaining low. The ability to predict outcome from resuscitation remains
elusive although several variables that are of value prearrest, intra-arrest, and postarrest have been identified. In the prearrest phase, initial rhythm is the most valuable
prognostic factor. Shockable rhythms show survival rates 5 to 10 times as high as nonshockable ones. Several other environmental and demographic factors have been
described, although many of them relate to the likelihood of the arrest being discovered early while the patient remains in a shockable rhythm. Intra-arrest prognostic
factors include the values of the PETCO2, trends in PETCO2, and the findings of
cardiac standstill on ultrasound. After ROSC, some early outcome measures include
lactate clearance and HRV. The ability to predict favorable or unfavorable neurologic
outcome requires a multivariate approach, combining clinical examination, biochemical markers, electrophysiological testing, and advanced neuroimaging. The influence
of TH in all of these prognostic factors has not been fully elucidated, and remains
a subject of intense research interest.
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103
Putting It All
To g et h e r t o I m p ro ve
Resuscitation Quality
Robert M. Sutton, MD, MSCEa,*, Vinay Nadkarni,
Benjamin S. Abella, MD, MPhilb
a
MD, MS ,
KEYWORDS
Cardiopulmonary resuscitation Cardiac arrest
Feedback Debriefing
Cardiac arrest is a major public health problem affecting thousands of individuals each
year in both the before hospital and in-hospital settings. However, although the scope
of the problem is large, the quality of care provided during resuscitation attempts
frequently does not meet quality of care standards, despite evidence-based cardiopulmonary resuscitation (CPR) guidelines, extensive provider training, and provider
credentialing in resuscitation medicine. Although this fact may be disappointing, it
should not be surprising. Resuscitation of the cardiac arrest victim is a highly complex
task requiring coordination between various levels and disciplines of care providers
during a stressful and relatively infrequent clinical situation. Moreover, it requires a targeted, high-quality response to improve clinical outcomes of patients. Therefore, solutions to improve care provided during resuscitation attempts must be multifaceted
and targeted to the diverse number of care providers to be successful.
In the 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care (AHA Guidelines),1,2 the focus of resuscitation priorities during cardiac arrest has shifted from early airway and breathing
management toward providing high quality uninterrupted chest compressions and
early defibrillation for shockable rhythms, which is exemplified in the acronym change
Financial Disclosures or Conflicts of Interest: Vinay Nadkarni receives unrestricted research

grant support from the Laerdal Foundation for Acute Care Medicine. Robert Sutton is supported through a career development award from the Eunice Kennedy Shriver National Institute of Child Health & Human Development (K23HD062629). Benjamin Abella receives research
funding from Philips Healthcare, the American Heart Association, and the Doris Duke Foundation, and has received speaking honoraria from Philips Healthcare.
a
Department of Anesthesiology and Critical Care Medicine, University of Pennsylvania and the
Childrens Hospital of Philadelphia, 7th Floor Central Wing: 7C09, 34th Street and Civic Center
Boulevard, Philadelphia, PA 19104, USA
b
Department of Emergency Medicine, Center for Resuscitation Science, University of
Pennsylvania, 3400 Spruce Street, Philadelphia, PA 19104, USA
E-mail address: suttonr@email.chop.edu
doi:10.1016/j.emc.2011.09.001
emed.theclinics.com
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Sutton et al
from Airway-Breathing-Circulation, or ABC, to Circulation-Airway-Breathing, or CAB.

There have been numerous studies supporting this simplified approach, including
a recent clinical trial demonstrating that even administration of advanced cardiac
life support (ACLS) medications may not provide a survival benefit to cardiac arrest
patients.3,4 Consequently, it seems that providing high quality CPR (summarized in
the AHA Guidelines catchphrase Push Hard, Push Fast) with minimal interruptions
and prompt defibrillation may be the most important actions during cardiac arrest
that will translate into a survival benefit.
Given the complexity of the care required during cardiac arrest resuscitation, it
should not be surprising that, even though in many locales cardiac arrest survival rates
have improved, overall, strategies to improve resuscitation quality and outcomes are
not fully implemented. An adult in-hospital cardiac arrest (IHCA) registry study has
documented a rate of survival to discharge for adult in-hospital arrest at 19%; pediatric rates of survival are slightly higher, exceeding 25%.510 Out-of-hospital cardiac
arrest (OHCA) survival rates are much lower for both groups at less than 10%, with
survival depending on location of arrest, initial rhythm, as well as patient and rescuer
factors.11,12 The variability of survival rates among different locations given the same
rhythm and same setting suggests that resuscitation performance may be a contributing factor.11 This variability in performance can be explained by several factors.
These events occur infrequently from the perspective of any given rescuer, most
rescuers are uncomfortable in these highly stressful situations,13 and this feeling of
unease is only magnified by the existing training programs that follow a lowfrequency paradigm (ie, certification every 24 years). Clearly, new approaches,
both technological and educational, are needed. In this article, we review some of
the new approaches to improving cardiac arrest resuscitation performance. The focus
will be on a continuous quality improvement paradigm (ie, before, during, after): to
improve resuscitation outcomes, we must improve training methods before actual
cardiac arrest events, monitor quality during resuscitation attempts, and feedback
care deficiencies to frontline care providers after the events using quantitative debriefing programs.
CURRENT STATE OF RESUSCITATION PERFORMANCE
Recent resuscitation literature, assisted by CPR-recording devices, large cardiac

arrest event registries, and high-fidelity ACLS simulation studies, have focused
on and provide a significant amount of objective data regarding rescuer performance during actual and simulated cardiac arrests. Unfortunately, a common
theme from these studies was that resuscitation performance frequently does
not meet established care guidelines during IHCA, OHCA, and simulated cardiac
arrests. Even more troubling, these deficiencies in care spanned the literature
on both pediatric and adult patients.1416 To illustrate, Wik and colleagues15 reported that during adult OHCA resuscitations, 33% of chest compressions were
too shallow and were being delivered only 48% of the time during the arrest (ie,
nearly half the time when the heart had stopped and there was little or no cardiac
output, no chest compressions were being performed). Although one might expect
such care deficiencies during the sometimes chaotic resuscitation of OHCA
victims, similar deficiencies (23% of chest compressions with incorrect rates;
36% of chest compressions too shallow) were also seen during adult in-hospital
arrest care.14 Sutton and colleagues,16 in the only pediatric report of actual arrest
resuscitation quality to date, demonstrated that even with the provision of defibrillator automated corrective feedback during the arrest, resuscitation efforts still did
Putting It All Together
not consistently meet established care guidelines. However, this pediatric study
did seem to demonstrate improved care compliance in comparison to previous
adult investigations. The investigators hypothesized that their improved care
was related to a bedside CPR training program instituted at their institution,17
highlighting a possible target for improving resuscitation outcomes (see later
discussion).
In addition to difficulties with chest compression delivery, ventilation rates
exceeding AHA recommendations have also been problematic.18,19 Why are incorrect ventilation rates troubling? During the low-flow state of CPR, cardiac output
and pulmonary blood flow are approximately 25% to 50% of that during normal sinus
rhythm. Therefore, much less ventilation is necessary for adequate gas exchange
from the blood traversing the pulmonary circulation. Furthermore, both laboratory
and clinical data indicate that a rapid rate of assisted ventilation (over-ventilation
from aggressive rescue breathing) during CPR is common and can substantially
compromise venous return and cardiac output by increasing intrathoracic pressure.18,19 These detrimental hemodynamic effects are compounded when one
considers the effect of interruptions in CPR to provide airway management and
rescue breathing.2022 Several studies have supported these results during adult
resuscitation attempts23,24 and, as a result, the AHA now recommends the CAB
approach, emphasizing that the rescuer should focus on providing high quality chest
compressions with minimal interruptions. However, given that most pediatrics arrests
are actually asphyxial in nature, controlled ventilation is still recommended. A recent
large pediatric series from Japan supported the need for ventilation in pediatric arrest
victims. In this study, favorable neurologic outcome 1 month after arrest was
improved in patients who received conventional CPR compared with compressiononly CPR for an arrest that was noncardiac in nature.25 In short, the resuscitation
technique should be titrated to the physiology of the patient to optimize patient
outcome.
Performance of actual chest compressions and ventilations is only one aspect of
resuscitation quality. In addition to deficiencies in these psychomotor skills, appropriate recognition and treatment of cardiac arrest rhythms has also been shown to
be problematic in actual practice. The treatment of choice for short-duration ventricular fibrillation (VF) is prompt defibrillation. Nevertheless, a large recent registry study
showed that defibrillation was delayed beyond 2 minutes in nearly one-third of inhospital VF-ventricular tachycardia (VT) arrests. In general, as the mortality rate
increases by 7% to 10% per minute of delay to defibrillation, such delays in treatment
must be avoided.26 Furthermore, the wrong treatment decisions are frequently made
with respect to defibrillation. In a study involving emergency medical providers (EMS)
providers and medical residents, although manual defibrillation decreased pauses in
chest compressions compared with semiautomatic defibrillation, more inappropriate
shocks were delivered (26%) with a manual approach. In this study, nearly 80% of
these shocks were delivered for an organized cardiac rhythm.27 Currently, the resuscitation literature is lacking a report of rhythm recognition and treatment during real
pediatric cardiac arrest. However, during simulated resuscitations, pediatric residents
at an academic teaching hospital delayed defibrillation by greater than 3 minutes after
onset of pulseless VT over half of the time.28 This is particularly troubling because
recent studies indicate that VF and VT (ie, shockable rhythms) occur in 27% of inhospital pediatric cardiac arrests at some time during the resuscitation,7 with as
many as 41% of pediatric cardiac intensive care arrests associated with VF or VT.29
Programs to improve rhythm recognition and treatment are needed in both the adult
and pediatric realm.
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IMPROVING PERFORMANCE IMPROVES OUTCOMES
Although numerous studies have documented that resuscitation quality frequently

does not meet established care guidelines, it also appears that this substandard
care is adversely affecting hemodynamics during, and outcomes from, cardiac arrest
resuscitation. For example, increasing chest compression depth to the AHA Guideline
standard results in favorable hemodynamic changes, such as an increased arterial
blood pressure, in adult humans30 and an increase in coronary blood flow in mature
pigs.31 In addition, in both human and animal studies of adult subjects, the minimal
interruption of chest compressions seems to be a critically important element of
CPR quality because even short pauses in chest compressions (45 seconds)
decreases coronary perfusion pressure, short-term clinical outcome (eg, defibrillation
success), and survival.23,32 Most importantly, studies in adults have established that
aggressive implementation of the AHA Guidelines substantially improves adult cardiac
arrest survival outcomes, including more favorable neurologic outcomes.33,34 Thus,
there seems to be evidence that improving resuscitation quality will translate to
improved outcomes for patients.
BEFORE: RESUSCITATION TRAINING
Because the quality of CPR is directly related to survival outcomes,23,35,36 several

studies have implicated the existing educational programs for teaching CPR skills as
a prime target for interventions to improve survival after cardiac arrest. Although
most hospitals in the United States require either basic life support or ACLS certification
for most care providers, this is often the only resuscitation training practitioners receive,
and there is a growing body of literature supporting the notion that basic life support and
ACLS certification may not necessarily even translate to adequate performance of
these resuscitation skills during actual arrest events, especially given that most
providers have poor retention of these skills 3 to 6 months after traditional training. Deficiencies with not only operational performance in simulated scenarios,3740 but also
with self-perceived rescuer confidence,13 are all too common. Better programs to
improve training success are desirable with the expectation that this would translate
into higher quality CPR performed during actual resuscitation attempts.
A multifaceted approach is needed to improve existing resuscitation training
methods. Alternative training strategies in addition to the standard certification courses
should be used to supplement existing resuscitation training. Techniques, such as
higher fidelity simulation,4143 automated quantitative feedback during training,44 postevent debriefing,45 and regular refresher training17,46,47 have shown promise. Individually or together, these techniques can be used to augment resuscitation performance
(Fig. 1) and will be discussed in more detail.
Simulation has shown to be an effective tool to teach resuscitation skills.4143
Moreover, there is a growing body of literature supporting that higher fidelity training
methods and scenarios achieve superior training targets (ie, the more realistic the
manikin and scenario, the better the educational outcomes).41 Importantly, the superiority of high fidelity training is not limited to simulated scenarios. For example, in the
realm of critical care and/or emergency medicine, recent simulation science has
demonstrated that training in central line insertion and daily maintenance not only
improves patient outcomes (eg, decreased complications with insertion48 and
catheter-related infections49) but, also, the cost50 associated with performance errors.
Furthermore, one recent study confirmed that simulation-based education could, in
fact, result in higher quality of care provided during an actual resuscitation events43
(ie, these studies have demonstrated that improving operational performance on
Fig. 1. Resuscitation quality after training. Curve A depicts quality decline after traditional
instruction. Note fall into gray shaded zone of poor quality several months after initial
training. Curve B represents the theoretical addition of high realism simulation and expert
debriefing. Although there is no change in rate of psychomotor skill quality decrement over
time, resuscitation quality is maintained longer owing to higher level of initial skill acquisition. Curve C represents addition of frequent refresher training in addition to simulation to
prevent decrement to poor quality.
manikins can improve operational performance in real life). Why does simulation
work? First, it provides the benefit of enhancing team work and increasing familiarity
with resuscitation equipment, thereby avoiding more frequent errors. As previously
mentioned, cardiac arrest resuscitations are relatively uncommon events for a given
care provider. Simulation provides the opportunity to make these stressful clinical situations more common, in a protected educational environment. Although the literature regarding simulation and improving team work is still evolving, it is likely that
simulation is among the best-suited instruments to observe and improve on team
dynamics and other human factors during rare-occurring, stressful situations, such
as cardiac arrests.51
In a study by Verplancke and colleagues,52 noncritical-care nurses reported an
average of 59 months since their last actual delivery of CPR and 18 months since their
last CPR training. It is likely that this gap in CPR training and experience is present in
other hospitals and care settings, which ultimately leads to a decline in resuscitation
performance. As a result, brief, but more frequent training refreshers may offer
one solution to this problem. Three pediatric studies, all evaluating health care
providers in both ICUs and general inpatient floors, have established that brief, intermittent refresher CPR training can improve both CPR skill acquisition as well as skill
retention in a simulated cardiac arrest scenario.17,46,47 The idea that a brief, relatively
infrequent training can improve CPR performance may seem illogical considering that
the high-intensity, standard, AHA programs demonstrate poor retention rates. The
success of these refresher training programs is grounded in educational precepts
and it takes into account the principles of adult learning. Adult learning theory states
that there are certain characteristics common to successful adult educational
programs: they must be focused, practical, and the need for obtaining the information
must be apparent.5355 Because the education can be concentrated in refresher trainings (<2 minutes in these pediatric investigations), participants do not have to attend
formal classroom instruction, making the program both practical and relevant.
However, although refreshers may improve CPR skill acquisition and CPR performance, the optimal frequency of these refreshers, length of refresher training modules,
and content of training still remains undetermined. Short and frequent refreshers may
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be more effective than more extensive refresher trainings on a less frequent basis.
However, requiring recertification at a shorter time interval could be time consuming
and impractical. It is likely that a multicenter trial will be needed to fully evaluate this
promising educational technique.
DURING: MONITORING CPR QUALITY WITH TITRATION TO PATIENT PHYSIOLOGY
The evaluation of the effectiveness of ongoing CPR efforts has proven difficult. Several
methods that are used commonly (eg, presence of femoral or carotid pulsations, pulse
oximetry) have not correlated with successful resuscitation and may even mislead
rescuers. The following is a discussion of real-time audiovisual feedback systems,
arterial blood pressure monitoring, and end-tidal carbon dioxide (CO2) capnography
as methods to guide resuscitation quality.
Real-time Audiovisual Feedback
Interest in improving CPR quality through real-time feedback devices has been
evolving since the early 1990s. Human,56,57 animal,58 and manikin studies5962 have
shown improvement in quantitative measures of CPR quality and surrogates of
survival outcomes (eg, end-tidal CO2) when CPR feedback devices were used. Given
the improvements seen in previous investigations, these technologies offer promise as
we look for ways to strengthen our training methods, particularly in light of the fact that
one of the problems highlighted concerning existing educational programs has been
the poor ability of instructors to actually perceive CPR error in class participants.63
As a result, the AHA now suggests that training programs consider use of automated
real-time feedback devices to improve overall training efficacy by providing a quantitative assessment of the CPR performed by trainees.64
During the past decade, innovative technologies have extended the ability to
monitor real-time CPR process from manikins used for training purposes to use in
actual cardiac arrest victims. Using force transducer and/or accelerometer technology
through pads placed between the rescuers hands and the patients chest, quantitative CPR quality information can be recorded, analyzed, and fed back to the rescuer
in an effort to correct CPR deficiencies. Feedback can be given on chest compressions rate, depth, ventilation rate, pauses, and incomplete chest wall recoil (leaning).
Feedback-enabled defibrillators, in before-and-after design trials (ie, studies with
retrospective controls) have shown to improve CPR quality delivered by EMS
providers and in-hospital care providers.36,65 In one study of adult OHCA, feedback
increased the mean compression depth from 34 mm to 38 mm and increased the
percentage of compressions within AHA Guidelines recommendations for depth
from 24% to 53%.36 In similar fashion, another clinical study demonstrated that feedback improved in-hospital CPR quality by reducing the variability of CPR, conforming
more to the AHA Guidelines recommendations.65 In the pediatric environment, two
studies from a single institution have further confirmed the positive effect of feedback
in improving CPR quality. In the study by Sutton and colleagues,16 compliance rates
for chest compression depth and rate approached 70%. Unfortunately, this study
was observational and lacked a before-period control group to fully evaluate the effect
of feedback technology. However, the compliance rates far exceed those published in
the adult-care and pediatric-care literature to date. Furthermore, in a small subset of
patients from this same cohort, the investigators demonstrated a marked reduction in
leaning because of feedback.66 In accordance with the 2010 International Liaison
Committee on Resuscitation recommendations, feedback technologies can improve
quantitative measure of CPR quality, in training and real cardiac arrest situations.
However, although automated feedback devices can support improvements in CPR

quality, questions have been raised regarding whether these devices actually improve
patient outcomes.44 None of the studies mentioned so far showed a significant
improvement in any type of survival, but they were also not powered to do so. So,
although it is clear that feedback technologies can coach providers to achieve quantitative feedback targets, whether achieving these targets through automated feedback technologies improves outcomes remains in question. A recent British Medical
Journal publication by Hostler and colleagues,67 using a cluster randomized design
from three sites within the Resuscitation Outcomes Consortium in the United States
and Canada, although demonstrating improvement in CPR quality, did not show
a difference in survival outcomes. Does this mean that CPR quality is not related to
clinical outcome? Unfortunately, the feedback targets used in this study were based
on 2005 guidelines and, as a result, even with feedback, the average chest compression depth reached only 40 mm. Currently the AHA Guidelines recommend a depth of
at least 50 mm to improve outcomes from adult cardiac arrest. In short, it seems that
feedback technologies are effective at getting providers to achieve the programmed
quality targets. It is the responsibility of resuscitation scientists to determine the
best targets for CPR quality that will translate into improved clinical outcomes.
A particularly helpful technology used in feedback enabled defibrillators is the ability
to display a signal that filters CPR artifact from the ECG tracing so that rhythm analysis
can occur during chest compressions. The obvious benefit is that a rescuer would no
longer have to pause chest compressions every 2 minutes to analyze cardiac rhythms.
As a result, with fewer interruptions, there would be improved coronary and cerebral
perfusion and likelihood of return of spontaneous circulation (ROSC). To date, there is
no published literature regarding the clinical use of this feature incorporated into defibrillators. There is a modicum of literature regarding the accuracy of similar technology.68 If this approach is shown to be reliable and not lead to incorrect rhythm
interpretations, it has the potential to enhance CPR performance by decreasing interruptions in chest compressions.
Arterial Blood Pressure and End-tidal CO2
Although CPR quality monitoring defibrillators have been highlighted in recent literature, older technology, such as monitoring of arterial blood pressure and end-tidal
CO2, during resuscitation can provide the rescuer with CPR quality information.
Why monitor arterial blood pressure? Diastolic blood pressure is a major determinant
of myocardial perfusion pressure (MPP), the driving force for myocardial blood flow
during CPR.6972 Aortic diastolic pressure (AoDP) is related to MPP by the following
equation: MPP 5 AoDP right atrial diastolic pressure (RADP). Because the right atrial
diastolic pressure does not change substantially during CPR,73,74 arterial diastolic
blood pressure is the most important variable affecting MPP and myocardial blood
flow. Because adequate myocardial blood flow is necessary for successful resuscitation from cardiac arrests,7577 it follows that increasing arterial diastolic pressure will
improve resuscitation outcomes. Evidence supporting diastolic blood pressure
augmentation to improve the chance of resuscitation comes from numerous studies
demonstrating that provision of vasoactive agents, such as epinephrine or vasopressin, or the application of abdominal binders, by raising AoDP, improve MPP
and resuscitation success.7883 These laboratory investigations show that arterial diastolic pressures of at least 30 mmHg during CPR are typically necessary for adequate
myocardial blood flow and successful resuscitation. Animals with arterial diastolic
pressures less than 25 mmHg rarely survived. There is also supporting evidence
from clinical adult arrest studies that diastolic pressures greater than 30 mmHg are
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Sutton et al
associated with return of spontaneous circulation.84 Therefore, an approach of goaldirected CPR, where a provider monitors arterial blood pressure and titrates chest
compression force and vasoactive agents to achieve hemodynamic goals, seems
reasonable.
Given the unexpected nature of many cardiac arrests and the sometimes chaotic
nature of resuscitation, particularly during OHCA, placement of invasive arterial monitoring is not always feasible. In these situations, continuous end-tidal monitoring CO2
(ie, capnography) can be used as an alternative to monitor CPR quality. In numerous
experimental models, noninvasive end-tidal CO2 correlates well with cardiac output,
MPP, and resuscitation success.8589 Furthermore, the utility of end-tidal CO2 monitoring during clinical investigations is not a new discovery and has been described
since the 1970s when Kalenda90 described three patients who were monitored for
expired CO2 during cardiac arrest. He described using CO2 levels to monitor for
rescuer fatigue and saw improvement in end-tidal CO2 levels when a new rescuer
started (presumably because the new provider was performing better CPR). He was
also the first to show that ROSC could be recognized by a sudden rise in expired
CO2. By recognizing ROSC without having to interrupt chest compressions to check
for a pulse or arterial blood pressure, one can anticipate that interruptions in chest
compressions can be minimized (Fig. 2). Finally, building on this work, other studies
have documented differences in end-tidal CO2 levels between survivors and nonsurvivors after adult cardiac arrest, suggesting that end-tidal CO2 can also be used as
a prognostic tool during cardiac arrest.86 As a result, continuous end-tidal CO2 monitoring is now recommended during cardiac arrest resuscitation when available.
In conclusion, several technologies, some old and some rather new, are available to
providers in both OHCA and IHCA settings. Although there can be arguments made
about the superiority of a given technology, the first step in developing plans to
improve resuscitation quality is to monitor the care provided during the arrest so
that targeted treatment plans can be developed.
Matching Cardiac Arrest Physiology to Resuscitation
Beginning in 2005, the AHA and European Resuscitation Council guidelines for
CPR were adjusted to better match the physiologic needs of the cardiac arrest
Fig. 2. Using end-tidal (ET) CO2 to detect ROSC. From onset of arrest (#), note slow increase
in end-tidal CO2 as compressions are delivered. With ROSC (arrow), organized ECG rhythm
begins to appear under chest compression artifact (asterisk) and end-tidal CO2 rises suddenly
to greater than 50 mmHg. Providers could have used the rapid rise in end-tidal CO2 as a clinical guide that there was a return of spontaneous circulation, without having to pause chest
compressions and risk interruption of CPR for a rhythm check.
victim, focusing on the delivery of high quality chest compressions with provision
of adequate ventilation. What defines adequate ventilation? Once cardiac arrest
has ensued and the heart has stopped beating, there is little to no blood flow
throughout the body. At that point, during the low-flow state of CPR, cardiac
output and blood flow are approximately 25% to 50% of that during normal sinus
rhythm. As a result, less ventilation is needed for adequate gas exchange. In addition, there is the concern that excessive ventilation from rescuers may have detrimental effects on hemodynamics during resuscitation and survival outcomes.18,19
These detrimental hemodynamic effects are compounded when one considers
the effect of interruptions in CPR to provide airway management and rescue
breathing. As a result, the chest compression to ventilation ratio was increased
from 15:2 to 30:2 in 2005 to ensure chest compressions were being delivered
for a greater proportion of the time during CPR. In 2009, a large prospective observational study corroborated the association between increased chest compression
fraction (the proportion of resuscitation time without spontaneous circulation
during which chest compressions are administered) and improved outcome,
with two highest groups of chest compression fraction more than twice as likely
to survive.91
The next obvious question raised by the developing body of literature supporting
increased chest compression fraction was whether ventilation was needed at all (ie,
compression-only resuscitation). Between 2005 and 2010, several studies were
focused on investigating an alternative resuscitation strategy, known as cardiocerebral resuscitation (CCR).9295 CCR entails providing more uninterrupted chest compressions to ensure optimal cerebral and cardiac perfusion. In Arizona, Bobrow and
colleagues94 described a variant of CCR termed minimally interrupted cardiac resuscitation, which minimizes interruptions in chest compressions by delaying endotracheal intubation and positive pressure ventilations, instead initially providing passive
oxygen insufflation via an oral pharyngeal airway and non-rebreather face mask.
The study demonstrated a significant improvement in survival to discharge for
OHCA. Since then, several other EMS systems have demonstrated comparable
improvements in survival by implementing similar protocols that emphasized uninterrupted chest compressions and delayed intubation.93,95
During the same period that CCR was being investigated for OHCA by EMS
providers, resuscitation scientists began to establish whether compression-only
CPR was preferable to standard CPR for bystanders. Because bystander CPR is
one of the most important determinants of resuscitation outcome,96 the hope was
by removing the need for ventilation delivery, more bystander CPR would be provided
and outcomes from OHCA would be improved. After several studies demonstrated the
efficacy of bystander-initiated compression-only CPR, this technique was endorsed in
the 2010 AHA and European Resuscitation Council guidelines for CPR as a reasonable
alternative to conventional CPR for adult OHCA.97,98 Most recently, using survival to
hospital discharge as the primary outcome, a meta-analysis was recently published
in Lancet and concluded that compression-only CPR is preferably to conventional
CPR with rescue breathing for adult OHCA.99 However, in pediatrics, given that
most arrests are actually asphyxial in nature, controlled ventilation is still recommended. A recent large pediatric series from Japan supported this approach and found
that favorable neurologic outcome 1 month after arrest was improved in patients
who received conventional CPR compared with compression-only CPR for an arrest
that was noncardiac in nature.25 In short, this is one of the take-home points of this
article: resuscitation technique and quality should be monitored and titrated to the
physiology of the patient to optimize outcome.
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Mechanical CPR Devices
As high-quality chest compressions with minimal interruptions seem to be a determinant of IHCA and OHCA survival, it follows that mechanical compression devices may
be useful during resuscitation attempts. Piston-type devices and circumferential
constriction band devices have been evaluated during cardiac arrest resuscitation
and they have shown promise in improving hemodynamic and short-term clinical
outcomes.100102 Although these devices can easily deliver high-quality chest compressions, rescuers must be cautious to limit interruptions in the deployment of said
devices.103 See discussion of these devices elsewhere in this issue.
AFTER: PERFORMANCE DEBRIEFING
Health care debriefing is defined as a facilitator-led participant discussion of events

with reflection and assimilation of learning into practice. Structured debriefing can
trace its origins back to the military in World War II. General George Marshall ordered
soldiers under his command to give an account of their experience on return home
from a mission. Although the initial intent was to gather tactical information or strategize for future battles, he noticed that debriefings were also spiritually healing and
morale building for his soldiers. The technique was further refined in the military and
aviation industries, and although initially used as a means to minimize the stress
response and improve psychological outcomes from traumatic and infrequent situations,104108 currently debriefing is conceptualized as a method to improve care during
rare and stressful events.
The value of debriefing starts with resuscitation training. Structured debriefing has
been established as a useful tool to improve compliance of in-hospital adult care
providers during simulated cardiac arrest. Although debriefing or automated feedback
alone improved CPR quality modestly in a study from the University of Pennsylvania,
the combination led to a more considerable improvement in quality.109 Similarly,
debriefing with pediatric in-hospital care providers has also shown the positive effects
of debriefing during resuscitation training. In a study from the Childrens Hospital of
Philadelphia, the combination of instructor-led training and debriefing with automated
defibrillator feedback improved CPR quality compared with either the training or
debriefing method alone.46 Therefore, in addition to quantitative monitoring of trainee
performance, it seems prudent to ensure that performance is fed back to trainees in an
attempt to achieve the best educational outcomes.
The first study published demonstrating efficacy of debriefing to improve outcomes
from cardiac arrest came from the University of Chicago where the combination of
resuscitation debriefing interventions and audiovisual feedback via defibrillators
produced a marked improvement in resuscitation performance and a 33% increase
in ROSC.45 This particular debriefing program consisted of weekly sessions that
reviewed transcripts of quantitative data downloaded from defibrillators, including
CPR-quality ECG data (Fig. 3). Although this study was a designed before-after study
using historical controls, the benefit of structured debriefing was apparent with
improved CPR quality target compliance and ROSC.
Although these investigations reported positive findings with the addition of debriefing, a European study in the pre-hospital setting failed to show any benefit after
incorporating performance evaluation.110 However, this study should not deter resuscitation scientists from recommending performance debriefing. Instead, this study
highlighted an important aspect of successful debriefing: the process must be
completed with front-line care providers. In the European study, CPR performance
data were presented to EMS leadership or local CPR instructors, not to front-line
Fig. 3. Representative CPR quantitative recording. Provides ability to review ECG, ventilation, and chest compression data after events to improve future resuscitation quality.
Note prompts given to rescuers to compress deeper when the chest compressions are
too shallow. The arrow heads indicate ventilations, in this recording provided at a rate of
approximately 60 per minute (too fast!). These recordings can be used to provide a structured quantitative postevent review for rescuers who participated in the resuscitation.
care providers. This prohibited the self-reflection and assimilation that is of paramount importance to debriefing success. Therefore, this study highlights the importance of having a highly structured debriefing process performed with front-line
providers.
EVIDENCE THAT PUTTING IT ALL TOGETHER IMPROVES OUTCOMES
Although this article is focused on techniques to improve resuscitation performance

(eg, innovative training methods, monitors to enable providers to titrate the resuscitation to arrest physiology, real-time feedback-enabled CPR monitoring defibrillators,
and a systematic post-cardiac arrest debriefing process), it is likely that a bundled
approach incorporating two to several of these techniques will be necessary to
improve long-term patient outcomes. As a promising recent example, the Take Heart
America program was a comprehensive, community-wide, systems-based approach
to the treatment of cardiac arrest.111 This program consisted of widespread cardiopulmonary resuscitation skills training in schools and businesses, retraining of all EMS
personnel in methods to deliver high quality CPR, deploying additional automated
external defibrillators in schools and public places (ie, enabling prompt defibrillation
when needed), and establishing treatment protocols regarding transport to and treatment by cardiac arrest centers. As a result of this intensive program, bystander CPR
rates increased from 20% to 29% (P 5 .086, odds ratio 1.7, 95% confidence interval
0.962.89), hypothermia therapy for admitted out-of-hospital cardiac arrest victims
increased from 0% to 45%, and, most importantly, survival to hospital discharge for
all patients after out-of-hospital cardiac arrest in these two sites improved from
8.5% to 19% (P 5 .011, odds ratio 2.60, confidence interval 1.196.26). Although
this study used historical controls, the magnitude of improvement in survival
outcomes provides strong evidence that initiation of a resuscitation care bundle or
system will be effective to improve outcomes from cardiac arrest.
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SUMMARY
In spite of the remarkable progress made in resuscitation science since

Kouwenhovens112 original description of closed chest cardiac massage, survival
from cardiac arrest continues to be very low. The reader should be convinced that
this could be attributed, in part, to the poor performance of resuscitation care. Furthermore, it should be clear that resuscitation of the cardiac arrest victim is a highly
complex task requiring coordination between multiple levels and disciplines of care
providers. In short, resuscitation is not easy and, despite improvements in care over
the past 50 years, there is substantial work to be done. The authors argue that using
a continuous quality improvement bundle (ie, improving training before, monitoring
and titrating quality during, and debriefing after events) seems to hold promise as
the resuscitation community strives to improve the care that we deliver to cardiac
arrest victims. In future investigations, with this approach, we expect resuscitation
scientists to begin to establish that improvements in performance will subsequently
translate into better survival rates for victims of sudden cardiac arrest.
ACKNOWLEDGMENTS
The authors would like to thank Dr Robert A. Berg and Dana Niles for their help in
preparation of this article. We would also like to acknowledge Marion Leary, Lori
Boyle, and Jessica Leffelman, who have supported resuscitation science at the
University of Pennsylvania and Childrens Hospital of Philadelphia.
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57. Kern KB, Sanders AB, Raife J, et al. A study of chest compression rates during
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58. Milander MM, Hiscok PS, Sanders AB, et al. Chest compression and ventilation
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60. Wik L, Thowsen J, Steen PA. An automated voice advisory manikin system for
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61. Wik L, Myklebust H, Auestad BH, et al. Retention of basic life support skills 6
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63. Kaye W, Rallis SF, Mancini ME, et al. The problem of poor retention of cardiopulmonary resuscitation skills may lie with the instructor, not the learner or the
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69. Voorhees WD, Babbs CF, Tacker WA Jr. Regional blood flow during cardiopulmonary resuscitation in dogs. Crit Care Med 1980;8(3):1346.
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84. Paradis NA, Martin GB, Rivers EP, et al. Coronary perfusion pressure and the
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85. Weil MH, Bisera J, Trevino RP, et al. Cardiac output and end-tidal carbon
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90. Kalenda Z. The capnogram as a guide to the efficacy of cardiac massage.
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96. Gilmore CM, Rea TD, Becker LJ, et al. Three-phase model of cardiac arrest:
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JAMA 1960;173:10647.
P o s t res u s c i t a t i o n
Care
Daniel Boutsikaris,
MD,
Michael E. Winters,
MD*
KEYWORDS

Postcardiac arrest Postcardiac arrest syndrome

Therapeutic hypothermia Cardiac arrest
Return of spontaneous circulation (ROSC)
Cardiac catheterization
Cardiac arrest accounts for approximately 350,000 resuscitations per year in North
America.13 The incidence of cardiac arrest requiring interventions by emergency
medical services (EMS) personnel is 50 to 55 per 100,000 population each year in
the United States and Canada.2 The primary goals of resuscitation are the return of
spontaneous circulation (ROSC) and meaningful neurologic recovery. Care of the
patient with ROSC after cardiac arrest is complex and challenging; it has a strong
impact on patient morbidity and mortality.1,35 Important components of postcardiac
arrest care are appropriate ventilation and oxygenation, hemodynamic optimization,
induction of therapeutic hypothermia, early cardiac catheterization, and correction
of metabolic derangements. It is imperative that the emergency physician (EP) be
knowledgeable of the systematic and multisystem approach to the patient with
ROSC following cardiac arrest. Given the urgency of treatment along with the
increasing emergency department (ED) lengths of stay for many critically ill patients,
it is the EP, rather than the intensivist, who can have the most significant impact on
morbidity and mortality in this select population of critically ill patients in the ED.6
This article focuses on the ED management of the patient with ROSC following cardiac
arrest. The information complies with the recently updated guidelines for postcardiac
arrest care, published by the American Heart Association (AHA).7
POSTCARDIAC ARREST SYNDROME
Following ROSC, a complex array of pathophysiologic processes begins to occur.

These processes, which constitute the postcardiac arrest syndrome (PCAS), are
grouped into 4 categories: systemic ischemia/reperfusion response, brain injury,
Funding support/financial disclosures/conflicts of interest: None.

Combined Emergency Medicine/Internal Medicine/Critical Care Program, University of
Maryland School of Medicine, 110 South Paca Street, 6th Floor, Suite 200, Baltimore, MD
21201, USA
E-mail address: mwint001@umaryland.edu
doi:10.1016/j.emc.2011.09.011
emed.theclinics.com
124
Boutsikaris & Winters
myocardial dysfunction, and persistence of the precipitating cause of the arrest

(Table 1).3
Systemic Ischemia-Reperfusion Response
With ROSC, ischemic tissue is reperfused, sending toxic substrates to the central
circulation and potentially perpetuating organ dysfunction. The systemic ischemia/
reperfusion response is thought to be mediated by increased cytokine production,
alterations in coagulation, oxygen free-radical formation, adrenal dysfunction, and
disruption of the blood-brain barrier.3,8,9 The extent of injury caused by reperfusion
depends on the duration of ischemia, existing comorbidities, and the cause of the
Table 1
Components of the postcardiac arrest syndrome
Pathophysiology
Clinical Manifestation
Potential Treatments
Brain injury
Reactive oxygen species

Protein oxidation
Lipid peroxidation
Impaired
cerebrovascular
autoregulation
Cerebral edema
Coma
Seizures
Myoclonus
Persistent
vegetative state
Stroke
Brain death
Therapeutic
hypothermia
Hemodynamic
optimization
Seizure control
Controlled
reoxygenation
Myocardial
dysfunction
Direct injury from CPR

and defibrillation
Catecholamine surge
Oxygen free radicals
Acute coronary
syndrome
Hypotension
Dysrhythmias
Global hypokinesis
Circulatory collapse
Early revascularization
Hemodynamic
optimization
Mechanical support
with IABP, LVAD,
ECMO
Systemic ischemia/
reperfusion
response
Mediated by cytokines
Impaired coagulation
Oxygen free-radical
formation
Adrenal dysfunction
Increased susceptibility
to infection
Hypovolemia
Hypotension
Circulatory collapse
Multiorgan failure
Hemodynamic
optimization
Temperature control
Persistent
precipitating
cause
ACS
COPD, asthma
CVA
PE
Overdose
Sepsis
Hypovolemia
Hemorrhage
Specific to cause
Disease-specific
interventions
Abbreviations: ACS, acute coronary syndrome; COPD, chronic obstructive pulmonary disease; CPR,
cardiopulmonary resuscitation; CVA, cerebrovascular accident; ECMO, extracorporeal membrane
oxygenation; IABP, intra-aortic balloon pump; LVAD, left ventricular assist device; PE, pulmonary
embolism.
Data from Neumar RW, Nolan JP, Adrie C, et al. Post-cardiac arrest syndrome: epidemiology,
pathophysiology, treatment, and prognostication. A consensus statement from the International
Liaison Committee on Resuscitation (American Heart Association, Australian and New Zealand
Council on Resuscitation, European Resuscitation Council, Heart and Stroke Foundation of Canada,
InterAmerican Heart Foundation, Resuscitation Council of Asia, and the Resuscitation Council of
Southern Africa); 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; and the Stroke Council. Circulation
2008;118:245283.
Postresuscitation Care
arrest.3 If ROSC can be achieved quickly, the systemic ischemia/reperfusion response

can be limited.3
The PCAS can be considered similar to sepsis.8,10 Like patients with sepsis, patients
with PCAS have a significant increase in the production of cytokines and inflammatory
mediators. This results in increased activation of neutrophils and the vascular endothelium leading to a potent pro-inflammatory response.10 More recently studies have indicated that ischemia may also stimulate such mediators as vascular endothelial growth
factor (VEGF), which was noted for its potential effects on vascular permeability.9 Overall, the increased presence of cytokines, activation of endothelium, and upregulation of
mediators such as VEGF is believed to lead to increased vascular permeability with
resultant volume loss, as well as vascular dysregulation.810 In addition, ischemia
disrupts coagulation, generally favoring an overall pro-coagulant state.3,1012 Finally,
increased cytokine production results in an entity called endotoxin tolerance, which
may initially be helpful against an overwhelming inflammatory response, but ultimately
leads to immune dysfunction and a heightened risk of infection.3,10
In addition to this proinflammatory, procoagulant state, adrenal dysfunction can
also develop in patients with reperfusion injury. The initial response to stress (eg,
cardiac arrest) is an increased secretion of cortisol from the adrenal glands. Following
ROSC after cardiac arrest, a relative adrenal insufficiency can emerge. This relative
insufficiency is common in patients after cardiac arrest and can contribute to circulatory collapse.13,14
Overall, the systemic ischemia/reperfusion response is characterized by intravascular volume depletion from increased vascular permeability, impaired vasoregulation,
prothrombotic state, and increased susceptibility to infection.3 An early, goal-directed
approach to resuscitation and management seems to limit the progression of the
systemic ischemia/reperfusion response.3,5,15,16
Brain Injury
Most deaths in patients with ROSC from out-of-hospital cardiac arrest occur from
neurologic injury.17 Although a detailed discussion of neuronal cell death is beyond
the scope of this article, it is important to briefly review the mechanisms that lead to it.
With ROSC, reactive oxygen species are generated by mitochondria in ischemic
neuronal tissues. These reactive oxygen species trigger a cascade of cellular and
molecular events, including protein oxidation, lipid peroxidation, and DNA damage,
all of which can induce neuronal cell death.18,19 Recent evidence suggests that sustained increases in arterial oxygen content (hyperoxia) may further increase the quantity of reactive oxygen species and increase the mortality.20 In addition to creating
reactive oxygen species, ischemia induces activation of transcription factors, resulting
in apoptosis, inflammation, and sustained oxidative stress.21 Many of these pathologic
processes occur hours to days following ROSC.3
The brain can also be injured following ROSC after cardiac arrest by impaired autoregulation of the cerebral vasculature and cerebral edema. Although data are limited,
vascular autoregulatory mechanisms may be either impaired or absent.22 As a result,
patients after cardiac arrest may need a higher mean arterial pressure (MAP) to sustain
cerebral perfusion pressure and oxygen delivery.22 Some degree of cerebral edema is
typically seen on imaging studies of comatose survivors of cardiac arrest. The clinical
significance of cerebral edema following ROSC remains controversial.2325 Torbey
and colleagues23 investigated the impact of cerebral edema by calculating the ratio
(in Hounsfield units) between the cerebral gray matter (GM) and white matter (WM).
They found that a GM/WM ratio of less than 1.18 at the level of the basal ganglia
was 100% predictive of death. The cause of cardiac arrest may contribute to the
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degree of cerebral edema. Morimoto and colleagues25 determined that cerebral

edema was more common when the arrest had respiratory causes. Based on the
available literature, the clinical relevance of impaired autoregulation and cerebral
edema cannot be determined. Consensus opinion suggests that transient cerebral
edema during the early postcardiac arrest period is rarely associated with clinically
relevant increases in intracranial pressure (ICP) or outcome.3
Myocardial Dysfunction
Although neurologic injury is the leading cause of death in patients after cardiac arrest,
myocardial dysfunction is common and may contribute to increased morbidity and
mortality.3,17,2629 Laurent and colleagues26 showed that 50% to 70% of patients after
cardiac arrest without evidence of coronary occlusion on angiography develop
myocardial dysfunction.30 Typically, myocardial dysfunction occurs within 8 hours
following ROSC and is manifested by increased cardiac filling pressures, decreased
cardiac index, and a decrease in both systolic and diastolic function.26,27 In most
patients, the cardiac index returns to baseline within 24 to 48 hours; however,
supportive treatment with vasoactive agents may be necessary for up to 72 hours
following ROSC. In rare cases, myocardial dysfunction persists for weeks or months
before returning to the patients prearrest cardiac function.30
Myocardial dysfunction is thought to occur from several factors. First, the myocardium may be injured directly from closed chest compressions or defibrillation. In addition, the surge in catecholamines that occurs following ROSC, or the use of
epinephrine during resuscitation, has been associated with myocardial dysfunction
in the postcardiac arrest period.30,31 At the cellular level, it is hypothesized that depletion of adenosine triphosphate stores diminishes myocardial performance, and several
days may be needed to restore it. Additional theories on myocardial dysfunction in the
postcardiac arrest period include the generation of oxygen free radicals, alterations in
sarcoplasmic calcium metabolism, and upregulation of heat shock proteins.27
Persistent Precipitating Cause
Following ROSC, the EP is challenged with identifying and treating the cause of the
cardiac arrest. Cardiac causes are most common for out-of-hospital arrests,
accounting for approximately 50% of cases.32 Importantly, ST-segment abnormalities
and complaints of chest pain are poor predictors of acute coronary occlusion in the
patient after cardiac arrest.32 It is estimated that 70% of deaths from acute myocardial
infarction occur as out-of-hospital cardiac arrests.33 Pulmonary embolism (PE) is
another common cause of cardiac arrest, accounting for 5% to 10% of cases.34,35
Although pulseless electrical activity is commonly associated with PE, asystole and
ventricular fibrillation can occur.34 Hess and colleagues35 found that respiratory failure
was the most common noncardiac cause of out-of-hospital cardiac arrest, accounting
for approximately 35% of cases. In their study, PE accounted for 13.3% of arrests.
Less common causes include drug overdose, electrolyte abnormalities, sepsis, near
drowning, hypothermia, environmental exposures, and intracranial catastrophes.3,35
ED MANAGEMENT OF THE PATIENT AFTER CARDIAC ARREST
To improve morbidity and mortality, ED management of the patient after cardiac arrest
should consist of a multisystem approach, with emphasis on appropriate oxygenation
and ventilation, hemodynamic optimization, institution of therapeutic hypothermia for
appropriate candidates, early cardiac catheterization when indicated, and management of metabolic derangements.
Oxygenation
Following ROSC, it is common practice to place all patients on 100% forced inspiratory oxygen (FiO2) regardless of intubation status. As previously discussed, there is
mounting evidence to suggest that high partial pressures of arterial oxygen (PaO2)
may be deleterious.3638 Kilgannon and colleagues20 evaluated more than 6000 adult
patients with ROSC after cardiac arrest and found that hyperoxia, defined in the study
as a PaO2 greater than 300 mm Hg, was associated with worsened outcome compared
with patients whose PaO2 ranged between 60 and 300 mm Hg. The optimal oxygen
saturation (SpO2) and PaO2 remain unknown. The most recent guidelines from the
AHA recommend titrating supplemental oxygen therapy to maintain an SpO2 greater
than 94% and a PaO2 around 100 mm Hg.7 For intubated patients, positive endexpiratory pressure (PEEP) can be titrated to maintain target oxygen saturation levels
while minimizing exposure to high levels of inspired oxygen.
Ventilation
Following cardiac arrest, patients are at risk of developing acute respiratory distress
syndrome.7 Although optimal settings for mechanical ventilation of the patient after
cardiac arrest have not yet been determined, current guidelines recommend implementing a lowtidal volume ventilatory strategy with the selection of initial tidal
volumes between 6 and 8 mL/kg of ideal body weight.7,3941 A respiratory rate that
avoids hyperventilation should be chosen. Hyperventilation increases intrathoracic
pressures, potentially worsening hemodynamic instability, and induces hypocapnia.7,42 Conversely, hypercapnia can increase ICP and exacerbate any preexisting
acidosis.3,41 An initial respiratory rate between 16 and 18 breaths per minute is suggested but must be followed with serial arterial blood gas measurements to determine
the partial pressure of carbon dioxide (PaCO2). Similar to PaO2, minute ventilation
should be adjusted to maintain normal levels of PaCO2 (4045 mm Hg).7 In recent years,
evidence has mounted in support of the efficacy of monitoring end-tidal carbon
dioxide concentration (PetCO2). The EP can use PetCO2, if it is available, as a method
to monitor ventilation, with the target being 35 to 40 mm Hg. To minimize ventilatorinduced lung injury, serial measurements of the plateau pressure should be obtained,
with the goal plateau pressure being less than or equal to 30 cm H2O.7,39,40 Tidal
volume may be decreased to as little as 4 mL/kg ideal body weight if the plateau pressure remains greater than 30 cm H2O.
Hemodynamic Optimization
Hemodynamic optimization of the patient after cardiac arrest focuses on restoring

intravascular volume, maintaining adequate perfusion pressure, monitoring oxygen
delivery, identifying and correcting precipitating causes, and providing supportive
care during the period of myocardial dysfunction.3 Early hemodynamic optimization
is essential to improving outcomes.5,43 In many ways, the approach to the patient after
cardiac arrest parallels that for other disease states, such as sepsis, with an early,
goal-directed approach to hemodynamic resuscitation.15,16 Therefore, many of the
recommended resuscitation end points for patients after arrest are extrapolated
from guidelines for the management of septic or critically ill postoperative patients.15,16
Restoring intravascular volume is an integral component of hemodynamic optimization. As discussed earlier, patients with PCAS are generally volume depleted as a result
of increased vascular permeability. Isotonic crystalloid fluids should be administered
to restore volume status and optimize right heart filling pressures.3,5,7,15,16 Between 3
and 5 L of crystalloid fluid may be required to maintain these filling pressures during
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the first 24 hours following ROSC.26 However, the best means of accurately assessing
volume status remains controversial. Previous guidelines recommended the use of
central venous pressure (CVP) to assess volume status, with a resuscitation end point
for CVP of 8 to 12 mm Hg.15,16 However, evidence for CVP as a reliable estimate of
intravascular volume status is lacking. Numerous conditions, such as tricuspid valve
abnormalities, PE, cardiac tamponade, tension pneumothorax, and right-sided
myocardial infarction, can increase CVP, thereby giving inaccurate information on
volume status.3 Current methods for assessing intravascular volume status include
respirophasic changes in the inferior vena cava, as measured with ultrasonography;
pulse pressure variation; and systolic pressure variation. These dynamic indices of
volume responsiveness provide a better estimate of volume status than CVP. In addition, urine output can be followed as an indirect marker of volume status and renal
perfusion. Current guidelines recommend targeting a urine output of greater than or
equal to 0.5 mL/kg/h.3
Maintaining adequate perfusion pressure is as important as restoring intravascular
volume. MAP, rather than systolic blood pressure, is a better physiologic surrogate for
organ perfusion pressure and should be followed. No prospective study designed to
identify the optimal MAP in these patients has been reported.3,7 Nevertheless, current
guidelines recommend a MAP greater than 65 mm Hg for patients after cardiac
arrest.7 Recognizing the limitations of the literature, the EP must determine the optimal
MAP for each patient. Some patients may require a higher MAP to maintain adequate
cerebral perfusion and oxygen delivery. Several studies have found that MAPs
between 90 and100 mm Hg give good outcomes.5,44,45 MAPs greater than 100 mm
Hg are unlikely to provide additional therapeutic benefit and may be detrimental.3,44
Given the importance of maintaining an adequate perfusion pressure, patients after
cardiac arrest should have an arterial line placed for continuous measurement of MAP.
If the MAP remains less than 65 mm Hg despite restoration of intravascular volume,
a vasopressor should be administered. To date, no vasopressor agent has been
shown to be superior. Current guidelines recommend the use of dopamine, norepinephrine, or epinephrine to maintain MAP greater than 65 mm Hg in the patient after
cardiac arrest.7 DeBacker and colleagues46 evaluated the use of norepinephrine and
dopamine in more than 1600 patients with undifferentiated shock. Although no survival
benefit was shown with either agent, dopamine was associated with an increased
number of adverse events and a trend toward a higher mortality for patients with
cardiogenic shock.
Titrating therapy to optimize hemodynamic parameters in the patient after cardiac
arrest also depends on assessing the adequacy of oxygen delivery. Oxygen delivery
is assessed via global markers of hypoperfusion, namely the serum lactate concentration and central venous oxygen saturation (ScvO2). ScvO2 is measured from a central
line placed in the internal jugular or subclavian vein. Values less than 70% indicate
inadequate oxygen delivery and indicate the need for continued aggressive resuscitation. Current guidelines recommend maintaining ScvO2 greater than or equal to
70%.3,7,15,16 Clinically, the interpretation of ScvO2 in the setting of cardiac arrest can
be difficult because of venous hyperoxia, which tends to occur in patients who have
received high doses of epinephrine (eg, during cardiopulmonary resuscitation
[CPR]).47 Recent evidence suggests that measuring serial lactate values and determining the lactate clearance rate is adequate for assessment of oxygen delivery.48,49
In a recent noninferiority trial, Jones and colleagues50 showed that titrating therapy in
accordance with the lactate clearance rate was comparable with therapy based on
ScvO2 values in patients with sepsis. However, lactate clearance can be impaired in
hepatic dysfunction, convulsive seizures, and hypothermia. Regardless of whether
ScvO2 or lactate clearance is used, the adequacy of oxygen delivery should be

assessed. For patients who have poor oxygen delivery, as shown by a lactate clearance rate of less than 10% for serial measurements or an ScvO2 of less than 70%
despite adequate intravascular volume and MAP, administration of an inotropic agent
should be considered. Dobutamine, the inotropic agent of choice, has been shown to
be effective in the reversal of systolic and diastolic dysfunction following cardiac
arrest.5153
If restoration of intravascular volume and the addition of vasopressor and inotropic
agents fail to maintain an adequate perfusion pressure or oxygen delivery, mechanical
assistance may be considered.3 In these circumstances, emergent cardiac catheterization is indicated to allow the placement of an intra-aortic balloon pump (IABP) or left
ventricular assist device (LVAD). However, the routine use of mechanical support is
not recommended, because studies have not shown a consistent survival
benefit.7,54,55 A summary of oxygenation, initial settings for the mechanical ventilator,
and hemodynamic goals are listed in Box 1.
Therapeutic Hypothermia
Although case reports on the potential benefits of therapeutic hypothermia date back
to the 1950s, it was not until after 2002, when 2 landmark studies were published in
The New England Journal of Medicine, that the AHA incorporated therapeutic hypothermia into its recommendations for postresuscitation care.7,5658 Current AHA
guidelines recommend the use of therapeutic hypothermia in all comatose survivors
of cardiac arrest.7 Comatose is defined by the AHA as a lack of meaningful response
to verbal commands.7
At present, knowledge gaps exist regarding patient selection, method of induction,
goal temperature, duration of the maintenance phase, and the rate of rewarming with
therapeutic hypothermia.3,7 Despite the recommendations to cool all comatose survivors of cardiac arrest, no prospective, randomized trials have evaluated the outcome
of therapeutic hypothermia in patients who had an initial cardiac arrest rhythm other
than pulseless ventricular tachycardia (VT) or ventricular fibrillation (VF). Literature
on patients with non-VT/VF rhythms is limited to case reports, case series, and
observation studies, which do seem to show a beneficial effect of therapeutic
hypothermia.5,5963
Patients receiving therapeutic hypothermia should be cooled as soon as possible.
Data from the 2 largest, prospective trials suggest that the window for therapeutic
hypothermia is between 2 and 8 hours following ROSC.56,57 Patients should be cooled
to a target temperature between 32 and 34 C.3,7,56,57 Although the ideal temperature
is not clear, a temperature less than 32 C may result in greater risk of complications
without a clear morbidity or mortality benefit. Patients can be cooled easily and inexpensively with the infusion of crystalloid fluid at a temperature of 4 C. Lactated Ringer
solution or 0.9% normal saline can be administered as a bolus between 500 mL and 30
mL/kg.7,64 In addition to cold intravenous fluids, surface cooling techniques such as
ice packs to the groin, axilla, head, and neck and cooling blankets can be
used.6567 Iced saline gastric lavage through a Salem Sump (Covidien, Mansfield,
Massachusetts) nasogastric tube is another strategy that can be used to achieve
the target temperature. More recent methods explored the use of endovascular cooling devices with feedback technology to assist with maintenance therapy.3,63 These
devices have not been shown to be superior in achieving or maintaining the target
temperature compared with cold intravenous fluids, ice packs, and cooling blankets.
Monitoring axillary, oral, or tympanic temperatures is not adequate in the patient in
whom therapeutic hypothermia is being induced.7 Instead, in nonanuric patients, core
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Box 1
Oxygenation, initial mechanical ventilation settings, and hemodynamic goals
Oxygenation
Titrate FiO2 to maintain SpO2 at greater than 94% and PaO2 around 100 mm Hg
Titrate PEEP to maintain target SpO2
Initial mechanical ventilator settings
Tidal volume: 6 to 8 mL/kg of ideal body weight
Respiratory rate: 16 to 18 bpm
PEEP: 5 cm H2O
Maintain
PaCO2: 40 to 45 mm Hg
PetCO2: 35 to 40 mm Hg
pH: 7.3 to 7.4
Monitor and maintain plateau pressure less than or equal to 30 cm H2O
Hemodynamic
Maintain euvolemia
Urine output: greater than or equal to 0.5 mL/kg/h
MAP: greater than or equal to 65 mm Hg
ScvO2: greater than or equal to 70%
Lactate clearance of greater than 10% at 2-hour intervals until normal
Vasopressors and inotropic agents as needed
Consider mechanical assist device (eg, LVAD, IABP)
Data from Neumar RW, Nolan JP, Adrie C, et al. Post-cardiac arrest syndrome: epidemiology,
pathophysiology, treatment, and prognostication. A consensus statement from the International Liaison Committee on Resuscitation (American Heart Association, Australian and New
Zealand Council on Resuscitation, European Resuscitation Council, Heart and Stroke Foundation of Canada, InterAmerican Heart Foundation, Resuscitation Council of Asia, and the Resuscitation Council of Southern Africa); 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; and the Stroke
Council. Circulation 2008;118:245283; and Peberdy MA, Callaway CW, Neumar RW, et al. Part
9: post-cardiac arrest care: 2010 American Heart Association Guidelines for Cardiopulmonary
Resuscitation and Emergency Cardiovascular Care. Circulation 2010; 22:S76886.
temperature should be monitored with a temperature-sensing Foley catheter or an

esophageal thermometer, provided that iced saline gastric lavage is not being
used.7 A pulmonary artery catheter can be used to monitor temperature if it has
been placed for other reasons.7,68 A rectal thermometer may be used if no other option
for core temperature monitoring is available.
Patient shivering can be problematic when attempting to reach goal temperature
and should be treated aggressively. Although there is sparse evidence to guide the
selection of medications to prevent shivering, current recommendations suggest an
opioid in combination with an anxiolytic. Additional medications used to treat shivering
in the patient after cardiac arrest receiving therapeutic hypothermia include propofol,
meperidine, fentanyl, and dexmedetomidine. If the patient continues to shiver despite
aggressive sedation and analgesia, neuromuscular blockade may be necessary in

intermittent bolus doses.3,7 Hypothermia can reduce medication clearance, which is
especially important when using neuromuscular agents and sedatives. Hypothermia
can reduce the clearance of these agents by as much as 30%.3,69 Shivering can
also be reduced by warming the skin: for every 4 C increase in skin temperature, there
is a 1 C decrease in the shivering threshold.3,69 Typically, warming the skin to treat
shivering is feasible only when using intravascular cooling devices.
Once patients achieve the target temperature of 32 to 34 C, the second phase, the
maintenance phase, of hypothermic therapy begins. The goal of this phase is to maintain a steady core body temperature, which is best achieved by methods that use
a closed-feedback temperature-sensing loop.3,7,66 Cold intravenous fluids alone
should not be used for the maintenance phase. Cooling blankets and ice packs,
although not optimal, are feasible.3,66 The optimal duration of the maintenance phase
of therapeutic hypothermia is unknown. Based on expert opinion and studies to date,
current guidelines recommend that the duration of therapy should be between 12 and
24 hours.3,7,56,57 Durations of hypothermia longer than 24 hours have not been studied.
Following 12 to 24 hours of hypothermia, patients should be rewarmed. Similar to the
induction and maintenance phases of therapeutic hypothermia, there is scant literature to
guide the rewarming phase. Current guidelines, based primarily on consensus opinion,
recommend rewarming patients at a rate of 0.25 C to 0.5 C per hour.3 Transitioning
from hypothermia to normothermia can result in significant effects on metabolism, electrolyte concentrations, medications levels, and hemodynamics.3 If rewarming speeds
are too high, the catabolic processes could be reinitiated, worsening patient outcome.69
Throughout the induction, maintenance, and rewarming phases of therapeutic hypothermia, it is important to continue to monitor oxygenation, ventilation, and hemodynamic optimization. All patients should remain on continuous cardiac monitoring,
pulse oximetry, and end-tidal carbon dioxide, with the goals of maintaining SpO2 greater
than 94%, euvolemia, MABP greater than 65 mm Hg, and a PetCO2 of 35 to 40 mm Hg.
The complications of therapeutic hypothermia include bradycardia, increased
systemic vascular resistance, and decreased cardiac output.69,70 Cooling also has
significant effects on the kidneys and can induce diuresis, resulting in hypophosphatemia, hypokalemia, hypomagnesemia, hypocalcemia, and hypovolemia.3,69,70 Electrolyte levels should be monitored frequently and replaced to high normal values.69
Hypothermia can also induce insulin resistance and decreased insulin secretion.
Significant hyperglycemia can be seen even in patients without a history of diabetes.3,69 Coagulopathy is another common effect of hypothermia, mediated through
platelet dysfunction and its effects on the clotting cascade.69 In addition, hypothermia
can suppress the immune system through inhibition of proinflammatory mediators.
Literature to date suggests a trend toward increased infections; however, values
have not reached statistical significance.3,69 A summary of the 3 phases of therapeutic
hypothermia is listed in Box 2.
Early Cardiac Catheterization
The rates of coronary artery disease in patients resuscitated from out-of-hospital

cardiac arrest are as high as 71%; up to 50% have an acute coronary occlusion.32,71
Cardiac catheterization provides definitive therapy for patients with an occlusion and
has been independently associated with improved outcome.3,7,32,71 Complaints of
chest pain and ST-segment increase seen on an electrocardiogram (ECG) are poor
predictors of acute arterial occlusion.3,7,32,71 Therefore, all patients with a presumed
cardiac cause of an arrest should be considered for emergent cardiac catheterization,
despite the absence of ST-segment increase on ECG.3,4,7,32,71 If PCI is not
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Box 2
Therapeutic hypothermia
Induction phase
Cool as early as possible, even if going for percutaneous coronary intervention (PCI)
Target temperature 32 to 34 C
Administer cold intravenous fluids (30 mL/kg bolus of isotonic crystalloid)
Use surface cooling methods
Place temperature-sensing Foley catheter, esophageal temperature probe, rectal probe, or
intravascular device
Control shivering
Maintenance phase
Maintain hypothermia at 32 to 34 C
Continue for 12 to 24 hours
Monitor electrolytes and replace to high normal values
Magnesium
Phosphate
Potassium
Calcium
Monitor glucose and treat hyperglycemia
Monitor coagulation parameters
Prothrombin time
Activated partial thromboplastin time
Platelets
Rewarming phase
Rewarm at a rate of 0.25 to 0.5 C/h
Monitor electrolytes and replace to high normal values
Rapid rewarming may reinitiate catabolic processes and worsening outcome
immediately available and ST-segment increase is present, or if there is strong suspicion for an ischemic cardiac event, thrombolytic therapy should be considered.3
PCI should not be delayed or withheld because of the use of therapeutic hypothermia. Rittenberger and colleagues60 and Wolfrum and colleagues72 showed that
the 2 procedures can be done together safely. The theoretic risk of increased bleeding
during hypothermia was not observed in either of these studies.60,72 Early PCI in the
setting of hypothermia is associated with improved survival and neurologic
outcome.32,60,71,73 Cardiac catheterization can also provide a means for advanced
hemodynamic monitoring and support as well as placement of mechanical assist
devices (ie, IABP or LVAD).
SUPPORTIVE CARE
Dysrhythmias
The treatment of dysrhythmias that occur during the postcardiac arrest period do not
differ from standard treatment of dysrhythmias in the patient who has not had a cardiac
arrest.7 These treatments can be electrical and medication therapies. Following

ROSC, all patients should be placed on continuous cardiac monitoring and a 12lead ECG should be obtained. Although patients may have received antidysrhythmic
therapy during resuscitation, current guidelines recommend against the use of
prophylactic antidysrhythmic medications.7
For stable patients with a normal QT interval who develop VT, procainamide or
amiodarone may be administered.3 Amiodarone has been shown to improve survival
to hospital admission, but not overall survival or survival to discharge.74,75 For patients
who develop VT in the setting of a prolonged QT interval, amiodarone can be administered. Patients with a prolonged QT interval who develop polymorphic VT should
receive magnesium sulfate.74 Magnesium is unlikely to be effective in the setting of
polymorphic VT with a normal QT interval.74
Because the underlying cause of a substantial number of out-of-hospital cardiac
arrests is cardiac ischemia, the definitive dysrhythmic therapy is reperfusion with
PCI or thrombolytics.32
Transfusions
Blood transfusion remains controversial outside the setting of hemorrhagic cardiac

arrest and in the critically ill. In the initial study on early goal-directed treatment of
sepsis, patients whose hemoglobin was less than 10 g/dL in the setting of an ScvO2
less than 70% received transfusions.16 The transfusion threshold of a hemoglobin
less than 10 g/dL in patients with potentially persistent hypoperfusion remains controversial. Currently, there are data to suggest that restrictive transfusion practices
(transfusion hemoglobin trigger <7 g/dL) may be beneficial.76 Blood transfusion should
be strongly considered in the patient after cardiac arrest whose hemoglobin concentration is less than 6 g/dL. There is almost no indication to transfuse patients after
cardiac arrest whose hemoglobin is greater than 10 g/dL.77
Seizure Management
Seizures are common in comatose survivors of cardiac arrest. It is estimated that the
clinical course of 5% to 20% of patients after cardiac arrest is complicated by
seizures.5,7 Prolonged seizure activity can have detrimental neurologic effects in the
patient after cardiac arrest and has been associated with increased mortality.78
Current guidelines recommend continuous electroencephalographic monitoring in
all comatose survivors of cardiac arrest.3,7
Patients who experience seizures during the postresuscitation period typically have
a poor response to antiepileptic medications, especially if myoclonus is present.79 If
myoclonus is observed, clonazepam is considered the drug of choice. Sodium valproate and levetiracetam may also be effective.80 Postcardiac arrest seizures have
also been treated with benzodiazepines, phenytoin, propofol, and barbiturates. Maintenance therapy with antiepileptic medications should be initiated once control of
seizure activity is achieved.3 For patients after cardiac arrest without seizure activity,
there is no benefit to the routine administration of antiepileptic medications.7,81,82
Hyperglycemia
Hyperglycemia is common in patients after cardiac arrest and may be detrimental.7,78

This topic has been investigated in critically ill patients and following cardiac
arrest.8385 In both settings, research has shown that glycemic control is important.83,84 However, the optimal glucose value remains controversial. In several studies,
intensive insulin therapy to aggressively target a normal serum glucose (80110
mg/dL) value did not affect the mortality rate and markedly increased the incidence
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134
of severe hypoglycemia.83,85 Therefore, current guidelines recommend moderate glycemic control, with a goal serum glucose between 144 and 180 mg/dL.7
Hyperthermia
Hyperthermia (>37.6 C) increases the risk of poor neurologic outcome in patients after
cardiac arrest.86 If hyperthermia develops, it should be treated aggressively with antipyretic medications or active cooling therapies.3,7 If hyperpyrexia develops during the
rewarming phase of therapeutic hypothermia, the patient must be monitored closely
and the temperature corrected as quickly as possible.3,7
A summary of supportive treatment is provided in Box 3.
REGIONALIZATION OF RESUSCITATION CENTERS
Out-of-hospital cardiac arrest (OOHCA) affects 236,000 to 325,000 people in the

United States each year.1 The national average survival rate to hospital discharge is
only 8.4%.1 This number does not describe neurologic status at discharge; many of
these patients probably have severe and permanent neurologic injury.
Regarding survival to hospital discharge, there is great variation between regions
and even among hospitals within the same region.13 There is roughly a fivefold
regional variation in outcome by EMS-treated patients of OOHCA.1,2 Seattle and
King County reached a 16.3% survival rate of EMS-treated patients with any initial
rhythm, and a 39.9% survival rate when the initial rhythm was VF. Rochester, Minnesota, reported a similar survival rate of 49% after bystander-witnessed VF arrest.1,2
Survival rates, as well as the likelihood of good neurologic recovery, are highly contingent on several interventions. Interventions such as bystander CPR and defibrillation
are beyond the control of the EP, but EMS transport to an appropriate facility can be
directed by the EP.87 Interventions such as emergent PCI, induction of therapeutic
hypothermia, and provider experience have all been shown to improve outcomes after
OOHCA.3,5,7,32,56,59,72
Similar to the current designation of trauma centers, ST-segment elevation myocardial infarction (STEMI) centers, and stroke centers, cardiac arrest center designation is
on the horizon.1,3,88 Cardiac arrest centers must be staffed with experienced
personnel who have access to the necessary resources to provide the efficient and
definitive care these patients require.1,3,32,59,71,72,89 The ability to perform emergent
coronary angiography is an independent predictor of improved outcome and must
be within the capabilities of a cardiac arrest center.1,3,32,71,89 The availability of cardiac
catheterization is also important, because some studies have shown rates of coronary
artery disease as high as 71% in the postarrest population.1
There is increasing evidence that it is safe to transport patients with ROSC to
a resuscitation center and bypass closer facilities.88,90 However, the nearest facility
should be bypassed only to provide primary transport to a cardiac arrest center. If
CPR remains in progress, EMS personnel should transport the patient to the nearest
facility for resuscitation. If the patient has ROSC during the prehospital phase of care,
transport to a cardiac arrest center should be arranged.90
Regionalization and designation decisions regarding cardiac arrest centers are
largely extrapolated from previous work done to establish designated trauma, stroke,
and STEMI centers. Longer primary transport times to reach these designated centers
has been shown to be safe for patients and to improve patient outcomes, and this is
likely the case for future cardiac arrest centers, which will be able to provide definitive
treatment under the direction of highly experienced care providers. However, many
EMS systems lack standard protocols for patients after cardiac arrest, many of
Box 3
Supportive care
Dysrhythmia
Obtain 12-lead electrocardiogram
Continuous cardiac monitoring
Standard medical and electrical therapies
Normal QT with VT: amiodarone or procainamide
Prolonged QT with VT: amiodarone
Prolonged QT with polymorphic VT: magnesium sulfate
Consider need for reperfusion therapy
Red blood cell transfusion
Strongly consider if:
Hemoglobin less than 7.0 g/dL and
ScvO2 less than 70% or lactate clearance less than 10% following 2 hours of resuscitation
Unlikely if hemoglobin greater than 10 g/dL
Seizure control
Initiate electroencephalogram monitoring for all comatose survivors
For myoclonic seizure activity:
Clonazepam drug of choice
Valproate and levetiracetam may also be used
For general seizure activity, all of the following are acceptable:
Benzodiazepines
Phenytoin
Propofol
Barbiturates
Initiate maintenance therapy once seizure controlled
No indication for routine administration of antiepileptic therapies in absence of seizure
activity
Hyperglycemia
Monitor glucose every 1 to 2 hours
Goal serum glucose 144 to 180 mg/dL
Administer insulin if serum glucose outside goal range
Hyperthermia
Aggressively control with antipyretics, surface cooling devices
whom are transported to the nearest facility, which may not have the resources
needed to adequately care for these complex patients.
SUMMARY
Caring for the ED patient with ROSC after cardiac arrest is challenging. A coordinated
and systematic approach to postcardiac arrest care can improve the mortality rate
135
136
and the chance of meaningful neurologic recovery. By achieving appropriate targets

for oxygenation, ventilation, and hemodynamic parameters, along with initiating
therapeutic hypothermia and arranging early PCI, the EP can have the most significant
impact on patients who have just been revived from death.
ACKNOWLEDGMENTS
The authors would like to thank Linda J. Kesselring, MS, ELS, the technical editor for
the Department of Emergency Medicine at the University of Maryland School of Medicine, for her assistance in the preparation of this article.
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Opportunities and pitfalls of a promising treatment modalityPart 2: Practical
aspects and side effects. Intensive Care Med 2004;30:75769.
Reynolds JC, Callaway CW, El Khoudary SR, et al. Coronary angiography
predicts improved outcome following cardiac arrest: propensity-adjusted analysis. J Intensive Care Med 2009;24:17986.
Wolfrum S, Pierau C, Radke PW, et al. Mild therapeutic hypothermia in patients
after out-of-hospital cardiac arrest due to acute ST-segment elevation myocardial
infarction undergoing immediate percutaneous coronary intervention. Crit Care
Med 2008;36:17806.
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73. Batista LM, Lima FO, Januzzi JL Jr, et al. Feasibility and safety of combined
percutaneous coronary intervention and therapeutic hypothermia following
cardiac arrest. Resuscitation 2010;81:398403.
74. Morrison LJ, Deakin CD, Morley PT, et al. Part 8: advanced life support: 2010
international consensus on cardiopulmonary resuscitation and emergency
cardiovascular care science with treatment recommendations. Circulation 2010;
122:S345421.
75. Kudenchuk PJ, Cobb LA, Copass MK, et al. Amiodarone for resuscitation after
out-of-hospital cardiac arrest due to ventricular fibrillation. N Engl J Med 1999;
341:8718.
76. Hebert PC, Wells G, Blajchman MA, et al. A multicenter, randomized, controlled
clinical trial of transfusion requirements in critical care. Transfusion requirements
in critical care investigators, Canadian Critical Care Trials Group. N Engl J Med
1999;340:40917.
77. Netzer G, Liu X, Harris AD, et al. Transfusion practice in the intensive care unit:
a 10-year analysis. Transfusion 2010;50:212534.
78. Nielsen N, Sunde K, Hovdenes J, et al. Adverse events and their relation to
mortality in out-of-hospital cardiac arrest patients treated with therapeutic hypothermia. Crit Care Med 2011;39:5764.
79. Hui AC, Cheng C, Lam A, et al. Prognosis following postanoxic myoclonus status
epilepticus. Eur Neurol 2005;54:103.
80. Caviness JN, Brown P. Myoclonus: current concepts and recent advances.
Lancet Neurol 2004;3:598607.
81. Randomized clinical study of thiopental loading in comatose survivors of cardiac
arrest. Brain Resuscitation Clinical Trial I Study Group. N Engl J Med 1986;314:
397403.
82. Longstreth WT Jr, Fahrenbruch CE, Olsufka M, et al. Randomized clinical trial of
magnesium, diazepam, or both after out-of-hospital cardiac arrest. Neurology
2002;59:50614.
83. Finfer S, Chittock DR, Su SY, et al. Intensive versus conventional glucose control
in critically ill patients. N Engl J Med 2009;360:128397.
84. Losert H, Sterz F, Roine RO, et al. Strict normoglycaemic blood glucose levels in
the therapeutic management of patients within 12h after cardiac arrest might not
be necessary. Resuscitation 2008;76:21420.
85. Oksanen T, Skrifvars MB, Varpula T, et al. Strict versus moderate glucose control after
resuscitation from ventricular fibrillation. Intensive Care Med 2007;33:2093100.
86. Zeiner A, Holzer M, Sterz F, et al. Hyperthermia after cardiac arrest is associated
with an unfavorable neurologic outcome. Arch Intern Med 2001;161:200712.
87. Iwami T, Kawamura T, Hiraide A, et al. Effectiveness of bystander-initiated
cardiac-only resuscitation for patients with out-of-hospital cardiac arrest. Circulation 2007;116:29007.
88. Nichol G, Soar J. Regional cardiac resuscitation systems of care. Curr Opin Crit
Care 2010;16:22330.
89. Callaway CW, Schmicker R, Kampmeyer M, et al. Receiving hospital characteristics associated with survival after out-of-hospital cardiac arrest. Resuscitation
2010;81:5249.
90. Hartke A, Mumma BE, Rittenberger JC, et al. Incidence of re-arrest and critical
events during prolonged transport of post-cardiac arrest patients. Resuscitation
2010;81:93842.
Rapid Response
Systems: Identification
a n d Ma n a g e m e n t of
t h e P re a r re s t St a t e
Michael T. McCurdy,
MD
a,b,
*, Samantha L. Wood,
MD
KEYWORDS
Rapid response Medical emergency team
Patient monitoring Cardiac arrest
Cardiac arrest occurs in up to 5 out of every 1000 adult hospital admissions.1 Despite
aggressive postresuscitation management, in-hospital cardiac arrest (IHCA) is associated with poor outcomes. In a review of 49,130 patients with IHCA, 84% died before
hospital discharge or suffered severe neurologic disability, with 55.2% dying during
the acute event.2 Disappointingly, rates of survival to hospital discharge for IHCA
patients have not changed over the last several decades.1,3,4 Although IHCA is more
common in children, they fare slightly better; cardiac arrest occurs in 7 to 30 out of every
1000 pediatric admissions,57 and survival to hospital discharge is 25% to 50%.8
Signs of deterioration usually precede IHCA,914 and over half of cases are preventable.15,16 Care for deteriorating ward patients awaiting intensive care unit (ICU) transfer is frequently inadequate.17 The improvements in morbidity and mortality attributed
to early, aggressive intervention in sepsis,18 trauma,19 stroke,20 and ST-elevation
myocardial infarction21 have led to a paradigm shift in how to best care for other critically ill patients as well. Rapid response systems (RRS) represent one way to intervene early on deteriorating patients in an attempt to prevent cardiac arrest and its
dismal outcome.

a
Division of Pulmonary & Critical Care Medicine, Department of Medicine, University of Maryland School of Medicine, 110 South Paca Street, 2nd Floor, Baltimore, MD 21201, USA
b
Department of Emergency Medicine, University of Maryland School of Medicine, Baltimore,
MD, USA
c
Combined Emergency Medicine/Internal Medicine/Critical Care Program, University of
Maryland Medical Center, 110 South Paca Street, Suite 200, Baltimore, MD 21201, USA
* Corresponding author. Division of Pulmonary & Critical Care Medicine, Department of Medicine, University of Maryland School of Medicine, 110 South Paca Street, 2nd Floor, Baltimore,
MD 21201.
E-mail address: DrMcCurdy@gmail.com
doi:10.1016/j.emc.2011.09.012
emed.theclinics.com
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McCurdy & Wood
THE RAPID RESPONSE SYSTEM
An RRS should provide emergent assessment and care for sick patients who require
a higher level of care. The system can be divided into afferent and efferent limbs.
The afferent limb refers to monitoring the patient, detecting crisis, and activating the
team. The RRS generally includes a protocol for monitoring patients and a list of
calling criteria. Calling criteria vary among institutions and may include vital-sign
abnormalities, changes in mental status, threatened airway, or other signs of deterioration. When a patient meets calling criteria, system activation is optional or mandatory. Most systems encourage nurses to activate the system when concerned about
potential patient deterioration regardless of whether calling criteria are met.
Once activated, a team of health care providers presents immediately to the
patients bedside to address the crisis; this team represents the efferent limb of the
RRS. There are several types of responding teams, including medical emergency
teams (METs), rapid response teams (RRTs), and critical care outreach (CCO) teams.
A 2006 consensus conference suggested using the term medical emergency team
for teams that are generally led by physicians and have the ability to: (1) prescribe
therapy; (2) place central vascular lines; (3) initiate ICU-level care at the bedside;
and (4) perform advanced airway management. The conference suggested the use
of the term rapid response team to describe a team without all 4 of those abilities
that performs a preliminary evaluation of a patient and summons additional help or
facilitates transfer to a higher level of care if warranted. Critical care outreach
team implies an outreach component such as proactively visiting hospital wards to
identify patients at risk for decompensation.22
Research on RRSs has focused primarily on the afferent limb, whereas studies
assessing the efficacy of the efferent limb are sparse. This difference can be attributed
to the ease of analyzing the afferent limb as compared with the complexity of studying
the efferent limb. For example, tracking RRS activation is fairly straightforward: teams
are either activated or not. On the other hand, the efferent limb is exceedingly difficult
to study because of the numerous variables involving different types of RRSs (eg,
MET, RRT, CCO), patient populations (eg, inner city, rural), disease processes (eg,
IHCA, hypotension, respiratory distress), care delivered (eg, antibiotics, fluids, vasopressors, intubation), and hospital resources (eg, nursing-to-patient ratios, ICU bed
availability, access to ancillary services). Because of the paucity of data on the efferent
limb, this review focuses exclusively on the afferent limb of the RRS.
THE AFFERENT LIMB
The afferent limb of the typical RRS comprises several steps. First, a patient clinically
deteriorates. Second, nursing staff detects the deterioration following patient assessment or monitoring. Third, nursing staff makes a decision to activate the team. Fourth,
the team is activated. Each of these seemingly simple steps presents challenges to the
effective and efficient functioning of the RRS.
Antecedents to IHCA
Warning signs precede 60% to 84% of IHCAs914 and are predictive of in-hospital, 30day, and 1-year mortality.12,2325 Most studies refer to these detectable signs of
patient deterioration as antecedents or abnormal indices, and include vital sign
abnormalities, changes in Glasgow Coma Scale (GCS) score, or other changes in
patient condition.
The majority of hospitalized patients remain stable throughout their stay,23,26 and
most of those who develop an abnormal vital sign or other concerning clinical
Rapid Response Systems
derangement will not experience cardiac arrest or death. In one prospective study of
ward patients, 66.7% of observed vital-sign abnormalities spontaneously resolved
and an additional 21.6% resolved with treatment. However, presence of a single
abnormality was associated with a significant increase in mortality, and mortality
risk further increased with every additional abnormality.23 Another study prospectively
evaluated abnormal indices in medical and surgical patients at a Veterans Affairs
Hospital. Thirty-five percent of those with at least one abnormality, compared with
2.5% of patients without any, later experienced cardiac arrest, death, or unexpected
ICU transfer.12 Use of an abnormal index oversimplifies a patients true risk for
cardiac arrest. However, vital signs and other basic findings, such as GCS score,
help to grossly estimate a patients risk of IHCA, death, or ICU transfer.
Antecedents to IHCA provide an opportunity for intervention, but they must be identified early enough to correct the underlying problem. Fortunately, adequate time
usually exists to intervene before patient deterioration.11,23 In one study, 48% of
non-Do Not Resuscitate (DNR) ward patients exhibited abnormal vital signs in the
8 to 48 hours prior to death.27 Patients with abnormal indices 8 hours preceding arrest
have higher in-hospital mortality (92% vs 81%), notwithstanding the higher likelihood
that patients with early abnormal vital signs are on monitored units and receive earlier
defibrillation.28,29 Physicians frequently document concern for patient deterioration
hours to days before requiring an unexpected ICU transfer.30 This alarming finding
may result from: (1) physician failure to recognize the prognostic significance of concerning data; (2) institution of inadequate interventions; or (3) failure to either get help
or successfully transfer the patient to a higher level of care. Regardless of the reason,
physician suspicion of patient deterioration is a harbinger of the eventual need for ICU
transfer, and sufficient time often exists for a meaningful preventive intervention if the
physician acts on such clinical suspicion.
Monitoring
Identification of appropriate RRS monitoring parameters is the subject of substantial

debate. Although the policies of most hospitals include monitoring of vital signs and
mental status, the specific parameters used to activate the RRS vary widely. In accordance with standards established at a recent RRS consensus conference, the afferent
limb should, at a minimum, monitor heart rate, blood pressure, respiratory rate,
temperature, and pulse oximetry. Airway patency, behavior change, capillary refill,
urine output, basic chemistry and hematology results, and clinical observations are
listed as additional possible monitoring parameters.9 In these studies, it is noteworthy
that telemetry analysis is not included as a routine monitoring parameter in patients
without dysrhythmias or suspected acute coronary syndrome.31
Determining the proper frequency of monitoring is also a significant challenge.
Continuous monitoring is associated with improved outcome in patients with
IHCA,32 whereas less frequent monitoring may delay the detection of impending instability. RRSs receive significantly more calls during the day and from monitored units,
reinforcing the concept that more intensive patient monitoring may increase the detection of critical events.33 Because good outcomes in critically ill patients depend on
how rapidly proper treatment is initiated, it logically follows that delay of RRS activation is associated with increased mortality.34
Although common sense and some studies suggest that more monitoring improves
patient outcomes, data do not consistently support this assertion.3537 Patient monitoring is also limited by practical concerns. Nursing resources, bed availability, and
cost may prohibit increased monitoring. Technological limitations also present challenges; one study showed that 40.6% of vital-sign abnormalities detected with
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continuous monitoring in a step-down unit were artifacts.26 Accurate vital signs are
sometimes challenging to obtain (eg, using a too-small blood pressure cuff in an obese
patient will result in an inaccurate blood pressure measurement), and an inappropriate
emphasis on absolute values rather than relative changes may limit monitoring
utility.38,39 The RRS consensus conference acknowledges that the ideal monitoring
frequency is still a matter of debate. The current recommendation is for individualized
monitoring plans for all patients, as long as indices are checked at least every 6 to 12
hours.9
RRS Activation
Since no standardized early warning score exists, different institutions employ various
scoring systems to activate the RRS. Regardless of the type of scoring system utilized,
the decision to active the RRS based on a score is ultimately the responsibility of the
bedside clinician. For example, a clinician may determine that despite the presence of
an abnormal vital sign, the patient does not warrant further evaluation. Whereas other
activation criteria can be quite subjective (eg, patient does not look good). Although
many track and trigger systems have been developed to guide this decision making
process40 none is sufficiently reliable to be adopted as the standard means of assessing the likelihood of clinical deterioration in either adults or children.4143
The simplest type of track and trigger system is the single-parameter track and
trigger system (SPTTS). In this system, a single vital sign or clinical abnormality outside
a specified range prompts RRS activation. A 2008 review examined 30 different
SPTTSs by retrospectively applying their criteria to a large database of patients
admission vital signs to evaluate their effectiveness in predicting in-hospital
mortality.44 Specificity ranged from 68.1% to 98.1%, but sensitivity was only 7.1%
to 52.8%.
Multiple-parameter track and trigger systems require more than one abnormality for
team activation. For example, the Patient-at-Risk score requires either 3 abnormal
indices or decreased mental status plus tachycardia or tachypnea for system activation.45 Sensitivity and specificity for ICU admission were poor (27% and 57%,
respectively).40
Aggregate-weighted track and trigger systems (AWTTSs) calculate a score based
on the degree to which a patients vital signs are abnormal. One frequently cited
AWTTS is the Modified Early Warning Score (MEWS). The MEWS assigns points
based on the degree of derangement of systolic blood pressure, heart rate, respiratory
rate, temperature, and mental status, with an elevated score correlating with
increased risk of death and ICU admission.46 The MEWS accurately identifies patients
at risk for deterioration when a score for age is included; unfortunately, its application
to acute medical admissions has not been shown to change outcomes.47 Dozens of
other AWTTs exist, but a recent review concluded that most did not perform well.48
Hospitals continue to use a variety of scoring systems, but clearly more research is
needed to identify the best-performing scoring system.
Several barriers to nursing activation of the RRS exist. Nurses may be reluctant to
call because they frequently witness patients who briefly exhibit abnormal signs
that spontaneously normalize.49 In addition, nurses may not know whom to contact
(eg, RRS vs primary team) in the event of patient decompensation or fear being reprimanded if a call is later deemed unnecessary.50 RRS activation rates improve with
supportive response by the RRS team and with increased nursing education,51,52
expertise, and patient familiarity. Mandatory RRS activation for all patients meeting
criteria also facilitates improved nursing activation.53 The relationship between nurse
workload and RRS activation is unclear, as studies have shown both increased and
decreased activation during busy shifts.54
As an alternative to nurse-triggered RRS activation, one study confirmed the feasibility of vital-sign data entry into a Personal Digital Assistant (PDA) that calculates an
early-warning score. This score is then transmitted to physicians who can access the
information online from anywhere in the hospital.55 Another study assessed the utility
of continuously calculating an instability index value; when this value exceeded
a certain cutoff, an alarm alerted nursing staff to determine the need for RRS activation.56 Although this system was associated with a decrease in episodes of patient
instability, its ability to alter outcomes and cost compared with simply increasing
nursing staffing level is unknown.57
Although family concern is frequently included in protocols as a trigger for nursing
activation of the RRS and often portends a decline in clinical status, experience with
direct activation of the RRS by a patients family is limited. Educational programs have
attempted to encourage family members to directly activate the RRS by calling
a phone number if they have any concern about the patients status. However, direct
activation remains rare and is frequently prompted by pain control or communication
issues rather than a patients clinical condition.55,5860
Criteria for RRS activation need to be more clearly defined to support decision
making. The heterogeneity of early-warning scores limits widespread implementation,
and difficulty exists in effectively identifying the most accurate one. As of yet, no
system has proved its ability to adequately substitute for the bedside clinicians vigilance in preventing a patients clinical deterioration.
RRS Efficacy
Outcome data for RRSs vary widely. In adults, some studies demonstrate reductions
in both IHCA and mortality,61,62 others demonstrate reductions in IHCA without
a significant change in mortality,6366 and still others show no significant differences
in either IHCA or mortality.59,67,68 One study showed decreased mortality in surgical
patients but increased mortality in medical patients after RRS implementation.69 Pediatric studies show decreases in IHCA only,5 decreases in IHCA and mortality,70,71
reductions in pulmonary arrest requiring intubation but no changes in IHCA or
mortality,72 and no significant decreases in IHCA or mortality.73
The inconsistent conclusions of these studies likely result from methodological
design flaws. Most are limited by historical controls, lack of randomization, inclusion
of DNR patients, and lack of standardized calling criteria and interventions. The International Liaison Committee on Resuscitation (ILCOR) has since called for consistency
and comparability of relevant collected and reported data regarding RRSs.74
Two randomized trials assessing the effect of RRSs yielded conflicting results. One
assessed the efficacy of a phased introduction of a nurse-led CCO service that
provided education on caring for critically ill patients and responded to emergent calls
prompted by a Patient-at-Risk score. Hospital wards randomized to CCO implementation reduced mortality compared with controls.75 The MERIT study, which randomized 23 Australian hospitals to either MET implementation or control, demonstrated
significant improvements in both the intervention and control arms, thus yielding no
differences in mortality, IHCA, or unplanned ICU admission at 6 months between
the arms.76 The findings of the MERIT study were affected by contamination between
the groups: RRSs in the intervention hospitals were often not activated, and preexisting cardiac arrest teams in control hospitals were frequently activated before actual
arrest. In addition, because the primary outcome was much lower than expected,
the study was underpowered to detect statistical significance. Therefore, a post hoc
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analysis of the MERIT database attempted to distinguish why before-and-after trials

show improved outcomes in hospitals implementing RRSs whereas the randomized
MERIT study showed no significant difference between treatment arms. Although
fraught with the typical limitations of a post hoc review of data from both intervention
and control hospitals, the reanalysis of the MERIT trial identified early RRS activation
(ie, calling for help before cardiac arrest) as the primary determinant of lower rates of
cardiac arrest and unexpected death.77
Follow-up studies involving MERIT hospitals offer possible explanations for the
initial negative results. For example, one participating hospital continued to follow
these outcomes beyond the 6-month study period and found significantly decreased
2- and 4-year IHCA and mortality with increased MET activation.78 The investigators
argued that hospital culture and institutional inertia impede rapid policy changes
and that MET efficacy may only be evident once hospital culture has time to adapt.
However, one study of a mature MET system demonstrated the persistence of
preventable cardiac arrests even after 16 years from its implementation.79 Experience
dictates that successful MET systems may not feasibly achieve a zero rate of
preventable IHCA.
A 2010 meta-analysis of 18 studies including over 1.2 million hospital admissions
assessed the effects of RRS implementation.80 Overall, RRSs were associated with
a 33.8% reduction in non-ICU adult IHCA. Mortality data varied widely among studies,
but no overall effect was demonstrated in adults, prompting concern that RRS implementation simply shifts patients who will likely die during their hospitalizations from the
ward to the ICU. Pediatric mortality from IHCA, however, was reduced by 37.7%. The
lower mortality rate was disproportionately large relative to the lower cardiac arrest
rate, raising doubt that decreased deaths were due to RRS interventions. This study
concluded that there was not robust evidence to support the ability of RRSs to reduce
in-hospital mortality. It also noted that study results over time trended toward the null
hypothesis, raising questions about initial publication bias.
One inconsistency common to several studies is that mortality rates decline out of
proportion to decreases in cardiac arrests.62,70,71 For example, 6-month periods
before and after implementation of an RRT in a Colorado hospital showed a decrease
in code blue calls from 70 to 55, indicating 15 fewer cardiac arrests; however, this
study also reported a significant decrease in mortality rate equivalent to 75 lives
saved.81
In summary, the data on RRS efficacy vary. Although some large studies fail to show
convincing results, others support RRS implementation when the system promotes
earlier calls. Further quality studies undoubtedly are needed to clarify what specific
aspects of the RRS are linked to improvement in meaningful outcomes.
CONTROVERSY
RRSs represent a highly controversial issue, and opinion pieces abound in the medical
literature. RRS supporters urge aggressive monitoring and evaluation.82 Skeptics
express concern that the rapid institution of RRSs may inhibit study and implementation of alternative and potentially superior ways to improve patient safety such as
educational initiatives, increased nursing staff, automated monitoring systems, or hospitalist presence on the floor.83 Concern also exists that the RRS may temporarily
mask underlying deficiencies in medical care for hospitalized patients, such as insufficient physician presence, patient admission to an inappropriate level of care, and
inefficient transfer of patients to a higher level of care.84,85 Others argue for a moderate
approach, acknowledging that RRSs are not supported by conclusive data, but
asserting that they are currently the best method to manage deteriorating patients.86
By taking an individualized approach to each patient, RRSs may optimize the use of
hospital resources by considering the appropriateness of invasive interventions in individuals unlikely to benefit from such care and by pursuing aggressive measures in
those who will.77
The major conflict surrounding RRSs reflects a problem commonly encountered in
medicine: how to reconcile the intuitive, logical appeal of an intervention with inconsistent and inconclusive evidence. This problem is perhaps most apparent in the Institute
for Healthcare Improvements (IHI) 100,000 Lives Campaign, which challenged hospitals to prevent accidental deaths by pursuing 6 initiatives for patient safety. Although
the campaigns success was questioned,87,88 the IHI supported its RRS advocacy by
highlighting the shortcomings of the MERIT study and argued against enforcing standards of evidence that in this case ignore accumulated reports, time-series data,
common sense, and sound logic.89 Explicitly or implicitly, policy continues to support
RRSs, as evidenced by the Joint Commissions recent patient safety goals. These
goals include a recommendation that hospitals select a suitable method that enables
health care staff members to directly request additional assistance from a specially
trained individual(s) when the patients condition appears to be worsening.90
SUMMARY
Bridging the divide between evidence-based and commonsense medical decision

making is challenging, especially when randomized, controlled study of the intervention is difficult and blinding is impossible. The benefit of RRSs is that intuitive and
supportive data exist, but the institution of an RRS is not a panacea for IHCA or unexpected deaths. RRS implementation should be one component of an effort to improve
patient safety that includes adequate nursing education and staffing, availability and
involvement of a patients primary caregivers, and hospital provision of sufficient
resources and efficiency. This coordinated approach facilitates appropriate admission
triage decisions and effective monitoring of stable patients, as well as rapid evaluation,
treatment, and transfer when necessary.
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36. Taenzer AH, Pyke JB, McGrath SP, et al. Impact of pulse oximetry surveillance on
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37. Watkinson PJ, Barber VS, Price JD, et al. A randomised controlled trial of the
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38. Edelson DP. A weak link in the rapid response system. Arch Intern Med 2010;
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39. Winters ME, McCurdy MT, Zilberstein J. Monitoring the critically ill emergency
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41. Subbe CP. Better ViEWS ahead? It is high time to improve patient safety by standardizing Early Warning Scores. Resuscitation 2010;81(8):9234.
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43. Gao H, McDonnell A, Harrison DA, et al. Systematic review and evaluation of
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47. Subbe CP, Davies RG, Williams E, et al. Effect of introducing the Modified Early
Warning score on clinical outcomes, cardio-pulmonary arrests and intensive
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48. Smith GB, Prytherch DR, Schmidt PE, et al. Review and performance evaluation of
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49. Buist MD, Shearer W. Rapid response systems: a mandatory system of care or an
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50. Shapiro SE, Donaldson NE, Scott MB. Rapid response teams seen through the
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53. Jones CM, Bleyer AJ, Petree B. Evolution of a rapid response system from voluntary to mandatory activation. Jt Comm J Qual Patient Saf 2010;36(6):26670, 241.
54. Jones L, King L, Wilson C. A literature review: factors that impact on nurses effective use of the Medical Emergency Team (MET). J Clin Nurs 2009;18(24):
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55. Smith GB, Prytherch DR, Schmidt P, et al. Hospital-wide physiological surveillancea new approach to the early identification and management of the sick
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58. Bogert S, Ferrell C, Rutledge DN. Experience with family activation of rapid
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61. Bellomo R, Goldsmith D, Uchino S, et al. A prospective before-and-after trial of
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63. Baxter AD, Cardinal P, Hooper J, et al. Medical emergency teams at The Ottawa
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66. Jones D, Bellomo R, Bates S, et al. Long term effect of a medical emergency
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68. Kenward G, Castle N, Hodgetts T, et al. Evaluation of a medical emergency team
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69. Jones D, Opdam H, Egi M, et al. Long-term effect of a medical emergency team
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70. Sharek PJ, Parast LM, Leong K, et al. Effect of a rapid response team on hospitalwide mortality and code rates outside the ICU in a Childrens Hospital. JAMA
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71. Tibballs J, Kinney S. Reduction of hospital mortality and of preventable cardiac
arrest and death on introduction of a pediatric medical emergency team. Pediatr
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72. Hunt EA, Zimmer KP, Rinke ML, et al. Transition from a traditional code team to
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(American Heart Association, Australian Resuscitation Council, European Resuscitation Council, Heart and Stroke Foundation of Canada, InterAmerican Heart
Foundation, Resuscitation Council of Southern Africa, and the New Zealand
Resuscitation Council); the American Heart Association Emergency Cardiovascular Care Committee; the Council on Cardiopulmonary, Perioperative, and Critical Care; and the Interdisciplinary Working Group on Quality of Care and
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76. Hillman K, Chen J, Cretikos M, et al. Introduction of the medical emergency team
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78. Santamaria J, Tobin A, Holmes J. Changing cardiac arrest and hospital mortality
rates through a medical emergency team takes time and constant review. Crit
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79. Galhotra S, DeVita MA, Simmons RL, et al. Mature rapid response system and
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80. Chan PS, Jain R, Nallmothu BK, et al. Rapid response teams: a systematic review
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81. Braaten J, Levin S, ORourke PT, et al. Saving lives at Centura. A Colorado
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83. Winters BD, Pham J, Pronovost PJ. Rapid response teamswalk, dont run.
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Pediatric Resuscitation
a n d C a rdia c Arre s t
William A. Woods,
MD
KEYWORDS
Pediatrics Cardiopulmonary resuscitation Emergencies
Critical care Cardiac arrest
Cardiac arrest (CA) in children is, fortunately, a relatively infrequent event. Because
adults are just big children, many of the principles discussed in this article also apply
to adults. Whereas the majority of articles in this issue focus on care specific to adults,
this article highlights the issues specific to the critical care and resuscitation of children. The article reviews the causes and conditions associated with pediatric CA
and pediatric care in the prearrest phase, and updates and reviews pediatric resuscitation for CA, including the 2010 updates by the American Heart Association (AHA).
Where controversy exists, alternative recommendations by the International Liaison
Committee on Resuscitation (ILCOR) and the European Resuscitation Committee
(ERC) are discussed. Finally, topics that may be of special interest are presented. A
recurring theme throughout this article is that, though infrequent, presentations and
complications during pediatric CA are predictable, and expected challenges can be
minimized through effective planning and education prior to patient presentation.
EPIDEMIOLOGY OF PEDIATRIC CARDIAC ARREST
Pediatric CA victims constitute a minor patient population in the emergency department (ED). Unfortunately, this can lead to unfamiliarity of staff with proper procedures
for pediatric CA. The review by Babl and colleagues1 describes the prehospital experience in Boston for 1 year; there were a total of 130,000 emergency medical services
(EMS) dispatches with 59,000 patient transports. Pediatric transports totaled only
5280 (8.9%) for the year with 13 children requiring cardiopulmonary resuscitation
and 15 requiring intubation. In-hospital arrests are also relatively infrequent. The
PECARN study by Moler and colleagues2,3 included 353 in-hospital and 138 out-ofhospital pediatric arrests from 15 hospitals over an 18-month period. On average,
the rate of pediatric CA was 15 in-hospital and 6 out-of-hospital arrests per hospital
per year. The most common presenting rhythm for in-hospital arrest was bradycardia
Funding: None.
Department of Emergency Medicine, University of Virginia, PO Box 800699, Charlottesville, VA
22908-0699, USA
E-mail address: waw9h@virginia.edu
doi:10.1016/j.emc.2011.09.013
emed.theclinics.com
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while asystole was most common during out-of-hospital arrests. Ventricular fibrillation
or tachycardia (VF/VT) was the presenting electrical rhythm in only 10% of in-hospital
arrests. Only 19% developed VF/VT sometime during the arrest phase.
A review of the epidemiology of pediatric CA can serve as a framework for planning
and preparation for pediatric CA victims. In the 1990s Schindler and colleagues4 and
Sirbaugh and colleagues5 found the most common cause of pediatric CA to be sudden
infant death syndrome (SIDS). These classic studies were done in the mid to late 1990s
before the successful Back to Sleep campaign.6 Subsequently, the number of
deaths due to SIDS has decreased dramatically, with more recent work by Moler
and colleagues2 showing a drop in the percentage of arrests caused by SIDS. The
most common reasons EMS crews will arrive to find a child in cardiopulmonary arrest
are trauma, drowning, sepsis, respiratory arrest, and cardiac abnormalities.4,5
Even after initiation of the Back to Sleep education program, pediatric out-ofhospital CA remained much more common in younger children. Nearly one-third of
the children in Molers out-of-hospital arrest series were younger than 1 year with
a survival rate of 30%. Another third of victims were age 1 to 8 years, and survival
was 50% in this population. Survival in the third of victims aged 8 through 18 was 36%.2
Analysis of pediatric CA in the ED pediatric patient population is typically included
in studies evaluating all in-hospital pediatric arrests. While inpatient pediatric CA has
some of the same causes as out-of-hospital arrest, it is more commonly a result of
respiratory failure/asphyxia. Children suffering an in-hospital CA are more likely to
have an underlying medical condition (88% for in-hospital vs 49% for out-of-hospital)
and to be younger.2,3 The average ages are 0.9 and 2.9 years old for in-hospital CA
and out-of-hospital, respectively. The most common chronic medical conditions are
prenatal conditions, congenital heart disease, and lung or airway disease.
In summary, pediatric CA is an infrequent event that occurs most commonly in children younger than 1 year. Outcomes are best in the 1- to 8-year-old population. Unlike
CA in adults, causes are frequently attributable to respiratory failure or trauma; VF/VT
occurs infrequently either as an initial rhythm or during resuscitation efforts. Thus,
though used infrequently, those that care for children with CA must have a broad skill
set because children with CA should not be expected to respond as readily to only
closed-chest compressions and early defibrillation, as may occur in adults.
PREVENTION OF CARDIAC ARREST (PREARREST)
In a comparison between in-hospital CA and out-of-hospital CA it was noted that of 37

pediatric CA due to trauma, 22 occurred in-hospital.3 In addition, 112 of the 149 pediatric CA due to respiratory failure were in-hospital.3 As these results demonstrate, children may continue to deteriorate after presentation to medical care. The landmark
study by Gausche and colleagues7 did not demonstrate a survival benefit with paramedic intubation in comparison with bag-valve-mask ventilation in 830 children
requiring advanced life support. The text also presents a description of the subgroups
and although the results did not achieve statistical significance, it is difficult not to
wonder whether expert clinical judgment can improve the survival of many children
requiring advanced life support. Acknowledging that children may continue to deteriorate after reaching ED care, what interventions may decrease the risk of subsequent
CA?
As a first step, emergency physicians should be familiar with emergency interventions that may be required for the children suffering CA who have an underlying
medical condition. Though often daunting to the emergency physician, the easiest
Pediatric Resuscitation and Cardiac Arrest
preexisting condition to review is inborn errors of metabolism. The emergency treatment of the metabolic disarray resulting from essentially all inborn errors of metabolism requires maintaining serum glucose levels and intravascular volume status
while temporarily suspending oral food intake by the child.8 The most notable exception to this rule is congenital adrenal insufficiency, which may present with hyperkalemia and may require stress-dose corticosteroids.
Children with congenital heart disease may require emergency care for several
reasons. First, the child with an undiagnosed ductal-dependent lesion may present
early in the newborn period with central or peripheral cyanosis as the ductus arteriosis
closes. Treatment involves the early initiation of a prostaglandin infusion to reopen the
ductus arteriosis and intensive care admission for definitive therapy. Complications of
prostaglandin infusion include apnea, hyperthermia, and irritability. Prophylactic
intubation may be considered, especially in consultation with the receiving intensivist.
The decision may depend on duration of transport, if necessary, and skill of transport
personnel.
Second, children who have undergone surgical repair of congenital heart disease
have an increased risk of sudden death from dysrhythmias. This risk is more common
in those with more complex primary lesions, and may not occur in those with atrial
septal and some ventricular septal defect repairs.9 In addition, there are no clear
data to define how long this risk persists. Thus, it is advisable to consider cardiology
consultation in those children with surgically corrected congenital heart disease who
present with significant chest pain or palpitations. All of these children with evidence of
dysrhythmia on their ED electrocardiogram require cardiology consultation.
Third, children with partially corrected congenital heart disease may present with an
alteration in their shunt fraction, or a change in the percentage of their cardiac output
directed toward the pulmonary artery. These children may have an increase in their
pulmonary blood flow, such as if volume overloaded from decreased compliance or
malabsorption of their home diuretic. Such children may have too little pulmonary blood
flow if their Blalock-Taussig shunt clots during mild dehydration or if the cardiac output
drops because of chronic hypoxia in the child with partial correction. Children with
a decrease in room air oxygen saturations may benefit from intravenous fluids if they
have a decrease in pulmonary blood flow, or may benefit from diuresis and positivepressure ventilation if they have an increased pulmonary blood flow. Obtaining a chest
radiograph and comparing with an old radiograph will help the emergency physician
decide if the child has a decrease or increase in his or her pulmonary blood flow
(decreased pulmonary vascularity or increased pulmonary vascularity, respectively,
compared with baseline). Children who become more hypoxic with agitation in the
ED may benefit from a small dose of intranasal fentanyl prior to intravenous cannulation
to prevent cardiovascular deterioration during attempts at peripheral vascular access.
Finally, children who have undergone cardiac transplantation may present to the ED
with episodes of acute rejection.10 Unfortunately, the symptoms of acute rejection are
vague, and diagnostic studies do not have high enough positive and negative predictive value to allow the emergency physician to exclude the diagnosis of acute rejection. Thus, it is reasonable to consult a childs cardiologist, especially if the childs
symptoms are nonspecific (especially nausea), if he or she has an increase in liver
function studies or shows signs of dehydration.
Children with severe acute exacerbations of bronchospasm require aggressive
therapy. Early administration of corticosteroids is recommended.11,12 While frequent
b-agonist dosing has been the mainstay of therapy, the optimal bronchodilator
regimen continues to be controversial. It is unclear whether continuous albuterol
therapy is more effective than sequential bolus dosing. Ipratropium is a potent
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bronchodilator alone, and its use can decrease the admission rate among children
with acute bronchospasm.1315 Rodrigo and Rodrigo16 reviewed the data on multiple
dosing of ipratropium. This review argues that multiple doses of ipratropium in the ED
can decrease the admission rate for those with severe asthma exacerbations, with
a number needed to treat of 5 to 11.
Treatment options for the child with bronchiolitis are limited. The key to early care of
these children is good supportive care: frequent effective nasal suction, supplemental
oxygen as needed, and repositioning for optimal air exchange. It is always tempting to
try a diagnostic and therapeutic trial of albuterol in children with bronchiolitis, as viral
respiratory infections are the most common trigger for acute bronchospasm in
children. Bronchodilator therapy should not be continued without objective findings
of clinical improvement. The role in the ED of therapies such as nebulized hypertonic
saline and high-flow humidified intranasal cannula is evolving.17,18
Sepsis protocols are proving to be beneficial in improving outcomes in adults with
sepsis syndromes. There is no reason to think that the outcome of children with sepsis
cannot be improved by aggressive, systematic care with attention to clinical details.
Clinically identifying sepsis in young children and determining resuscitation end points
may be challenging, as children in warm shock may have bounding peripheral
pulses and an adequate blood pressure. Serial, careful clinical examinations are vital.
Physicians should pay attention to relative changes in vital signs, mental status, relative change in pulse character and perfusion, as well as respiratory rate and effort. The
clinician should suspect that tachypnea is a compensatory effort due to metabolic
acidosis. Early dosing with antipyretics is indicated to attempt to separate examination findings resulting from fever from those due to sepsis. Aggressive fluid resuscitation is indicated for septic shock. Young children may require up to 80 to 100 mL/kg of
isotonic solution during their initial resuscitation phase.
Fortunately, care of the newborn infant is typically not complicated. Keys to successful
transition to extrauterine life are: adequately stimulate and dry; adequately position for
easy respiration; and ensure an adequately warm environment. The AHA recommends
not separating the newborn from the mother if a term gestation is crying and/or breathing
and has good muscle tone.19 Airway suctioning need only be performed for excessive
secretions. If performed, care must be taken to detect any episode of bradycardia that
may result from stimulation of the posterior nasopharynx. The pulse at the base of
the umbilical stump is the most reliable location to palpate a pulse in a newborn.
Guidelines for newborn resuscitation have changed over recent years to deemphasize the use of oxygen in the resuscitation of a newborn.19 Most newborns, even those
requiring some bag-valve mask ventilation, can be effectively treated with room air. In
fact, room air or blended oxygen is recommended for normal newborn resuscitation in
the AHA 2010 Guidelines.19 If supplemental oxygen is supplied, the concentration
should be aggressively weaned as soon as is practical. It is reasonable to consider
withholding resuscitation efforts if a newborn is so premature that the eyelids are still
fused; otherwise the emergency physician should consider the child of viable age and
attempt resuscitation. It is appropriate to stop resuscitation efforts if there is no
detectable heart rate after 10 minutes of resuscitation efforts.19 However, this decision
should also consider the presumed etiology of the arrest of the newborn.
CARE OF THE CHILD IN CARDIAC ARREST
In 2010, the ILCOR, AHA, and ERC provided updates to the 2005 recommendations.2022 Box 1 summarizes the new changes in the 2010 AHA recommendations.19,20 Optimal care of the child in CA demands a prepared system and skilled
Box 1
Changes to the 2010 AHA Guidelines for resuscitation and emergency care of children
Resuscitation techniques:
Retraining is emphasized to ensure familiarity with equipment
Cricoid pressure is deemphasized as a method to prevent aspiration during intubation
attempts
Minimizing rescuer fatigue is emphasized to maintain the quality of chest compressions
Chest compressions without ventilation is encouraged in cases of nonasphyxial arrest
during bystander rescue (more common in adults)
Medications:
Medication dosing is controversial: use of lean body weight versus actual body weight is
unknown
The dose of intratracheal administration of medications should, in general be 2 to 3 times
the intravenous dose
The dose of intratracheal administration of epinephrine is suggested to be 10 times the
intravenous dose.
The dose of intratracheal administration of atropine is increased to 0.040.06 mg/kg
The routine use of sodium bicarbonate is discouraged during resuscitation
The routine use of calcium is discouraged during resuscitation
The role of vasopressin is not clear, but there is more support for its use during refractory CA
Lidocaine use is no longer specifically recommended for the treatment of VF/VT
Protocols:
With refractory bradycardia, epinephrine and isoproterenol infusions are no longer
advocated
Adenosine may have a role in the treatment of wide complex tachycardia
Postresuscitation hyperoxemia should be avoided
There is no longer a lower age limit to the use of automated external defibrillators
Special resuscitation situations:
The AHA gives treatment and protocol suggestions for children with:
Septic shock
Single-ventricle anatomy
Pulmonary hypertension
providers who are familiar with guidelines and equipment. An optimally prepared
system should have appropriate equipment, and organizational and consultation
patterns in place before the arrival of the critically ill child. To aid preparation the
American Academy of Pediatrics (AAP), the American College of Emergency Physicians (ACEP), and the Emergency Nurses Association produced a joint policy statement that can be used as a starting reference to ensure an optimally prepared
system for those who provide emergency care for children.23
The 2010 recommendations from AHA and ILCOR recognize the importance of
rapid intervention and aggressive implementation of resuscitation protocols.20,21,24
Medical emergency teams or rapid response teams are gaining favor for inpatient
units because use of these teams brings aggressive skilled resources to the
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bedside.25 Literature continues to support the conventional teaching that rapidly

and effectively declaring an emergency is often the biggest barrier to effective
resuscitation.26
EQUIPMENT
The aforementioned collaborative policy statement defines the equipment needed to

obtain vascular access in children of all sizes.23 Vascular access is essential for
optimal pediatric resuscitation. Peripheral venous access is relatively easy to obtain
and has the advantage of low-resistance catheters that allow rapid infusion of isotonic
solution or blood products. The easiest veins to cannulate include the antecubital
fossa, the dorsum of the hand, and the scalp (using a rubber band tourniquet with
a tab of tape to ease removal).
Central venous access is typically more difficult to obtain in the young child. Preambulatory children may have relatively smaller femoral veins, as the metabolic requirement of the lower extremities is lower than a walking age child. When performing
a blind attempt at femoral venous access in adults, classic teaching says that the
femoral vein is one-third of the distance from the symphysis pubis toward the anterior
superior iliac spine. In young children the femoral vein may be closer to halfway
between the symphysis pubis and anterior superior iliac spine. ED ultrasound assists
emergency physicians in central venous cannulation of adults and should be helpful in
infants and children, although data are not yet convincing.27 Once obtained, central
venous catheters can be used for higher-dose infusions of vasoactive agents.
Intraosseous (IO) catheters are relatively simple to place, have landmarks unaltered
by volume status, and can be used to administer all drugs commonly used during
a resuscitation. The relatively new intraosseous catheter drills are much more elegant
and problem free than previous manual IO catheters. IO catheters can be used for
volume resuscitation, vasoactive infusions, and most laboratory studies. When
training practitioners to use IO needles it is imperative to emphasize that fluid may
not infuse easily. In fact, a syringe on a 3-way stopcock to provide a bolus of fluid is
frequently required. Box 2 lists the most commonly used sites for IO catheter placement. Educators must also train providers on acceptable methods to secure the catheter, to prevent dislodging the catheter during resuscitation efforts.
Airway equipment should include masks, airway adjuncts, and intubation equipment appropriate for all sizes of children. Providers differ on the choice of
Box 2
Sites and contraindications of IO catheter placement
Site of placement
Proximal medial tibia
Distal medial tibia
Distal medial femur
Anterolateral proximal humerus
Contraindication to placement
Fracture of the same bone
Previous intraosseous needle placement attempt in the same bone
Cellulitis overlying placement site
Osteogenesis imperfecta
laryngoscope blades (curved, straight, and so forth) when intubating children. Many
experts will use a straight blade when intubating young children because of the anterior larynx and floppy epiglottis. As devices such as video-assisted intubating laryngoscopes are becoming more widely available, further research will be needed to
determine the optimal equipment for securing the pediatric airway in the critically
unstable child. The 2010 AHA Pediatric Advance Life Support Guidelines do not
comment on laryngoscope choices. Providers should use the laryngoscope they are
most comfortable with during pediatric intubations, as first-pass success rates are
lower in ED intubations of young children than in adults.28
Whereas traditionally uncuffed endotracheal tubes (ETTs) were considered to be
preferable in younger children, cuffed and uncuffed ETTs are both acceptable according to the 2010 recommendations.2022 A cuffed ETT may be more desirable in cases
where a child has high airway resistance or poor lung compliance. Cuffed ETTs have
the advantage of smaller air leak in comparison with uncuffed tubes. However, cuffed
ETTs are also sized one-half size smaller internal diameter than their uncuffed counterparts. Thus, suction catheters may be more difficult to use in smaller-cuffed tube
sizes. If placing cuffed tubes, physicians and respiratory therapy must be properly
oriented to accurate cuff inflation pressure, as overfilling the cuff may cause airway
injury. It would not be unreasonable to consider cuffed tubes for children older than
1 year, while considering uncuffed tubes for younger children if suctioning will be
important. When intubating a child a good rule of thumb is the depth of intubation
should be 3 times the tube diameter when measured at the lips. Endotracheal tube
placement must be confirmed with exhaled carbon dioxide detection. Acceptable
methods include capnography or colorimetry, with continuous capnography being
preferable, if available, as it can guide effective chest compressions and signal tube
dislodgment. Providers should be oriented to the equipment and understand the
scenarios whereby false-positive and false-negative results may occur.
Equipment storage and organization may be unique to many different EDs.
However, all providers (physicians and nurses) should be knowledgable of the local
organizational system used. A reliable resupply system ensures that proper functioning equipment is fully stocked and not beyond expiration dates, as this equipment
will be used relatively infrequently. Staff should have in-house call schedules and
referral destinations organized. Transportation teams should be properly educated
as to the pediatric critical care that may be required during anticipated transports.
Policies and equipment should be in place to estimate a childs weight and to ensure
accurate equipment and medication dosing based on that childs size. Reference
material should include suggested sizes of ETTs, thoracostomy tubes, and laryngeal
mask airways, as well as expected drug doses and rates of infusions. Radiology
resources specific to pediatric care should be organized and defined.
It is essential to ensure accurate medication dosing and the ability to deliver appropriate medication doses and infusion rates. Controversy exists over whether to use
actual weight or ideal body weight in obese children. In fact, recent recommendations
vary between publications on this topic. The AHA recommends basing medication
doses on ideal body weight estimates in obese children to prevent drug toxicity.20
The ILCOR recommends using length-based estimates in trying to approximate lean
body mass.21 Regardless of the method embraced, medication dosing should not
exceed adult dosages.
To aid in maintaining dosing accuracy, the authors institution uses a written
resource manual to enhance communication between physicians and nurses. Each
page of the manual is dedicated to a particular weight, providing the weight-based
dose of a medication and the volume to be administered for each drug, and
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concentration currently available in the ED medication dispensing formulary (eg, midazolam comes in different concentrations in this hospital). If infusions are to be mixed
in a central pharmacy, communication and preparation is required to ensure that any
vasoactive infusions will be prepared and transported in time to meet clinical requirements. It is important to plan in advance which vasoactive infusions will require
a continuous infusion pump versus which can be delivered via intermittent bolus
pumps. In the authors institutions ED, all vasoactive infusions are delivered via
syringe pump if the child weighs 10 kg or less.
Professional education appears to improve performance during resuscitation.2932
There are many sources of professional education: self-directed education, skills practice, high-fidelity simulation, lower-fidelity simulation, Pediatric Advanced Life Support
(PALS) courses, and so forth. There is a growing body of literature to suggest that many
of these choices can increase care providers confidence in their ability to perform
a skill.30 There is also a growing body of literature to suggest that many of these choices
can increase a providers recall of information and performance on subsequent tasks
using that information.30 Providers should take an honest, periodic assessment of their
skills and recent clinical experiences to determine the appropriate education necessary. An area of research interest is starting to document that outcomes are improved
if providers are more experienced.32 ED leadership should ensure that educational
opportunities exist for those that will care for children. Education should also reinforce
the clinical examination necessary to identify an impending deterioration, including
detection of the typical signs of compensated and decompensated shock.
THE AMERICAN HEART ASSOCIATION GUIDELINES 2010
Chest Compressions and Defibrillation
The 2010 AHA Guidelines on basic life support for adults stress the importance of
rapid onset of chest compressions while deemphasizing the benefit of mouth-tomouth rescue breathing.33 As many pediatric CA are not a result of a dysrhythmia
but rather a respiratory arrest, the AHA recommends chest compressions with ventilations in infants and children.20 Keys to pediatric chest compressions are to push
fast (100 compressions per minute) and push deep (at least one-third the depth
of the chest). For the health care provider the AHA recommends a ratio of compressions to ventilations for lone rescuers of 30:2 and for 2 rescuers of 15:2. Ventilations
should be delivered in such a fashion as to minimize any interruption in chest
compressions. Rescuers should focus on minimizing common errors: allow the chest
to completely recoil between compressions, minimize interruptions of compressions,
avoid excessive ventilation, avoid rescuer fatigue, and ensure proper hand placement.
The two-thumb encircling hands method is preferred for infants when there are two
rescuers present.20
Defibrillation for ventricular fibrillation should be done using infant paddles for children less than 10 kg (approximately 1 year).20,22 If greater than 10 kg the adult size
paddles should be used. Biphasic shocks may be preferred, as they are less harmful
than monophasic shocks and appear to be at least as equally effective. The initial defibrillation dose for VF is 2 to 4 J/kg. The AHA recommends increasing the second dose
to 4 J/kg and considering increasing to a maximum of 10 J/kg or adult maximum
dosing.20 The International Consensus report recommends initial dosing of 2 to 4
J/kg and does not discourage the use of higher doses.21 The European Resuscitation
Council recommends all doses of 4 J/kg.22 Further research clearly is needed in this
area. Cardioversion should be performed with initial doses of 0.5 to 1 J/kg. If unsuccessful, the dose may be increased to 2 J/kg. When considering the use of an
automated external defibrillator (AED), standard settings can be used for children
older than 8 years. An AED with a dose attenuator is preferred for those aged 1 to 8
years. Manual defibrillation is preferred for patients younger than 1 year. An AED
without a dose attenuator can be used for all ages if no other options are available;
however, EDs designed to care for children should have manual defibrillators capable
of dose adjustment.34
Airway Intervention
Effective bag-mask ventilation is a complicated skill. Rescuers should be skilled in

airway-positioning maneuvers (jaw lift) and should deliver enough gas (oxygen or
room air) volume to just make the chest rise.20 Excessive ventilation can result in
increased intrathoracic pressure with decreased venous return, air trapping with barotrauma, and increased risk of aspiration and regurgitation. Ventilation of the child in
CA should be performed with 100% oxygen. After return of spontaneous respiration,
the inspired concentration of oxygen should be weaned to achieve saturations of at
least 94%.20,22
If further airway intervention is required, endotracheal intubation should be performed. A laryngeal mask airway is an option if prolonged bag-mask ventilation and
intubation are not possible. Endotracheal tube size may be better estimated by child
length than by child weight in obese children; otherwise age-based formulas, weightbased tables, and comparison of external tube diameter with that of the patients fifth
finger are all appropriate initial references.20 A cuffed ETT should be one-half size
smaller than an appropriate uncuffed ETT. Rapid sequence intubation may be performed to eliminate the risk of gastric inflation with bag-mask ventilation. The use of
cricoid pressure is not universally supported, and is deemphasized in the 2010 recommendations.2022 These recommendations state that cricoid pressure should be performed only if it does not interfere with ventilation or prolong intubation. If gastric
inflation occurs, decompression with a nasogastric or orogastric tube may improve
oxygenation and ventilation. Venting a gastrostomy tube, if present, can effectively
decompress the stomach.
Medication dosing and choice are controversial when intubating a child in or near
CA. Based on AHA PALS, medication dosing should be based on actual body weight
rather than lean body weight, if using medications to rapidly sedate and provide neuromuscular blockade to ease intubation.20 Etomidate provides rapid intubating conditions while maintaining hemodynamic status (ie, cardiac and cerebral perfusion
pressures).3537 A single dose of etomidate has been noted to decrease adrenal function when used in septic adults, and the International Consensus discourages the
routine use of etomidate for septic children.21 Ketamine also provides rapid, predictable sedation while maintaining mean arterial pressure.37 Traditionally ketamine has
been thought to increase intracranial pressure. However, further study is certainly indicated to determine under which physiologic conditions ketamine may cause an
increase in intracranial pressure, as some recent data suggest that no significant
elevation occurs.3840 Succinylcholine has the advantage of rapid neuromuscular
blockade of brief duration. As succinylcholine is a depolarizing neuromuscular
blocker, clinically significant hyperkalemia may result in children with undiagnosed
muscular dystrophy. Thus, rocuronium may also be considered because it is the nondepolarizing neuromuscular blocker with the most rapid onset and briefest duration of
action.
Choosing to intubate a child requires a plan to react to expected complications.
Complications can include failure to achieve intubation, desaturation, hypotension,
bradycardia, vomiting, and laryngospasm.28,4143 In anticipation of possible failure
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to achieve intubation, physicians should always have alternative airway maneuvers

and equipment in mind and immediately available. This aspect is particularly important
when intubating younger children, as the intubation success rate is lower for young
children than teenagers.28 Hypotension with subsequent CA may occur during intubation.44 Conventional wisdom states that the use of induction agents can result in hypotension. Various mechanisms have been postulated but remain unproved. Good
clinical practice dictates special attention to the child with distributive shock, severe
hypovolemic shock, or significant acidosis. If time permits, aggressive volume expansion prior to intubation should be administered, and adrenergic medications should be
immediately available prior to intubation.
Once the child is intubated, the emergency physician should carefully consider
initial ventilator settings and ventilation strategy. Hyperventilation should be avoided
during CA. During the immediate postintubation period, the physician should handventilate the child or work very closely with respiratory therapy to determine the
most appropriate ventilator settings for the child who is not yet in CA. While hyperoxemia and hyperventilation are to be avoided, there are clinical scenarios that may
require specialized ventilation strategies. Children who are intubated and have
a concomitant severe metabolic acidosis will require a very rapid ventilatory rate (ie,
at least the preintubation respiratory rate) to provide the necessary compensatory
respiratory alkalosis. Sudden, fatal CA may occur with an insufficient minute volume,
due to rapid changes in acidemia. Children with bronchospasm or bronchiolitis may
require very prolonged exhalation times or slow inhalation periods to allow adequate
gas exchange without excessive peak inspiratory pressures. Either venous or arterial
blood gases are adequate for assessing the response to the ventilation strategy. Box 3
describes the mnemonic DOPE for possible causes of a sudden deterioration in an
intubated patients condition.
Fluids and Medications Used in Resuscitation
Early aggressive fluid resuscitation in children may be required in the child with normal
blood pressure. As children often maintain systolic blood pressure despite significant
volume depletion, the most useful clinical features for detecting dehydration in a young
child are absence of tears, dry mucous membranes, prolonged capillary refill, and
abnormal general appearance.45 Isotonic solution, such as normal saline or lactated
Ringer solution, can be safely administered in sequential doses of 20 mL/kg. A review
of children presenting to the ED in shock noted that children with septic shock
received a mean dose of 58 mL/kg of crystalloid while in the ED.46 Although most children are not overly sensitive to excessive volume resuscitation, common volumesensitive conditions are children with diabetic ketoacidosis (potential risk of cerebral
edema), children with sickle cell disease and suspected acute chest syndrome, and
children with partially surgically corrected congenital heart disease with an excess
of pulmonary blood flow. When treating children with these acute conditions it is
Box 3
DOPE pneumonic for those intubated patients who deteriorate
D Displacement of the tube
O Obstruction of the tube
P Pneumothorax
E Equipment failure
imperative to provide only the resuscitation fluid required to reestablish perfusion

while not administering an excessive dose that may increase the risk of complication.
Epinephrine is the most frequent medication administered during resuscitation
efforts after CA.2,3 The a-adrenergic activity of epinephrine increases aortic diastolic
and coronary perfusion, due to vasoconstriction. Epinephrine may be administered
intravenously, intraosseously, intramuscularly, subcutaneously, or intratracheally.
Current recommendations for all intravenous doses during resuscitation are 0.01
mg/kg with a maximum dose of 1 mg.20 The optimal intratracheal dose is unknown,
although the AHA recommend administration of 10 times the intravenous dose if
epinephrine is given intratrachially.20 Sodium bicarbonate and other alkaline solutions
may inactivate catecholamines if administered simultaneously. Historically, high-dose
epinephrine (10 times typical dose) was considered in cases of refractory CA;
however, high-dose epinephrine has fallen out of favor. Epinephrine is recommended
for the treatment of pediatric CA (with or without electrical activity), pediatric bradycardia with a palpable pulse, and anaphylaxis.12,20 Smaller intravenous doses (5%
10% of intravenous dosing) may be initially administered intravenously to patients
with anaphylaxis.12 Rapid intravenous bolus doses of epinephrine should be avoided
in the conscious patient.
Atropine has traditionally been the second most common medication administered
during resuscitation efforts after pediatric CA.2,3 Atropine sulfate accelerates the atrial
pacemaker and increases the speed of atrioventricular conduction. Atropine is recommended for use in the child with bradycardia with a pulse and with poor perfusion.
However, atropine is no longer in the algorithm of pediatric CA, even in the presence
of pulseless electrical activity.20 The minimum dose of atropine is 0.1 mg because
smaller doses may cause a paradoxic bradycardia. Dosing of intratracheal atropine
is somewhat controversial. The AHA recommends 0.04 to 0.06 mg/kg whereas the
European Resuscitation Council recommends 0.03 mg/kg.20,21
Sodium bicarbonate is often administered in cases of pediatric CA.2,3 Current AHA
recommendations warn that excessive sodium bicarbonate may impair tissue oxygen
delivery and decrease the ventricular fibrillation threshold. It also may induce electrolyte abnormalities such as hypernatremia, hyperosmolality, hypocalcemia, and hypokalemia. Current recommendations state that routine use of sodium bicarbonate is not
recommended in the treatment of CA.20 Sodium bicarbonate, however, may have
a role in the treatment of acute intoxications or hyperkalemia.
Vasopressin is an endogenous peptide initially isolated from the posterior pituitary.
The V1 receptor in vascular smooth muscle is of the most interest, as stimulation
results in vasoconstriction. Trials of vasopressin for the treatment of CA began after
it was noted that survivors of CA had substantially higher serum levels of endogenous
vasopressin than nonsurvivors. Hypothetical adverse effects of vasopressin include
increased myocardial oxygen demand and dysrhythmias, as well as decreasing
splanchnic blood flow.47 Rarely, hyponatremia may result during infusion therapy,
typically when being used for sepsis. Current recommendations state that bolus doses
can be administered during refractory CA; however, there is insufficient evidence
demonstrating that use of vasopressin results in an increased rate of survival to
discharge for children.20 Vasopressin infusions may have a role in the treatment of
septic or hemorrhagic shock, but more data are required to demonstrate a benefit
in children.48,49 Vasopressin boluses can be administered via intravenous, intraosseous, or endotracheal routes.
Amiodarone may be considered in the treatment of CA due to pediatric VF or VT. The
AHA recommends expert consultation before the administration of amiodarone or procainamide in children with tachycardia without shock, hypotension, and acutely altered
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mental status.20 Adenosine can also be considered for use in cases of tachycardia. The
AHA notes that adenosine may be useful in cases of wide complex tachycardia as long
as the child is without known Wolff-Parkinson-White syndrome, the rhythm is regular,
and the QRS is monomorphic.20 Adenosine can be administered in cases of supraventricular tachycardia (SVT); however, the AHA recommends vagal stimulation or Valsalva maneuvers before pharmacologic therapy in cases of stable SVT.20
Infusion protocols for vasoactive agents do not differ significantly from adults. In
younger children with decompensated shock, epinephrine or norepinephrine infusions
are preferred over dopamine. b-Adrenergic actions predominate with epinephrine
infusion rates of less than 0.3 mg/kg/min, whereas a-adrenergic actions causing vasoconstriction occur at doses greater than 0.3 mg/kg/min. Norepinephrine is a potent
vasoconstrictor used to treat shock, with low systemic vascular resistance.
SPECIAL SITUATIONS
Family Presence During Resuscitation
Current literature and recommendations note that family presence during resuscitation efforts may aid in the grief process for family members of the child undergoing
resuscitation.2022 This practice is typically more effective if there is an ED team
member who can be assigned to the family to answer questions, attend to needs,
and pay attention to nonverbal cues from the family. Ideally the team member
assigned will be a skilled clinician who can interpret the context of the resuscitative
efforts for the family. Preparing an ED for this practice may require orientation sessions
with nonclinicians (chaplains, social workers) who may also be assigned to the family.
Further instruction should be directed toward staff to anticipate conflicts or likely clarifications that may arise during resuscitation, and plan how to handle them in front of
the family. For instance, nurses should practice vocabulary and phrases that will allow
for clarification of drug doses while not being perceived by the family as questioning
the competence of the team leaders. Similarly, physicians need to be aware that safe
practice includes the verification of medication doses, and they should expect such
requests for clarification from nursing and pharmacy. Expecting these requests
ensures that physicians are more attentive to unusually worded or repetitive questions
from staff during the emotional stress of a pediatric CA.
Procedures on the Newly Dead
Occasionally children arrive at the ED in CA after presenting with a history consistent

with a contagious illness. Typically the organism of concern is Neisseria meninigitidis,
as close family members may require antibiotic prophylaxis. In this scenario, the child
is pronounced dead prior to obtaining blood cultures (and/or cerebrospinal fluid
cultures). Although individual states may vary, in the Commonwealth of Virginia the
Medical Examiner has charge of a body after an unexplained death.50 Consent from
the Medical Examiner would be required before postmortem blood and/or cerebrospinal fluid for culture is obtained. Failure to obtain consent from the Medical Examiner
may be considered unlawful. However, obtaining cultures while in the ED should be
considered if a delay might occur when the procedure is deferred to the Medical
Examiner. Thus, knowledge of local laws and communication with the Medical Examiner is imperative in this scenario.
Disaster Preparation
Branas and colleagues51 reviewed all of the multiple casualty incidents (MCIs) occurring within the state of Maryland during a 3-year period. An MCI was defined as at least
10 simultaneous victims. Four of the 10 incidents included at least several children.

Branas work suggests that 5 or 6 children would seem to be a reasonable maximum
number of critically injured children to expect during a typical MCI. The New York
City Department of Health provides thorough suggestions for infrastructure to plan
for multiple injured children.52 Special pediatric considerations include care for those
children who are separated from caregivers (consent issues, identification, emotional
care, and so forth), setting up a pediatric safe area for those who are medically clear,
and training and equipment in preparation for multiple injured children. Pediatric
specific equipment may include medications, decontamination, and transportation
equipment. Though infrequent, resources and challenges that will occur during
MCIs are predictable. Anticipated challenges ideally can be minimized through preevent preparation.
Prevention of Pediatric Cardiac Arrest through Advocacy
Emergency physicians are uniquely positioned to view the tragedy of avoidable illness
and injury within our society. Many of the deaths in children fall into predictable patterns.
For example, with regard to drowning, young children are more likely to drown in bathtubs or after falling into bodies of water when unwitnessed; adolescents aged 15 to 19
are more likely to drown in a rural environment with friends during warm months.53 What
steps are available to advocate and educate to prevent further injury? Rimsza and
colleagues54 reviewed the deaths of children in Arizona in the later 1990s to identify
the proportion of preventable deaths. The investigators, from the Arizona Child Fatality
Review Program, determined that 29% of all pediatric deaths were preventable.54 The
review identified unintentional injuries that could have been prevented, typically through
patient education about appropriate safety procedures. ED teams are very familiar with
important safety information, such as pool safety, bicycle helmets, and pediatric motor
vehicle restraint recommendations. Parents of patients presenting to the ED are willing
to apply educational information provided during the ED visit.55 The review by Rimsza
and colleagues also determined that 253 of the 2983 deaths due to medical causes
could have been prevented.54 The investigators believed that suboptimally prepared
EMS and delays in seeking medical care because of lack of health insurance contributed to these deaths. It appears from all available data that emergency physicians
can have an impact on children during daily clinical interactions, within our individual
medical system, and through the advocacy of our national organizations.
SUMMARY
The AHA, ILCOR, and ERC have recently published updates on pediatric resuscitation. There have been subtle changes to recommended protocols. The most notable
shift in the guidelines has been the increased emphasis on provider training and
education, and a heightened attention toward the prearrest period. For the emergency
physician, these changes point to opportunities to prepare in advance for the critically
ill child in order to aggressively bring maximum resources to the bedside of the ill child.
Through comprehensive planning, optimal care can be delivered in the most timely
fashion.
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Card iac A rrest in

S p e c i a l Po p u l a t i o n s
Jeffrey D. Ferguson,
MD, NREMT-P
a,b,
*, Jocelyn De Guzman,
MD
c,d
KEYWORDS
Cardiac arrest Traumatic injury Asthma Pregnancy
Poisoning Toxicology Electrical injury Submersion injury
The following situations present unique challenges in resuscitation of the patient in

cardiac arrest. Specific situations were chosen for inclusion based on their likelihood
of presentation to the emergency department. These situations not only require modifications to basic adult resuscitation, they house the potential for severe time and
resource use. The decision to apply these modifications to standard care for the
cardiac arrest patient may be obvious in some cases or may be applied due to suspicion from the presenting medical history, history of present illness, or physical examination. Some of the therapeutic interventions discussed here are applicable to the
patient in a near arrest condition and may be considered to prevent progression to
cardiovascular collapse in the gravely ill patient. With rare exception, general care
of any cardiac arrest patient should include continuous high-quality chest compressions and appropriate airway and ventilatory management.
TRAUMATIC INJURY
Multiple pathologies can lead to cardiac arrest in the setting of traumatic injury and
may occur individually or in combination. Etiologies include: severe head injury,
hypoxia (airway obstruction or disruption, pulmonary contusion, hemothorax, or pneumothorax), distributive shock (spinal cord injury), or diminished cardiac output (exsanguination, tension pneumothorax, pericardial tamponade, or myocardial contusion).
In cases of traumatic arrest where a clear etiology is not readily apparent, an AirwayBreathing-Circulation (ABC) approach to heroic interventions may be reasonable.

a
Department of Emergency Medicine, Brody School of Medicine, East Carolina University,
3ED-330 PCMH ED Tower, Greenville, NC 27834, USA
b
EastCare Critical Care Transport, Pitt County Memorial Hospital, Greenville, NC, USA
c
Department of Emergency Medicine, Brody School of Medicine, East Carolina University,
Greenville, NC, USA
d
Disaster Services, Pitt County Memorial Hospital, Greenville, NC, USA
* Corresponding author. Department of Emergency Medicine, Brody School of Medicine, East
Carolina University, 3ED-330 PCMH ED Tower, Greenville, NC 27834.
E-mail address: fergusonjef@ecu.edu
doi:10.1016/j.emc.2011.09.014
emed.theclinics.com
170
Ferguson & De Guzman
Unfortunately, the prognosis of out-of-hospital cardiac arrest due to trauma is poor,

particularly in the setting of blunt injury. Cervical spinal immobilization should be maintained throughout resuscitation unless there is a clear mechanism of injury that
excludes the potential for spinal injury.
The airway should be immediately assessed and stabilized. Conventional direct laryngoscopy and endotracheal intubation remain the standard of care for definitive airway
control. Rates for successful endotracheal tube placement may be augmented with
cricoid maneuvers such as Sellick; backward, upwards, rightwards pressure (BURP);
or 2-handed laryngoscopy or with tube introducers like the gum elastic bougie.14 Video
or optical laryngoscopic modalities have shown promise for successful airway management with decreased times for tube placement and minimizing cervical spine manipulation.1,57 Supraglottic blind insertion airway devices (King LT [King Systems, Noblesville,
IN, USA] LMA [LMA North America, Inc, San Diego, CA, USA], and others) may also be
useful in difficult airway or failed intubation.8 These devices may also be in place as
part of prehospital resuscitation efforts. In these cases, the decision to remove them
and attempt endotracheal intubation should be guided by the ability to oxygenate, ventilate, and prevent aspiration. Surgical cricothyrotomy equipment should be readied at the
earliest identification of a potentially difficult airway and should proceed if the previously
described methods are ineffective at airway control.
Following trauma, ventilation difficulty may be the result of pneumothorax, hemothorax, or gastric distention. For patients in extremis, bilateral needle decompression
or tube thoracostomies should be empirically performed. Orogastric tube placement
should also be performed if gastric distension is suspected based on physical examination, poor ventilator compliance after pleural decompression, or if a history of prolonged or aggressive bag valve mask use was present before airway control.
External hemorrhage control should be performed to prevent additional volume
depletion. This may occur through a combination of clamping visible vessels, tourniquet application to extremities with severe wounds, and pressure application with or
without commercially available hemostatic agents. If used, nongranular, low heatgenerating hemostatic products are recommended.9,10 Large-bore peripheral venous
access should be obtained with rapid infusion of 2 L of isotonic crystalloid followed by
uncross-matched packed red blood cells if available. Peripheral access remains superior for infusion rates required in traumatic arrest; however, intraosseous and central
lines should be placed if peripheral access is difficult to obtain. Needle pericardiocentesis may be therapeutic for pericardial tamponade; however, it will likely prove only to
be a temporizing measure.
If definitive surgical intervention is readily available, a subset of patients may benefit
from resuscitative thoracotomy. A proposed subset includes any witnessed posttraumatic arrest in the emergency department, arrest less than 5 minutes for penetrating cardiac injury, less than 15 minutes for penetrating thoracic injury, or any
exsanguinating abdominal vascular injury where secondary signs of life are present
(eg, pupillary reflexes, spontaneous movement, organized electrocardiographic
(ECG) activity).11 While these indications have not been universally accepted, subsequent literature affirms high mortality rates in patients who undergo emergency
department thoracotomy, particularly for blunt trauma.12,13 Internal cardiac massage
and defibrillation, relief of pericardial tamponade, direct control of cardiac or thoracic
hemorrhage, and cross-clamping of the aorta can be performed during the thoracotomy; however, these interventions require a high degree of technical skill, and
should only be attempted by experienced providers.
Ventricular fibrillation (VF) and ventricular tachycardia (VT) should be defibrillated
immediately upon their recognition. Advanced cardiac life support (ACLS) algorithms
Cardiac Arrest in Special Populations
for these and other dysrhythmias should be considered, with the likelihood of successful
chemical conversion of these being small if their underlying etiology is hypovolemia.
The use of bedside ultrasound may provide rapid diagnosis of many of the conditions discussed previously in the hands of an experienced practitioner. There is,
however, no evidence to support delaying the previously described empiric interventions for ultrasonography in the setting of traumatic arrest.
ASTHMA
There were 1.75 million asthma-related emergency department visits and nearly 3500
deaths in 2007.14 There are 2 general scenarios for which cardiac arrest can occur.
The first is a severe exacerbation that progresses rapidly to arrest. The second is
when a patient experiencing an exacerbation is already receiving maximal therapy
and deteriorates to arrest. This section addresses the first scenario; however, therapies discussed may be applied in either situation if not already in place.
The primary therapies in treating asthma-induced arrest are aimed at overcoming
hypoxia and bronchoconstriction. To that end, endotracheal intubation should be
rapidly established. The largest possible endotracheal tube should be inserted to limit
air flow resistance through the airway adjunct. In most adults, an 8 mm or 9 mm diameter
tube can be used. Ventilation techniques should avoid breath stacking or auto-positive
end-expiratory pressure (PEEP) situations caused by the prolonged expiratory phase
inherent to bronchospastic conditions.15,16 A proposed ventilatory strategy includes
a tidal volume of 6 to 8 mL/kg with a slower ventilatory rate, short inspiratory times
(80100 mL/min), and inspiratory to expiratory times of 1:4 or 1:5.17
Nebulized beta-2 agonists can be administered continuously (albuterol 1015 mg/h
or equivalent) or intermittently (2.55 mg every 20 minutes) through the endotracheal
tube.18 Nebulized anticholinergic agents (ipatroprium bromide 0.5 mg) may have
added benefit with albuterol, but the onset of action is delayed as much as 20
minutes.18 Corticosteroids should be administered early; however, they have
a delayed onset of action (612 hours) and will likely only benefit the patient if resuscitation is successful.17
While external compression of the thorax during the expiratory phase to maximize
exhalation has been proposed, its use remains controversial and is difficult to coordinate during compressions of cardiopulmonary resuscitation (CPR).19 Needle or tube
thoracostomy decompression should be performed if pneumothorax is suspected
based on worsening ventilatory compliance or lateralizing signs of chest wall movement, breath sounds, or tracheal deviation. Bilateral decompression for refractory
patients is warranted given the potential for masking of these lateralizing signs.
Standard ACLS/pediatric advanced life support (PALS) algorithms apply to
dysrhythmias. Epinephrine is likely to be the most useful of the standard drug therapies due to its bronchdilatory effect and should be repeated every 2 to 5 minutes.
Correction of acidosis may be necessary to achieve responsiveness to sympathomimetics given the potential for severe respiratory, and later, metabolic acidosis. Empiric
use of 50100 mEq (12 ampules) of sodium bicarbonate, or administration guided by
arterial pH less than 7.0 is appropriate. The addition of isoproterenol, aminophylline,
terbutaline, or magnesium may be considered for improved bronchodilation; however
their benefit in asthma-induced cardiac arrest has not been validated.
PREGNANCY
Resuscitation of the pregnant cardiac arrest victim provides added stress to the clinician due to the idea of caring for 2 patients simultaneously. Alleviation of this concern
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is best dealt with by accepting the conventional wisdom that the best care of the
unborn fetus is optimal care for the mother.
Etiologies of cardiac arrest unique to the pregnant patient include maternal hemorrhage, preeclampsia/eclampsia, HELLP syndrome (hemolysis, elevated liver
enzymes, low platelet count), amniotic fluid embolus, and adverse effects of maternal
care including tocolytic and anesthetic therapies. The likelihood of some nonobstetric
etiologies of cardiac arrest also increases in pregnancy including pulmonary embolus,
septic shock, cardiovascular diseases such as cardiomyopathy and myocardial
infarction, endocrine disorders, and collagen vascular disease. Traumatic causes of
arrest should also be considered due to documented increased rates of abuse and
homicide in pregnant women.20,21
Preparation for emergent cesarean delivery should be made as soon as cardiac
arrest is identified in a pregnant patient. Deliveries performed within 5 minutes of arrest
of the mother result in the highest survival rates for infants above 24 to 25 weeks
gestational age.17,22 Early delivery may also benefit the successful resuscitation of
the mother. Removing the fetus allows for decompression of the inferior vena cava
and abdominal aorta, allowing for improved venous return and cardiac output in the
mother. Additional staff, including a neonatal intensive care team, should be available
to assume care of the fetus after delivery. Obstetric or surgical consultants should be
contacted for definitive management after resuscitation if not already present for the
perimortem cesarean section.
Initial resuscitation efforts of the pregnant patient should focus on securing a protected airway and removal of blood flow obstruction caused by the gravid uterus.
Because of anatomic and physical changes that occur during pregnancy, the likelihood
of regurgitation of gastric contents is increased. Bag valve mask ventilation with
supplemental oxygen is recommended before intubation attempts due to faster desaturation in pregnant patients.23 Smaller ventilatory volumes should be used given the
diaphragm elevation and increased potential for gastric insufflation due to decreased
lower esophageal sphincter tone.17,22 Endotracheal intubation should occur as soon
as possible while maintaining cricoid pressure. Verification of endotracheal placement
should be performed by colormetric carbon dioxide detection or waveform capnometry, as decreased lower esophageal sphincter tone may lead to erroneous results or
misinterpretation of suction-based esophageal intubation detector devices.
Displacement of the gravid uterus away from the inferior vena cava and aorta likely
improves hemodynamics beyond 20 weeks gestation.22 A one or two-handed technique can be used to move the uterus toward the left upper quadrant of the abdomen.
This allows the patient to remain supine for other procedures including chest
compressions and intubation. Manual displacement has been shown to be superior
to placing the patient in a left lateral tilt position; however, tilting the patient 30 to
the left from supine using blanket rolls or a commercially available wedge should be
attempted if manual displacement is not successful.17
Standard ACLS algorithms require no modification in the care of the pregnant
patient. A theoretic need for increased dosing exists due to increased volumes of
distribution and higher glomerular filtration; there is no evidence to support this, but
some advocate that higher doses of medications should be considered if no response
to initial dosing is seen.24 Whenever possible, venous access and subsequent medication administration should be performed at sites above the diaphragm to avoid
failure of the medication to reach central circulation due to decreased venous return.17
Cardiac arrest occurring during magnesium infusion for treatment of preeclampsia or
premature labor requires discontinuing the magnesium infusion and administering 1 g
of calcium gluconate intravenously.25
POISONING
Cardiac arrest due to poisoning presents a complex challenge to even the most astute
clinicians. Information provided from often scant history of present illness may identify
toxins suspected in the poisoning, but often multiple drugs are encountered in the
case of intentional overdose or an unknown agent is involved in a workplace incident
or chemical exposure. In these cases, toxidromes are relied upon to determine the
culprit. Masking of clinical toxidromes may be present in the setting of cardiac arrest
due to prolonged hypoxia, hypoperfusion, or prehospital management (eg, dilated
pupils after atropine administration or cold, wet skin after field decontamination).
This may further complicate the choice of specific antidotes or therapies. Once
poisoning is suspected in cardiac arrest, immediate consultation with a medical toxicologist or poison control center should occur.
Provider safety should also be a paramount consideration in chemical ingestion or
exposures. Gross decontamination including removal of clothing and copious irrigation
should occur before entrance to the emergency department. Exposure to ingested or
inhaled chemicals may also pose a threat through exhaled air, vomitus, or fecal material.
As with all cardiac arrest patients, immediate resuscitative efforts should begin with
assessment and immediate management of the ABCs. Standard ACLS/PALS protocols should be followed. Once these initial interventions have been started, the
provider may then address any suspected toxidromes and consider their respective
antidotes. Gastrointestinal decontamination therapies including activated charcoal
administration, gastric lavage, and whole-bowel irrigation are not recommended in
the setting of cardiac arrest. These interventions can, however, be considered if resuscitative efforts are successful, preferably after expert consultation. Immediate consideration for antidote therapy is appropriate in some cases where an agent exposure or
ingestion is known or reasonably assumed based on the available history.
Victims in cardiac arrest from smoke inhalation or who are removed from a fire in
a confined area should be treated for cyanide toxicity. Hydroxocobalamin (Cyanokit;
Meridian Medical Technologies, Inc, St Louis, MO, USA) should be immediately
administered (510 g over 1530 min) intravenously if available.17,26 Additionally,
sodium thiosulfate administered intravenously may offer benefit over hydroxocobalamin alone.17 If hydroxocobalamin is not available, other cyanide antidotes kits may be
useful. The effectiveness of classic cyanide antidotes for smoke inhalation is limited,
as amyl nitrite administration requires an inhaled route. Additionally, both amyl and
sodium nitrite may result not only in hypotension, but also in functional anemia if
excessive methemaglobinemia is produced in the setting of concomitant
carboxyhemoglobinemia.27
Cholinergic agent exposure should be treated primarily with atropine sulfate. Pralidoxime chloride can also be administered for cholinergic poisonings when the offending agent is speculated to be an organophosphorous compound. Both antidotes can be
found in the commercially available Mark 1 kit or other similarly packaged nerve agent
antidote kit. Adequate patient decontamination and ventilation of the treatment area
should be ensured to provide safety for the health care providers during resuscitation.
Opioid overdose that results in respiratory arrest may respond naloxone administration through intravenous, intramuscular, or intranasal routes. While titrated 0.4 mg
doses are recommended, higher doses may be necessary if large ingestions are
present or if ultrapotent opioids are involved. If a mixed ingestion has occurred or is
suspected, the provider may opt for supportive care including intubation to await
metabolism of the medication. In situations where cardiac arrest occurs, naloxone
is unlikely to provide return of spontaneous circulation.
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In contrast to opioid reversal, overdoses involving benzodiazepines should not be

treated with a reversal agent such as flumazenil in the emergent setting. This therapy
could theoretically precipitate seizures in chronic benzodiazepine use or mixed ingestions. Supportive measures should be the mainstay of therapy.
Antihypertensive agents including beta-blockers and calcium channel blocker overdoses may result in profound hypotension with or without bradycardia. Antidotes such
as glucagon, calcium gluconate, or insulin/D50 have had some success in the symptomatic, prearrest patient.17 There are no data to support their use in cardiac arrest;
however, if they are to be successful in aiding in resuscitation, their administration
should occur early in arrest rather than waiting to the end of the ACLS algorithm.
In the suspected poisoned patient, wide complex tachycardia may be secondary to
conduction delays caused by myocardial sodium channel blocking agents. While
unstable wide complex tachycardia should be treated with standard ACLS protocols,
1 to 2 mEq/kg of sodium bicarbonate should be considered improve cardiac function.
This is particularly important in suspected poisonings when wide complex tachycardia
is refractory to electrical therapy.
ELECTRICAL/LIGHTNING INJURY
As the heart is an electrically driven organ, it is particularly sensitive to electrical injury.

Alternating current (AC), standard in household and commercial power supply, is reported to produce VF through a mechanism similar to the R-on-T phenomenon. Lightning is a massive direct current discharge and can produce asystole or VT by
depolarizing the myocardium. In addition, secondary arrest can occur in lightning
injury, as a patients spontaneous cardiac activity may return only to suffer a secondary
hypoxic arrest due to disruption of central nervous system (CNS) respiratory centers or
thoracic muscle paralysis.28
No modifications of standard ACLS/PALS algorithms are needed in electrically
induced cardiac arrest. The potential for successful resuscitation is higher than other
etiologies for arrest given that the patients are typically younger and lack coexisting
cardiopulmonary disease, as long as immediate treatment is available and initiated.
As opposed to standard care of multiple casualty incidents, patients in respiratory
and/or cardiac arrest after a lightning strike should have priority triage and treatment
over those victims not in arrest.
Trauma and burn care are often required as they are common sequelae of electric
shock and lightning injury. Cervical spine immobilization should be maintained during
intubation and resuscitation efforts of these patients.
HYPOTHERMIA
In severe hypothermia, marked depression occurs in all critical organ systems. This
may lead to cardiovascular collapse, but may also have a protective effect, allowing
for successful resuscitation after prolonged arrest times. For this reason, many feel
that a patient cannot be pronounced dead until rewarming has occurred and resuscitative efforts remain futile. However, clinical judgment should still prevail in the decision to attempt resuscitation. Efforts should be withheld in the presence of obvious
lethal injuries, lividity, blockage of airways with ice, or if chest compressions are
impossible due to advanced freezing.17 If drowning occurs before hypothermia, chances of resuscitation are reduced. Other etiologies of injury and illness often accompany hypothermia (eg, overdose, hypoglycemia, and trauma) and should be
considered and treated appropriately.
If the decision is made to attempt resuscitation, the patient should be immediately

intubated and chest compressions begun. Core body temperature should be obtained
as soon as possible, which will guide further resuscitation efforts. If available, needletype electrodes are preferred for cardiac monitoring.
For severe hypothermia (core temperature <30 C), aggressive active internal
rewarming should be undertaken, including warmed, humidified oxygen, warmed
intravenous fluids, pleural or peritoneal lavage, and partial or complete cardiopulmonary bypass. Hypothermic myocardium may be refractory to defibrillation and ACLS
medications. One attempt at defibrillation should be made for VF/VT. Further attempts
at defibrillation for VF/VT refractory to the initial shock may be reasonable according to
standard basic life support (BLS) algorithm concurrent with rewarming. Similarly, the
current recommendation for ACLS drugs suggests it may be reasonable to administer
these medications in accordance with standard ALS algorithm concurrent with
rewarming.17
For moderate hypothermia (3034 C) or once rewarming has raised the core
temperature to 30 C, defibrillation and medication administration should occur per
ACLS/PALS guidelines. At this temperature, active internal rewarming should be
undertaken or continued. If hypothermia is mild (>34 C) or when rewarming raises
core temperature to 34 C, standard ACLS/PALS guidelines may be applied, including
decisions regarding termination of resuscitation efforts. During rewarming, intravascular volume expansion will likely be necessary secondary to vasodilation.
SUBMERSION INJURY/DROWNING
Cardiac arrest from submersion is usually due to hypoxia. This may result from suffocation, but it may also be secondary to head or spinal cord injury. For this reason, early
intubation is required and should be performed with manual stabilization of the
cervical spine. Aspiration of large volumes of fluid with submersion is rare, but
increased inspiratory and PEEPs may be required to achieve adequate ventilation
and oxygenation due to pulmonary edema or acute lung injury. The beneficial use of
pulmonary surfactant has been documented in case reports of fresh water drowning
and may be considered.17
Standard ACLS/PALS algorithms should be used for cardiac arrhythmias without
modification. Electrolyte and acidbase disturbances are unlikely the etiology of
cardiac arrest in early presentations of submersion injury and do not warrant empiric
correction; however, this should be a consideration in patients who later deteriorate
during observation. Hypothermia and trauma are common confounders of submersion
injury; treatment of these issues was previously discussed.
Prognosis depends on duration of submersion and the duration and severity
hypoxia. In 1 pediatric study, submersion or resuscitative efforts greater than 25
minutes and pulseless arrest on arrival to the emergency department reportedly
were associated with universal mortality.29 A second study correlated the severity of
respiratory involvement with mortality, citing 93% mortality for those presenting in
arrest.30
ELDERLY
The number of people in the United States aged 55 and older continues to rapidly rise.
The US Census Bureau reported a 13% increase to 67.1 million between 2000 and
2005, more than 4 times the rate of growth (3%) of the population under 55. In accordance with that trend, the number of senior citizens, aged 65 and older, increased by
a factor of 11 in the 20th century, from 3.1 million to 33.2 million. It is estimated that by
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176
the year 2030, 20% of Americans will be senior citizens. While most of the aging baby
boomers live independently, a growing subset of the population is in nursing home
care. Data from the US Centers for Disease Control and Prevention report approximately 1.5 million nursing home residents in over 16,000 nursing homes across the
United States.
As age increases, so does the likelihood of having more than 1 disease process.
Cardiac disease, cancer, and stroke remain the leading causes of death in the elderly,
accounting for 70% of all deaths in this age group.31 Debilitating conditions like stroke
and dementia often leave these patients poor historians and unable to give complete
medical information to the health care providers. Therefore, providers often rely on
medical records, emergency medical services (EMS), and family for supplemental
information. Multiple illnesses, both acute and chronic, often lead to multiple medications, resulting in polypharmacy. Special attention should be paid to the medications
of this patient group during resuscitation efforts to look for contributors and possible
dysrhythmia-attributing side effects.
ACLS algorithms should be initiated unless the patient has advanced directives
stating contrary. Airway management should include attention to any dental apparatus, which may assist in bag valve ventilation, but should be removed before intubation. Early recognition of a potentially difficult airway is crucial in elderly patients with
severe kyphosis and degenerative joint disease of the neck and torso. Despite
changes in muscle mass and fat composition, along with potentially decreased
glomerular filtration rates in this population, there are no current recommended medication adjustments for ACLS therapy.
Advanced directives such as a living will, do not resuscitate order, and durable
power of attorney should be ascertained as soon as possible in efforts to honor the
wishes of the patient. Early discussion with any available family regarding continuing
versus termination of resuscitative efforts and family presence during the resuscitation
should occur.
SUMMARY
In certain cardiac arrest situations, modifications to current cardiac resuscitation algorithms may improve patient outcome. These situations are often rare, but when they
occur, they house the potential for severe time and resource use, and in some cases
specialized skill sets. The decision to apply these modifications to standard care for
the cardiac arrest patient may be obvious in some cases or may be applied due to
suspicion from the presenting medical history, history of present illness, or physical
examination. However, with rare exception, general care of any cardiac arrest patient
should include continuous high-quality chest compressions and appropriate airway
and ventilatory management.
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2008;36:216373.
2. Sellick BA. Cricoid pressure to control regurgitation of stomach contents during
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3. Marco CA, Marco AP. Airway adjuncts. Emerg Med Clin North Am 2008;26:
101527.
4. Levitan RM, Kinkle WC, Levin WJ, et al. Laryngeal view during laryngoscopy:
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5. Serocki G, Bein B, Scholz J, et al. Management of the predicted difficult airway:

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6. Byhahn C, Iber T, Zacharowski K, et al. Tracheal intubation using the mobile CMAC video laryngoscope or direct laryngoscopy for patients with a simulated
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7. Malik MA, Subramaniam R, Maharaj CH, et al. Randomized controlled trial of the
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8. Cook TM, Hommers C. New airways for resuscitation? Resuscitation 2006;69:
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10. McManus J, Hurtado T, Pusateri A, et al. A case series describing thermal injury
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content/112/24_suppl/IV-146.full.pdf+html. Accessed September 2, 2011.
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American College of Surgeons. Practice management guidelines for emergency
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15. Oddo M, Feihl F, Schaller MD, et al. Management of mechanical ventilation in
acute severe asthma: practical aspects. Intensive Care Med 2006;32:50110.
16. Corbridge TC, Hall JB. The assessment and management of adults with status
asthmaticus. Am J Respir Crit Care Med 1995;151:1296.
17. Vanden Hoek TL, Morrison LJ, Shuster M, et al. Part 12. Cardiac arrest in special
situations: 2010 American Heart Association guidelines for cardiopulmonary
resuscitation and emergency cardiovascular care. Circulation 2010;122:
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18. National Asthma Education and Prevention Program. Expert Panel Report 3
(EPR-3): guidelines for the diagnosis and management of asthmasummary
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19. Watts JI. Thoracic compression for asthma. Chest 1984;86:505.
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25. Munro PT. Management of eclampsia in the accident and emergency department. J Accid Emerg Med 2000;17:711.
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Devices Used in
Card iac A rrest
Steven C. Brooks, MD, MHSc, FRCPCa,b,c,*, Alina Toma,
Jonathan Hsu, BHScf
MD, FRCPC
d,e
KEYWORDS
Cardiac arrest Cardiopulmonary resuscitation
Medical devices Extracorporeal life support
High-quality cardiopulmonary resuscitation (CPR), with an emphasis on adequate

compression depth, rate, and consistency, is important in optimizing vital organ
perfusion and survival from cardiac arrest.1 However, even the best-quality conventional CPR is inefficient, resulting in only 25% of normal cardiac output.2 Over the
past several decades, many therapeutic devices have been designed to improve
on conventional CPR and increase the probability of survival. This article does not
provide a comprehensive review of all devices proposed for this purpose, but reports
on a selection of those that have received attention in the medical literature and the
most recent 2010 American Heart Association (AHA) guidelines for Emergency
Cardiovascular Care and CPR.3
This article reviews devices in two main sections. The first section describes devices
that are adjuncts to conventional manual chest compressions. These devices include
those that provide prompts to the rescuer to guide conventional CPR. This section
This chapter discusses the several devices that may be used in the treatment of cardiac arrest.
The ResQPod, Autopulse, Zoll Pocket CPR, Q-CPR, LUCAS, Lifestat, and ECMO devices are
approved for use as described in this chapter. At the time of writing, the CPRGlove, Lifestick,
ResQPump, and CPRmeter devices have not received FDA approval for use on patients in
cardiac arrest as described in the chapter.
a
Division of Emergency Medicine, Department of Medicine, University of Toronto, 2075
Bayview Avenue, C7-53, Toronto, Ontario, Canada, M4N 3M5
b
Rescu, Li Ka Shing Knowledge Institute, St Michaels Hospital, 30 Bond Street, Toronto,
Ontario, Canada, M5B 1M8
c
Program for Trauma, Emergency and Critical Care, Sunnybrook Health Sciences Centre, 2075
Bayview Avenue, Toronto, Ontario, M4N 3M5
d
Department of Internal Medicine, Sunnybrook Health Sciences Centre, University of Toronto,
2075 Bayview Avenue, Toronto, Ontario, Canada, M4N 3M5
e
Emergency Department, St Michaels Hospital, 30 Bond Street, Toronto, Ontario, Canada,
M5B 1M8
f
Undergraduate Medical Education Program, Faculty of Medicine, University of Toronto,
Toronto, Canada
* Corresponding author. Rescu, St. Michaels Hospital, 30 Bond Street, Toronto, Ontario, M5B 1W8
E-mail address: brooksst@smh.ca
doi:10.1016/j.emc.2011.09.002
emed.theclinics.com
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Brooks et al
also reviews devices used to augment conventional manual chest compressions

through improving the physics of the chest wall translation during the compression
maneuver or improving the dynamics of the chest cavity pump through other mechanisms. The second section describes devices that have been designed to entirely
replace manual chest compressions during CPR as a method of maintaining vital
organ perfusion.
DEVICES USED AS ADJUNCTS TO MANUAL CHEST COMPRESSIONS
Devices Used to Prompt CPR Providers
CPR prompting devices are designed to focus the providers attention on accepted
standards of CPR quality. Prompting devices range from basic metronomes to guide
the rate of chest compressions to more sophisticated accelerometer or impedance
technology that can provide real-time audio and visual feedback in response to other
important components of CPR quality. Prompting devices are either stand-alone or
incorporated into defibrillator-monitor units. Examples of stand-alone devices are
the Zoll PocketCPR (Zoll Medical Corporation Technologies, Chelmsford, MA, USA)
and the CPRmeter (Laerdal Medical, Stavanger, Norway), which are puck-like devices
that can be placed under the hands of the rescuer during chest compressions. These
devices measure aspects of dynamic chest compression and provide audio or video
feedback. Prompting devices can be used on mannequins as educational tools during
CPR training or as adjuncts during actual resuscitations.
Metronomes
A metronome is a device used to mark time using an auditory or visual stimulus at

regular intervals. The use of a metronome during CPR has been studied in the hospital
and out-of-hospital settings. Most studies show that metronomes can improve the rate
of chest compression delivery closer to recommended rates, and one study reported
an associated improvement in survival.46 No studies have shown harm with the use
of metronomes.
Force transducers and accelerometers
Force transducers are devices that can measure the force applied to the chest wall
during CPR. Accelerometers can detect movement of the chest wall. Data from these
devices can be translated into audio or visual feedback on the depth, rate, consistency,
and recoil of chest compressions. Supportive evidence for these devices was first
reported in a case series of patients using a position-sensing arm that showed encouraging hemodynamic effects when used during in-hospital cardiac arrests. Abella
and colleagues7 showed a reduction in variability of compression rate and ventilation
rate in a prospective cohort study of 156 patients using the Q-CPR system (Philips
Medical, Andover, MA, USA), which uses an accelerometer for feedback on compression depth and impedance measurements across the chest for feedback on ventilation rate. A prehospital before-and-after study of 284 patients performed with
a similar device found that average compression depth increased from 34 9 mm to
38 6 mm (P<.001), percent of adequate depth compressions increased from 24%
to 53% (P<.001), and mean compression rate decreased from 121 18 to 109 12
(P<.001).8 Survival was not significantly different between the groups, with 2.9%
surviving to discharge versus 4.3% in the intervention group (P 5 .2).
Edelson and colleagues9 also used the Q-CPR device in 224 patients and were able
to show a decrease in ventilation rate (13 7 vs 18 8; P<.001) and an increase in
compression depth (50 10 mm vs 44 10 mm; P<.001) when the device was used.
Niles and colleagues10 were also able to show that audiovisual feedback in a pediatric
Devices Used in Cardiac Arrest
arrest population decreases the amount of detrimental leaning performed during chest
compressions and therefore promotes better chest recoil. When using an accelerometer, placing a stiff backboard behind the patient experiencing cardiac arrest is important for feedback. One study showed that the feedback can be inaccurate when
chest compressions are performed on soft surfaces without a backboard, resulting in
delivery of chest compressions with suboptimal compression depth.11
Accelerometer and pressure sensing technologies have also been incorporated into
novel feedback devices, such as a CPR glove and CPR board. The CPR glove (Altreo
Medical, Burlington, Ontario, Canada) is designed to be worn on the hand of the
provider giving chest compressions. A small visual display and built-in speaker on
the back of the glove provide the user with instructions on the sequence of CPR
and feedback about quality of chest compressions. No studies reporting use of the
glove have been published at the time of writing. A single Chinese case report
described a pressure-sensitive CPR board placed under the patients body during
CPR, which provides feedback about the quality of chest compresssions.12 No
published studies have directly compared feedback devices.
Devices Used to Augment Manual Chest Compressions
Active compression-decompression devices
Active compression-decompression devices have been designed to improve the

mechanics of standard chest compressions through facilitating an exaggerated recoil
phase of the chest compression cycle. For example, the CardioPump ACD-CPR Device
(Advanced Circulatory Systems, Inc., Roseville, MN) uses a suction cup component
that attaches to the patients chest and allows lifting of the chest wall beyond neutral
position causing active decompression (Fig. 1). This device also includes a force gauge
to encourage adequate compression and decompression by the user. Other more
simple devices, such as a modified oven mitt with Velcro, have also been developed
for this purpose.13 The intended physiologic mechanism common to all active
Fig. 1. The CardioPump ACD-CPR Device (Advanced Circulatory Systems, Inc., Roseville, MN,
USA) is an active compression-decompression CPR device that uses a suction cup to facilitate
active decompression during the recoil phase of manual chest compressions during cardiac
arrest. (Courtesy of Advanced Circulatory Systems, Inc., Roseville, MN, USA; with permission.)
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compression-decompression CPR (ACD-CPR) devices is to create a negative intrathoracic pressure and increased venous return during the active decompression phase.
Several studies have shown that improved hemodynamics are possible with this technique compared with standard chest compressions.14 Evidence for the effectiveness of
these devices in humans is mixed, but no data suggest they are harmful.1527
A Cochrane systematic review and meta-analysis (updated in 2010) pooled the data
from 12 randomized and pseudo-randomized comparisons involving 4988 patients
and found no evidence of mortality benefit with the use of ACD-CPR compared with
standard manual chest compressions.14 The recent American Heart Association
(AHA) guidelines for CPR and Emergency Cardiovascular Care concluded that
evidence is insufficient to recommend for or against the routine use of these devices
in cardiac arrest, but suggest that these may be considered for use when providers are
adequately trained and monitored.
Impedance threshold device
During the compression phase of CPR, pressure in the heart chambers and intrathoracic vascular structures increases as external pressure is applied to the chest. The
pressure gradient directs blood out of the heart and to the periphery. The recoil of
the chest wall during the decompression phase is equally important. The decrease
in intrathoracic pressure to subatmospheric levels assists in the venous return of
circulation to the heart. This phase is critical for cardiac preload and is thus essential
for optimal cardiac output, blood pressure, and vital organ perfusion. However, as the
intrathoracic vacuum draws blood back to the heart, it simultaneously draws air into
the lungs. This influx of inspiratory gases takes away from the potential hemodynamic
benefit of the decompression phase of CPR.
First described in 1995,28 the impedance threshold device (ITD) is designed to limit
this influx of air, increase the negative intrathoracic pressure, and thus enhance circulation during CPR. This device is commercially available as the ResQPOD ITD
(Advanced Circulatory Systems, Inc., Roseville, MN) (Fig. 2). The ITD is a pressuresensitive valve that can be attached to the respiratory circuit via an endotracheal
tube, supraglottic airway, or facemask. The negative intrathoracic pressure in an intubated patient has been documented to be up to 13 mm Hg, contrasted with a pressure of only 3 mm Hg without the use of an ITD.29 When used with a facemask, a tight
seal between the face and the mask must be continuously maintained during CPR to
hold the vacuum. A two-person ventilation technique can be used to maintain this
continuous seal, with one person delivering ventilations and another securing the
mask against the patients face. Because of its flexibility in attachment to the respiratory circuit and its portable nature, the ITD is appropriate to use for basic life support in
the field and for emergency department resuscitation.
During individual chest compressions, air is allowed to move freely out of the chest
and through the device, just as during active ventilation by the rescuer. The lumen within
the ITD will remain open, creating no resistance to ventilation. Spontaneous inspiration
through the ITD is possible but may be difficult for a recently resuscitated patient.
Thus, immediate removal of the ITD once pulse has been restored is recommended.
Besides providing augmentation of negative intrathoracic pressure during CPR
decompression to increase venous return, the ResQPOD ITD comes equipped with
ventilation timing assist lights that flash at a rate of 10 times a minute to prevent overventilation. Studies have shown that even professional rescuers responding to out-ofhospital cardiac arrests may excessively ventilate patients,30 which can lead to
decreased venous return to the heart, decreased coronary perfusion pressure, and
increased intracranial pressure.
Fig. 2. The ResQPOD impedance threshold device (Advanced Circulatory Systems, Inc.,
Roseville, MN, USA) is used on the patients airway to prevent passive influx of respiratory
gases during the recoil phase of chest compressions and increase the negative intrathoracic
pressure generated. (Courtesy of Advanced Circulatory Systems, Inc., Roseville, MN, USA;
with permission.)
A systematic review and meta-analysis published in 2008 identified five randomized

controlled trials that tested the effectiveness of the ITD in treating out-of-hospital
cardiac arrests. The included studies were heterogeneous in that three of them
included the use of ACD-CPR in the ITD group and two used conventional CPR. The
meta-analysis of these studies found that patients in the ITD group were more likely
to experience return of spontaneous circulation (relative risk,1.29; 95% CI, 1.10
1.51) and early survival, defined as survival at 24 hours or intensive care unit admission
(relative risk, 1.45; 95% CI, 1.161.80). No evidence showed a positive effect on neurologic outcome in survivors or longer-term survival (eg, survival to hospital discharge).
The 2010 AHA guidelines suggested that an ITD may be considered as a circulatory
adjunct during CPR by trained personnel in adults in cardiac arrest.1,3 The moderate
strength of recommendation (level IIb) balances the biologic plausibility for benefit
with ITD use and the heterogeneous results from clinical studies. Soon after these
guidelines were published, preliminary results from the Resuscitation Outcomes
Consortium (ROC) PRIMED study were published in abstract form.31 The PRIMED
study was a large multicenter, double-blind, randomized, controlled trial comparing
the ITD with a sham device during standard CPR for patients experiencing
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nontraumatic out-of-hospital cardiac arrest. More than 8700 patients were randomized in this study. The Data Safety and Monitoring Board stopped the trial early
because of futility. No difference was seen between groups regarding the primary
outcome of survival to discharge with a good neurologic function (modified Rankin
score 3). At the time of writing, full analysis of the study, including that of important
subgroups, had not been published.
Combined use of ACD-CPR and an ITD
Adding the use of an ITD during ACD-CPR may synergistically improve the effectiveness of chest compressions during resuscitation from cardiac arrest. In one small
randomized controlled study in humans, airway pressures were not significantly
reduced during ACD-CPR alone because inspiratory gases were allowed to flow
into the airway during the decompression phase. When an ITD was used on an endotracheal tube during ACD-CPR, significant negative airway pressures were generated
(mean, 7.3 mm Hg; SD, 4.5).29
Building on data from several smaller studies showing an improvement in short-term
survival with combined ACD-CPR and ITD use, Aufderheide and colleagues32 recently
published a multicenter randomized controlled study comparing the use of ACD-CPR
with an ITD versus standard CPR without an ITD. In this study of more than 1200
patients who experienced nontraumatic out-of-hospital cardiac arrest, the investigators showed a 53% improvement in survival to hospital discharge with favorable
neurologic function in the group treated with ACD-CPR and ITD. The study showed
that 47 (6%) of 813 controls survived to hospital discharge with favorable neurologic
function compared with 75 (9%) of 840 patients in the intervention group (odds ratio,
1.58; 95% CI, 1.072.36; P 5 .019). Similar results were found when assessing 1-year
survival rates, with 9% in the ACD group and 6% of the standard CPR group (P 5 .03).
Both survival groups had equivalent cognitive skills, disability ratings, and emotionalpsychological statuses. The overall major adverse event rate did not differ between
groups, but more patients had pulmonary edema in the intervention group (94
[11%] of 840) compared with controls (62 [7%] of 813; P 5 .015).
This study was well-designed but had some limitations. The ACD-CPR device (the
ResQPump) also included a pressure gauge feedback device for providers to monitor
chest compression quality, and the ITD device included a metronome light to standardize ventilation rate. These two additional sources of feedback should be considered cointerventions. Furthermore, the study was stopped early because of a
funding shortage, and early termination of trials can lead to inflated estimates of
outcomes.33 Lastly, the authors declared potential conflicts of interest, which include
the fact that one is the coinventor of both tested devices and Chief Medical Officer of
the company that sells the devices (Advance Circulatory Systems).
Despite these limitations, in the context of previous studies showing the effective
generation of negative intrathoracic pressure and numerous smaller clinical studies
showing a short-term survival advantage, this study supports the concept that
combining ACD-CPR and ITD to augment negative intrathoracic pressure generation
is a viable strategy for resuscitating patients in cardiac arrest and may be associated
with improved longer-term survival with good neurologic function. Reproduction of
these results in future independent studies will clarify whether this strategy should
be broadly implemented.
Interposed abdominal compression devices
The Lifestick resuscitator (Datascope, Fairfield, NJ, USA) is a device that combines
ACD-CPR and interposed abdominal compression techniques, which, when used in
animal studies, showed an increased coronary perfusion pressure and total cerebral
blood flow, higher end-tidal carbon dioxide, and better survival compared with standard CPR.34,35 One randomized trial and one prospective study investigated
outcomes with the Lifestick device in patients experiencing cardiac arrest. The
randomized trial included only 50 patients and was not powered to detect differences
in survival outcomes, but it did show that the device was not associated with any
increase in CPR-related injuries and was well accepted by users.36 The 2010 AHA
guidelines for emergency cardiovascular care and CPR do not include a specific
recommendation for the use of this type of device because there is insufficient data
supporting or refuting effectiveness.3
Devices Used as an Alternative to Manual Chest Compressions

Mechanical chest compression devices
Traditional cardiopulmonary resuscitation for cardiac arrest victims includes the

delivery of rhythmic manual chest compressions by a human rescuer. However,
several types of mechanical chest compression devices using a variety of mechanisms can provide an alternative to the human chest compressor, including pneumatic
vests, load-distributing bands (LDB), and pistons. The feature common to all of them is
that a deforming force is applied rhythmically and automatically to the chest wall,
simulating the action of manual chest compressions.
Numerous studies have shown that even well-trained, experienced rescuers tend to
provide suboptimal compressions with respect to depth, rate, and consistency.3740
Human chest compressors are also prone to fatigue and dwindling compression
quality over time.41 In theory, mechanical chest compression devices are not susceptible to these problems. With the understanding that CPR quality and consistency are
associated with patient outcomes, mechanical chest compression devices have been
proposed as an alternative to imperfect manual CPR. The benefit of these devices may
be their ability to provide consistent, high-quality chest compressions with minimal
interruptions while liberating rescuers from this duty to tend to other tasks associated
with resuscitation and transportation. Mechanical chest compression devices may be
particularly useful in scenarios where a prolonged resuscitation may be necessary or
where manual chest compressions may be technically difficult (eg, accidental hypothermia, toxicologic causes of cardiac arrest or intra-arrest cardiac catheterization).
Available devices use a variety of mechanisms. Several papers report on the use of
a pneumatic vest to facilitate chest compression during cardiac arrest. Similar to an
oversized blood pressure cuff, the pneumatic vest is placed circumferentially around
the patients thorax, and chest compression is achieved with the rapid introduction of
pressurized air into and out of the vest.42 The pneumatic vest concept has since
evolved into a load-distributing band cardiopulmonary resuscitation device called
the AutoPulse (Zoll Medical Corporation, Chelmsford, MA, USA) (Fig. 3). The commercially available AutoPulse uses a wide band of material attached to a short backboard.
The band is connected to a mechanism that can shorten the band under force in
a rhythmic fashion such that the band squeezes the entire chest with each cycle.
Other devices use compressed gas or an electric mechanism to drive a piston
placed over the lower sternum of the patient. For example, the Life-Stat (formerly
the Thumper) device (Michigan Instruments, Grand Rapids, MI, USA) is a gaspowered piston device with a built-in transport ventilator. Other piston devices,
such as the Lund University Cardiac Assist System (LUCAS; Jolife AB, Lund, Sweden),
incorporate a suction cup attachment for the piston to facilitate active compressiondecompression CPR (Fig. 4).
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Fig. 3. The AutoPulse Non-Invasive Cardiac Support Pump (Zoll Medical Corporation,
Chelmsford, MA, USA) is a mechanical CPR device that uses a load-distributing band that
encircles the patients chest and rhythmically shortens and lengthens to facilitate chest
compressions. (Courtesy of Zoll Medical Corporation, Chelmsford, MA, USA; with
permission.)
The relative effectiveness of mechanical chest compression devices as an alternative to manual chest compressions for improving clinical outcomes after cardiac arrest
is not clear. Data suggesting clinical benefit with the use of mechanical chest
compression devices are mostly derived from animal and human observational
studies. Animal studies have shown that mechanical chest compressions can produce
improved cerebral, central, and coronary blood flow4345 and improved survival46,47
Fig. 4. The LUCAS2 (Jolife AB, Lund, Sweden) is a mechanical chest compression device that
incorporates a suction cup attachment for the piston to facilitate active compressiondecompression CPR. (Courtesy of Jolife AB, Lund, Sweden; with permission.)
compared with manual chest compressions. Several observational studies in humans

have shown improved outcomes with the use of mechanical chest compression
devices.4852 The study by Ong and colleagues52 was a before-and-after comparison
of the AutoPulse device with manual chest compressions in patients with out-ofhospital cardiac arrest treated by paramedics. When comparing 499 patients who
received manual chest compressions with 284 patients who received treatment with
the AutoPulse device, the authors showed an adjusted odds ratio of 2.27 (95% CI,
1.114.77) for survival to hospital discharge favoring the AutoPulse. They report
a number-needed-to-treat of 15.
The ASPIRE trial was published in the same issue of the Journal of the American
Heart Association. In this multicenter, cluster-randomized trial, Hallstrom and
colleagues53 studied 767 patients with out-of-hospital cardiac arrest. They compared
the effectiveness of chest compressions delivered by the AutoPulse with that of standard manual chest compressions delivered during advanced life support and basic life
support procedures by prehospital personnel. Clusters were based on ambulance
station or group of stations, with crossover occurring at intervals ranging from 4 weeks
to 2 months. The study recruited patients in five cities, and the protocol for CPR was
not uniform across all sites. In fact, the CPR protocol was changed part way through
the study at one site. The change involved a 2-minute delay in applying the mechanical
device to the patient while paramedics administered manual CPR and a first defibrillation if needed. This change was incorporated in response to quality assurance data
from the local emergency medical services system showing prolonged time without
compressions in the load-distributing band device group. The primary outcome of this
study was survival to 4 hours after the 911 call. The Data Safety and Monitoring Board
stopped the trial early because of decreased survival to hospital discharge in patients
who received mechanical chest compressions (9.9% in the manual CPR group vs
5.8% in the mechanical CPR group). The proportion of patients with a cerebral performance category of 1 or 2 (good neurologic function) at discharge was lower in the
mechanical CPR arm of the study (3.1% in the mechanical CPR group vs 7.5% in
the manual CPR group).
The results of this study, which is the largest randomized comparison to date, were
unexpected. The bulk of previous animal, human physiologic, and observational clinical data had suggested benefit. Many commentators and a more recent reanalysis of
the original trial data54 suggested that the protocol change at one of the sites (resulting
in a delay in the application of the device) had been responsible for the negative
results. This controversy has highlighted the importance of how devices are incorporated into the sequence of CPR and the need to monitor CPR quality in both arms of
the study. The risk is that the use of the devices may introduce interruptions in chest
compressions or delay other interventions, such as defibrillations, which may negate
any beneficial effects from the mechanical chest compressions that are ultimately
provided once the device is in place.
Reflecting on these heterogeneous data, the 2010 AHA guidelines for emergency
cardiovascular care and CPR3 concluded that evidence is insufficient to recommend
the routine use of mechanical CPR devices for cardiac arrest, but recommended that
properly trained personnel may considered their use in specific settings of cardiac
arrest. More clarity is likely to come soon from two ongoing, large, multicenter,
randomized studies comparing mechanical chest compression with manual chest
compressions.
The PaRAMeDIC study in the United Kingdom (trial registered at http://www.
controlled-trials.com/ISRCTN08233942) plans to randomize 4200 patients with outof-hospital cardiac arrest treated by paramedics to either chest compressions with
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the LUCAS device or manual chest compressions. They will measure survival to
hospital discharge as the primary outcome, and a variety of neurologic and functional
outcomes at short- and long-term end points as secondary outcomes. Enrollment is
planned to end in 2013.
The Circulation Improving Resuscitation Care (CIRC) study is a multicenter,
randomized study enrolling patients with nontraumatic out-of-hospital cardiac arrest
from several locations in the United States and Europe. This study will compare the
use of the AutoPulse device with manual chest compressions with respect to survival
to hospital discharge and several other outcomes, including neurologic outcome. The
investigators are planning to recruit 5000 patients in the study, which will be
completed sometime in 2012.
The hope is that, with attention to uniform training, early application of the device
into the sequence of CPR with minimal interruptions, and careful monitoring of CPR
quality in both study arms, these trials will provide a definitive answer regarding the
effectiveness of mechanical chest compression devices for cardiac arrest.
Extracorporeal life support
Advances in technology have enabled the rapid deployment of cardiopulmonary

bypass since it was first proposed in 1966.55 The extracorporeal membrane oxygenation (ECMO) device has shown to be effective in the neonatal population for respiratory
failure56 and congenital cardiac defects.57 More recently, ECMO has been studied in
chidren and adults with prolonged arrest after conventional measures have failed.5861
A basic ECMO circuit consists of a gas-exchange device, such as an oxygenator;
vascular cannulae to access and return blood; circuit tubing; a pump; and a heater
cooler that regulates blood temperature.62 ECMO is typically a temporary means of
providing oxygenation, carbon dioxide removal, and hemodynamic support to
patients with cardiac or pulmonary failure. In instances of cardiac arrest, this device
can buy valuable time for resolution of underlying pathophysiologic problems.
When ECMO is used on a patient, blood is removed from the venous system via
a catheter, which can be attached to the right atrium. It passes through a membrane
oxygenator and is delivered back to the patients circulatory system through a catheter
in the arterial system. Points of attachment can be the aorta or common carotid artery.
Besides the risk of complications, another challenge with ECMO is its deployment
during ongoing conventional CPR. Interruptions in chest compressions should be
minimized to facilitate favorable outcomes, including best possible coronary perfusion
and chance of regaining spontaneous circulation. Thus, a rapid, simple cannulation
technique is necessary. Choices for arterial cannulation include the carotid artery or
femoral artery, and for venous cannulation include the internal jugular or the common
femoral vein. Percutaneous cannulation of the femoral arteries during cardiac arrest
has also been shown to be successful in adults.63
Although several observational studies and case reports have shown an association
between extracorporeal life support for cardiac arrest and increased survival compared with conventional CPR,64,65 no data are available from randomized controlled
trials. The emergent, unexpected nature of cardiac arrest and the complicated nature
of deploying this intervention threaten the feasibility of a randomized controlled trial. In
the most recent observational report from Seoul, Korea, Shin and colleagues65 undertook a retrospective analysis of 406 patients with in-hospital cardiac arrest. Using
a propensity scoreadjusted analysis, which attempted to control for prearrest conditions and CPR variables, the investigators observed that the use of ECMO in 120 adult
patients who had greater than 10 minutes of CPR was associated with a reduced risk
of mortality and less neurologic impairment (odds ratio, 0.17; 95% CI, 0.040.68).
Currently, the practical deployment considerations and high resource use will
prohibit the implementation of this therapy in most centers. Data are sparse and from
nonrandomized comparisons, but support the feasibility, safety, and effectiveness of
extracorporeal life support. The 2010 AHA guidelines found that evidence was insufficient to recommend the routine use of extracorporeal life support but that it may be
considered when it is readily available for patients who have a brief period without blood
flow and when the condition leading to cardiac arrest is reversible (eg, accidental hypothermia, drug intoxication).3
SUMMARY
Good-quality CPR and chest compressions are essential to maximize a patients

chances of survival after cardiac arrest. Even the best manual chest compressions
are inefficient at replacing normal cardiac output. This article reviewed several technologies and devices proposed to improve survival after cardiac arrest through optimizing
the physics of CPR and vital organ perfusion. Despite promising results from laboratory studies or observational human studies, no single strategy or device has consistently shown improvement in survival over conventional CPR. Recent data supporting
the combined use of the ITD and ACD-CPR in cardiac arrest32 provide rationale for
investigating investigating combination strategies that simultaneously use multiple
devices with complimentary mechanisms to improve cardiac output during CPR.
The benefit of mechanical chest compression devices remains unclear. Evidence
from randomized studies is mixed, with the largest study suggesting harm. Using these
devices in cardiac arrest has the potential for delaying or interrupting good-quality
manual CPR. For clinicians choosing to use any of these devices, caution and attention
to overall CPR quality must be used during the deployment of devices. The answer to
the long-debated question of whether human or machine provides the best life-saving
chest compressions is likely to be answered shortly as two large randomized trials of
mechanical chest compression close enrollment within the next 1 to 2 years. However,
regardless of the results, this and other questions around the effectiveness of devices
in the treatment of cardiac arrest will likely need to be readdressed continuously as
technology and understanding of resuscitation advance.
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Immediate recognition and activation of the emergency response team;

1. Scherman N, editor. 2 Kings 4:32-35. Brooklyn, NY: Mesorah Publications Ltd;

Safar P. History of cardiopulmonary cerebral resuscitation. In: Kaye W, Bircher N,

Department of Internal Medicine, University of Washington, 1959 NE Pacific Street, Box

Cardiac Arrest: A Public Health Perspective

population considered.18 Among 39 sites worldwide that published their outcomes

Out-of-hospital cardiac arrest affects approximately 490,000 individuals in Europe

Fig. 2. Leading causes of death in United States.

Cardiac Arrest: A Public Health Perspective

Dilated or hypertrophic cardiomyopathy accounts for about 10% to 15% of cases of

Cardiac Arrest: A Public Health Perspective

The exact mechanism of collapse in an individual patient is often difficult to establish

phenomenon, such as increased clotting or increased parasympathetic instability.

Survival from cardiac arrest varies tremendously across communities. As noted

A cardiac resuscitation system is an interconnected community, EMS, and hospital

Cardiac Arrest: A Public Health Perspective

InterAmerican Heart Foundation, Resuscitation Councils of Southern Africa).

22. Iwami T, Nichol G, Hiraide A, et al. Continuous improvements in chain of survival

Cardiac Arrest: A Public Health Perspective

ACCESS AND PRESENTATION

The authors have nothing to disclose.

Boyd & Perina

Out-of-Hospital Cardiac Arrest

Boyd & Perina

an approximate 1% (0.7%2.1% range) absolute increase in survival. In addition to

Out-of-Hospital Cardiac Arrest

Boyd & Perina

Out-of-Hospital Cardiac Arrest

compressions. Pressure-sensing devices placed between the chest and a providers

Boyd & Perina

Out-of-Hospital Cardiac Arrest

8. Rosamond W, Flegal K, Furie K, et al. Heart disease and stroke statistics2008

Boyd & Perina

Out-of-Hospital Cardiac Arrest

45. Mosier J, Itty A, Sanders A, et al. Cardiocerebral resuscitation is associated with

Cardiopulmonary resuscitation (CPR) developed in different environments from the

Epidemiologic analysis of sudden cardiac death is challenging. In the out-of-hospital

Department of Medicine, University of Virginia, PO Box 800136, Charlottesville, VA

Monteleone & Lin

In-Hospital Cardiac Arrest

Monteleone & Lin

In-Hospital Cardiac Arrest

Monteleone & Lin

or surgical knowledge often function as team leaders on CATs. Leadership, team

In-Hospital Cardiac Arrest

1. Eftestol T, Sunde K, Steen PA. Effects of interrupting precordial compressions on

Monteleone & Lin

2. Andreka P, Frenneaux MP. Haemodynamics of cardiac arrest and resuscitation.

In-Hospital Cardiac Arrest

Monteleone & Lin

Circulation, specifically, high-quality chest compressions, is the most critical portion of

Emerg Med Clin N Am 30 (2012) 3549

If the patient is unresponsive and has no

ABC becomes CAB

Circulation is to be addressed first with the

Push Hard, Push Fast

100 compressions/min at a depth of at least