ICU

557

Table of contents
Topic Page/reference
1 ICU 559 – 560

2 Factors increasing incidence of infection in ICU 560

3 Modes of transmission of organism 561

4 ICU admission criteria/levels of ICU care 561

5 Critically ill pt recognition 562

6 Inv requiring urgent corrective actions 562

7 I HUG FAST/assessment & initial resuscitation 563

8 Impending resp arrest/distress; inadequate oxygenation/ventilation 564

9 Monitoring in ICU/chest physio/general care/daily clinical mx 565

10 Pressure sore 566

11 Ind/contraind/complic tracheal intubation 567

12 Muscle weakness in ICU 568

13 Advanced ventilation 569

14 Aims of resp support/signs suggestive of failing tissue perfusion/ 570

flapping tremor
15 Mechanical ventilation/types/goals/red flags/ind/complic 571 – 572

16 Complic of prolonged artificial ventilation/prolonged stay in ICU 573

17 Mode 574

18 Cycling/initial ventilator settings/PIP/Plateau pressure 575

19 NIV 576

20 PEEP 577

21 CPAP 578

22 BiPAP 579

23 Weaning 580

24 SBT 581

25 Pneumonia/CURB-65/nosocomial/HCAP 582 – 583

26 VAP 584 – 587

27 Mechanisms of respiratory failure 588

28 Resp failure/def/type/cause/ 589

29 Principal goals in the mx of acute resp failure/assessment of resp failure 590

30 Mx type 1 RF 591

31 Mx type 2 RF 592

Dr. K H Mozumder
 558

32 Monitoring in resp failure 592

33 Cardiogenic vs non-cardiogenic edema 592

34 ALI/ARDS 594 – 599

35 Prone positioning 598

36 ICU care bundles 598

37 Universal precautions against infectious diseases (HIV, HBV, HCV) 600

38 Antisepsis/disinfection/sterilization/autoclave/spore killing 600 – 601

39 Vascular catheters/cannulation/Seldinger’s 602

40 Adv of using ultrasound for vascular access 602

41 Approaches for IJV/SCV/FV 603

42 Why Right IJV cannulation is generally preferred over the left IJV? 603

43 Ind/relative contraind/complic CVC 604

44 CVP 605

45 CVP measurement techniques/uses of CVP/ 607

Causes of raised and decreased CVP
46 Artefacts caused by technical problems related to CVP measurements 607

47 JVP/ScvO2/SvO2 608

48 Arterial catheterization 611

49 Hyperdynamic circulation 614

50 Cardiac output (CO) measurement techniques 614

51 Principles/periop modalities/uses of echo 615

52 Mechanisms of antimicrobial resistance/ 616

factors promoting antimicrobial resistance/origin of drug resistance
53 Classification of antimicrobial agents/beta-lactam compounds 617

54 Antimicrobial prophylaxis against infective endocarditis 618

55 Severity assessment scoring systems in ICU 618

56 Organ system failure definitions 619

57 New onset of fever in ICU 620

58 Common causes of different respiratory patterns 621

59 Sounds production 621

60 Bedside PFTs 622

61 Inflammation/infection/cross inf/nosocomial inf/sepsis/SIRS/SHOCK 624 – 642

62 DIC 643

63 Physiological effects/physical signs of malnutrition 647

64 Essential nutrients/benefits of proper nutrition in critical illness 647

Dr. K H Mozumder
 559

65 TPN/immunomodulation & feeding 648 - 654

66 Acid-base disorders/AG/Tonicity/Delta ratio/Electrolyte imbalances 656 – 678

67 ABG analysis/classification of ABD/Allen’s test/MEN 679 – 684

68 Analgesia & sedation in ICU/PCA/Ramsay/Richmond 685 – 688

69 Scenarios/previous questions 689

Dr. K H Mozumder
 560

ICU
An Intensive Care Unit is a specially staffed & equipped ward dedicated for management of patients with life-threatening
illness, injuries or complications. 1950: concept from post-operative recovery or polio epidemic;
1960: developed from respiratory and cardiac care.

Role of an ICU:
1) Physiological optimization of patients to prevent the onset of organ failure.
2) Facilitation of complex surgery.
3) Support of failing organ system by providing-
 Intensive nursing
 Invasive and non-invasive monitoring
 Therapeutic measures otherwise not possible in ward level.
 Opportunity for live organ transplantation.

Different levels of ICU:

1) Level-1: -adult ICU
-district hospital
-like HDU; can provide CPR & short term cardiorespiratory support (<24 hr).
-Monitor or prevent complication of at risk pt (ECG).

2) Level-2: -Medical college/Divisional hospital

-Provide all sorts of multisystem life support.
-Has access to physiotherapy, pathology & radiological support facilities.
-No complex investigation & therapy like CT scan, MRI

3) Level-3: -Tertiary level hospital

-Provide all aspect of ICU service by referral system.
-Designed by specialists- intensivist, trainees, nurses.
-All sorts of investigation & therapies available at all times.

Types of ICU:
1) Multi-disciplinary; e.g. medical ICU, surgical ICU, Burn ICU, etc.
2) Uni-disciplinary; e.g. Neuro ICU, Cardiac ICU, etc.

OR,
1) Open:
 Have access to all doctors/specialists for admission and management of patients.
 The patients are managed & coordinated by anaesthetist group day to day & co-managed by referring specialist.
 Line of responsibilities are unclear.
2) Closed: Admission, mx, discharge and referral policies under the control of intensivist or critical care specialist.
3) Semi-open/Semi-closed

Trait Open ICU Closed ICU

Responsible physician A patient’s Primary physician is responsible An Intensivist is primarily
for full time ICU care. responsible for full time ICU care.

Consultancy Primary physician may consult with an No need, an intensivist is all in all.
intensivist.

Chance of nosocomial infection More Less

Referral system Good Lack of enough trained intensivist

Dr. K H Mozumder
 561

Design of ICU
1) Site: close proximity to relevant acute areas, i.e. operating rooms, emergency departments, CCU, labour wards and
investigation departments.

2) Size: ranges from 1 – 4 bed per 100 total hospital beds (depends on type, availability of HDU and admission policy)

3) Reception area: reception foyer + waiting room for visitors + distressed or interview room+ overnight relatives’ room.

4) Patient areas:
 Open multi-bed wards (Single Bed area 150 – 215 sq. feet)
 Single bed isolation room (Cubicle)
 Mixed 5 bed in cubicle
 Specialized rooms/beds if necessary for procedures/surgeries, hemodialysis, burns, use of IABP machines, etc.
 Utilities port for each patient bed:
 O2 port :3
 Medical air ports :2
 Suction port :3
 Electrical power outlet : 16
 Bed side light :1

5) Technical areas: laboratory & workshop for repairing, maintenance and development.

6) Central station:
 Communication, Monitoring, Drugs
 Storage of notes, radiographs
 Emergency trolley/ Crash cart
 Security control

7) Nurse 1:1
8) 24 hours on site dedicated cover by medical staff
9) An identifiable consultant
10) Staff areas: Lounge/rest rooms, changing rooms, conference rooms, etc.

Causes/Factors for increased incidence of infection in ICU

1) Variety of patients mixed in a closed environment.

2) Multiple working team/visitors.

3) Immunocompromization:
a) Poor local organ defenses:
 Respiratory
 Poor cough reflex
 Poor ciliary movement
 Poor laryngeal reflex
 Alimentary
 Organism converted to a part of flora
 Increased pH may colonize bacteria.
 Eye: loss of blinking drying of sclera  infection
 Genitourinary: Urinary catheterization

b) Poor body defenses:

 Depressed reticuloendothelial system
 Depressed cell mediated immunity
 Depressed humoral immunity

4) Structure of ICU:
 Closed environment
 Lack of well ventilation
 Lack of high efficiency particulate air (HEPA) system
 Inadequate humidification
 Cubicles/open space

Dr. K H Mozumder
 562

Modes of transmission of organisms

 Aerosolized droplets (> 5 microns)
 Airborne transmission (< 3 microns), usually viral.
 Contact transmission.

ICU admission criteria

1) Patient’s condition should be potentially reversible.
2) Patient requiring or likely to require endotracheal intubation and invasive mechanical ventilatory support.
3) Patient requiring support for ≥ 2 organ systems (e.g. inotropes, hemofiltration, etc.)
4) Patient with comorbidity who require support for acute reversible failure of another organ system.
5) Patient requiring optimum monitoring.
6) Patient with critical condition.

Levels of ICU care

Level 0
 Requires hospitalisation
 Patient’s needs can be met through normal ward care.

Level 1
 Patients recently discharged from a higher level of care
 Patients in need of additional monitoring/clinical interventions
 Patients requiring critical care outreach service support, clinical input or advice

Level 2
 Patients needing preoperative optimisation.
 Patients needing extended postoperative care.
 Patients stepping down to from level 3 care.
 Patients receiving single organ support including basic cardiovascular, renal or respiratory support

Level 3
 Patients receiving advanced respiratory support alone.
 Patients requiring a minimum of two organs supported.

Dr. K H Mozumder
 563

A critically ill pt can be recognized by following signs

Respiratory
1) Respiratory arrest
2) Threatened or obstructed airway
3) Stridor, intercostal recession, paradoxical breathing (seesaw)
4) RR <8 or >30 breaths/min
5) Respiratory distress: use of accessory muscle; unable to speak in complete sentences.
6) SpO2 <90% on high concentration oxygen
7) Rising PaCO2 >7 kPa (52.5 mmHg) or >2 kPa above normal with acidosis.

Cardiovascular
1) Cardiac arrest
2) Pulse rate <50 0r >150 bpm
3) SBP <90 mmHg; MAP <60 mmHg
4) Poor peripheral perfusion
5) Evidence of inadequate O2 delivery
6) Metabolic acidosis
7) Hyperlactataemia
8) Poor response to volume resuscitation
9) Urine output <0.5 ml/kg/Hour (check urea, creatinine, K+)

Neurological
1) Threatened or obstructed airway.
2) Repeated or prolonged seizures.
3) Absent gag or cough reflex
4) Failure to maintain normal PaO2 and PaCO2.
5) Failure to obey commands.
6) GCS <12
7) Sudden fall in level of consciousness (GCS by <2 points than previous)

Investigations requiring urgent corrective action include:

Blood sugar <80 or >600 mg/dl
Sodium <110 or >160 mmol/L
Potassium <2.5 or >6.0 mmol/L
pH <7.2
Bicarbonate <16 mmol/L

Dr. K H Mozumder
 564

I HUG FAST is a continuous quality improvement (CQI) checklist to ensure reliable application of evidence-based
measures to reduce complications in the ICU.
 Infection control
 Hand hygiene and head of bed elevation, Ulcer prophylaxis, Glycemic control
 Feeding, Analgesia, Sedation, Thromboprophylaxis

Assessment and initial resuscitation of critically ill patients:

a) Airway: Considering intubation and ventilation, if needed; more oxygen supplementation.

b) Breathing
 Assessment : -RR, Pattern of breathing, VT
-Chest auscultation
-Use of accessory muscles or not
-Chest wall movement symmetry

 Monitoring: SpO2, ABG, CXR

 Considering high concentration oxygen therapy and invasive or noninvasive MV.

c) Circulation
 Assessment: -Pulse, BP, signs & symptoms of shock
 Monitoring: -ECG
 Considering -large bore intravenous access
-volume resuscitation
-arterial cannulation
-central venous cannulation
-vasopressors may be needed.

d) Disability
 Assessment: -GCS
 Considering: -exclusion of hypoglycemia and reviewing airway, breathing and circulation.

e) Exposure & Evidence: Should look for targeted clinical examination and evidence, the information provided by any
recent investigations, prescriptions or monitoring sheets.

Dr. K H Mozumder
 565

C/F of impending respiratory arrest/distress:

 Breathlessness
 Marked tachypnea or hypoventilation, exhausted.
 Inability to talk
 Open-mouth breathing
 Flaring of ala nasi
 Use of accessory muscles of respirations
 Paradoxical breathing
 Cyanosis or desaturation, especially if on supplemental oxygen.
 Tachycardia or bradycardia if periarrest.
 Sweaty, cool/clammy peripheries
 Mental changes, confusion and lading to coma in extreme conditions.

C/F of inadequate oxygenation or ventilation:

(These are very late features of respiratory failure and imply impending cardiorespiratory arrest)
 Restlessness
 Delirium
 Drowsiness
 Cool extremities
 Cyanosis
 Tachycardia
 Arrhythmia
 Hypotension
 Flapping tremor (asterixis)

e-FAST = extended focused assessment with sonography in trauma

RUSH = rapid ultrasound for shock and hypotension
FATE = focus assessed transthoracic echocardiography.

VA ECMO = veno-arterial ECMO (for refractory cardiogenic shock)

VV ECMO = veno-venous ECMO (for refractory severe hypoxia in ARDS)

Dr. K H Mozumder
 566

Monitoring in ICU
a) Respiratory:
1. ABG & Pulse oximetry
2. Lung function: PaO2, P/F ratio, etCO2, airway pressure & VT for lung compliance & airway
resistance.

b) Circulatory:
1. Pulse; BP (NIBP, ABP); ECG; CVP
2. PAWP
3. Cardiac output; Urine output
4. Peripheral skin temperature
5. Blood lactate, [H+], Base excess & Base deficit.

c) Neurological: GCS, ICP, EEG

d) Renal: Clinical & Biochemistry
e) Hepatic: Clinical & Biochemistry

f) Homeostasis: Drug therapy, Anticoagulant & Thrombolytic

Components of chest physiotherapy

1. Administering aerosol.
2. Clearing pulmonary secretion.
3. Re-expansion of atelectatic alveoli.
4. Preserving normal lung function.

General care options for ICU pt:

1. Care of eyes, mouth, bowel-bladder & skin.
2. Posture changing- 2 hourly.
3. Chest & Limb physiotherapy.
4. Nutritional support.
5. Prophylactic antibiotic.
6. Prevention of stress ulcer.
7. DVT prophylaxis.
8. Sedation. And Analgesia.

Daily clinical mx of a pt in ICU

1) Review progress reports from nursing and medical staff and any specialist opinions.
2) Review of 24-hour charts.

3) General examination & specific examination including:

a) CVS: Haemodynamics, fluids, inotropes.
b) Respiratory: ventilator settings, ABGs.
c) GIT: nutrition, nasogastric aspirate, bowel function.
d) Renal: urine output, overall fluid balance, Urea, Creatinine, Electrolytes, RRT.
e) Neurological: sedation level, GCS, pupillary responses.

4) Laboratory reports
a) Hematological including coagulation & biochemistry.
b) Microbiological including culture and sensitivity.

5) Drug therapy response

6) Imaging
7) Monitoring
8) Assessment and plan

Dr. K H Mozumder
 567

Dr. K H Mozumder
 568

Pressure sore/Decubitus ulcer/Bed sore

Necrosis with ulceration due to pressure, usually over a bony prominence.
Stage-1: -Sore are not open wound.
-Skin may be painful but it has no breaks or tear.
-Reddened skin, doesn’t blanch.

Stage-2: -Skin breaks open, wears away or form an ulcer.

-Extend into deeper layer of skin.

Stage-3: -Extend into tissue beneath the skin.

-Fat may be seen in the sore but not muscle, tendon or bone.

Stage-4: -Very deep

-Extend into muscle, bone, joint or tendon.

In stage-3 & 4, there may be little or no pain due to significant tissue damage.

Usual sites: Ischium, greater trochanter, sacrum, heel, malleolus, occiput, etc.

Causes/Factors predispose to pressure sore:

1) Inadequate peripheral perfusion (Hypotension, PVD, use of vasopressor drugs).
2) Malnutrition, including minerals deficiency.
3) Reduced sensation.
4) Immunocompromization.
5) Inadequate posture changing.
6) Poor support of limbs.
7) Diarrhoea/urinary incontinence.
8) Systemic disease (DM)

Mx & prevention of pressure sore

1) Frequent posture changing- 2 hourly.
2) Adequate nutritional support.
3) Proper skin care.
4) Use of pneumatic bed (air mattresses which vary the pressure points continuously).
5) Raising the affected limb/area.
6) Regular dressing & clearing.
7) Negative pressure dressing (Vacuum-Assisted Closure).
8) Systemic antibiotic
9) Aquasil silver- apply locally (excellent healing)
10) Honey dressing

Dr. K H Mozumder
 569

Indications for tracheal intubation

ANAESTHETIC:
1) Restricted access to the pt, e.g. head and neck surgery, prone position.
2) To protect against tracheal soiling by gastric contents and blood, e.g. Dental, ENT and emergency surgery.
3) To secure the airway, e.g. in airway obstruction.
4) When muscle relaxation is required, e.g. abdominal surgery.
5) When IPPV is required, e.g. respiratory disease, cardio-thoracic surgery, neurosurgery and prolonged
surgery.

NON-ANAESTHETIC:
1) Protection of airway, e.g. in unconscious pts, impaired protective laryngeal reflexes, in airway obstruction.
2) Removal of sputum/secretions.
3) CPR
4) Respiratory arrest or RR <8 breaths/min
5) Tachypnoea >35 breaths/min
6) Inability to tolerate oxygen mask/CPAP/NIV; e.g. agitation, confusion.
7) Hypoxaemia (PaO2 <60 mmHg, SpO2 <90%) despite CPAP with FiO2 >0.6
8) Hypercapnia if conscious level is impaired or risk of raised ICP.
9) Worsening respiratory acidosis.
10) Removing the work of breathing in exhausted pts.

Contraindications for tracheal intubation:

1) Acute epiglottitis
2) Laryngeal edema
3) Laryngo-tracheo-bronchitis

Complications of tracheal intubation

A. During laryngoscopy and intubation:
1) Malposition: esophageal/bronchial intubation, laryngeal cuff position.
2) Airway trauma: dental damage; lip, tongue or mucosal laceration; sore throat; dislocated mandible;
retropharyngeal dissection.
3) Physiological reflexes: hypoxia, hypercarbia, HTN, tachycardia, raised ICP & IOP, laryngospasm.
4) Tube malfunction: cuff perforation.

B. While the tube is in place:

1) Malposition : unintentional extubation, bronchial intubation, laryngeal cuff position.
2) Airway trauma : mucosal inflammation and ulceration; excoriation of nose.
3) Tube malfunction : Fire/explosion; Obstruction.

C. Following extubation:
1) Airway trauma : edema and stenosis (glottic, subglottic or tracheal); hoarseness (vocal cord
granuloma or paralysis); laryngeal malfunction and aspiration.
2) Laryngospasm
3) Negative-pressure pulmonary edema.

Complications of laryngoscopy
1) Airway trauma: dental damage; lip, tongue or mucosal laceration; sore throat; dislocated mandible;
retropharyngeal dissection.

2) Physiological reflexes: hypoxia, hypercarbia, HTN, tachycardia, raised ICP & IOP, laryngospasm.

Dr. K H Mozumder
 570

Dr. K H Mozumder
 571

Muscle weakness in ICU patients

Potentially treatable causes:
1) Nutritional deficiency: prolonged catabolism with loss of muscle mass.

2) Electrolyte abnormalities: K+, Mg2+, PO43-

 Hypokalaemia
 Hypo- and hyper-magnesaemia
 Hypophosphataemia

3) Myasthenia gravis and myasthenic syndrome

4) Infection or post-infective polyneuropathy

 GBS
 Poliomyelitis (unlikely)

Non-treatable causes:
1) Polyneuropathy of critical illness
 Sepsis
 Multi-organ failure
 Burns
 Trauma
 Axonal degeneration of motor & sensory nerves

2) Disuse atrophy (prolonged assisted ventilation)

3) Prolonged (> 5 days)use of NMBA

4) Peripheral neuropathies due to DM, HIV/AIDS, and Alcohol abuse, etc.

5) Corticosteroid myopathy

6) Cervical cord pathology such as trauma, sepsis, vascular accident, etc.

Dr. K H Mozumder
 572

Advanced ventilation
Aims: To minimize further pulmonary damage due to barotrauma, volutrauma and biotrauma.

Strategies are:
1) Low tidal volume (4 – 6 ml/kg of IBW) and airway pressure as low as possible while achieving adequate
oxygenation.
2) Permissive hypercapnia (PaCO2 upto 60 – 70 mmHg).
3) Higher levels of PEEP to achieve adequate alveolar recruitment and oxygenation.
4) Prone ventilation
5) High-frequency oscillatory ventilation (HFOV)
6) Inhaled nitric oxide (NO)
7) Extracorporeal membrane oxygenation therapy (ECMO)
8) Corticosteroids [risks of secondary infection and muscle weakness]

Rescue therapies for refractory hypoxaemia in ARDS patient

1) Prone ventilation
2) High-frequency oscillatory ventilation (HFOV)
3) Inhaled nitric oxide (NO)
4) Extracorporeal membrane oxygenation therapy (ECMO)
5) Corticosteroids [though there are risks of secondary infection and muscle weakness]

Approaches for weaning from respiratory support

1) Spontaneous breathing trials (SBTs)
2) Progressive reduction in pressure support ventilation.
3) Individualized weaning plans, with regular periods of training followed by rest, to enable respiratory
muscles to regain strength.

SBTs involve
 Removing all respiratory support, typically on a daily basis.
 And observing how long the pt is able to breathe unassisted.

Signs of failure of SBTs

 Rapid shallow breathing
 Hypoxaemia
 Rising PaCO2
 Sweating
 Agitation

Dr. K H Mozumder
 573

Aims of respiratory support

1) To maintain the patency of the upper airway.
2) To correct hypoxaemia and hypercapnia.
3) To reduce the work of breathing (WOB).

Signs suggestive of failing tissue perfusion

 Tachycardia
 Confusion or diminished conscious level.
 Poor peripheral perfusion (cool, cyanosed extremities; poor capillary refill; poor peripheral pulses)
 Poor urine output (< 0.5 ml/kg/hr)
 Metabolic acidosis
 Increased blood lactate concentration

Causes of flapping tremor

1) Hypercapnia (type-2 respiratory failure)
2) Hepatic failure
3) Renal failure
4) Drug toxicity
5) Acute focal parietal or thalamic lesions.

Dr. K H Mozumder
 574

Mechanical ventilation
MV is any means in which physical devices or machines are used to either assist or replace spontaneous respiration. When it
is continued for >21 consecutive days for >6 hours/day, then it is called prolonged mechanical ventilation.

Types:
1) Negative pressure ventilation (Tank ventilator, Iron lung, Cuirass ventilator)
2) Positive pressure ventilation

GOALS: -To treat hypoxaemia

-To treat acute respiratory acidosis
-Relief of respiratory distress
-Prevention or reversal of atelectasis
-Providing rest to ventilatory muscles.

RED FLAGS for pending intubation:

RR >25 b/min
PaCO2 >50 mmHg
PaO2 <50 mmHg
SpO2 <90%

General indications for MV:

1) Need for high levels of inspired oxygen e.g. hypoxic respiratory failure.
2) Need for assisted ventilation e.g. hypercapnic respiratory failure; surgical procedures.
3) Protection of airway against aspiration.
4) Relief of upper airway obstruction.

Dr. K H Mozumder
 575

Indications for artificial/controlled/mechanical ventilation:

A. Clinical signs and conditions
1) Postoperative: after major abdominal, cardio-thoracic or neurosurgery operations.

2) Respiratory failure: -ARDS, ALI

-Acute severe asthma
-Acute pneumonia
-Aspiration pneumonitis
-acute exacerbation of COPD
-Smoke inhalation & Burn

3) Circulatory failure: -Cardiogenic shock

-Pulmonary edema
-Post-cardiac arrest resuscitation

4) Neurological diseases:-Coma of any cause

-Status epilepticus
-Drug overdose
-respiratory failure due to muscle failure, e.g. GBS, Poliomyelitis, Myasthenia gravis
-Head injury (to avoid hypoxaemia and hypercapnia and to reduce ICP)
-Bulbar abnormalities causing risk of aspiration (e.g. stroke)

5) Multiple trauma

B. Respiratory parameters:
1) Direct measurements: PaO2 <50 mmHg on room air
PaCO2 >50 mmHg in absence of metabolic alkalosis

2) Derived indices: PaO2/FiO2 ratio <300 mmHg

(A-a)O2 gradient >350 mmHg [A–a gradient = PAO2–PaO2; normally <15 mmHg
but
progressively increases with age upto 20–30 mmHg]
VD/VT >0.6

3) Clinical indices: RR >35 or <8 breaths/min

4) Mechanical indices: VT <5 ml/kg

Vital capacity <15 ml/kg
Maximum inspiratory pressure >-25 cmH2O

Dr. K H Mozumder
 576

Complications of mechanical ventilation

1) During intubation
 Injury to teeth, mouth and bleeding.
 Esophageal & Bronchial intubation
 Obstruction of tube due to kinking or secretion

2) Complication of positive pressure ventilation

 Pneumothorax, Barotrauma
 ↑ ICP; ↓ Cardiac output
 Altered gas exchange

3) Complication of artificial ventilation

 Hypo-/hyperventilation, apnoea
 O2 toxicity
 Ventilator disconnection
 Nosocomial infection
 Aspiration

4) Late complications: laryngeal injury, tracheal narrowing, tracheomalacia, sinusitis etc.

Complications of prolonged artificial ventilation

 Microaspiration of oral secretions or feed.
 Pressure from the tracheal cuff can cause ischaemic damage to the underlying tracheal mucosa.

Complications of prolonged stay in ICU

Dr. K H Mozumder
 577

MODE
The method by which the patient and the ventilator interact to perform a ventilatory cycle is called the
mode.

They include:
1) CMV Continuous/Controlled mandatory/mechanical ventilation (the simplest form)
2) ACV Assist control ventilation
3) IMV Intermittent mandatory ventilation
4) SIMV Synchronized intermittent mandatory ventilation
5) MMV Mandatory minute ventilation
6) PCV Pressure control ventilation
7) PSV Pressure support ventilation
8) IRV Inverse I:E ratio ventilation
9) APRV Airway pressure release ventilation
10) HFV High frequency ventilation
11) DLV Differential lung ventilation

Spontaneous ventilatory modes:

 Pure spontaneous
 CPAP
 PSV
 Volume Target Pressure Support Ventilation

In controlled ventilation, the ventilator initiates the breath and perform all the work of breathing (WOB).

In assisted ventilation, the pt initiates or terminates all or some of breathing with variable amount of support
from ventilator.

Inverse ratio ventilation is the ventilation in which the inspiratory phase time is longer than the expiratory phase time.

Alveolar gas equation, PAO2 = FiO2 (Patm – PH2O) – PaCO2/RQ

= FiO2 (760 – 47) – PaCO2/0.8

Dr. K H Mozumder
 578

Cycling
Inspiratory to expiratory change over or the mechanism that cycle ventilation from inspiratory to expiratory
phase is called cycling.

4 phases of respiratory/ventilatory cycle include:

1) Inspiration
2) Inspiration to expiration change over
3) Expiration
4) Expiration to inspiration change over

Initial ventilator settings

1) FiO2 : starting with 0.7 – 1, then gradually reducing to 0.5

2) VT : 6 – 10 ml/kg, greater than spontaneous ventilation VT (5 – 8 ml/kg)

3) RR : 12 – 20 breaths/min

4) Sensitivity : Pressure triggering initial setting: -2 cmH2O

High sensitive: auto cycling
Low sensitive: Lock out

Flow triggering  0.5 of base flow (L/min)

5) Flow rate (Speed with which the VT is delivered): 40 – 60 L/min

If not adjusted properly causes air hunger, increased WOB.
If flow rate is increased ↓ TINS (helps in COPD); ↑TEXP (causes turbulence & ↑ PIP)
If flow rate is decreased ↑ TINS, ↓TEXP, flow becomes laminar, ↓PIP (helpful in ARDS)

6) I:E ratio: ↓ I: E ratioapplied in COPD (air trapping)

↑ I: E ratio (inverse) applied in ARDS

7) Sigh: (1.5 × VT), prevent small airway closure, 10/hour

8) PEEP : 5 – 20 cmH2O

PIP is the maximum pressure during the inspiratory phase time, and it provides an indication of dynamic
compliance.

Plateau Pressure is the resting pressure measured during the inspiratory pause (a time of no gas flow), and it
mirrors static compliance. Airway pressure usually falls when there is an inspiratory pause. This lower pressure
is called the plateau pressure.

Dr. K H Mozumder
 579

Non-Invasive Ventilation (NIV)

It is a ventilatory support by nasal or full face-mask. It can be delivered by:
1) A simple BiPAP turbine ventilator
2) A complex ICU ventilator using a simple breathing circuit with a leak.

Uses:
 First-line therapy in patients with type-2 respiratory failure secondary to acute exacerbation of COPD.
 It can also be used to support selected patients with hypercapnia secondary to pulmonary edema or
pneumonia or during weaning from invasive ventilation.

Dr. K H Mozumder
 580

PEEP
Application of positive pressure (5-20 cmH 2O) during expiration as an adjunct to mechanically delivered breath
is referred as PEEP (Positive End Expiratory Pressure).

Indications: Atelectasis, ARDS, Pulmonary edema.

Relative contraindications
 Unilateral lung disease.
 Pneumothorax
 Hypovolaemia
 Intracardiac shunt
 Obstructive lung disease
 Raised ICP

Advantages
1) Recruits atelectatic alveoli.
2) Counteracts small airway closure.
3) Redistributes lung water.
4) ↓ Intrapulmonary shunt
5) Maintains FRC
6) Improves lung compliance
7) ↑ Oxygenation

Disadvantages:
1) Haemodynamic instability due to increased intrathoracic pressure at higher PEEP (↓ cardiac output, ↓BP)
[Decreased venous return due to increased Right atrial pressure and Increased Pulmonary Vascular
Resistance causes Right ventricular pressure overall impaired diastolic filling of Left ventricle]
2) Barotrauma
3) ↑ ICP
4) ↓ Hepatic and renal blood flow.
5) If intrinsic PEEP is high, the concentration of additional extrinsic PEEP can become crucial as there is a
potential risk of sustained lung hyperinflation if external PEEP is greater than the concentration of intrinsic
PEEP.

Dr. K H Mozumder
 581

CPAP
Continuous Positive Airway Pressure (CPAP) is defined as ventilation that maintains the airway pressure
above ambient throughout the patient’s breathing cycle. The term is commonly used in reference to
spontaneous ventilation.

 Pt must have the drive to produce adequate VT.

 Pt must be cooperative, able to protect the airway.

 Pt must have the strength to breathe spontaneously and cough freely.

 High flow (inspiratory) gas source is provided.

 Airway pressure never touch baseline.

 CPAP pressure should be 5 – 10 cmH2O (less than lower esophageal sphincter pressure)

Methods
 Tightly fitting full face mask
 Nasal mask
 High-flow nasal cannula
 Nasal pillows (Adam’s circuit)
 Nasal prongs (for neonate)
 Hoods

Indications
 Hypoxaemia due to decreased lung volume secondary to abdominal or thoracic surgery (hypoventilation)
 ARDS
 Pulmonary edema
 Pulmonary atelectasis (post-operative)
 Sleep apnoea syndrome

Advantages
1. Increased FRC & VT.
2. Prevent alveolar collapse.
3. Increased oxygenation (helps correct hypoxaemia).
4. Increased muscle strength.
5. Decreased intrapulmonary shunting.
6. May be alternated with SIMV during weaning.
7. Monitoring of Expiratory VT and apnoea alarm prevent hypoxia.
8. Reduce WOB and improve hypercapnia in type-2 respiratory failure.

Disadvantages
1. Increased intrathoracic pressure causes decrease in venous return.
2. Decreased cardiac output.
3. Increased ICP.
4. Barotrauma.
5. Decreased hepatic and renal blood flow.
6. Decreased urinary output & GFR.

Dr. K H Mozumder
 582

BiPAP
 Bi-level Positive Airway Pressure (Turbine ventilator).
 iPAP= 15 – 25 cmH2O
 ePAP= 4 – 10 cmH2O

Dr. K H Mozumder
 583

Weaning
The process of withdrawing a patient from ventilator support in a staged manner is called weaning. It is a
dynamic process

Pathophysiology of weaning failure

1) Respiratory muscle fibres are of two types:
 Slow (type-I)/Endurance : prolonged performance; resistant to fatigue; e.g. quite breathing.
 Fast (type-II)/Strength : rapid contraction for short term.

2) Muscle fatigue signs are: ↑RR, ↓VT, ↑VE, ↓Vital capacity, paradoxical respiration

3) Increased demand of energy: e.g. ↑resistance, ↓compliance, hypoxaemia

4) Decreased supply of energy: e.g. hypoxaemia, anaemia, electrolyte imbalance, ↓cardiac output.

Methods of weaning
1) SIMV
2) PSV
3) SBT (Spontaneous Breathing Trial) BiPAP, CPAP, T-piece
4) SIMV + PSV

Readiness for weaning

A. RESPIRATORY parameters:
1) Oxygenation: PaO2 > 70 mmHg
FiO2 < 0.5
P/F ratio > 200 mmHg
QS/QT < 20%
PEEP ≤ 8 cmH20

2) Ventilation: PaCO2 35 – 45 mmHg

pH 7.35 – 7.45 (no ongoing respiratory/metabolic acidosis)
VD/VT < 0.6

3) Ventilatory demand: VE > 5 L/min but <10 L/min

4) Respiratory mechanics:
 Endurance: Maximum Voluntary Ventilation (MVV): twice VE
VT > 5 ml/kg

 Strength: Vital capacity: 10 – 15 ml/kg

Maximum inspiratory pressure (MIP) : <-20 cmH2O

5) Respiratory frequency & patterns: RR < 25 breaths/min; RSBI <105 breaths/min/L

6) Lung compliance: CST 70 – 100 ml/cmH2O; CDYN 50 – 80 ml/cmH2O

B. Stable cardiovascular function with minimal requirements for inotropic or vasopressor drugs.
C. Appropriate mental status: pt is arousable or GCS ≥13
D. OTHERS:
 Patient should be awake and co-operative with intact neuromuscular and bulbar function.
 Primary pathology should have resolved.
 Precipitating illness and complicating factors adequately treated.
 Low sputum production.
 Minimal sedation with absence of severe pain.
 Adequate nutritional status.
 No fever.
 No significant electrolyte imbalance.

Dr. K H Mozumder
 584

Spontaneous breathing trial (SBT):

Weaning from the ventilator includes a few forms of partial ventilatory support. SBT is one of these. This
involves allowing the patient to breathe spontaneously with the application of PEEP only, ideally for 30 min and
up to a maximum of 2 h.

A successful spontaneous breathing trial usually indicates that tracheal extubation will be successful, and if not,
a repeat trial can be performed daily.

A gradual form of weaning is to allow a short period of spontaneous breathing without ventilatory assistance
(e.g. initially 1–5 min) with close observation and monitoring of the patient. The duration and frequency of
these trials is increased as the patient’s condition improves.

Disadvantages of IRV:
Increased gas trapping
Decreased venous return/cardiac output

Dr. K H Mozumder
 585

Pneumonia

Pneumonia is an acute respiratory illness associated with recently developed radiological pulmonary shadowing,
which may be segmental, lobar or multilobar.

Or,
Pneumonia is an inflammation of the pulmonary substances of the lungs.

It may be classified as:

Clinically  CAP
 HAP
 Pneumonia occurring in immunocompromised patients
 Pneumonia occurring in patients with underlying
damaged lung (including suppurative and aspirational
pneumonias)

Site involved Lobar pneumonia Homogenous consolidation

of one or more of the lung
lobes, often with associated
pleural inflammation.

Bronchopneumonia More patchy alveolar

consolidation associated
with bronchial and
bronchiolar inflammation,
often affecting both lower
lobes.

Aetiology Infective Bacterial, viral, parasitic,

fungal
Chemical induced
Radiotherapy induced
Allergic

Inflammatory response in lobar pneumonia evolves through following stages:

Congestion Alveolar units are flooded by a proteinaceous exudate, neutrophils, RBCs and pneumococci.

Red hepatisation Fibrin forms on the cut surfaces of the affected lobe and it resembles liver.

Grey hepatisation Congestion resolves and lung tissues become grey.

Resolution Clearance and repair mechanisms restore the normal architecture of the lung.

Dr. K H Mozumder
 586

Hospital-acquired or nosocomial pneumonia is a new episode of pneumonia occurring at least 2 days after
admission to hospital. It is the second most common hospital-acquired infection (HAI) and the leading cause of
HAI-associated death. The elderly are particularly at risk, along with patients in intensive care units, especially
when mechanically ventilated (VAP).

Healthcare-associated pneumonia (HCAP) is the development of pneumonia in a person who has spent at least
2 days in hospital within the last 90 days, or has attended a hemodialysis unit, received intravenous antibiotics,
or been resident in a nursing home or other long-term care facility.

Factors predisposing to development of hospital acquired pneumonia:

1) Reduced host defences against bacteria
 Reduced immune defences (e.g. corticosteroid treatment, diabetes, malignancy)
 Reduced cough reflex (e.g. post-operative)
 Disordered mucociliary clearance (e.g. anaesthetic agents)
 Bulbar or vocal cord palsy

2) Aspiration of nasopharyngeal or gastric secretions

 Immobility or reduced conscious level
 Vomiting, dysphagia (N.B. stroke disease), achalasia or severe reflux
 Nasogastric intubation

3) Bacteria introduced into lower respiratory tract

 Endotracheal intubation/tracheostomy
 Infected ventilators/nebulisers/bronchoscopes
 Dental or sinus infection

4) Bacteraemia
 Abdominal sepsis
 IV cannula infection
 Infected emboli

Dr. K H Mozumder
 587

Ventilator-associated pneumonia (VAP)

Ventilator-associated pneumonia (VAP) is a common nosocomial infection characterized by a new or

progressive infiltrate in the chest X-ray along with fever and leukocytosis in patients receiving mechanical
ventilation for more than 48 h.

This can be attributed partly to the prevalence of infection with MDR pathogens like Enterobacter,
Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa and
Enterobacteriaceae (ESKAPE bugs).

Mortality is in the order of 30%.

Pathophysiology:Free passage of pathogens into lungs-

1) Through endotracheal tube (ETT) in a person with underlying lung or immune problem.
2) By droplet through ETT and around cuff.
3) By deep suctioning.

D/Ds of VAP:
Atelectasis
Aspiration
Pulmonary embolism with infarction
Pulmonary hemorrhage
Cardiogenic pulmonary edema
ARDS
Fluid overload
Hypersensitivity pneumonitis
Drug reactions: cyclophosphamide, methotrexate
Cryptogenic organizing pneumonia (H/O recent viral infection)
Radiation pneumonitis
Lung contusion

Risk factors predisposing to VAP:

Patient related Extremes of age
Cardiovascular diseases
ARDS
MODS
Coma

Ventilator related Duration of IPPV > 7 days

Tracheal cuff pressure <20 cmH2O
Reintubation
Tracheostomy

General ICU care related Supine position

Invasive monitoring devices
Aspiration of gastric contents
Indiscriminate use of broad spectrum antibiotics

Dr. K H Mozumder
 588

Dx of VAP:
There is no gold standard for diagnosis. Clinical scores use focal infiltrates on chest x-ray increased FiO 2
requirements, sputum production, temperature, and inflammatory markers to suggest the presence of VAP.

The modified clinical pulmonary infection score (CPIS) at baseline is calculated from the first five variables.
For positive Gram stain and culture, two points are added to the CPIS baseline score. A score of more than six at
baseline or after incorporating the Gram stain or culture result is considered suggestive of pneumonia. CPIS has
low sensitivity and specificity for diagnosing VAP.

Dr. K H Mozumder
 589

Mx:
Pertinent history taking, physical examination, sending investigations and resuscitation need to be carried out
simultaneously.

1) The patient should be resuscitated with

- Airway,
- Breathing,
- Circulation & Consciousness

2) Sending paired blood culture and endotracheal aspirate or bronchoalveolar lavage (BAL) for Gram stain
and quantitative aerobic culture.

3) Starting empiric antibiotic therapy for suspected infection following local guidelines and it should cover for
MRSA with linezolid or vancomycin.
4) Sending further investigations
 FBC
 Serum Procalcitonin
 C-reactive protein (CRP)
 Urea, creatinine
 Serum electrolytes
 Prothrombin time
 Blood culture—two sets (if not sent earlier)
 Endotracheal aspirates or fiberoptic bronchoscopy with protected specimen brush (PSB) or
bronchoalveolar lavage (BAL) (in selected cases like immunosuppressed)
 Arterial blood gas, lactate
 Urine for microscopy
 Chest X-ray
 ECG or echocardiogram (optional) if the patient is in septic shock

5) De-escalation of antibiotic when a causative pathogen is identified.

6) Prevention of VAP in the ICU.

A paired blood culture setwas defined as two separate sets of blood cultures drawn from different peripheral
venous sites or two separate sets of blood cultures where one was taken from a peripheral site and the other from
a central catheter.

Selective decontamination of the digestive tract (SDD) is a technique designed to eradicate aerobic, potentially
pathogenic bacteria colonising the oropharynx and upper gastrointestinal tract, thus eliminating an important
risk factor for nosocomial pneumonia. It has not been widely adopted because of its inconsistent effects on
mortality and concerns about the potential for selecting antibiotic-resistant pathogens.

Dr. K H Mozumder
 590

Prevention of VAP:
Pharmacological methods Non-pharmacological methods
1) Scrupulous hand hygiene with alcohol 1) Use of noninvasive mask ventilation
based solution

2) Good oral care with chlorhexidine 2) Avoid reintubation

3) Short course of antibiotic therapy (when 3) Orotracheal and orogastric intubation

clinically applicable)

4) Management without sedation whenever 4) Use of heat moisture exchanger

possible or interruption of sedation daily

5) Restricted blood transfusion 5) Closed endotracheal suction

6) Vaccines (influenza and pneumococcal) 6) Subglottic secretion drainage

7) Prophylactic probiotic 7) Automated control of endotracheal tube cuff pressure

8) Mechanical tooth brushing

9) Ultrathin polyurethane endotracheal tube cuff

10) Saline installation before endotracheal suctioning

11) Change of ventilator circuit only for each new patient

12) Nursing the patient semirecumbent

13) Shortening duration of mechanical ventilation (assess

readiness to extubate daily/perform spontaneous
breathing trials with sedatives turned off/facilitate early
mobility)

14) Adequate intensive care staffing

15) Use of ICU care bundles

16) Education and training

Dr. K H Mozumder
 591

Mechanisms of respiratory failure:

Reduced central drive Airway obstruction Neuromuscular defects
 Brainstem injury Tumour  Spinal cord lesion
 Stroke Infection  Phrenic nerve disruption
 CVA Sleep apnoea  GBS, Myasthenia Gravis, MND, MS
 CNS trauma Foreign body  Poliomyelitis
 SAH  Critical illness polyneuropathy
 Drug effects (e.g. opioids)  Electrolyte disorder (Hypophosphataemia,
 Metabolic encephalopathy Hypomagnesaemia, Hypokalaemia)

Musculoskeletal Gas exchange unit dysfunction

& pleural function  Pulmonary contusion
 Trauma  Pulmonary edema
 Severe scoliosis  Pneumonia
 Flail chest  ARDS
 Pleural effusion  Aspiration
 Pneumothorax  ILD/DPLD
 Haemothorax  Near drowning
 Smoke inhalation

Dr. K H Mozumder
 592

Respiratory Failure
It may be defined as impairment of normal gas exchange severe enough to require acute therapeutic
interventions.

The term respiratory failure is used when pulmonary gas exchange fails to maintain normal PaO 2 & PaCO2
levels.

Respiratory failure is defined as inadequate gas exchange by the respiratory system with the result of
hypoxaemia (PaO2 <60 mmHg) with or without hypercapnia (PaCO2 >50 mmHg).

Types of respiratory failure

A. According to presence or absence of hypercapnia
1) Type-I: Only hypoxaemia
(Failure of oxygenation due to V/Q mismatch) PaO2↓
PaCO2 normal or ↓
A-aDO2 ↑

2) Type-II: Hypoxaemia with hypercapnia

(Alveolar hypoventilation) PaO2↓;
PaCO2 ↑;
A-aDO2 normal;
pH ↓

B. According to onset/duration/relation of PaCO2 with pH

1) Acute RF : pH usually decrease.
2) Chronic RF : pH usually normal.

Causes of
Type-I RF Type-II RF
 High altitude (low ambient O2)  COPD
 Pneumonia  Reduced respiratory drive, e.g. drug overdose, head
 Pulmonary edema injury
 Pulmonary embolism  Upper airway obstruction e.g. edema, infection, FB
 Pulmonary fibrosis  Late severe acute asthma
 Pulmonary contusion (blunt chest  Peripheral neuromuscular diseases, e.g. GBS,
trauma) Myasthenia gravis
 Pneumothorax  Flail chest injury
 Bronchial asthma  Exhaustion
 ARDS, Aspiration, Lung collapse

Dr. K H Mozumder
 593

Principal goals in the Mx of acute respiratory

failure are:
1) Maintenance of a patent upper airway
2) Correction of hypoxaemia
3) Removal of excess carbon dioxide
4) Rx of cause.

Dr. K H Mozumder
 594

Mx of Type-I RF

C/F:
1) Stimulation of carotid body chemoreceptor leading to dyspnoea, tachypnoea and hyperventilation.

2) Central or peripheral cyanosis

3) Hypoxic effect: alteration of mental status

 Seizure, Somnolence
 Coma, Permanent hypoxic brain damage

4) Sympathetic nervous system stimulation leading to tachycardia, diaphoresis, systemic vasoconstriction and
hypertension.

5) In the severe form of respiratory failure:

 Bradycardia
 Vasodilation
 MI
 Arrhythmia
 Cardiac failure

INV:
1) ABG (Hypoxaemia)
2) X-ray chest

Rx:
1) Maintenance of airway.
2) High flow oxygen therapy
3) Nebulized bronchodilators; Corticosteroids
4) Leukotriene receptor antagonist: Montelukast
5) Respiratory stimulant
6) Treatment of specific precipitating cause.
7) Frequent physiotherapy.
8) Pharyngeal suction, if needed.
9) Antibiotics (if there is evidence of infection).

Dr. K H Mozumder
 595

Mx of Type-II RF
C/F:
1) Central cyanosis
2) Depressed consciousness level
3) Warm periphery
4) Full bounding pulse
5) Flapping tremor/asterixis
6) Vasodilation
7) Wheeze, prolonged expiration, Hyperinflation, intercostal drawing, pursed lips.
8) Peripheral oedema, raised JVP, Hepatomegaly, ascites

INV:
1) ABG (Hypoxaemia, Hypercapnia and Acidosis)
2) X-ray chest

Rx:
1) Maintenance of airway
2) Treatment of specific precipitating cause
3) Controlled oxygen therapy (low flow) 24 – 28%
 Start with 24% controlled-flow venturi mask.
 Aim for a PaCO2 >7 kPa (52 mmHg); a PaCO2 <5 kPa (37 mmHg) is dangerous.

4) Nebulized bronchodilators
5) Frequent physiotherapy
6) Pharyngeal suction, if required.
7) Antibiotics (if there is evidence of infection)
8) Diuretics (if there is evidence of fluid overload)

Monitoring of a pt with respiratory failure:

 ABG
 Capnography
 Lung function (PaO2, PaO2: FiO2 ratio)
 Airway pressure
 V/Q mismatch
 VD/VT ratio

Trait Cardiogenic edema Non-cardiogenic edema

1) Prior H/O heart disease Yes No

2) 3rd heart sound Yes No

3) Cardiomegaly Present Absent, normal sized heart

4) Distribution of infiltrates Central Peripheral

5) Width of vascular pedicle Widening Normal width

6) PAWP Increased Normal or decreased

7) Fluid balance Positive Negative

Dr. K H Mozumder
 596

Dr. K H Mozumder
 597

Acute Lung Injury

Acute lung injury (ALI) is a spectrum, with non-cardiogenic pulmonary edema at the mild and ARDS at the
severe end. A PaO2/FiO2 ratio < 300 mmHg is suggestive of ALI, though this term is obsolete now by the 2012
Berlin guidelines of ARDS.

ARDS
Sponge lung, shock lung, non-cardiogenic pulmonary edema, capillary leak syndrome, traumatic wet lung, &
adult hyaline membrane disease.

Berlin definition of ARDS (2012)

1) Onset within one week of a known clinical insult, or new or worsening respiratory symptoms.

2) Bilateral opacities on chest x-ray, not fully explained by effusions, lobar/lung collapse or nodules.

3) Respiratory failure not fully explained by cardiac failure or fluid overload. Objective assessment (by
Echocardiography) must exclude hydrostatic edema if no risk factor is present.

4) Impaired oxygenation:

Mild PaO2:FiO2 >200 mmHg but ≤300 mmHg with PEEP or CPAP ≤5 cmH2O

Moderate PaO2:FiO2 >100 mmHg but ≤200 mmHg with PEEP ≤5 cmH2O

Severe PaO2:FiO2 ≤100 mmHg with PEEP ≤5 cmH2O

Conditions predisposing to ARDS

Inhalational (direct) Blood-borne/Indirect/Extra-pulmonary
 Aspiration of gastric contents  Sepsis
 Toxic gas/burn injury  Necrotic tissue, particularly bowel.
 Pneumonia  Fluid overload
 Blunt chest trauma  Multiple trauma/major trauma
 Smoke inhalation & Near drowning  Severe burns
 Pneumocystis jiroveci and viral pneumonia  Acute pancreatitis
 Pulmonary contusion  Cardiopulmonary bypass
 Air, fat and amniotic fluid embolism  Carcinomatosis
 Drug overdose- Bleomycin, salicylate  Drugs (heroin, barbiturates, thiazide)
 Radiation  Major transfusion reaction
 Anaphylaxis
 Fat embolism
 Obstetric crises (amniotic fluid embolism, eclampsia)

Dr. K H Mozumder
 598

Pathophysiology of ARDS
Damage of either lung epithelium or endothelium due to direct insult on lung cells or indirect effect resulting
from systemic inflammation.
↓
Sequestration of neutrophil and macrophages in pulmonary capillaries with the release of oxygen free radicals
(OFRs), proteases and leukotrienes.
↓
Increased capillary permeability (capillary leak syndrome)
↓
Damage of type-II pneumocytes leading to surfactant depletion
↓
Exudation & accumulation of protein rich cellular fluid within alveoli (alveolar flooding) and formation of
‘hyaline membranes’.
↓
Combination of loss of surfactant and fluid accumulation leading to ventilation impairment.
↓
V/Q mismatch
↓
Increased intra-pulmonary shunt
Inflection point is defined as the pressure level on a pressure –
↓ volume curve at which collapsed alveoli are recruited (opened) and
Hypoxaemia.
with small changes in pressure, large changes in volume take place.

The principal M/A for both PEEP and CPAP appears to be expansion
of partially collapsed alveoli & this recruitment (re-expansion) of
collapsed alveoli occurs at PEEP or CPAP levels above the inflection
point.

C/F of ARDS
 H/O predisposing factors
 Acute onset
 Unexplained tachypnoea
 Sever breathlessness and labored respirations.
 Central cyanosis
 Fine crepitation throughout both lung fields.

D/Ds of ARDS
 Cardiogenic pulmonary edema
 Diffuse pneumonia
 Alveolar hemorrhage
 Acute interstitial lung diseases
 Acute immunologic injury (e.g. hypersensitivity, pneumonia)
 Toxin injury e.g. radiation, etc.
 Neurogenic pulmonary edema.

Dr. K H Mozumder
 599

Diagnostic criteria of ARDS

 Hypoxaemia, defined as P:F ratio < 200 mmHg.[When hypoxaemia is resistant to O 2 therapy alone is called
refractory hypoxaemia]

 Chest x-ray showing diffuse non-homogenous bilateral infiltrates (cotton wool appearance); dependent
areas tend to be most affected.

 Absence of raised LVEDP or, PCOP <15 mmHg [normal 3 – 12 mmHg]

 Impaired lung compliance (≤50 ml/cmH2O)

 Acute onset (usually 2 – 3 days of the predisposing event).

Phases of ARDS
Exudative 1 week ↑RR, ↓PaO2, dyspnoea; CXR diffuse infiltrates

Proliferative Early in the 2nd Replacement of fibrin and cell debris by collagen.
week ↑PaCO2, persistent hypoxaemia,
CXR diffuse infiltrates + air bronchogram.

Fibrotic After 10 days CXR linear opacity with fibrosis

Permanent scarring

Characteristic CXR findings of cardiogenic pulmonary edema:

1) Patchy infiltrates from the hilum
2) Prominent pleural effusions
3) Cardiomegaly and cephalization.

Investigations for ARDS

 CXR
 ABG
 BAL (broncho-alveolar-lavage)
 Echo
 HRCT of chest
 FBC
 Others: urea-creatinine-electrolytes; LFT; S. acute phase protein

Investigations for monitoring an ARDS pt in ICU

 Routine investigation as dictated by clinical condition.
 Consider repeat CXR daily.
 Daily creatine kinase level (especially for paralyzed pt).
 Monitor inflammatory markers (CRP, WBC count)
 Echo
 12-lead ECG

Dr. K H Mozumder
 600

Rx of ARDS
1) GENERAL mx:
 Early recognition and treatment of underlying medical and surgical disorders (e.g. sepsis, aspiration,
trauma, etc.)
 Empirical treatment of sepsis when indicated and of secondary nosocomial infection.
 Good nutritional support.
 Strict glycemic control.
 Prophylaxis against DVT, GIT bleeding and central venous catheter infections.
 Other general care- stress ulcer prevention, physiotherapy, etc.
 Minimizing procedures and their complications.
 Use of sedatives and NMBA
 Haemodynamic management

2) Oxygen therapy: target SpO2 >90% or PaO2 >60 mmHg and reduce FiO2 ≤0.6 to prevent toxicity.

3) Ventilatory support:
 When CPAP fails, IPPV with high PEEP

 Lung protective strategies to counteract both pathophysiology of ARDS & ventilator associated lung
injury:
a) Low tidal volume (4 – 6 ml/kg of IBW)
b) Permissive hypercapnia (Low VT ventilation with elevated PaCO 2 upto 70 mmHg with pH
>7.2).
c) Inverse I:E ratio
d) Use of higher PEEP (to improve alveolar recruitment, limit atelectasis and reduce
hypoxaemia)
e) FiO2 < 0.6

4) Prone ventilation may improve oxygenation.

5) Vasodilator drugs (NO, prostacyclin) to reduce pulmonary vascular resistance.

6) Fluid restriction and use of diuretics

7) Corticosteroids may have some role in refractory ARDS.

8) Free radical scavenger, anti-prostaglandins and anti-proteases may have some role.

Adverse effects of PEEP in ARDS:

 Decrease venous return
 Decrease cardiac output
 Impaired ventilator performance
 Increased pulmonary vascular resistance
 Decrease left ventricular compliance
 May cause barotrauma.

Causes of iatrogenic lung injury in ARDS:

1) Increased Pplt >30 cmH2O
2) Increased VT >6 ml/kg and
3) Increased FiO2 >0.5

First two factors cause over distension of alveoli.

Morbidity/mortality from ARDS take place usually from the precipitating cause or complications like sepsis,
renal failure, gastrointestinal hemorrhage, etc.
Dr. K H Mozumder
 601

Prone positioning
 The volume of the lung compressed by the mediastinal structures decreases.
 Pleural pressure becomes more uniform.
 Ventilation-perfusion mismatch is reduced.
 Improve gas exchange
 Reduce ventilator induced lung injury (VILI)
 Recruitment of collapsed lung field by redistribution of edema.
 Increased diaphragmatic motion enhances ventilation.

The evidence base is mixed; it appears to depend on the specific cohort of patients, timing and duration of prone
therapy.

Care bundles

Care bundles consist of a number of evidence-based practices each of which has been found to improve outcome
and are easily achievable. When performed collectively, reliably and continuously these bundles confer a greater
probability of survival.

There is an increasing evidence for the utility of care bundles for specific conditions in the intensive care setting.

The most familiar bundles are the Surviving Sepsis campaign resuscitation (6 h) and management (24 h)
bundles and ventilator care bundles.

The ventilator care bundle comprises the following components to reduce VILI or ALI or ARDS:
 Low tidal volumes (4 – 6 ml/kg of ideal body weight)
 Plateau airway pressure less than 30 cmH2O
 Limiting peak inspiratory pressure to 30 cmH2O
 Sedation holds and use of sedation scores
 Permissive hypercapnia (acceptance of higher than normal PaCO2 with pH > 7.2)
 Acceptance of PaO2 7 – 8 kPa, SaO2 >90%
 Semirecumbent positioning (head up by 30 – 45 degrees unless contraindicated) during ventilation to
reduce the incidence of VAP
 Lung recruitment using higher PEEP to prevent alveolar collapse
 Use of longer inspiratory times as with IRV or airway pressure release ventilation (APRV)
 Using ventilation modes that allow and support spontaneous respiratory effort.
 Avoidance of NMBAs
 Protocol-driven weaning

Dr. K H Mozumder
 602

Dr. K H Mozumder
 603

Universal precautions against infectious diseases (HIV, HBV, and HCV)

Universal precautions refers to the practice of avoiding contact with patients' bodily fluids, by means of the
wearing of nonporous articles such as medical gloves, gowns, goggles, and face shields.

1) Simple hygiene.
2) Frequent hand washing.
3) No recapping and the immediate disposal of contaminated needles.
4) Use of gloves and other protective barriers during contact with open wounds & body fluids.
5) Use of disposable equipments where possible.
6) Minimum equipment in OT.
7) Careful disposal of sharps and other equipment.
8) Use of proper techniques for disinfection or the disposal of contaminated materials.
9) Filters on breathing tubing if not disposable.
10) Non-disposable equipment should be decontaminated with 2% glutaraldehyde; washed with soap &
water and then left in glutaraldehyde for a further 3 hours.
11) Contaminated floors and surfaces should be washed with 1% hypochlorite solution.

Antisepsis is the process of prevention of infection by inhibiting or arresting the growth & multiplication of
microorganisms on the surface of the living objects. Antiseptic agents are as follows:
 10% povidone-iodine
 2% chlorhexidine gluconate (CHG)
 70% alcohol
 0.5% CHG in 70% isopropyl alcohol

Disinfection is the process of killing of non-sporing microorganisms on the surface of an inanimate object.

Sterilization is the process of killing of all forms of living microorganisms including bacteria, viruses, prions,
fungi and their spores present in inanimate objects by means of physical, chemical or gaseous procedures.

Methods of sterilization:
1 Heat Low temperature Water bath, Vaccine bath & Inspissator

High temperature Dry heat

Flaming, Incineration & Hot air oven

Boiling (100 ºC)

Holding & Flashing method

Pasteurization
Moist heat With pressure  Autoclave

Steaming Without pressure  Koch’s steamer

 Ernold’s steamer
 Tyndallization
2 Filtration
3 Radiation: x-ray, γ-ray, cathode-ray, ß-ray, UV-ray, Infrared-ray

4 Chemical 2% glutaraldehyde; Formaldehyde; Ethylene oxide (EO); Chlorine; Iodine; Chlorhexidine

Phenol 1 – 5 %
Hydrogen peroxide
70% ethyl alcohol

Dr. K H Mozumder
 604

Autoclave
An autoclave is a device used to sterilize equipment and other supplies by subjecting them to high pressure
saturated steam (moist heat) at 121 ºC at 1 atmospheric pressure for around 15 – 20 min depending on the size
of the load and contents. It was invented by Charles Chamberland in 1884, although a precursor known as the
steam digester was created by Denis Papin in 1679.

Principles of autoclaving
In autoclave, the temperature is increased by increasing the pressure. Steam is used. The moisture portion of the
steam is removed and replaced by sterile air. Indicator tape or tubes are used to be confirmed that the correct
condition is reached. It is useful for metals and fabrics. But there is deterioration of rubber & plastic. The sharp
instruments become blunt. 121 ºC at 1 atmospheric pressure for around 15 – 20 min is required, depending on
the size of the load and contents.

Methods of spore killing:

Physical: Autoclave Chemical: Halogens (chlorine, iodine)
Hot air oven Ethylene oxide
Tyndallization Formaldehyde
Ionizing radiation Glutaraldehyde
Fumigation

Dr. K H Mozumder
 605

Vascular catheters

Vascular catheter or intracatheter is a plastic tube, usually attached to a puncturing needle, inserted into a blood
vessel for infusion, injection, or pressure monitoring. First introduced by Werner Forssmann in 1929 and was
awarded Nobel Prize in medicine in 1956 for performing the first right-heart catheterization in a human subject.

Types of vascular catheters:

1) Peripheral vascular catheters (venous & arterial)
2) Central venous catheters:
3) Peripherally inserted central venous catheters (PICCs) ----mostly made of silicone.
4) Special catheters: hemodialysis catheters, introducer sheaths, PA catheters, etc.

Accessible central veins: Internal jugular, Subclavian & Femoral vein; Basilic, external jugular vein.
Advantages Disadvantages
 Bleeding can be recognized and Risk of carotid artery puncture
controlled
Internal
 Malposition is rare
Jugular
 Less risk of pneumothorax

 Most comfortable for conscious patients Highest risk of pneumothorax

Should not be done if age < 2 yrs.
Subclavia
The vein is non-compressible, if bleeding
n
occurs.

 Easy to identify Highest risk of infections

Femoral  Preferred site for emergencies & CPR Risk of DVT
 No risk of pneumothorax Not suitable for ambulatory patients.

In a patient with coagulopathy: prefer Femoral > IJV > SC

To reduce risk of infection: prefer SC > IJV > Femoral

Techniques of cannulation
1) A catheter over a needle
2) A catheter through a needle
3) A catheter over a guidewire (Seldinger’s technique)

Seldinger’s technique
This is a technique of cannulation where the catheter is inserted over a guidewire. In this technique,
1) Introducer needle is used to locate the vein.
2) Guidewire is threaded through the needle and Needle is removed.
3) Skin & vessel are dilated with the help of a dilator.
4) Catheter is placed over the guidewire and Guidewire is removed.
5) Catheter is secured in place.

Advantages of using ultrasound for vascular access:

 Fewer complications
 Fewer attempts for successful cannulation
 Fewer failed procedure
 Shorter time for procedure
 Can be used in patient with contraindication to blind technique; patient with coagulopathy
 Can be used in difficult access category; obesity, short neck, swollen neck, burns/post-
radiotherapy/postsurgical contracture, etc.

Dr. K H Mozumder
 606

Dr. K H Mozumder
 607

Approaches for
 Trendelenburg position (to reduce the risk of air embolism & to distend the vein)
 Patient’s head turned slightly away from the side of venepuncture.
 Triangle formed by the clavicle and sternal & clavicular heads of the SCM muscle is
Internal
located.
Jugular
Needle direction: along the medial border of the lateral head of the SCM, toward the
ipsilateral nipple, at an angle of 30º to the skin, lateral to the carotid artery pulsation.

Right IJV cannulation is generally preferred over the left due to:
1) The larger diameter of the right-sided vein
2) Its more direct path to the SVC
3) The lower dome of the right pleura
4) Absence of the thoracic duct
5) Lower rate of catheter malposition with right-sided access and
6) The relative ease of access for a right-handed operator

 Subclavian vein lies posterior to the medial portion of the clavicle and in between the 1 st rib & the clavicle
(though, invariable anatomic position).
 Subclavian artery is located posterior to the vein and anterior scalene muscle lies between them.
 Optimal location of the catheter tip: just superior to or at the junction of the SVC and the RA

 Trendelenburg position (to reduce the risk of air embolism & to distend the vein)
 Patient’s head turned slightly away from the side of venepuncture.

Needle direction:
Subclavian
 1 – 2 cm inferior to the junction of medial & middle thirds of the clavicle.
 Needle is held 5 – 10º to the coronal plane of the body and is directed towards the
suprasternal notch.
 Constantly pull back on the plunger as it needle advances.

 Femoral artery lies at the junction of the medial & middle thirds of the inguinal ligament.
Pt lies supine.

Needle direction:
Femoral
 2 – 3 cm inferior to the inguinal ligament and 1 – 1.5 cm medial to the femoral artery at
the inguinal ligament. 45º with the skin, parallel to the thigh and directed cephalad.
 Take care not to advance the needle past the inguinal ligament.
 Right femoral vein offers an ergonomic advantage for Rt-handed clinicians and vice versa.

Post-catheter placement jobs

 Aspirate blood from each port.
 Flush with normal saline or distilled water.
 Secure catheter with sutures.
 Cover with sterile dressings (Tega-derm).
 Obtain CXR for internal jugular and subclavian lines.
 Write a procedure note.

Dr. K H Mozumder
 608

Indications for central venous catheterization

1) Difficult peripheral vascular access.
2) For appropriate fluid management in:
 Shock
 Severe sepsis and septic shock
 Low urine output
 Intraoperative, etc.

3) Large-bore venous access for rapid administration of fluids.

4) Simultaneous multiple drug administration.
5) Concentrated vasoactive agent administration (e.g. norepinephrine >0.2 mcg/kg/min)
6) For administration of agents irritating to peripheral veins (e.g. amiodarone, phenytoin, mannitol,
potassium)
7) Interventions like thrombolysis, venous stenting, cardiac stenting, etc.
8) Total parenteral nutrition (TPN)
9) Chemotherapy
10) Prolonged antibiotic therapy (e.g. infective endocarditis)
11) Temporary hemodialysis (HD)
12) Temporary transvenous pacing.
13) During cardiopulmonary resuscitation (CPR)
14) ECMO
15) For haemodynamic monitoring (ScvO2, CVP).
16) Aspiration of air emboli.
17) Cardiac catheterization (PA catheter), pulmonary angiography.

Relative contraindications for central venous catheterization

 Local site infections or burns
 Anatomic abnormalities
 Coagulopathy or thrombocytopenia
 Combative patients
 Vasculitis, cellulitis, severe dermatitis at site, etc.

Risks/Complications of central venous cannulation

Vascular:
 Air embolism or thromboembolism
 Arterial puncture
 Arteriovenous fistula
 Hematoma, blood clot

Infectious:
 Line infection; Blood stream infection
 Sepsis, Cellulitis
 Osteomyelitis
 Septic arthritis

Miscellaneous:
 Pneumothorax, Haemothorax, hydrothorax, haemomediastinum
 Chylothorax (on left side)
 Cardiac perforation, cardiac tamponade
 Trauma to nearby nerves & arteries
 Dysrhythmias
 Catheter knotting or malposition

Dr. K H Mozumder
 609

Central Venous Pressure (CVP)

CVP is the pressure recorded from the RA or SVC and is representative of the filling pressure of the right side
of the heart. CVP or right atrial pressure is monitored using a catheter inserted via either IJV or subclavian vein
with the distal end sited in the upper RA. CVP should be recorded at the end-expiration.

Normal CVP measurements:

 Normal = 0 – 5 mmHg
 Normal (if ventilated) = 5 – 10 mmHg
 Target of volume resuscitation (usual) = 6 – 10 mmHg
 Target of volume resuscitation (if ventilated) = 10 – 15 mmHg

P = atrial depolarization
QRS = ventricular depolarization
T = ventricular repolarization

Dr. K H Mozumder
 610

 a wave is the pressure increase secondary to atrial contraction. It is the tallest wave.

 c wave represents the increase in atrial pressure caused by the closing & bulging of the tricuspid valve
into the RA during ventricular contraction.

 v wave denotes passive atrial filling (by closed tricuspid valve).

 x descent occurs during relaxation of the atrium.

 y descent demonstrates passive ventricular filling (opening of tricuspid valve).

Cannon 'a waves' are seen when the atrium contracts against a closed tricuspid valve.

Irregular cannon 'a waves' : Complete Heart Block

Regular cannon 'a waves' : Nodal Rhythm
Increased 'a wave' : Atrial Hypertrophy
Absent 'a wave' : Atrial Fibrillation

Absent 'x descent' & Large 'v wave': Tricuspid Incompetence

Dr. K H Mozumder
 611

CVP measurement techniques

 Non-invasive: distended jugular veins in the absence of thoracic inlet obstruction indicates a raised CVP.
 Invasive: by central venous catheterization with using a manometer.

Uses of CVP: Values & waveform assists with

diagnosis of and in determining
 Right heart failure, cor pulmonale  Mechanical atrial capture & AV pacing
 Cardiac tamponade  Presence of p wave in case of SVT
 Right ventricular infarction  Differential diagnoses of shock state
 Tricuspid regurgitation or stenosis  Correct central line placement.
 Complete heart block (cannon ‘a’)
 Constrictive pericarditis

Causes of
Raised CVP decreased CVP
RVF Venodilators
Tricuspid stenosis & regurgitation Hypovolaemia
Pericardial effusion (cardiac tamponade) Effective hypovolaemia (vasodilatation)
Constrictive pericarditis Dehydration
SVC obstruction; Fluid overload; vasopressors Artefact: transducer is raised inadvertently.
Hyperdynamic circulation
High PEEP settings, positive pressure ventilation
Pulmonary Embolism (PE)
COPD/cor pulmonale
Increase in intrathoracic pressure

Artefacts caused by technical problems related to CVP measurements

1) Line malpositioning:
 Catheter tip in the RV
 Internal jugular line in axillary vein or
 Subclavian line in IJV.

2) Transducer not in alignment with phlebostatic axis (mid-axillary line).

3) Inaccurate calibration of transducer system.

4) Infusion attached to monitoring line.

5) Clot/occlusion in the line.

Dr. K H Mozumder
 612

Jugular venous pressure (JVP)

JVP is the vertical height between the manubrio-sternal angle & the top of the jugular venous wave while the
patient is positioned at about 45º to the horizontal line.

Continuous fiberoptic venous oximetry is a valuable tool for monitoring the balance between oxygen delivery
and consumption at the bedside. Continuous venous oximetry is a sensitive real-time indicator of this balance,
which can be applied as a global or regional indicator – with mixed venous oxygen saturation (SvO 2) and central
venous oxygen saturation (ScvO2) being the most commonly monitored. SvO 2 is a true reflection of the global
balance between oxygen delivery and consumption since it is measured in the pulmonary artery, where venous
blood returning to the right heart from the superior vena cava (SVC), inferior vena cava (IVC) and the coronary
sinus (CS) have mixed. SvO2 has been extensively studied and used clinically to monitor the global balance
between DO2 and VO2.

ScvO2
It is the oxygen saturation of venous blood coming from the head and upper body. It is measured from the
superior vena cava (SVC), that drains blood from the head and upper body to the heart and thus, it is called as
central venous oxygen saturation.

ScvO2 is usually 2 – 3% lower than SvO2.  Because it contains predominantly SVC blood from the upper body
 Blood from the upper body has a higher oxygen extraction ratio, and thus a lower SO2 than IVC blood.
 Of major organs at rest, the brain has high oxygen extraction ratio and the kidneys have the lowest.

Situations where ScvO2 > SvO2:

 Anaesthesia (because of increase in CBF and depression of metabolism)
 TBI (cerebral metabolism depressed)
 Shock (because of diversion of blood from splanchnic circulation; and increased oxygen extraction).

SvO2 (Mixed venous O2 saturation)

It is the oxygen saturation of blood returning to right side of the heart. It is measured from PA catheter or RV.
SvO2 = O2 delivery to tissues – O2 consumption
= DO2 – {(CaO2 – CvO2) × CO}

 Normal value = 60 – 80%; average 75%

 Measurement is non-specific.
 Value < 50% is considered as critical tissue O2 delivery.
 Value < 30% suggests anaerobic metabolism.

Significantly elevated levels of SvO2 (>80%) may indicate:

 Inability to use oxygen delivered to the tissues (sepsis)
 Significantly high cardiac output
 Shunting of oxygenated blood past tissue
 Technical errors

Use of SvO2
 As an early indicator of imminent haemodynamic failure.
 As an indicator of O2 supply or demand in critically ill patients.

Dr. K H Mozumder
 613

Factors that influence SvO2 & ScvO2

1) Cardiac output
2) Hemoglobin
3) Arterial oxygen saturation (SaO2) and
4) Oxygen consumption

PvO2 (mixed venous oxygen pressure) = 35 – 45 mmHg

Dr. K H Mozumder
 614

Dr. K H Mozumder
 615

Arterial catheterization

Indications for intraarterial blood pressure monitoring:

1) Haemodynamic instability
2) For frequent blood pressure (BP) monitoring during vasopressor therapy.
3) For frequent ABG analysis
4) Assessment of fluid responsiveness using pulse pressure variation (PPV) or stroke volume variation (SVV)
5) Fine tuning of target BP in management of hypertensive emergencies using vasodilator.

Contraindications for intraarterial catheterization:

Inadequate circulation to the extremity.
Uncontrolled severe coagulopathy.
Extremities with full thickness burn or trauma.
Skin infection over the insertion site.
Raynaud’s phenomenon.
Multiple punctures or arterial cannulation in the past.
Thromboangiitis obliterans (Buerger’s disease)
Locations near arteriovenous fistula.

Phlebostatic axis is the junction of the fourth intercostal space and midpoint between the anterior and posterior
chest walls. It is used as the reference point for the level of pressure transducer while measuring intraarterial
pressure.

Normal arterial waveform

The main components of an arterial blood pressure measuring system include:

1) Intra-arterial cannula
2) Fluid filled tubing
3) Pressure transducer
4) Pressurised flushing system
5) Microprocessor and display

Dr. K H Mozumder
 616

Advantages of direct arterial pressure measurement:

 Accuracy of pressure measurement
 Beat-by-beat observation of changes when blood pressure is variable or when vasoactive drugs are used
 Accuracy at low pressures
 Ability to obtain frequent blood samples

Problems relating to arterial cannulation:

 Requires skill to insert
 Bleeding
 Pain on insertion
 Arterial damage and thrombosis
 Injury to nearby nerves (e.g. superficial radial nerve)
 Embolisation of thrombus or air
 Misplaced (retained) guidewire
 Ischaemia to tissues distal to puncture site
 Local infection and bacteraemia
 Inadvertent injection of drugs
 Late development of fistula or aneurysm

Why should a pressure transducer be positioned at the same level as the patient’s heart?
To avoid introducing error by reading hydrostatic pressure (the pressure exerted by a column of fluid) in
addition to blood pressure. For every 10 cm the transducer is below the heart, the system will overread by
7.4mmHg (and will under-read by the same amount if the transducer is above the heart)

What features of an arterial blood pressure measurement system help to reduce errors from excessive damping?
1) The cannula and tubing should be wide-bore, short (no longer than 48 inch), high-pressure (non-compliant)
and kink free.
2) Avoiding tubing extensions and stopcocks.
3) All connections should be tight.
4) The fluid within the tubing should be non-compressible and of low density.
5) 0.9% saline or heparinised saline is usually used, and it must be free of air bubbles and clots.
6) 3-way taps and extra lengths of tubing should be kept to a minimum.
7) The flush system should be pressurised to 300mmHg to allow an infusion at 2 – 4ml/hr to reduce thrombus
formation and also to allow the ‘fast flush test’ to be performed.
8) The waveform should also be displayed so that the waveform changes associated with excessive damping
may be quickly detected and appropriate alterations made to the system.
9) Keeping the cannulated extremity in neutral or slightly extended position.

Why should an intra-arterial blood pressure measurement system have a high natural frequency?
The arterial waveform consists of a fundamental wave and at least eight harmonic waves of increasing
frequency. Should any of those waves oscillate at a similar frequency to the natural frequency of the measuring
system, resonance will occur, resulting in inappropriate amplification of the waves, distorting any readings. For
this reason a system should have a natural frequency which is greater than eight times the maximal anticipated
heart rate.

Dr. K H Mozumder
 617

Damping is an influence within or upon an oscillatory system that has the effect of reducing or preventing its
oscillation. In physical systems, damping is produced by processes that dissipate the energy stored in the
oscillation.

It indicates the tendency of an oscillating system to return to its resting state. Anything that takes energy out of
the system results in a progressive diminution of amplitude of oscillations.

Damping can be checked by performing a ‘ square wave test’. This is done by activating the flush device, then
quickly releasing it and observing the waveform on the monitor. The waveform will sharply rise and ‘square
off’ at the top when the flush is activated and then the tracing returns to the baseline after it is released. Then
checking the number of oscillations to get an idea about damping:

Optimally damped : one or two oscillations before returning to tracing.

Underdamped : more than two oscillations before returning to trace.
Overdamped : less than one oscillations before returning to tracing.

The square wave test is usually repeated every 8 – 12 hour, or whenever the waveform looks over- or
underdamped, or when the accuracy of the measurement is doubtful.

Whether the system is underdamped or overdamped, MAP always remains the same.

Following haemodynamic interpretations can be made from the arterial waveform:

1) More accurate and real-time recording of arterial pressure, particularly mean arterial pressure (MAP).
2) Calculation of pulse pressure variation (PPV) to see fluid responsiveness.
3) Steep slope of upstroke means good contractility and vice versa.
4) Area under the curve represents the stroke volume (SV).
5) Position of the Dicrotic notch – low (low SVR) and high (high afterload).
6) Steep slope of descent means low SVR.

Complications of arterial catheterization:

1) Ischaemia of hand: presents with absent pulse, dampened waveform, blanched or mottled skin, delayed
capillary refill, painful and cold hands or fingers with motor weakness.
2) Infections: blood stream infections, sepsis.
3) Bleeding, hematoma
4) Nerve damage
5) Pseudoaneurysm.

Dr. K H Mozumder
 618

Hyperdynamic circulation

This is defined as abnormally increased circulatory volume. Systemic vasodilation and the associated decrease

in SVR results in decreased pulmonary capillary wedge pressure (PCWP) and decreased BP, presenting usually
with a collapsing pulse, but sometimes a bounding pulse.

In effort to compensate, the heart will increase cardiac output (CO) and heart rate (HR), which accounts for the
increased pulse pressure (PP) and sinus tachycardia. The condition sometimes accompanies septic
shock, preeclampsia, and other physiological and psychiatric conditions.

Possible causes of hyperdynamic circulation:

Anemia AV fistulae Aortic Regurgitation
Exercise Pregnancy Pyrexia
Thyrotoxicosis Paget's disease Beriberi
Portal hypertension Vasodilator drugs Hypervolemia
Hypercapnia Anxiety
Kidney disease Liver failure Adrenal Crisis-especially after fluid replacement
Hydrocephalus Dysautonomia Erythroderma

Purposes of cardiac output measurement:

 To detect congenital & acquired heart disease.
 To detect cardiac septal defects.
 To monitor the patients with cardiogenic or hypovolaemic shock not responding to initial treatment.

Cardiac output (CO) can be measured with the following:

A. CLINICAL assessment
 Peripheral perfusion
 HR
 Respiratory rate
 Urine output

B. NON-INVASIVE measurements
 BP
 Ultrasound
 Transthoracic echocardiography
 Thoracic bioimpedance

C. INVASIVE measurements
 Direct arterial pressure
 Oesophageal Doppler
 Transoesophageal echocardiography (TOE)
 LiDCO (Lithium dilution CO)
 PiCCO (Pulse index continuous CO)
 Pulmonary artery (Swan-Ganz) catheter.

PiCCO combines pulse contour analysis and transpulmonary thermodilution technique.

Dr. K H Mozumder
 619

Principle of echocardiography
Echocardiography employs ultrasound of 2 – 10 MHz. A piezoelectrode in the probe transducer converts
electrical energy delivered to the probe into ultrasound waves. These waves then travel through the tissues,
encountering the blood, the heart, and other structures. Sound waves pass readily through tissues of similar
acoustic impedance; however, when they encounter different tissues, they are scattered, refracted or reflected
back toward the ultrasound probe. The echo waves then interact with the ultrasound probe and generate an
electrical signal. By knowing the time delay between the transmitted and the reflected sound wave, the location
of the source of the reflected wave can be determined and the electrical signal can be reconstructed as an image.

Perioperative echocardiographic modalities:

1) Transthoracic Echo (TTE)
2) Transoesophageal Echo (TOE/TEE)
3) Epiaortic & epicardiac ultrasound
4) Three-dimensional Echo

Uses of echocardiography
1) Diagnosis of the source of the haemodynamic instability, including
 Systolic & diastolic heart failure
 Valvular abnormalities
 Hypovolaemia
 Pericardial tamponade

2) Estimation of hemodynamic parameters, such as SV, CO, intracavitary pressure, etc.

3) Diagnosis of structural diseases of the heart, such as valvular heart disease, shunts, aortic diseases, etc.

4) Guiding surgical interventions, such as mitral valve repair.

Dr. K H Mozumder
 620

Mechanisms of antimicrobial resistance

Microorganisms have evolved in the presence of naturally occurring antibiotics, and have therefore developed
resistance to all classes of antimicrobial agents. Intrinsic resistance is an innate property of a microorganism,
whereas acquired resistance arises by spontaneous mutation or horizontal transfer of genetic material from
another organism in a phage or plasmid. Some examples of antimicrobial resistance are as follows:

1) Active efflux of antimicrobial agent:

 Tetracycline resistance in Gm (+ve) and Gm (-ve) bacteria
 Fluconazole resistance in Candida species

2) Impermeability/reduced permeability:
 Carbapenem resistance in Pseudomonas species.
 Aminoglycosides resistance in Anaerobes

3) Target modification:
 Altered penicillin binding protein : ß-lactam resistance in MRSA
 RNA polymerase mutation : Rifampicin resistance in M. Tuberculosis
 DNA gyrase mutation : Ciprofloxacin resistance in Enterobacteriaceae

4) Enzymatic degradation of agent:

 ß-lactam resistance in many organisms. E.g. penicillinase in Staph. aureus; ESBL, AmpC and
NDM-1 in enterobacteriaceae
 Chloramphenicol resistance in Staphylococci.

Factors promoting antimicrobial resistance

1) Inappropriate use of antibiotics, e.g. in viral infections.
2) Inadequate dosage or treatment duration.
3) Use of antimicrobials as growth-promoters in agriculture.
4) Overuse of potent, broad-spectrum antibiotics.
5) Indiscriminate prophylaxis.

Origin of drug resistance

1) GENETIC:
a) Chromosomal, e.g. RNA polymerase mutation (Rifampicin resistance in M. Tuberculosis).
b) Extra-chromosomal, e.g. plasmid resistance (ß-lactamases) and transposon resistance.

2) NON-GENETIC:
a) Metabolic inactivity
b) Loss of specific target structure
c) Infection at sites where antimicrobials are excluded or are not active.

Dr. K H Mozumder
 621

Classification of antimicrobial agents

ANTIBIOTICS
1) Cell wall synthesis inhibitors, e.g. Penicillins, Cephalosporins, Monobactams, Carbapenems, Bacitracin,
Vancomycin
2) Protein synthesis inhibitors:
30 S: Tetracyclines, Aminoglycosides and Spectinomycin.
50 S: Macrolides, Clindamycin, Chloramphenicol, linezolid.
3) Folic acid synthesis inhibitors, e.g. Sulphonamides
4) Nucleic acid synthesis inhibitors, e.g. Quinolones, Rifampicin.
5) Interfering with transport through cell membrane, e.g. Polymixin and polyene antibiotics.

ANTIFUNGALS
1) Systemic (oral/parenteral) agents for systemic infections
 Amphotericin B
 Flucytosine
 Azoles: Imidazolesketoconazole, miconazole, clotrimazole
Triazoles Itraconazole, Fluconazole.
 Echinocandins, e.g. Caspofungin, Micofungin, Anidulafungin.
2) Oral systemic agents for mucocutaneous infections, e.g. Griseofulvin, Terbinafine.
3) Topical: Nystatin
Topical azoles, e.g. clotrimazole, miconazole
Topical allylamines, e.g. Terbinafine, Naftifine.

ANTIVIRALS
1) Anti-herpes agents, e.g. Acyclovir, Ganciclovir, Famciclovir, Foscarnet
2) Anti-HIV nucleoside and nucleotide reverse transcriptase inhibitors,
e.g. Zidovudine, Lamivudine, Stavudine
3) Anti-HBV agents: Adefovir, Entecavir
4) Anti-influenza agents: Oseltamivir, Zanamivir, Amantadine, Rimantadine
5) Others: Interferons, Palivizumab, Ribavirin, Imiquimod.

ANTI-PROTOZOALS
Chloroquine, Quinine, Pyrimethamine, Miltefosine, Primaquine, Mefloquine, Sodium stibogluconate,
Proguanil, Sulfadoxine, Metronidazole, Tinidazole

ANTI-MALARIALS: Artemether, Artesunate, Atovaquone

ANTI-HELMINTHICS: Albendazole, Mebendazole, Levamisole, Pyrantel pamoate, Ivermectin.

ß-lactam compounds:
1) Penicillins:
a) Penicillin-G, Penicillin-V.
b) Anti-staphylococcal penicillins; e.g. Naficillin.
c) Extended-spectrum penicillins; e.g. Ampicillin and the antipseudomonal penicillins.
2) Cephalosporins: 1st gen : Cefazolin, Cephalexin, Cefadroxil, Cephradine
2nd : Cefaclor, Cefuroxime, Cefoxitin
3rd : Ceftriaxone, Cefpodoxime, Ceftazidime
4th : Cefepime
3) Monobactams, : Aztreonam
4) Carbapenems : Doripenem, Ertapenem, Imipenem, Meropenem.
5) ß-lactamase inhibitors : Clavulanic acid, Sulbactam, Tazobactam.

Dr. K H Mozumder
 622

Antimicrobial prophylaxis against Infective Endocarditis:

Antimicrobial prophylaxis is now recommended only for those patients who are at highest risk of adverse
outcomes if they were to develop infective endocarditis.
Regimen: single dose 30 – 60 min before procedure
Situation Agent Children
Adult
(per kg of body weight)
Oral Amoxicillin 2 gm IV/IM 50 mg IV/IM
Unable to take oral medication Ampicillin 2 gm IV/IM 50 mg IV/IM
Or, Ceftriaxone 1 gm IV/IM 50 mg IV/IM
Allergic to penicillins or Clindamycin 600 mg oral 20 mg oral
Azithromycin/Clarithromycin 500 mg oral 15 mg oral
ampicillin
Allergic to penicillins or Ceftriaxone 1 gm IV/IM 50 mg IV/IM
Clindamycin 600 mg IV/IM 20 mg IV/IM
ampicillin and unable to take
oral medication

Severity assessment scoring systems in ICU

1) APACHE-II: (Acute Physiology Assessment and Chronic Health Evaluation; version-II):

12 mandatory physiological variables including GCS with each variable point from 0 to 4. (12 × 5 = 60)
 Temperature (rectal)
 MAP, HR, RR
 Arterial pH
 Oxygenation
 Na+, K+, creatinine,
 Hct, WBC
 GCS

Age= 6 points; Chronic health evaluation= 5 points; Total points= 71; Computed after 24 hours of ICU
care.

2) APACHE-III
3) SAPS= Simplified Acute Physiology Score

4) TISS= Therapeutic Intervention Score System

5) ISS= Injury Severity Score

6) GCS
7) SOFA, q-SOFA= quick Sepsis-related Organ Failure Assessment Score

8) RASS=Richmond Agitation Sedation Scale

9) Ramsay Sedation Scale

10) RIFLE= Risk, Injury, Failure, Loss and End-stage kidney classification.
11) Murry lung injury scoring

12) Child-Pugh for patients with liver failure

13) Ranson score for patients with pancreatitis

14) CMM= Cancer Mortality Model

15) MPM= Mortality Probability Model

16) MODS= Multiple organ Dysfunction Score

Dr. K H Mozumder
 623

Dr. K H Mozumder
 624

Organ system failure definitions

Cardiovascular failure Presence of ≥1 of the following:

 Use of vasoconstrictors
 MAP< 50 mmHg
 Episodes of VF/VT
 HR< 40 bpm
 Inadequate DO2 causing base deficit >-10
 CI <2 L/min/m2

Respiratory failure  RR> 40 breaths/min

 PaCO2 >6.65 kPa in the absence of opioids
 (A-a)O2 >350
 Dependence on mechanical ventilation for >3 days

Renal failure Presence of ≥1 of the following:

 Urine output <0.5 ml/kg/hour for 24 hours

 S. urea >35 mmol/L; S. creatinine >1.5 mg/dl

Hematological failure Presence of ≥1 of the following:

 WBC <1,000/microliter of blood

 Platelet <20,000/microliter of blood
 Hct <20% in the absence of bleeding

Neurological failure Best GCS <8 in the absence of drugs

Hepatic failure  Encephalopathy

 Child-Pugh score >3
 S. Bilirubin >30 mmol/L
 INR >1.5 in the absence of DIC

Metabolic failure  Uncompensated non-cardiac base deficit >-10

 Acute serum electrolyte shift requiring intravenous therapy

GIT failure  Ileus or uncontrollable diarrhoea

 GIT hemorrhage
 Pancreatitis

Dr. K H Mozumder
 625

New onset of Fever in ICU

Fever is a temperature that exceeds the normal daily variation in temperature for each individual patient. The
current recommendations for the definition of a fever in ICU patients are as follows:

1) A body temperature of 38.3ºC (101ºF) or higher represents a fever, and deserves further evaluation.
2) A lower threshold of 38ºC (100.4ºF) can be used for immunocompromised patients, particularly those with
neutropenia.

Potential sources/causes of new onset nosocomial fever in ICU

INFECTIOUS:
1) Sinusitis
2) Blood transfusions
3) Catheter sepsis
4) Drug fever
5) Surgical site infection (SSI)
6) Urinary tract infection (UTI)
7) Deep venous thrombosis (DVT)
8) Pneumonia
9) MI, Infective endocarditis
10) Bowel translocation, bowel infarction, Clostridium difficile infection

Non-INFECTIOUS:
1) SIRS
2) Early postoperative fever
3) Pulmonary embolism
4) Platelet transfusions
5) Drug fever caused by amphotericin, penicillins, cephalosporins, phenytoin, procainamide, quinidine, etc.
6) Thyrotoxicosis
7) Adrenal crisis
8) Acalculous cholecystitis
9) Iatrogenic

Removal of secretions of airway can be facilitated by

1) Hydration
2) Humidification of inspired gas
3) Chest physiotherapy
4) Postural drainage
5) Tracheal suction with sterile catheter
6) CTSS (Closed Tracheal Suction System)
7) Fibreoptic bronchoscopy (in inspissated secretion)

Normal saline use into tracheal tube prior to introduction of catheter serves two purposes:
a) Stimulates active expiratory effort and
b) Removal of secretion.

Dr. K H Mozumder
 626

Common causes of different respiratory patterns:

Tachypnoea  Anxiety, Pain
 Chest injury
 Pneumothorax
 Pulmonary embolism
 Br. Asthma
 Metabolic acidosis
 Brainstem stroke

Bradypnoea/apnoea  Cardiac arrest

 Opioids
 Central neurological causes (stroke, head injury)

Cheyne-Stokes breathing  LVF

 Central neurological causes (stroke, head injury)
 Overdose (barbiturates, ɤ-hydroxybutyrate, opioids)

Kussmaul breathing  DKA

 Lactic acidosis
 Uraemia
 Hepatic failure
 Overdose (methanol, ethylene glycol, salicylates)

Paradoxical breathing  Respiratory failure

 GBS
 High spinal cord lesions

Sounds production:
Breath Originate mainly from the rapid turbulent airflow in the larynx, trachea and main bronchi.

Bowel Produced by passage of air through small intestine and it requires gastric emptying.

Heart 1st Closure of mitral and tricuspid valves

2nd Closure of aortic and pulmonary valves

3rd From ventricular wall due to abrupt cessation of rapid filling

4th Ventricular origin (stiff ventricle and augmented atrial contraction) related to atrial
filling.

Opening Opening of stenosed leaflets of mitral valve.

Snap Prosthetic heart sounds.

Dr. K H Mozumder
 627

Bedside pulmonary function tests

CLINICAL ASSESSMENT
1) Ability to walk upstairs

2) RR

3) Cough test
(Cough following a deep breath):
 Inadequate cough, if FVC <20 ml/kg; FEV1 <15 ml/kg; PEFR <200 L/min
 A wet productive cough/self-propagated paroxysms of coughing indicates that patient is susceptible to
pulmonary infections.

4) Sabrasez Breath Holding test

(Take a full but not too deep breath and hold it as long as possible):
 > 25 sec : normal cardiopulmonary reserve (CPR)
 15 – 25 sec : limited CPR
 < 15 sec : very poor CPR (contraindication for elective surgery)

OTHERS
1) Schneider’s match blowing test: It measures maximum breathing capacity (MBC).
(Blow a match stick from a distance of 6 inches with-
 Mouth wide open
 Chin rested/supported
 No purse lipping
 No head movement
 No air movement in the room
 Mouth and match at the same level)

Interpretation:
Able to blow out the match : MBC > 60 L/min; FEV1 >1.6 L
Cannot blow out : MBC < 60 L/min; FEV1 <1.6 L

Modified match blowing test:

Able to blow out the match from 9 inch distance indicates : MBC > 150 L/min
From 6 inches : MBC > 60 L/min
From 3 inches : MBC > 40 L/min

2) Forced expiratory time

(After a deep breath, exhale maximally and forcefully and keep stethoscope over trachea and listen)
Normal : 3 – 5 sec
Obstructive lung disease : > 6 sec
Restrictive lung disease : < 3 sec

3) Wright Peak Flow meter: (measures PEFR)

Normal Male : 450 – 700 L/min

Female : 350 – 500 L/min

4) De-Bono whistle blowing test: (measures PEFR)

5) Micro-spirometers: (measures vital capacity)

6) Pulse oximetry & Arterial Blood Gas (ABG)

Dr. K H Mozumder
 628

Dr. K H Mozumder
 629

Inflammation is a complex reaction to injurious agents (such as microbes and damaged, usually necrotic,
cells) that consists of vascular responses, migration and activation of leukocytes and systemic reactions.
Cardinal signs of inflammation are: rubor, calor, tumor, dolor & functio laesa.

Infection is invasion of normally sterile tissue by microorganisms.

Cross infection is the transfer of an infectious agent or disease from one pt to other in a hospital.

Nosocomial infection It refers to a new episode of infection that developed at least 2

or, days (48 hours) after admission to hospital.
Health care-associated infection (HAI, HCAI)
Common nosocomial infections are:
1) Blood stream infection (BSI)/Bacteremia
2) Hospital acquired pneumonia (HAP)
3) Surgical site wound infection (SSI)
4) Urinary tract infection (UTI)
5) Gastrointestinal and skin infections

Common pathogens that cause nosocomial infection are:

 Staphylococcus aureus
 Methicillin resistant Staph aureus (MRSA)
 Pseudomonas aeruginosa
 Acinetobacter baumannii.
 Klebsiella species
 Staphylococcus epidermidis
 Escherichia coli
 Anaerobes (Clostridium difficile)
 Candida albicans and aspergillus
 Respiratory Syncytial Virus
 Influenza virus.

Dr. K H Mozumder
 630

Prevention of nosocomial infection

A. Target-oriented approach:
1) Increasing awareness about consequences of infection among the staffs.
2) Isolation of the already infected patients.
3) Restriction of the patient attendants.
4) Limiting the number of specialist or doctor or trainees from different disciplines.

B. Appropriate nursing care:

1) Reducing the available route of entry of infection.
 Changing all catheters, cannula, and tubes as early as possible.
IV cannula— 48 hours
Central venous catheter— 3–7 days
Tracheostomy—14 days
Urinary catheter— 21 days

 Subclavian CVC is preferable.

2) Preventing transfer of organisms by-

 Proper hand hygiene with soap and antiseptic solutions.
 Strict aseptic measures must be carried out with all invasive procedures.
 Breathing circuit, bacterial filter, dome of humidifier should be disposable.

3) Improving host defence:

 Adequate nutritional support.
 Early drainage of wound.
 Active or passive immunization.

4) Reducing risk of endogenous infection from gut

 Early enteral feeding
 Improving gut flow
 Selective decontamination of digestive tract (SSD)

5) Infection control team:

 Surveillance and investigation of infection outbreak.
 Educating the staffs.
 Review of antibiotics in use.
 Review of microbial antibiotic resistance pattern.
 Infection control protocol.
C.

Dr. K H Mozumder
 631

Sepsis A life-threatening organ dysfunction caused by a dysregulated host response to

infection.
Or, (SIRS + documented infection by C/S report)

Severe sepsis  Sepsis with any one of the organ dysfunction.

 Hypotension: SBP <90 mmHg or decrease >40 mmHg or MAP <65 mmHg.
 Hyperlactatemia: S. lactate >2 mmol/L or >18mg/dl
 S. creatinine >2 mg/dl or >176 µmol/L or urine <0.5 ml/kg/hr
 ALI with P/F ratio <300 mmHg
 S. bilirubin >34 µmol/L
 Platelet <1,00,000/mm3
 INR >1.5 or APTT >60 sec

Bacteraemia Presence of viable bacteria in the blood without multiplication and specific
symptoms.

Septicaemia Presence of viable bacteria in the blood with multiplication and specific
symptoms and signs.

Systemic inflammatory It is defined by the presence of ≥2 of the following:

response syndrome 1) RR >20 breaths/min
(SIRS) 2) HR >90 bpm
3) WBC >12 × 109 /L or <4 × 109 /L
4) Temperature >38ºC or <36ºC
5) PaCO2 <32 mmHg or ventilated
 Hypothermia and septic neutropenia indicate more severe infection.
 Wide pulse pressure may be an early pointer to systemic sepsis, because due
to vasodilation afterload is reduced.

Causes of SIRS:
 Pancreatitis
 Trauma
 Cardio-pulmonary bypass
 Vasculitis, etc.

MODS It is the presence of two or more altered organ functions in acutely ill patients
such that homeostasis can’t be maintained without intervention.

Shock The defining feature of shock is a level of oxygen delivery (DO 2) that fails to
meet the metabolic requirements of the tissues.

Shock is a systemic state of low tissue perfusion that is inadequate for normal
cellular respiration. With insufficient delivery of oxygen and glucose, cells switch
from aerobic to anaerobic metabolism. If perfusion is not restored in a timely
fashion, cell death ensues.

Septic/Hyperdynamic/ It is defined as sepsis associated with hypotension (SBP<90 mmHg, MAP<60

warm shock mmHg, or systemic blood pressure <40 mmHg from baseline) despite adequate
fluid resuscitation and vasopressors required to maintain MAP ≥65 mmHg
and serum lactate level >2 mmol/L.

q-SOFA Presence of ≥2 of the following:

 Hypotension (SBP ≤ 100 mmHg)

Dr. K H Mozumder
 632

 Altered mental status (GCS ≤ 13)

 Tachypnoea (≥ 22 breaths/min)

Common mechanism of tissue hypoperfusion include:

 Hypovolaemia (e.g. Haemorrhage and burns);
 Septic shock (e.g. Pneumonia);
 Cardiogenic shock (e.g. Myocardial infarction);
 Neurogenic shock (e.g. High cervical spinal cord injury); and
 Adrenocortical insufficiency.

Principles of mx of shock:
1) Treatment of the underlying pathological condition;
2) Optimisation of circulating blood volume;
3) Optimisation of cardiac output;
4) Optimisation of blood pressure;
5) Restoration of vascular tone;
6) Optimisation of oxygen delivery; and
7) Support of any organ failure.

Ischaemia–reperfusion syndrome
During the period of systemic hypoperfusion, cellular and organ damage progresses due to the direct effects of
tissue hypoxia and local activation of inflammation. Further injury occurs once normal circulation is restored to
these tissues. The acid and potassium load that has built up can lead to direct myocardial depression, vascular
dilatation and further hypotension.

The cellular and humoral elements activated by the hypoxia (complement, neutrophils, microvascular thrombi)
are flushed back into the circulation where they cause further endothelial injury to organs such as the lungs and
the kidneys. This leads to acute lung injury, acute renal injury, multiple organ failure and death.

Reperfusion injury can currently only be attenuated by reducing the extent and duration of tissue hypoperfusion.

Endocrine shock
Endocrine shock may present as a combination of hypovolaemic, cardiogenic or distributive shock. Causes of
endocrine shock include hypo- and hyperthyroidism and adrenal insufficiency.

Hypothyroidism causes a shock state similar to that of neurogenic shock due to disordered vascular and cardiac
responsiveness to circulating catecholamines. Cardiac output falls due to low inotropy and bradycardia. There
may also be an associated cardiomyopathy.

Thyrotoxicosis may cause a high-output cardiac failure.

Adrenal insufficiency leads to shock due to hypovolaemia and a poor response to circulating and exogenous
catecholamines. Adrenal insufficiency may be due to pre-existing Addison’s disease or be a relative
insufficiency due to a pathological disease state, such as systemic sepsis.

Dr. K H Mozumder
 633

Monitoring for patients in shock

Minimum
ECG
Pulse oximetry
Blood pressure
Urine output

Additional modalities
Central venous pressure
Invasive blood pressure
Cardiac output
Base deficit and serum lactate

Dr. K H Mozumder
 634

Classification of shock
The causes of circulatory failure or shock may be categorized as either low flow or stroke volume, or low
peripheral arteriolar resistance (vasodilation).

Examples
Low flow or SV Hypovolaemic Internal or external hemorrhage, severe burns, salt & water
depletion, etc.

Cardiogenic MI, acute MR, cardiogenic pulmonary edema, etc.

Obstructive Major PE, cardiac tamponade, tension pneumothorax, etc.

Low peripheral Sepsis/SIRS Infection or other causes of systemic inflammatory response

arteriolar resistance producing widespread endothelial damage with vasodilatation,
(vasodilation) arteriovenous shunting, microvascular occlusion, capillary leak
and tissue edema.

Anaphylactic Inappropriate vasodilatation triggered by an allergen (e.g. bee

sting), often associated with endothelial disruption and capillary
leak.

Neurogenic Major brain or spinal injury, high cervical cord trauma, GBS, etc.

Objective markers of inadequate tissue oxygen delivery which can aid earlier identification of shock:
 Increasing base deficit.
 Elevated blood lactate level and
 Reduced urine output.

Clinical courses of shock:

Compensated,
Decompensated &
Low flow or stroke volume Low peripheral arteriolar resistance
Hypovolemic,
Sepsis/SIRS,
Cardiogenic & Neurogenic
Anaphylactic
Obstructive.
Cold peripheries. Warm peripheries. Vasodilated.
Bounding pulses
Reduced or absent peripheral pulses. Features of high cardiac output. Hypotension
with a
Weak central pulses. In early stagewide pulse pressure (normal paradoxically
SBP, low DBP); because afterload is reduced slow HR.
Evidence of low cardiac output. and thus SV is maintained.

In early hemorrhagic shock: narrow In more advanced stage SBP falls and
pulse pressure (↓ SBP, ↑ DBP). peripheries become cool (due to hypovolemia
associated with capillary leak)

In advanced stage, fluid resuscitation works

usually; but if no improvement, then myocardial
depression may be present.
Irreversible.

Dr. K H Mozumder
 635

Dr. K H Mozumder
 636

Dr. K H Mozumder
 637

SEPTIC shock
Predisposing factors:
Intrinsic factors  Age <10 yr and >70 yr
 Co-morbidities: DM, IHD, Malignancy
 Immunosuppression

Surgery  Wound, Dirty procedures, Prosthetic material

Procedures:  Urinary catheterization, Intravenous cannulation, Wound dressing

Hospital factors:  Prolonged hospital stay (especially in ICU), Outbreaks

Community factors  Travelling, Disease outbreaks

Genetic polymorphism:  Cytokine response, Coagulation

Both Gram (+ ve) and Gram (- ve) bacteria can cause septic shock but traditionally more associated with Gram
(-ve) bacteria.

Gram (-ve) Gram (+ve) Fungi

Escherichia coli Streptococcus
Klebsiella Staphylococcus
Pseudomonas
Proteus
Acinetobacter

C/F: INITIALLY:
1) Hyperthermia, chills
2) Nausea, vomiting
3) Tachycardia, Tachypnoea
4) Flushing, warm periphery
5) Vasodilation, hyperdynamic circulation
6) High cardiac output
7) Hypotension
8) Oliguria
9) Acute mental instability

LATER:
1) Hypotension (due to hypovolemia or poor myocardial function)
2) Low cardiac output
3) Feeling cool and cold periphery.

Dr. K H Mozumder
 638

Pathophysiology of septic shock:

 The reaction is elicited by the interaction between bacteria or their product with normal host defence. Most
common are endotoxin producing Gram negative bacteria (e.g. E. coli, Proteus, Pseudomonas, etc.)

 The endotoxin (a component of LPS) and exotoxin (if present) bind with CD4 receptor on leukocyte’s
(especially monocyte and phagocyte) endothelial cell and other cell types.

 Initiation of synthesis, release and activation of cascade of mediators derived from plasma or cell.

 Endogenous mediators involved are:

 Cytokines: TNF, IL2,6,8, NO, PAF
 Arachidonic acid metabolites: Prostaglandins, Thromboxane A2, Leukotrienes.
 Plasma proteases: Complement compounds (C3a), Kinins.

 Action of the mediators on different organ systems of body are:

Heart: diminished myocardial contractility
Blood vessels: systemic vasodilation, thrombosis, DIC.
Lungs: ARDS
Generalized organ dysfunction.
↓
Septic shock
↓
- Hyporesponsive (overwhelming sepsis) Death
- Hyperresponse (SIRS and MODS)  Death
- Balanced (compensated anti-inflammatory response syndrome/CARS)  resolution

Typical hemodynamic pattern in septic shock:

 Low CVP or wedge pressure (due to low cardiac filing pressure)
 High cardiac output (CO)
 Low SVR/ peripheral vasodilatation.

But, in the advanced stages of septic shock, cardiac dysfunction is more prominent and the CO is reduced,
resulting in haemodynamic pattern that resembles cardiogenic shock, i.e. High CVP, High SVR and Low CO.

Lab. Findings of septic shock:

1) Thrombocytopenia (early sign)
2) Leucocytosis; but leucopenia in overwhelming sepsis.
3) Elevated serum lactate level
4) Elevation of S. aminotransferase and S. bilirubin.
5) Increase Prothrombin time and FDP
6) Hyperglycemia (insulin resistance)
7) ABG reduced PaO2; metabolic acidosis
8) Microbial evidence of specific organism may be found in blood culture.

Principles of treatment of septic shock:

1) Control and eradication of the infection by
 Appropriate and in time I/V antibiotics
 Drainage of abscesses
 Debridement of necrotic tissues and
 Removal of infected foreign bodies.

2) Maintenance of adequate perfusion with intravenous fluids and inotropic and vasopressor agents.

3) Supportive treatment of complications such as ARDS, Renal failure, GIT bleeding, DIC, etc.

Dr. K H Mozumder
 639

Treatment of septic shock:

1) Initial resuscitation: Therapeutic goals: CVP 8 – 12 mmHg
MAP ≥ 65 mmHg
SvO2 ≥ 65%
ScvO2 ≥7 0%
Hb > 8 gm/dl
Glucose < 180 mg/dl
Urine output ≥ 0.5 ml/kg/hour
 Airway maintenance
 Breathing: Endotracheal intubation with mechanical ventilation may be needed. Target SpO 2 >97%.
 Obtain plasma lactate level.
 Circulation:
a) Fluid administration: Targeted and rapid I/V fluid; continued until BP, tissue perfusion and O 2
delivery acceptable.
b) Vasopressors: if hypotension persists despite fluid resuscitation.

Norepinephrine 0.1 – 1 mcg/kg/min [α1, ß1]

Dopamine Start @ 5 mc/kg/min and titrate upward as needed

(1 – 20 mcg/kg/min); [α1, ß1 and dopamine receptors]
 Renal dose <5
 Cardiac dose 5 – 10 and
 Vasoconstrictor dose >10 mcg/kg/min

Phenylephrine 20 – 300 mcg/min [only α1 effect]

Dobutamine upto 40 mcg/kg/min
Vasopressin 0.03 units/min

2) Antimicrobial therapy:
 Blood cultures should be obtained prior to administration of antibiotics.
 Broad spectrum antibiotic is appropriate.
 Removal of infection source: catheters, abscess, etc.

3) Strict glycemic control

4) Corticosteroids: Inj. Hydrocortisone 50 mg I/V 6 hourly for 7 days [N.B. Beneficial for who had relative
adrenal insufficiency]
5) Activated protein C

6) Others:
 Prevention of venous thrombosis by LMWH.
 GIT care- H2 blocker, PPI.
 Renal support- Haemofiltration or hemodialysis (if needed)
 Nutritional support- start early and preferably through enteral route.
 Maintaining plateau pressure at ≤30 cmH2O in ventilator-dependent patients.

Some clinical conditions attributed to inflammatory injury:

Brain Septic encephalopathy
Bone marrow Anaemia of chronic illness
Cardiovascular Septic shock
Kidneys AKI
Lungs ARDS
Peripheral nerves Critical illness polyneuropathy
Skeletal muscle Critical illness myopathy

Dr. K H Mozumder
 640

HYPOVOLAEMIC shock
It is an emergency condition in which excessive blood and fluid loss make the heart unable to pump enough blood to the
body.

Causes
1) Blood loss due to
 Bleeding from cut injury
 Bleeding from other injuries
 Internal bleeding such as in the GIT.

2) Loss of body fluid leading to decrease in blood volume

 GIT loss (diarrhoea, vomiting, naso-gastric secretion)
 Renal loss (Diabetes insipidus)
 From skin due to burn

3) Sequestration of body fluid within abdominal viscera or peritoneal cavity.

Classification and C/F

Mild hypovolaemia Decreased perfusion of organs that can tolerate ischaemia (skin, fat, skeletal muscle, bone,
(<20% blood volume loss) etc.)
 Cold feeling
 Postural hypotension
 Dry tongue
 Concentrated urine

Moderate hypovolaemia Decreased perfusion of organs that can withstand ischemia poorly (pancreas, spleen, kidney,
(20 – 40%) etc.)
 Thirst, Tachycardia, Oliguria

Severe hypovolaemia Decreased perfusion to brain and heart.

(>40%)  CVS: rapid thready pulse, low BP
 CNS: restless, agitated, confused, obtunded
 Respiratory: ↑RR
 Renal: anuria
If progresses further, cardiac arrest & death.

Laboratory findings:
1) Hematocrit: may be normal if rapid blood loss occurs and assessed early.
2) Lactate: Increased
3) ABG: ↓pH, ↓HCO3-, ↑Base deficit
4) Urine osmolality increased (>1.010)
5) Urinary Na+ <10 mmol/L
6) Blood urea, S. creatinine, S. electrolytes

Dr. K H Mozumder
 641

Effects of hypovolaemic shock:

CVS a) Starling law of fluid shift towards interstitium.
b) Compensation: fluid movement towards vascular space due to constriction of capacitance vessels.

c) Neuroendocrine response:

On venous end:
 Angiotensin & vasopressin enhance sympathetic effecttachycardia
 Adrenergic discharge causing constriction of large venules & small veins divert to heart
increased diastolic filling increased SV.

On arteriolar end:
 Constriction of precapillary sphincter & arterioles lead to redistribution of blood to vital organs
(brain, heart)

Metabolic a) Decreased O2 supply to tissues

b) Anaerobic metabolism
c) Increase in arteriovenous O2 content difference.

Cellular & 1) Increased apoptosis in CNS

immunologic 2) Release of TNF, free radicals, leukotrienes
3) Activation of coagulation cascade and complement system

Renal  Decreased afferent blood flow & filtration pressure

 Acute tubular necrosisAKI

Monitoring of a pt with hypovolaemic shock:

 Pulse, BP
 Urine output
 Blood urea, S. creatinine, S. electrolytes
 Blood sugar
 CVP
 Pulse oximetry & Capnography

Treatment:
1) General principles:
 Airway, breathing & circulation
 I/V access: two large bore cannula
 A quick search should be made for source of blood and fluid loss.
 Central venous catheter insertion.

2) Fluid resuscitation: choice of initial fluid therapy is determined by availability & patient’s condition.
a) Crystalloids:
 Isotonic fluid: Ringer’s lactate is the best (contains more physiological electrolytes). 0.9% NaCl and 5% DNS
can also be used.
For adult initial bolus of 1- 2 liters.
For paediatrics 20 ml/kg bolus and assess response.
 Hypertonic saline (3% NaCl)

b) Colloids:
 Natural: 20% albumin, purified protein fraction, FFP
 Synthetic: Hydroxyethylstarch 6%, Dextran – 70, Dextran – 40

3) In acute blood loss, blood transfusion is the choice of replacement.

4) Inotropes and vasopressors, if needed.

Dr. K H Mozumder
 642

CRYSTALLOIDS:
Advantages Disadvantages
 Readily available  Short lived haemodynamic effect (<30 min)
 Less expensive  Pulmonary edema and peripheral edema may develop.
 Simple to infuse large volume  Hartmann’s solution is contraindicated in DM.
 Balanced salt solution approximate ECF  Large Na+ and H2O load.
composition.  No O2 carrying capacity.

COLLOIDS:
Advantages Disadvantages
 Small volume is required  Expensive and less available
 Longer-lived hemodynamic effect (4  Reduced platelet aggregation
hours)  RBC sludging
 Minimum peripheral edema  Allergic reaction
 Renal dysfunction

Dr. K H Mozumder
 643

Dr. K H Mozumder
 644

CARDIOGENIC shock
Systemic hypoperfusion secondary to severe depression of cardiac output and sustained systolic arteriolar
hypotension despite elevated filling pressure.

Classic criteria for diagnosis include:

1) SBP <80 mmHg
2) Persistent hypotension for at least 30 minutes.
3) Reduced systolic cardiac function: Cardiac index <1.8 L/m2/min
4) Tissue hypoperfusion: oliguria, cold extremities, confusion, etc.
5) Increased left ventricular filling pressure: PCWP >18 mmHg.

Etiologies
1) Acute MI or ischemia
2) LVF
3) Ventricular septum rupture
4) Papillary muscle or chordal rupture; in severe MR.
5) Ventricular free wall rupture with subacute tamponade.

Pathophysiology:
Myocardial infarction and/or myocardial dysfunction

Systolic dysfunction Diastolic dysfunction

↓SV & ↓CO ↑LVEDP & pulmonary congestion

Hypotension Hypoxia

Systemic hypoperfusion and reduced coronary perfusion pressure (CPP)

Ischemia

Progressive myocardial dysfunction

Death
STAGES of cardiogenic shock:
1) Compensated
2) Decompensated hypotension
3) Irreversible shock: activation of complement cascade and irreversible myocardial & peripheral tissue
damage.

C/F:
of the low cardiac output state  Cold, clammy grey skin
 Slowed capillary refill time
 Oliguria, Sweating, Confusion
 Hypotension, Tachycardia

of heart failure Elevated JVP & other signs of heart failure

Pulmonary edema & 3rd heart sound

Investigations:
1) 12 lead ECG, Echocardiography, CXR
2) Swan Ganz catheterization: SvO2

Dr. K H Mozumder
 645

Rx of cardiogenic shock:
1) General measures:
 Oxygen supplementation
 Propped up position
 Opioids: Morphine (Relieve pain & anxiety; Provide sedation; Lessen cardiac stress)

2) Resuscitation:
 If PAWP <10 mmHg, provide balanced salt solution.
 GTN: Reduce both preload & afterload finally reduce EDPIncrease O2 delivery to ischemic areas.

3) Pharmacological support:
a) Inotropes:
Dobutamine Improves ventricular performance without increasing O2 demand. Dose: upto 40 µg/kg/min
(ß1)
Dopamine D1 & D2 stimulation at low dose; α and ß stimulation at high dose.

Renal dose (D1) : < 5 µg/kg/min (Improves renal function; Inhibit noradrenaline release)
Intermediate/Cardiac dose : 5 – 10 µg/kg/min (Improves cardiac function without increasing O 2
demand)
Vasoconstrictor dose (α) : >10 µg/kg/min (Increased O2 demand; Increase HR; Decrease renal
function)

Digoxin Has little importance in cardiogenic shock.

b) Vasodilators: GTN @ 10 – 100 µg/min

c) Other modalities:
 Anti-ischemic
 Anti-coagulation
 Thrombolytics
 Percutaneous coronary intervention (PCI)
 Intra-aortic Balloon Pump (IABP)
 Left ventricular assist device
 Emergency CABG.

Dr. K H Mozumder
 646

NEUROGENIC shock
Produced by peripheral vasodilation due to vasomotor tone loss as a result of spinal cord injury, regional
anaesthesia or administration of autonomic blocking agents.

Effects:
1) Blood pooled in periphery decrease venous returndecrease CO
2) Above the level of injury:
 Adrenergic system activated increase HR Increase force of contraction.
 Bradycardia, if cardiac sympathetic flow affected.
3) Loss of vasomotor tone causes impaired cellular metabolism.

Causes:
1) Spinal cord injury at spinal cord T3 or above.
2) Regional anaesthesia
3) Administration of autonomic blocking agents.

C/F:
 Extremities: warm above & cool below injury.
 BP low
 HR rapid, thready, may be bradycardia
 Sign of spinal shock & spinal cord injury
 Absent all voluntary reflexes & neurogenic activity below level of injury.
 Loss of sensation
 Flaccid paralysis below injury.

 Poikilothermia (unable to regulate temperature)

Imaging studies:
 To find out any trauma: radiograph of cervical, thoracic & lumbosacral spine.
Review after being transferred to ICU.

 To find out vertebral fragment compressing spinal cord: CT scan or MRI.

Rx:
1) Supportive
 Secure airway, oxygenation, & ventilation
 I/V access
 Assess bladder function, if needed.

2) Fluid: may need several liters of balanced salt solution.

3) Pharmacological: α-adrenergic support (e.g. Phenylephrine, Ephedrine, Noradrenaline);

Target MAP = 60 – 80 mmHg

4) Surgery: If spinal transection due to fracture of vertebra stabilization of vertebra.

5) Rehabilitation:
 Nursing and support personnel
 Prevent pressure sore.
 Prevent UTI
 Early consultation and counselling by physiatrist.

Dr. K H Mozumder
 647

SPINAL shock
The term ‘spinal shock’ applies to all phenomena surrounding physiologic or anatomic transection of spinal cord
that result in temporary loss or depression of all or most spinal reflex activity below the level of injury.

Causes:
1) Spinal cord injury following trauma and surgery.
2) Inflammatory lesion of spinal cord.
3) Infective cause
4) Metastatic lesion in spinal cord.

Dr. K H Mozumder
 648

DIC/Consumption coagulopathy
Pathological activation of coagulation by a disease process leading to fibrin clot formation, consumption of
platelet and clotting factors (I, II, XIII) and secondary fibrinolysis. Consequence is initial thrombosis followed
by increased bleeding tendency due to consumption of clotting factors and fibrinolytic activity.

Causes: 4STEM B2PIR

Burn Pre-eclampsia
Pulmonary embolism Amniotic fluid embolism
Extracorporeal circulation Intrauterine death (IUD) Obstetric
Haemolysis Placental abruption
Malignancy Retained product of conception.
Shock
Sepsis
Major surgery
Snake bite
Trauma

Pathophysiology of DIC:

Massive tissue destruction. Endothelial injury

↓ ↓
Release of tissue factor Activation of subendothelial
Collagen and contact factor
↓ ↓
Activation of extrinsic Activation of intrinsic Platelet aggregation
Coagulation pathway coagulation pathway

DIC

Activation of plasmin Consumption of clotting factors and platelet

Microthrombi

Breakdown of fibrin & proteolysis Microangiopathic Vascular occlusion

of factor V & VIII hemolytic anaemia
↓
FDP and Platelet aggregation Ischaemic tissue damage
↓
Fibrin polymerization Multiorgan failure (MOF)

Bleeding
C/F
 Bruising
 Bleeding from wounds, venipuncture sites, GIT,
lung, uteroplacental bed.
 Capillary microthrombosis may lead to
MOF/MODS/TOF (total organ failure)/MSOF
(Multisystem OF).

Dr. K H Mozumder
 649

 Shock, acidosis and hypoxaemia may occur.

Lab. Findings
 Thrombocytopenia
 Low titre of fibrinogen, coagulation factor and antithrombin-III.
 High titre of FDP
 Prolonged PT, APTT & TT.

Rx
1) Directed as underlying cause: antibiotic, blood transfusion and other treatments, wound dressing, etc.
2) Supportive: Oxygen therapy and treatment of respiratory failure, if present.
3) Administration of FFP, platelet & possibly cryoprecipitate.
4) Inj. Antithrombin-III
5) Heparin in chronic DIC & major coagulopathy.
6) Administration of activated protein C should be considered in sepsis related DIC.

Dr. K H Mozumder
 650

Dr. K H Mozumder
 651

Dr. K H Mozumder
 652

Physiological effects of malnutrition

 Pulmonary:
 Decreased diaphragmatic contractility
 Decreased hypoxic drive
 Decreased ventilatory response to CO2.

 Cardiac:
 Decreased myocardial contractility
 Decreased response to inotropes
 Ventricular dilatation

 Renal: Decreased GFR, Impaired Na+ excretion

 Hepatic:
 Altered metabolism of CHO, fat & protein.
 Decreased protein synthesis
 Decreased drug metabolism
 Impaired bilirubin excretion

 Hematological: Anaemia, Coagulopathy

 Immune system:
 Decreased T-cell function
 Impaired chemotaxis & phagocytosis.

Physical signs of malnutrition:

Loss of subcutaneous fat
Muscle wasting
Peripheral edema
Ascites

Essential nutrients:
Nutrients that cannot be synthesized from other nutrients inside the body and that’s why must be supplied from
outside are called the essential nutrients. They are as follows:
 8–10 AAs: PVT TIM HALL: Phenylalanine, Valine, Threonine, Tryptophan, Isoleucine, Methionine, Histidine,
Arginine, Leucine, and Lysine.

 3 FAs: Linolenic, linoleic and arachidonic acid.

 13 Vitamins

 16 minerals

Benefits of proper nutrition in critical illness:

 Promote glycogenolysis
 Increase gluconeogenesis
 Inhibit glycolysis
 Increase synthesis & breakdown.

Dr. K H Mozumder
 653

Total Parenteral Nutrition (TPN)

Total parenteral nutrition is a way of supplying all the nutritional needs of the body by bypassing the digestive
system and dripping nutrient solutions directly into a vein.

Indications:
ABSOLUTE
1) Gut failure or severe gut dysfunction.
2) Inability to tolerate enteral feeding.

RELATIVE
1) Moderate to severe malnutrition.
2) Abdominal sepsis.
3) Prolonged ileus.
4) Severe necrotizing pancreatitis.
5) Severe inflammation of bowel.
6) Massive bowel resection.

Complications:
1) CATHETER related
 Catheter sepsis
 Pneumothorax
 Haemothorax
 Chylothorax (left side)
 Air embolism
 Thromboembolism
 Cardiac tamponade

2) ELECTROLYTE imbalance (PO43-, K+, Mg2+)

 Hypophosphataemia
 Hypokalaemia
 Hypomagnesaemia

3) METABOLIC
 Hyperchloremic acidosis
 Hyperglycemia
 Rebound hypoglycemia (if stopped suddenly)
 Hyperlipidaemia
 Excess CO2 production
 Fat embolism
 Azotaemia
 Pancreatitis

4) HEPATIC dysfunction
 Steatosis
 Intrahepatic cholestasis

Dr. K H Mozumder
 654

Monitoring:
1) CLINICAL SIGNS
 Body weight and fluid balance daily.
 Triceps skin fold thickness
 Abdominal girth
 Mid arm circumference
 Handgrip strength

2) INVESTIGATION
 Serum urea, creatinine, electrolytes and osmolality daily.
 Urine urea and osmolality daily.
 Blood glucose should be measured frequently.
 Liver function and plasma Ca2+, PO43-, Mg2+ should be done twice a week.
 FBC every 1 – 3 days.
 Prothrombin Time (PT) once a week.
 Iron, folate, vit-B12 should be measured at least weekly.
 24 hours nitrogen balance.

Dr. K H Mozumder
 655

Immunomodulation & Feeding

Critically ill patients have impaired gastrointestinal function (motility, secretion, mucosal atrophy, altered flora
& bacterial translocation, etc.) secondary to an acute phase response. Increased bacterial translocation is
associated with increased risk of sepsis.

To reduce that, there has been interest to dietary components with immunomodulatory properties:

1) Glutamine:
 The most abundant amino acid in the body.
 Fuel for electrolytes and some lymphoid cell.
 Maintain gut mucosal integrity & cellular function.
 Precursor of glutathione.
 Can significantly reduce mortality & length of hospital stay.

2) Arginine
 Proliferation of T-cell.
 Increase NK cell function.
 Improves cell mediated immunity & survival.

3) Taurine
 An abundant amino acid with role of membrane stabilization & Ca2+ influx regulation.
 Has antioxidant properties.

4) Omega-3 fatty acids (anti-inflammatory activity)

5) Ribonucleotides (promote protein synthesis)

Immunonutrition:
Combination of omega-3 fatty acids, arginine, nucleotides and glutamine in enteral feeding is called
immunonutrition. Study shows reduction of mortality with immunonutrition.

Role of ALBUMIN in nutrition in critical illness:

 Shortens inflammatory phase
 Helps in angiogenesis, collagen synthesis & wound remodeling.

Dr. K H Mozumder
 656

Assessment of nutritional status:

A. Traditional objective assessment tools:
1) Weight loss: mild (10%), moderate (30%) in 6 months
2) BMI
3) Anthropometric measurement
 Triceps skin fold thickness
 Mid arm circumference
 Hand grip strength
4) Biochemical test:
 S. albumin < 3 gm/dl
 S. prealbumin
 S. Transferrin < 150 mg/dl
 Total lymphocyte count <1200/µL
 Hb concentration
 TIBC

B. Subjective global assessment tools:

1) History:
 Weight loss (acute/chronic)
 Poor diet
 Change in food intake
 Gastrointestinal symptoms including vomiting, diarrhoea & functional impairment
2) Physical examination may reveal loss of subcutaneous fat, muscle wasting, edema and ascites.

Causes of anaemia in critically ill patients:

1) Erythropoietin (Ep) deficiency.
2) Reduced RBC production.
3) Blood loss due to venesection.
4) Blood loss due to gastric stress ulcer.
5) Coagulopathy associated with systemic inflammatory response.

Causes of thrombocytopenia:
1) Sepsis
2) Dilutional thrombocytopenia
3) Thrombotic thrombocytopenic purpura (TTP)
4) Idiopathic thrombocytopenic purpura (ITP)

Dr. K H Mozumder
 657

Total daily energy requirement depends on:

1) Basal Metabolic Rate (BMR)
2) Specific Dynamic Action (SDA)
3) Activity level

And these are the components of metabolism.

BMR It is the amount of energy expended while at rest in a neutrally temperate environment,
in the post-absorptive state (meaning that the digestive system is inactive, which
requires about 12 hours of fasting).

It is the minimum rate of energy expenditure per unit time at rest. It is usually expressed
as Joules/hour-kg body mass. It is calculated by Harris-Benedict equation and Schofield’s
equation.

Harris-Benedict It is a method used to estimate an individual’s BMR and daily kilocalorie requirements.
equation or The estimated BMR value is multiplied by a number that corresponds to the individual’s
principle activity level. BMR calculation:

For male= 66.5 + (13.75 ×body wt in kg) + (5 ×height in cm) – (6.8 ×age in yr)
For female=655 + (9.6 ×body wt in kg) + (1.8 ×height in cm) – (4.7 ×age in yr)

Normal BMR= 35 – 40 Kcal/m2 body/Hour

SDA/TEF/DIT Specific Dynamic Action/Thermic Effect of Food/Dietary Induced Thermogenesis:

It is the amount of energy expenditure above the resting metabolic rate due to the cost of
processing food for use and storage.

Total daily energy expenditure (TDEE) = BMR × activity factor

Amount of
exercise/activity Description TDEE/maintenance
Sedentary Little or no exercise (desk job) BMR × 1.2
Lightly active Light exercise/sports; 1-3 days/week BMR × 1.375
Moderately active Moderate exercise/sports; 3-5 days/week BMR × 1.55
Very active Heavy exercise/sports; 6-7 days/week BMR × 1.725
Extremely active Very heavy exercise/physical job/training; 2 times per day BMR × 1.9

Dr. K H Mozumder
 658

Routes of feeding:
1) ENTERAL:
 Oral
 Naso-gastric (with fine bore catheter or wide bore catheter)
 Naso-duodenal
 Naso-jejunal
 Percutaneous gastrostomy
 Percutaneous jejunostomy
 Percutaneous endoscopic gastrostomy (PEG)
 Radiologically inserted gastrostomy (RIG)

2) PARENTERAL:
 Dedicated central venous line
 Peripheral polyurethane catheter
 Peripherally inserted central catheter.

Indications for nutritional support in the critically ill patients:

Critical or prolonged illness during which a pt will be unable to maintain their nutritional requirements by
mouth.

Enteral feeding
Indication:
1) Swallowing is inadequate or impossible.
2) Presence of normal working gut is essential.

Contraindications:
1) Non-functioning gut: obstruction, anatomical disruption, ischemia, etc.
2) Generalized peritonitis.
3) Severe shock state.

Enteral nutrition
Advantages Disadvantages
1) Cheaper 1) Patients require a functioning and intact
2) Non-invasive gastrointestinal tract.
3) Bowel integrity & function is maintained 2) Diarrhoea (upto 40% patients)
4) Normal intestinal flora are preserved 3) Nausea and vomiting (associated with ileus,
5) Bacterial translocation is minimized or prevented gastric stasis, abdominal distention)
and reduced risk of sepsis 4) Risk of aspiration and pulmonary injury.
6) Normal gastric acidity and gastrointestinal barrier 5) Risk of direct pulmonary instillation of feed.
function is preserved.
7) Enhanced secretion of IgA.
8) Reduced stress ulceration.
9) Nitrogen uptake and incorporation, carbohydrate
and lipid utilization all favour anabolism and
weight retention.

Dr. K H Mozumder
 659

Parenteral nutrition
Advantages Disadvantages
1) Useful in short bowel syndrome and intestinal 1) Expensive
obstruction 2) Invasive
2) Useful in any cause of failure to establish 3) Catheter infection risk
enteral feeding. 4) Risk of electrolyte imbalance, hepatic steatosis,
3) Helpful in prolonged ileus. azotemia, etc.
5) Hyperglycaemia, which impairs immune
response as well as promote osmotic
dehydration.
6) Fluid and lipid overload.

Refeeding syndrome:
Feeding of malnourished patient particularly after a period of starvation may result in severe metabolic
disturbance, most notably hypophosphataemia. Hypophosphataemia developing after initiating parenteral or
enteral nutrition has been termed as the refeeding syndrome.

Mechanism: Total body phosphorus depletion plus influx of phosphorus during refeeding lead to severe
decrease in extracellular phosphorus.

Benefits of early enteral feeding:

1) Improved wound healing.
2) Decreased susceptibility to infection.
3) Increase lymphocyte count.
4) Increase S. albumin.

Causes of hypoproteinemia:
1) Lack of protein in diet.
2) Malabsorption (in gastro-enteropathy).
3) Liver diseases: hepatitis, cirrhosis & fibrotic changes in liver.
4) Renal failure: nephrotic syndrome, AGN.
5) Congenital deficiency of one or more plasma proteins.

Dr. K H Mozumder
 660

Dr. K H Mozumder
 661

Dr. K H Mozumder
 662

ACID-BASE DISORDER
Primary change Compensatory change
Respiratory acidosis ↑PaCO2 ↓pH ↑HCO3-
Respiratory alkalosis ↓PaCO2 ↑pH ↓HCO3-
Metabolic acidosis ↓ HCO3- ↓pH ↓PaCO2
Metabolic alkalosis ↑ HCO3- ↑pH ↑PaCO2

Compensatory responses:
Expected changes
Disturbance
pH HCO3-
Acute
↓0.08 ↑ 1 mmol/L per 10 mmHg PaCO2 rise
Respiratory acidosis
Chronic
↓0.08 ↑ 4 mmol/L per 10 mmHg PaCO2 rise
Respiratory acidosis
Acute
↑0.03 ↓ 2 mmol/L per 10 mmHg PaCO2 fall
Respiratory alkalosis
Chronic
↑0.03 ↓ 5 mmol/L per 10 mmHg PaCO2 fall
Respiratory alkalosis

pH PaCO2
Metabolic acidosis ↓0.015 ↓1.2 mmHg per 1 mmol/L HCO3- fall
Metabolic alkalosis ↑0.015 ↑0.7 mmHg per 1 mmol/L HCO3- rise

Standard averages: pH= 7.4; PaCO2= 40 mmHg; HCO3- = 24 mmHg

Compensatory member pH result

Normal range Out of range (OOR) Uncompensated
OOR OOR Partial compensation
OOR Normal range Full compensation

pH pH (potential of hydrogen) is the negative logarithm (base 10) of hydrogen ion concentration.

Acid A chemical substance that dissociates in the water to produce H+, then can acts as a proton
[H+] donor. e.g. HCl, H2CO3
 Strong acid dissociates more completely (100%).

Base A chemical substance that accept or receive proton. e.g. NaHCO3

Buffer A weak acid or its conjugate base which acts to minimize any change in [H+]. e.g.
 Bicarbonate buffer (H2CO3/HCO3-)
 Phosphate buffer (H2PO4-/HPO42-)
 Protein buffer (PrH/Pr-)
 Haemoglobin buffer (HbH/Hb-)
 Ammonia buffer (NH3/NH4+)

Compensation The body’s attempt to return the acid base status to normal, i.e. pH closer to 7.4

Dr. K H Mozumder
 663

Compensatory mechanisms:
1) Blood and tissue buffers (within seconds)

2) Pulmonary buffers (within minutes) (+)/(-) respiratory centers (↑)/(↓) alveolar ventilation (↓)/(↑)
PaCO2pH becomes normal.

3) Renal (within hours):

During Respiratory acidosis: ↑reabsorption of HCO3-
↑excretion of titratable acids
↑formation of ammonia

During Respiratory alkalosis: rapid excretion of large amount of HCO3- through kidneys.

Physiological responses to changes in [H+]:

1) Immediate chemical buffering.
2) Respiratory compensation (whenever possible) and
3) A slower but more effective renal compensatory response that may nearly normalize arterial pH even if the
pathological process remains present.

Dr. K H Mozumder
 664

Respiratory acidosis
CAUSES:
1) Alveolar hypoventilation:
 CNS depression: drug overdose, sleep disorder, obesity hypoventilation syndrome
 Neuromuscular disorder: myopathy, neuropathy (e.g. GBS, MND, Myasthenia, etc.)
 Chest wall deformity: flail chest, kyphoscoliosis
 Pleural abnormality: pneumothorax, pleural effusion
 Airway obstruction: COPD, Br. Asthma, FB, etc.
 Parenchymal lung disease: pulmonary edema, pulmonary embolism.
 Ventilator malfunction.

2) Increased CO2 production:

 Carbohydrate load
 MH
 Prolonged seizure
 Thyroid storm
 Burn
 Vigorous exercise

Rx:
1) Reverse the imbalance between CO2 production and alveolar ventilation.
2) Increase alveolar ventilation with an aim to reduce PaCO2 (carbon dioxide production).
3) Mechanical ventilation.
4) Tromethamine.

Dr. K H Mozumder
 665

Metabolic acidosis
Mechanisms:
1) Consumption of HCO3- by strong nonvolatile acids.
2) Renal or gastric wasting of HCO3-.
3) Rapid dilution of ECF compartment with bicarbonate–free fluid.

CAUSES:
A. HIGH Anion Gap Metabolic Acidosis (HAGMA):
1) Failure to excrete endogenous non-volatile acid, e.g. renal failure (GFR <20ml/min).
2) Increased endogenous non-volatile acid production
 Ketoacidosis (DM, starvation) & Lactic acidosis
 Mixed acidosis (HONK, Alcoholism)
 Inborn errors of metabolism.
3) Ingestion of toxins, e.g. salicylates, methanol, ethylene glycol, paraldehyde, toluene, sulfur, etc.
4) Rhabdomyolysis.

B. Normal Anion Gap (hyperchloremic) Metabolic Acidosis (NAGMA):

1) Increased GIT loss of HCO3-.
 Diarrhoea
 Anion exchange resins (cholestyramine)
 Ingestion of CaCl2, MgCl2, etc.
 Fistula (pancreatic, biliary, small bowel)
 Ureterosigmoidostomy, Ileostomy
2) Increased renal loss of HCO3-
 Renal tubular acidosis
 Carbonic anhydrase inhibitor
 Hypoaldosteronism
3) Increased intake of chloride containing acids, e.g. NH4Cl, Lysine HCl, Arginine HCl, etc.
4) TPN
5) Dilutional (use of 0.9% NaCl)

Dr. K H Mozumder
 666

Rx of metabolic acidosis:

Dr. K H Mozumder
 667

0.3 ×body weight × base defic it

NaHCO3 administration formula: = corrected (ml). It acts within 15 min.
2

In 8.4% NaHCO3 : 1 ml = 1 mmol.

In 7.5% NaHCO3 : 1 ml = 0.89 mmol.

Problems with NaHCO3 administration:

 Highly osmotically active substance
 Risk of intracellular acidosis
 Vasodilation
 Hypotension
 Corrosive effect
 Inhibits release of O2 at tissue level (shifts ODC to left)
 Impairs myocardial contractility
 Impairs action of adrenaline
 Causes Hypernatremia

That’s why NaHCO3 should not be administered if pH is more than 7.25.

Dr. K H Mozumder
 668

Anion gap It is the difference between unmeasured anions and unmeasured cations (UA – UC) and calculated
by the difference between primary measured cations (Na +, K+) and the primary measured anions
(Cl-, HCO3-) in serum.

[Na+ - (Cl- + HCO3-)]

Normal AG= 10 –18 mmol/L

Advantage:
1) Simple to measure and evaluate acid base disorder.
2) Can be done at bedside.

Disadvantage:
1) Reduced anions i.e. hypoalbuminaemia, which is common in critical illness, will reduce AG
and may mask an elevated AG.
2) Unmeasured cations (such as lithium and hyperglobulinaemia), hypercalcaemia and
hypermagnesaemia will reduce AG.
3) Calculations of AG involves measurement of electrolytes, therefore is dependent on the
accuracy of measurement process.

Bicarbonate gap AG + patient’s [HCO3-]

Bicarbonate space The volume of distribution of HCO3- when given intravenously, equals to ECF space.

Standard It is the concentration of HCO3- in plasma, equilibrated for temperature 37ºC, PaO 2 ≥100 mmHg,
Bicarbonate (SBC) PaCO2=40 mmHg.

Aim is to eliminate the respiratory component of the acid-base status. Therefore, Low SBC 
true metabolic acidosis & High SBC  true metabolic alkalosis.

Base excess/deficit A measure of metabolic alkalosis/acidosis expressed as the amount of acid or base required to
return pH of blood to 7.4 and PaCO2 to 40 mmHg at full oxygen saturation and 37ºC.

Normal = -2 to +2 mmol/L;
Positive value = Metabolic Alkalosis &
Negative value = Metabolic Acidosis.

Osmolal gap The discrepancy between the measured and calculated plasma osmolality is referred to as an
Osmolal gap. Normal Osmolal gap = 10 – 15 mOsm/L.

Importance: Significant Osmolal gap indicates a high concentration of an abnormal osmotically

active molecule in plasma such as ethanol, methanol, acetone, mannitol, ethylene glycol or
isopropyl alcohol.

Osmolal gaps may be present in:

 CKD
 Ketoacidosis
 Patients those receiving large amounts of glycine
 Marked hyperlipidaemia
 Marked hyperproteinaemia

Glucose(mg/dl) BUN (mg/dl)

Plasma osmolality = 2[Na+] + + [normal = 280 – 290 mOsm/L]
18 2.8
For every 100 mg/dl increase in plasma glucose concentration, plasma sodium decreases approximately 1.6 mmol/L.

Glucose(mg/dl)
Effective plasma osmolality= 2[Na+] +
18

Dr. K H Mozumder
 669

Tonicity refers to effect of solution on cell membrane.

 Isotonic solution : no effect
 Hypotonic solution : increases cell volume
 Hypertonic solution : decreases cell volume.

the Increase ∈anion gap ( AG−12)

It is defined as following: Delta ratio= =
Delta ratio
the decrease∈¿ ¿ ¿¿
The delta ratio is sometimes useful in the assessment of HAGMA to determine if a mixed acid
base disorder is present.
Assessment guideline
< 0.4 Hyperchloremic NAGMA
0.4 – 0.8 Combined HAGMA + NAGMA
Pure HAGMA
1–2 Lactic acidosis: average value 1.6
DKA likely to have a ratio closer to 1 due to urine ketone loss (especially if pt is not dehydrated).
>2 HAGMA + concurrent metabolic alkalosis or a pre-existing compensated respiratory acidosis.

Dr. K H Mozumder
 670

Hyponatremia
Causes/Classification:
A. Decreased total sodium content: (Hypovolaemic; preservation of circulatory volume takes place at the
expense of plasma osmolarity)

Renal: Diuretics (thiazides)

Mineralocorticoid deficiency
Salt-losing nephropathies
Osmotic diuresis (glucose, mannitol)
Renal tubular acidosis

Extra-renal: Vomiting
Diarrhoea
Integumentary loss (sweating, burns)
Third-spacing

B. Normal total sodium content: (Euvolaemic)

Primary polydipsia
Glucocorticoid deficiency
SIADH
Hypothyroidism
Drug-induced (Chlorpropamide, cyclophosphamide)

C. Increased total sodium content: (Hypervolaemic; edematous)

Congestive heart failure
Cirrhosis of liver
Nephrotic syndrome
Renal failure

C/F:
Mild – moderate (Na+ >125 mEq/L): usually frequently asymptomatic.
 Early symptoms (non-specific): anorexia, nausea, weakness.
 Progressive cerebral edema
 Lethargy, confusion, seizures, coma, death.
 Non-cardiogenic pulmonary edema.

Moderate (Na+ 115 – 125 mEq/L)

Severe (Na+ <115 mEq/L): serious manifestations develop.

Dr. K H Mozumder
 671

Rx of hyponatremia:
 Treatment of the underlying cause. Mild (oral); moderate (oral + 0.9% NaCl IV); Severe (3% NaCl)

 0.9% NaCl is generally the treatment of choice for hyponatremic patients with decreased total body sodium
content.

 Water restriction is the primary treatment for hyponatremic patients with normal or increased total body
sodium content.

 Hormone replacement in patients with adrenal or thyroid hypofunction.

 Measures to be taken aimed at improving CO in patients with heart failure.

 Demeclocycline (antagonizes ADH activity at the renal tubules) is a useful adjunct to water restriction in
the treatment of patients with SIADH.

 Correction of plasma Na+ to greater than 125 mEq/L is usually sufficient to alleviate symptoms.

 The rapidity at which hyponatremia to be corrected should be tailored to the severity of symptoms.

Sodium deficit or requirement= TBW × (Desired Na+ - Present Na+) = X mEq

X
 Because 0.9% NaCl contains 154 mEq sodium per Litre of solution, so the pt should receive Litre of
154
0.9% NaCl to correct the deficit. Correction rate for:
Mild symptoms: 0.5 mEq/Hr or less
Moderate: 1 mEq/Hr or less
Severe: 1.5 mEq/Hr or less

 Infusion rate =?

 Hypertonic saline (3% NaCl) may be indicated in markedly symptomatic patients with plasma Na+ <115
mmol/L.

 Any co-existing isotonic fluid deficits should be replaced with an isotonic solution.

Glucose(mg/dl) BUN (mg/dl)

Plasma osmolarity= 2[Na+] + +
18 2.8

Dr. K H Mozumder
 672

1 gram (1000 mg) sodium contains = 43 mmol Na+ [1 mmol Na+ = 23 mg sodium]
1 gram (1000 mg) NaCl contains = 17 mmol Na+ = 390 mg sodium

1 tablet 300 mg NaCl = 5.1 mmol Na+.

1 TSF NaCl = 6 gram NaCl ≈ 2400 mg sodium = 104 mmol Na+.

pH of 3% and 5% NaCl = 5.8

Risks of 3% NaCl infusion:

 Central pontine myelinolysis
 It can precipitate pulmonary edema, hypokalaemia, hyperchloremic metabolic acidosis and may cause
transient hypotension.
 Bleeding associated with prolongation of PT & aPTT.

 Plasma or extracellular Na+ concentration is more indicative of water balance than total body sodium
content.

Dr. K H Mozumder
 673

Dr. K H Mozumder
 674

Hypernatremia
 Hyperosmolarity is usually, but not always, associated with hypernatremia.

 Hyperosmolarity without hypernatremia may be seen-

 During marked hyperglycemia or
 Following accumulation of abnormal osmotically active substances in plasma.

 Hypernatremia is most commonly seen in

 Debilitated patients who are unable to drink
 Extremes of age
 Patients with altered consciousness

Major causes of Hypernatremia:

1) Impaired thrust: coma, essential hypernatremia
2) Osmotic diuresis: DKA, HONK, Mannitol administration.
3) Excessive water losses:
Renal: Central neurogenic DI, Nephrogenic DI
Extra-renal: sweating
4) Combined disorders: coma + hypertonic NG feeding

C/F:
 Cellular dehydration causing restlessness, lethargy, hyperreflexia, seizures, coma & death.
 Focal intracerebral hemorrhage or SAH due to rapid decrease in brain volumes causing rupture of the
cerebral veins.
 Acute hypernatremia is the worst.
 Chronic hypernatremia is usually better tolerated than the acute form. Because 24 – 48 hours later,
intracellular osmolarity begins to rise as a result of increases in intracellular inositol and amino acid
(glutamine & taurine) concentrations. As intracellular solute concentration increases, neuronal water
content slowly returns to normal.

Rx:
 Aim : to restore plasma osmolarity to normal as well as correcting the underlying cause.
 Target : to reduce plasma Na+ concentration not at a rate faster than 0.5 mmol/L/Hr
 Water deficit should generally be corrected over 48 hr with a hypotonic solution such as 5% DA.
 Rapid correction can result in seizures, cerebral edema, permanent neurological damage & death.

Normal TBW ×140

Fluid or water deficit= Normal TBW - ( ) [Normal TBW= body wt × 0.6
Present ¿ ¿
or 0.55]

 Infusion rate =
 Any co-existing isotonic fluid deficits should be replaced with an isotonic solution.

Anaesthetic considerations:
 Associated fluid deficits in hypernatremia (i.e. hypovolaemia) accentuates any vasodilation or cardiac
depression from anaesthetic agents and predisposes to hypotension and hypoperfusion of tissues.

 As Vd is reduced, dose reduction for most IV agents are necessary.

 Elective surgery should be postponed in patients with significant hypernatremia (Na + >150 mmol/L) until
the cause is established and fluid deficits are corrected.

 Hypovolaemic patients are particularly sensitive to sympathetic blockade from spinal or epidural
anaesthesia. If an anaesthetic must be administered prior to adequate correction of hypovolaemia, ketamine
may be the choice of induction agent.

Dr. K H Mozumder
 675

Dr. K H Mozumder
 676

Central neurogenic DI Nephrogenic DI

Administration Causes increase in urinary osmolarity Failure of the kidneys to produce hypertonic
of exogenous urine.
ADH

Aetiology Due to lesion in or around the May be congenital or secondary to CKD,

hypothalamus and the pituitary stalk. hypokalaemia, hypercalcaemia, sickle cell
Often develops with brain death. disease, hyperproteinaemia, etc.
Transiently commonly seen following
neurosurgical procedures and head
trauma.

C/F H/O polydipsia, polyuria (often >6 L/day) and absence of hyperglycemia.
Urinary osmolarity < plasma osmolarity.
Marked polyuria without glycosuria.

Rx Aqueous vasopressin (ADH): Treatment of underlying causes

5 – 10 units SC/IM every 4 – 6 hour. Adequate fluid intake
Sodium and protein restriction
Desmopressin (synthetic analogue of
ADH): Volume depletion by a thiazide diuretic
10 – 40 mcg/dose intranasal either as a can paradoxically decrease urine output by
single dose or divided into two doses. reducing water delivery to collecting
tubules.

Dr. K H Mozumder
 677

Dr. K H Mozumder
 678

Potassium balance
Inter-compartmental shifts of potassium occurs due to changes in:
 Extracellular pH: (acidosis increases extracellular and plasma [K+] approx. 0.2 – 1.2 mEq/L per 0.1 unit
pH changes).

 Circulating insulin and catecholamine: directly affect Na+ - K+ - ATPase activity and decreases plasma
[K+] by increasing cellular uptake of potassium in the liver and skeletal muscle by insulin & activation of ß2
receptors. Alpha-adrenergic activity may impair the intracellular movement of K+.

 Plasma osmolarity: increased osmolarity (hypernatremia, hyperglycemia, mannitol, etc.) increases plasma
[K+] 0.6 mEq/L per 10 mOsmol/L increases in plasma osmolarity.

 Hypothermia: decreases plasma [K+]

 Exercise: increases plasma [K+].

Renal potassium excretion parallels its extracellular concentration:

 Nearly all the potassium filtered in glomeruli is normally reabsorbed in PCT and LH.

 Kidneys can excrete as much as 500 mEq potassium/day when potassium intake is increased slowly.

 Hyperkalaemia stimulates aldosterone secretion.

 Potassium secretion in the distal tubules is coupled to aldosterone-mediated reabsorption of sodium.

 High renal tubular flow rates (as during osmotic diuresis) increase potassium secretion by keeping the
capillary-to-renal tubular gradient for potassium secretion high and thus excretion of potassium
becomes high.

 Main source of K+ elimination is kidney. Main source of K+ intake are fruits and nuts.

Dr. K H Mozumder
 679

Dr. K H Mozumder
 680

Hypokalaemia
Causes: C/F:

Mild hypokalaemia
= 3 – 3.5
mmol/L
Moderate
hypokalaemia =
2.5 – 3 mmol/L
Severe hypokalaemia
< 2.5
mmol/L

Rx:
1) Oral
replacement over several days using a potassium
chloride solution, 60 – 80 mmol/day when serum
[K+] is > 3 mmol/L.
(1 TSF syrup KT = 6.7 mmol K+)

2) IV correction, if serum [K+] <3 mmol/L:

(1 amp = 10 ml KT = 20 mmol K+)
 Reserved for patients with, or at risk for,
significant cardiac manifestations or severe muscle weakness.
 Goal is to remove the patient from immediate danger (arrhythmias), not to correct the entire
potassium deficit.
 Peripheral IV replacement : maximum 8 mmol/hr.
 Central IV replacement : maximum 10 – 20 mmol/hr and require close ECG monitoring.
 Total IV replacement : maximum 240 mmol/day.

Deficit × weight × 0.4

Potassium chloride is preferred when metabolic alkalosis also present.

Potassium bicarbonate or equivalent (K+ acetate or K+ citrate) is preferred with metabolic acidosis.

Potassium phosphate is suitable alternative with concomitant hypophosphataemia (DKA).

Anaesthetic considerations in hypokalaemia:
Preoperative:
 The decision to proceed with elective surgery is based on:
 Serum K+ = 3 – 3.5 mmol/L;
 Rapidity at which hypokalaemia has developed and
 Presence or absence of secondary organ dysfunction.

 Chronic mild hypokalaemia (K+ = 3 – 3.5 mmol/L) without ECG changes does not substantially increase
anaesthetic risk.

Dr. K H Mozumder
 681

Intraoperative:
 Vigilant ECG monitoring.
 IV potassium should be administered only if atrial or ventricular arrhythmias develop.
 Glucose-free IV solutions should be used.
 Hyperventilation should be avoided. (alkalosis will cause further hypokalaemia)
 Dosage of NMBAs should be reduced by 25 – 30%.
 Peripheral nerve stimulator (PNS) should be used to follow both the degree of NMB and the adequacy of
reversal from neuromuscular blockade.

Dr. K H Mozumder
 682

Hyperkalaemia
Causes:

C/F:
1) Cardiac manifestations: [K+] > 7 mmol/L;
 VFasystoleheart stops at diastole.
 Hypocalcaemia, hyponatremia and acidosis accentuate the cardiac effects of hyperkalaemia.

2) Skeletal muscle related: [K+] > 8 mmol/L;

 Due to sustained spontaneous depolarization and inactivation of Na+ channels of muscle membrane.
 Weakness, paraesthesia, muscle cramp.

3) GIT: ANV, abdominal cramps, diarrhoea, paralytic ileus.

Causes of decreased renal excretion of potassium:

1) Marked reductions in GFR (<5 ml/min/1.73 m2)
2) Decreased aldosterone activity or
3) A defect in potassium secretion in the DCT.

Dr. K H Mozumder
 683

ECG changes characteristically progress sequentially as following:

Symmetrically peaked T-waves (often with a shortened QT interval)
↓
Widening of the QRS complex
↓
Prolongation of the PR interval
↓
Loss of P-wave
↓
Loss of R-wave amplitude
↓
ST-segment depression (occasionally elevation)
↓
ECG resembles a sine wave
↓
VFasystoleheart stops at diastole (sudden depolarization of the cell without the ability to repolarize)

 K+ is mostly intracellular cation. So, normally it has a tendency to move outside the cells due to the
concentration gradient.

 As plasma [K+] rises, this concentration gradient gets reversed. So, potassium will move into the cells and
RMP can become more positive, to the point of even causing contraction. When RMP gets so high that it
is above the threshold potential, meaning that once the myocardial cells depolarizes and contracts, it
cannot repolarize to allow another contraction.

 That means all myocardial cells are depolarized and this inactivates Na+ channels in the heart.

 So, there will be no spontaneous firing by myocardial cells and heart cannot contract anymore and it stops
at diastole.

Ischaemic tissue does not receive oxygen. So, there is lack of ATP and Na + - K+ - ATPase does not work. Once
K+ leaves the cell, it cannot be pumped back into the cell. That’s why potassium rises in the surrounding
interstitium of ischaemic tissues.

Calcium rigor (Hypercalcaemia tends to stop the heart at systole):

Raised Ca2+ causes increased binding with troponin, actin and myosin. And increased interaction stops the heart
at systole.

Dr. K H Mozumder
 684

Rx of hyperkalaemia:
1) Reduction of potassium intake and correction of underlying abnormalities.

2) Stabilization of cell membrane potential: Inj. Calcium gluconate 10%, 10 ml IV slowly over 10 min.
(Rapid effect but short lived; calcium can potentiate digoxin toxicity)

3) Shifting of potassium into cells:

 Inhaled ß2-agonist as nebulization (e.g. Salbutamol)
 IV glucose (50 ml of 50% solution) + Insulin (5 unit) or
 IV 10% or 25% glucose 2 ml/kg + Insulin 0.1 unit/kg
(Takes one hour for achieving peak effect)

 IV NaHCO3 (if acidosis is present)

4) To remove potassium from the body:

 IV frusemide and 0.9% NaCl, if residual renal function is adequate.
 Ion-exchange resin (non-absorbable cation-exchange resin):
E.g. Ca-resonium powder 15 gram sachet orally or rectally – 8 hourly or
Rectal sodium polystyrene sulfonate (Kayexalate) 20 gram in 100 ml of 20%
sorbitol.
(Each gram of resin binds upto 1 mmol of K+ and releases 1.5 mmol of Na+)

 Hemodialysis or hemofiltration, if [K+] >6 mmol/L despite medical treatment.

(Maximum potassium removal capability of HD = 50 mmol/hour)

Anaesthetic considerations in hyperkalaemia:

 Elective surgery should not be undertaken in patients with significant hyperkalaemia.
 Vigilant ECG monitoring.
 Avoiding succinylcholine and potassium containing IV solutions such as lactated Ringer’s solution.
 Avoiding acidosis (metabolic or respiratory).
 Mild hyperventilation may be desirable.
 Peripheral nerve stimulator (PNS) should be used to follow both the degree of neuromuscular blockade
(NMB) and the adequacy of reversal NMB.

Dr. K H Mozumder
 685

ECG changes due to ionic changes in blood

Hyponatremia may be associated with low-voltage ECG.

Hypokalaemia: (ECG manifestations are primarily due to delayed ventricular repolarization)

K+ Events
± 3.5 Prominent U wave; actual QT interval remains 0.4 sec.
If T & U waves merge, the apparent QT interval is often prolonged.
If T & U waves are separated, true QT interval is seen to be of normal.

<3 T wave flattening and inversion

2.7 Increasingly prominent U wave

± 2.5 ST depression (<1.3 mEq/L); T inversion in precordial leads;

increased P wave amplitude and Prolonged PR interval;
Prominent U wave; true QT interval remains normal.

Hyperkalaemia: (ECG manifestations are primarily due to delayed ventricular depolarization)

Heart stops at diastole.
K+ Events
± 7.0 Very tall, slender peaked T waves (a manifestation of altered
repolarization); PR and QRS intervals within normal limit.

± 8.5 Atrial paralysis (no evidence of atrial activity); broad and slurred QRS
complex; QRS interval approximates to 0.2 sec; T-wave remains tall and
slender.
Further hyperkalaemia may result in VT, VF.
Hypercalcaemia (calcium rigor): heart relaxes less during diastole and eventually stops in
systole.

Hypocalcaemia: Prolongation of ST segment and QT interval.

Dr. K H Mozumder
 686

ABG analysis
An arterial blood gas is a blood test that is performed using blood from an artery and it measures the arterial
oxygen tension, PaCO2 and pH.

Blood collection sites:

 Radial artery at the wrist
 Femoral artery at the groin
 Brachial artery
 Dorsalis arteria pedis
 Axillary artery

Radial artery is the common choice for ABG, because-

1) It’s more superficial.
2) It has substantial collateral circulation, (though 5% of patients have incomplete palmar arches and lack
adequate collateral blood flow) and
3) Easily compressible.

Indications:
1) To evaluate the adequacy of ventilatory support.
2) To evaluate the acid base status and management plan.
3) To evaluate O2 carrying capacity of blood (PaO2, HbO2, Hb %).
4) To quantitate the pt’s response to therapeutic intervention and/or diagnostic evaluation.
5) To monitor severity and progression of a documented disease process.

Contraindications:
1) Bleeding diathesis.
2) Severe PVD; absence of peripheral pulse.
3) Infection over site of needle puncture.
4) AV fistula of same limb
5) Abnormal modified Allen’s test

Information obtained from ABG:

 Acid base status
 Oxygenation: PaO2, SaO2
 CO2 elimination
 Level of carboxyhemoglobin & methemoglobin.

Parameters of ABG:
Measured Calculated
Normal values Normal values
pH 7.35 – 7.45 Standard Bi Carbonate 22 – 28 mmol/L
PaO2 80 – 100 mmHg Base excess - 2 to +2 mmol/L
PaCO2 35 – 45 mmHg Anion gap 10 – 18 mmHg
SaO2 95 – 100% P50 25 – 27 mmHg
Lactate 0.5 – 2 mmol/L (A – a)O2 < 30 mmHg
Electrolytes: Na+, K+, Cl-, Ca2+ CaO2 15 – 24 ml/dl

Hazards of ABG analysis:

 Haemorrhage; Hematoma; Air or clotted blood
 Arteriospasm
 Pain; Trauma to the pt
 Infection
 Vasovagal response

Classification of acid-base disorder

Dr. K H Mozumder
 687

Functional classification:
 Respiratory acidosis
 Respiratory alkalosis
 Metabolic acidosis
 Metabolic alkalosis

Technical classification:
 Uncompensated
 Partially compensated
 Fully compensated

Characteristic classification:
Single disorder:
 Respiratory disorder
 Metabolic disorder
 Compensating disorder

Mixed disorder:

 Same direction disorder:

 Respiratory & metabolic acidosis
 Respiratory & metabolic alkalosis

 Opposite direction disorder:

 Respiratory acidosis & metabolic alkalosis
 Respiratory alkalosis & metabolic acidosis.

Dr. K H Mozumder
 688

Allen’s test
(Designed by Dr. Edgar Van Nuys Allen; professor of cardiovascular medicine, Mayo Clinic, Rochester,
Minnesota)

Allen’s test is a simple, but not reliable, method for assessing the safety of radial artery cannulation. In this
test, the patient exsanguinates his or her hand by making a fist. While the operator occludes the radial &
ulnar arteries with fingertip pressure, the patient relaxes the blanched hand.

Collateral flow through the palmar arterial arch is confirmed by flushing of the thumb within 5 sec after pressure
on the ulnar artery is released. Delayed return of normal color (5–10 s) indicates an equivocal test or insufficient
collateral circulation (>10 s). The Allen’s test is of such questionable utility that many practitioners routinely
avoid it.

a) Sufficient collateral flow: flushing of the thumb within 5 sec after pressure on the ulnar artery is released.
b) Equivocal test: delayed return of normal color (5 – 10 sec) of the thumb after pressure on the ulnar artery is
released.
c) Insufficient collateral circulation: requiring > 10 sec for returning normal color of the thumb after pressure
on the ulnar artery is released.

Alternatively, blood flow distal to the radial artery occlusion can be detected by palpation, Doppler probe,
plethysmography, or pulse oximetry. Unlike Allen’s test, these methods of determining the adequacy of
collateral circulation do not require patient cooperation.

Dr. K H Mozumder
 689

The modified three-digit Allen’s test

a) The ulnar artery is located by palpation at the proximal skin crease of the wrist and then compressed with
three digits.

b) With both arteries compressed the subject is asked to clench and unclench the hand 10 times. The hand is
then held open, ensuring that the wrist and fingers are not hyperextended and splayed out. The palm is
observed to be blanched.

c) The ulnar artery is released and the time taken for the palm and especially the thumb and thenar eminence
to become flush is noted.

Capillary refill time > 6 seconds is considered as positive.

The modified Allen's test is performed by simultaneously compressing both the radial and ulnar arteries,
followed by exsanguination of blood from the palm by repeated clenching and unclenching of the fist. The
pressure over the ulnar artery is then released while continuing to maintain pressure over the radial artery. A
delay in flushing of the palm by 5 – 6 seconds is suggestive of abnormal ulnar-artery patency.

Dr. K H Mozumder
 690

(Ref:http://www.nejm.org/action/showMediaPlayer?
doi=10.1056%2FNEJMicm1001091&aid=NEJMicm1001091_attach_1&area=)

Dr. K H Mozumder
 691

Multiple Endocrine Neoplasia

These are rare autosomal dominant syndromes characterized by hyperplasia and formation of adenomas or
malignant tumours in multiple endocrine glands.

They fall into two groups:

1) MEN 1 (Werner’s syndrome):
1º hyperparathyroidism
Pituitary tumours (chromophobes)
Pancreatic neuro-endocrine tumours (e.g. insulinomas, gastrinomas)

2) MEN 2 (Sipple’s syndrome):

1º hyperparathyroidism (type 2a)
Medullary carcinoma of thyroid
Phaeochromocytoma or
Multiple mucosal neuromas (type 2b or 3)

Pathogenesis:
MEN 1: It results from inactivating mutations in ‘menin’, a tumour suppressor gene on chromosome 11.
MEN 2: Mutations in the RET proto-oncogene on chromosome 10 cause constitutive activation of a membrane-
associated tyrosine kinase.

Dx:
MEN 1:
Annual history & Physical examination
Measurement of S. Calcium, gastrointestinal hormones and prolactin.
MRI of the pituitary gland is performed at less frequent intervals.

MEN 2:
Annual history & Physical examination
Measurement of S. Calcium, S. Calcitonin and urinary catecholamine metabolites.

[Because MEN syndromes are hereditary, family members should be screened for early signs of
Phaeochromocytoma, thyroid cancer, and hyperparathyroidism.]

Dr. K H Mozumder
 692

Analgesia & sedation in ICU

Opioids : Fentanyl, morphine, remifentanil.

Non-opioids : Acetaminophen, ketorolac, ibuprofen.

Narcotic is the term which refers to a general class of drugs that blunt sensation and depress consciousness.

Advantages of fentanyl over morphine as analgesic in ICU or for long term analgesia:
 More rapid onset of action (as lipid solubility of fentanyl is 600 times more than that of morphine).
 Less risk of hypotension (no histamine release)
 Absence of active metabolites.

Advantages of Remifentanil:
 Analgesic effect upto 10 min.
 Broken down by non-specific esterases in tissue and RBC.
 No dose adjustments necessary for renal or hepatic failure.

Dose of remifentanil:
Bolus = 1.5 mcg/kg
Continuous infusion = 0.5 – 15 mcg/kg/hr

Morphine Fentanyl
Onset of action 5 – 10 min 1 – 2 min

Bolus 2 – 4 mg every 1 – 2 hourly 0.35 – 0.5 mcg/kg every 30 – 60 min

Infusion 2 – 30 mg/hr 0.7 – 10 mcg/kg/hr

PCA
demand (bolus) 0.5 – 3 mg 15 – 75 mcg
lockout interval 10 – 20 min 3 – 10 min

Lipid solubility - 600 times that of morphine

Active metabolites Morphine-3-glucoronide Absent

Morphine-6-glucoronide

Histamine release Yes No

Dose adjustment for renal 50% dose reduction None

& hepatic failure

Pethidine/meperidine is not favored as analgesic in ICU:

Pethidine is metabolized in the liver to norpethidine/normeperidine, a metabolite that is slowly excreted by the
kidneys. Its elimination half-life is 15 – 40 hours. Its accumulation can produce:
 CNS excitation
 Agitation
 Myoclonus
 Delirium
 Generalized seizures, etc.

Since renal dysfunction is more prevalent in ICU patients, there is a high risk for accumulation of the neurotoxic
metabolite.

Dr. K H Mozumder
 693

Patient – Controlled Analgesia (PCA):

It is an effective method of controlling pain and may be superior to intermittent opioid dosing in patients who
are awake and capable of drug self-administration.

This method uses an electronic infusion pump that can be activated by the patient. When pain is sensed, the pt
presses a button connected to the pump to receive a small intravenous bolus of drug. After each bolus, the pump
is disabled for a mandatory time period (lockout interval) to prevent overdosing. The minimum lockout interval
is determined by the time required to achieve peak drug effect.

Anxiety is characterized by exaggerated feelings of fear or apprehension that are sustained by internal
mechanisms more than external events.

Agitation is a state of anxiety accompanied by increased motor activity.

Delirium is an acute confusional state that may, or may not, have agitation as a component.

Sedation is the process of relieving anxiety and establishing a state of calm.

Ramsay sedation scale

Score description
1 Anxious & Agitated
2 Co-operative, oriented and tranquil
3 Respond to verbal command only
4 Asleep but brisk response to loud auditory stimulus (LAS)
5 Asleep but sluggish response to LAS or light glabellar tapping
6 Asleep, no response.

Dr. K H Mozumder
 694

Sedation with BDZs

Advantages Disadvantages
1) Dose-dependent amnesic effect (anterograde  Drug accumulation with prolonged sedation.
amnesia)  Apparent tendency to promote delirium.
2) Anticonvulsant effect
3) Sedatives of choice for drug withdrawal syndromes,
including alcohol, opiate, BDZ withdrawal.

A continuous infusion of midazolam will result in progressive drug accumulation in tissues. To avoid
excessive sedation from drug accumulation, midazolam infusions should be limited to ≤ 48 hr.

Midazolam
 Highly lipid soluble.
 Metabolized by CYP450 enzyme system in liver.
 Active metabolite (1- hydroxy midazolam) is cleared by kidneys.
 Loading dose = 0.01 – 0.05 mg/kg
 Continuous infusion = 0.02 – 0.1 mg/kg/hr
 Onset of action = 2 – 5 min
 Duration (after bolus) = 1 – 2 hr

Other sedatives used in ICU:

Propofol : has sedative + amnesic effect; but no analgesia.

Dexmedetomidine : sedative + amnesic + mild analgesic.

Haloperidol : antipsychotic; inhibit dopamine receptors in CNS.

Dr. K H Mozumder
 695

Problems and potential consequences of excessive sedation in ICU patients:

Problems Potential consequences
1 Accumulation with prolonged infusion Delayed weaning from supportive care

2 Detrimental effect on cardiovascular system Increased requirement for vasoactive drugs

3 Detrimental effect on pulmonary function Increased ventilation/ perfusion (V/Q) mismatch

4 Tolerance Withdrawal on stopping sedation

5 No rapid eye movement (REM) sleep Sleep deprivation, delirium and psychosis

6 Reduced intestinal motility Impairment of enteral feeding

7 Potential effects on immune/endocrine Drugs such as opioids may have a role in

function immunomodulation and risk of infection

8 Adverse effects of specific drugs For example, propofol infusion syndrome

Dr. K H Mozumder
 696

Scenarios (previous questions)

Page/reference
a) A 25-year-old male with severe head injury following RTA is admitted in
ICU. Unresponsive but breathing spontaneously.
 What is GCS? Significance of GCS.
 Assessment
 Primary management
 Different inv with reasoning
 Indications & complications of artificial ventilation
 Ventilation strategy
 Assess progress
 Anesthetic mx of pt having extradural hematoma
 Prevent bed sore

 Goal of mx in emergency room

 Primary goals of mx in ICU
 Indications for immediate tracheal intubation and artificial ventilation in the
emergency room......(Smith-840)
 Common complications of artificial ventilation
 What is cricothyrotomy?
 Tracheostomy care in ICU
 Nosocomial infection
 Assessment for weaning
 Steps followed for weaning

b) A 30-year-old male is admitted in the casualty ward following RTA. He needs

emergency exploratory laparotomy.
 Preoperative assessment
 Prepare for surgery
 Steps of RSI
 Mx of aspiration pneumonia
 Indications for artificial ventilation

c) A 50-year-old male was admitted in medicine ward with fever and cough for
last 10 days. Now he became confused, dyspnoeic and hypotensive.
 Evaluate
 Criteria for referring to ICU
 Criteria for immediate artificial ventilation
 How will you monitor in ICU
 Mention the parameters to be monitored of a ventilatory patients in ICU
 What the haemodynamic supports usually used in ICU.

d) A 55-year-old male with severe respiratory distress and hypertension is

admitted in ICU.
 Investigations
 Indications for mechanical ventilation
 Modes of ventilation
 Complications of a prolonged stay in ICU
 Weaning criteria

e) A 40-year-old male with high fever, respiratory distress and hypotension is

admitted in ICU.
 Investigations with reasoning
 Mx of hypotension
 How will you choose antibiotic for the patient?
 Assess the patient for requirement of mechanical ventilation
 Indications for tracheostomy.
 General care of a patient on ventilator.*

Dr. K H Mozumder
 697

f) A 12-year-old girl with rapid shallow breathing and progressive paresis

starting from lower limbs with H/O fever few days back is admitted in ICU.
 Approach/proceed to dx
 Investigations
 PEEP- ind, contraind
 Complications of long term ventilation.
 Mx of VAP.*
 Indications & complications of tracheostomy
 Factors predisposing to thromboembolism

g) A 60-year-old male with fever, hypotension and difficulty in breathing is

admitted in ICU. He underwent a Whipple’s operation 5 days back.
 Approach/proceed to dx
 Define SIRS, sepsis, septic shock
 Principles of mx of septic shock

Dr. K H Mozumder
 698

Dr. K H Mozumder
 699

Dr. K H Mozumder
 700

Dr. K H Mozumder
 701

Dr. K H Mozumder
 702

Dr. K H Mozumder
 703

Dr. K H Mozumder
 704

Dr. K H Mozumder
 705

Dr. K H Mozumder
 706

Dr. K H Mozumder
 707

Dr. K H Mozumder