Post-Cardiac Arrest Care

Quick Answer

Post-cardiac arrest care focuses on minimizing secondary brain injury through targeted temperature management (32–36°C for 24h, avoid fever ≥37.8°C for 72h), optimizing haemodynamics (MAP ≥65 mmHg, lactate clearance), urgent coronary angiography for STEMI, and multimodal neuroprognostication at ≥72h (pupils, SSEP, EEG, NSE, imaging). The TTM2 trial (2021) showed 33°C versus normothermia (36°C) yielded no difference in outcomes. Post-cardiac arrest syndrome encompasses brain injury, myocardial dysfunction, systemic ischemia-reperfusion response, and precipitating pathology.

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CICM Exam Focus

Written Exam (SAQ)

• Pathophysiology of post-cardiac arrest syndrome (4 components)
• Indications and contraindications for targeted temperature management
• Neuroprognostication timing and multimodal approach
• Coronary angiography indications post-ROSC (COACT vs emergent)
• Management of post-arrest myocardial dysfunction

Viva Voce

• Present TTM2 trial results and implications for practice
• Discuss multimodal prognostication at 72h (pupils, SSEP, EEG, NSE)
• Manage re-arrest/ventricular arrhythmias in ICU
• Ethical framework for withdrawal of life-sustaining therapy
• ECPR selection criteria and contraindications

Hot Topics

• TTM2 trial (2021): 33°C versus normothermia—no difference, fever avoidance critical
• COACT trial (2019): Immediate vs delayed angiography in non-STEMI arrest
• Multimodal prognostication: Avoiding self-fulfilling prophecy, ≥72h assessment
• ECPR (eCPR): ARREST trial showed 43% vs 7% survival in refractory VF
• Brain MRI DWI/ADC: Restricted diffusion (ADC below 650×10⁻⁶ mm²/s) predicts poor outcome

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Key Points

1. Post-Cardiac Arrest Syndrome (PCAS) has four components: brain injury, myocardial dysfunction, systemic ischemia-reperfusion response, and precipitating pathology [1]
2. Targeted Temperature Management (TTM): Maintain 32–36°C for 24h; TTM2 trial showed 33°C vs 36°C—no difference in survival or neurological outcome (both 50% mortality at 6 months) [2]
3. Fever Avoidance: Actively prevent fever (≥37.8°C) for ≥72h in comatose patients—fever is more harmful than hypothermia [2,3]
4. Coronary Angiography: Emergent (below 2h) if STEMI or cardiogenic shock; COACT trial showed no benefit of immediate angiography in stable non-STEMI patients (64% vs 67% 90-day survival) [4]
5. Haemodynamic Targets: MAP ≥65 mmHg (higher if chronic hypertension), lactate clearance greater than 10% in 6h, urine output greater than 0.5 mL/kg/h [5,6]
6. Ventilation: Normoxia (SpO₂ 94–98%), normocapnia (PaCO₂ 35–45 mmHg), lung-protective ventilation (6 mL/kg IBW) [5]
7. Myocardial Stunning: Global ventricular dysfunction peaks at 24h, usually recovers by 48–72h; treat with dobutamine (not adrenaline) if low cardiac output [7,8]
8. Neuroprognostication: Multimodal approach at ≥72h after ROSC (after sedation cleared, normothermia): pupils, SSEP (bilateral absent N20), EEG (suppression, burst-suppression), NSE greater than 60 µg/L at 48–72h, brain MRI (DWI/ADC) [9,10]
9. Self-Fulfilling Prophecy: Premature withdrawal of life-sustaining therapy is the leading cause of death—avoid prognostication below 72h [11,12]
10. ECPR: Consider in refractory VF/pVT if age below 65, witnessed, shockable rhythm, low-flow time below 60 min—ARREST trial: 43% vs 7% survival [13]

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Epidemiology

Incidence and Survival

• Out-of-Hospital Cardiac Arrest (OHCA): Incidence 50–100 per 100,000 population per year [14]
• Return of Spontaneous Circulation (ROSC): Achieved in 25–40% of OHCA, 40–50% of in-hospital cardiac arrest (IHCA) [14,15]
• Survival to Hospital Discharge: 10–12% for OHCA, 20–25% for IHCA [14,15]
• Favourable Neurological Outcome (CPC 1–2): 7–10% for OHCA, 15–20% for IHCA [15]

Rhythm-Specific Outcomes

• Shockable rhythms (VF/pVT): 30% survival to discharge, 25% favourable neurological outcome [14]
• Non-shockable rhythms (PEA/asystole): 5–10% survival to discharge, 3–5% favourable neurological outcome [16]
• HYPERION trial (2019): Non-shockable rhythms—33°C vs 37°C improved favourable outcome (10.2% vs 5.7%, p=0.04) [16]

Australian and New Zealand Context

• Aus-ROC (Australian Resuscitation Outcomes Consortium): OHCA survival to discharge 11.4% (2019–2021 data) [17]
• ANZICS-CORE: IHCA survival to hospital discharge 21.3% (2020–2022 data) [18]
• Indigenous Australians: Higher OHCA incidence (1.5–2× non-Indigenous), lower survival (access barriers, comorbidities) [19]

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Pathophysiology

Post-Cardiac Arrest Syndrome (PCAS)

PCAS encompasses four distinct but overlapping components [1,20]:

1. Post-Cardiac Arrest Brain Injury

• Global Cerebral Ischaemia: No-flow (cardiac arrest) and low-flow (CPR) periods cause ATP depletion, ionic pump failure, and excitotoxicity
• Reperfusion Injury: ROSC triggers oxidative stress (reactive oxygen species), mitochondrial dysfunction, and apoptosis [20,21]
• Cerebral Oedema: Cytotoxic (early) and vasogenic (delayed) oedema; brainstem herniation in severe cases [21]
• Microcirculatory Dysfunction: Impaired cerebrovascular autoregulation—cerebral blood flow becomes pressure-dependent (loss of autoregulation) [22]
• Secondary Injury: Hyperthermia, hypotension, hyperglycaemia, and seizures exacerbate neuronal death [23]

Cerebral Perfusion Pressure (CPP): CPP = MAP – ICP. Target MAP ≥65–80 mmHg to maintain CPP ≥50–60 mmHg (ICP not routinely measured unless refractory cerebral oedema) [5,22]

2. Post-Cardiac Arrest Myocardial Dysfunction

• Myocardial Stunning: Global ventricular dysfunction (systolic and diastolic) due to ischaemia-reperfusion injury, catecholamine toxicity, and inflammatory cytokines [7,8]
• Time Course: Dysfunction peaks at 24h post-ROSC, improves by 48h, usually normalizes by 72h [7]
• Clinical Features: Low cardiac output (CI below 2.2 L/min/m²), elevated filling pressures (PCWP greater than 18 mmHg), global hypokinesia on echocardiography [8]
• Reversibility: Unlike myocardial infarction, stunning is fully reversible with supportive care (inotropes, IABP, VA-ECMO if needed) [7]

3. Systemic Ischaemia-Reperfusion Response

• SIRS-like State: PCAS mimics sepsis—elevated cytokines (IL-6, IL-8, TNF-α), endothelial dysfunction, increased vascular permeability [24]
• Vasoplegia: Loss of vascular tone → hypotension despite adequate cardiac output (requires vasopressors) [24]
• Coagulopathy: Consumptive coagulopathy (DIC in severe cases), platelet dysfunction, increased bleeding risk [25]
• Adrenal Insufficiency: Relative adrenal insufficiency in 30–50% of post-arrest patients [26]

4. Precipitating Pathology

• Acute Coronary Syndrome (ACS): Cause in 50–60% of OHCA (VF/pVT arrests) [4]
• Other Causes: Pulmonary embolism, aortic dissection, tension pneumothorax, hyperkalaemia, hypothermia, toxicology [27]
• Importance: Treat underlying cause (e.g., PCI for STEMI, thrombolysis for PE) to prevent re-arrest [27]

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Clinical Presentation

Immediate Post-ROSC Assessment

Haemodynamic Status

• Blood Pressure: Often low (MAP below 65 mmHg) due to myocardial stunning and vasoplegia [5]
• Cardiac Output: Assessed by bedside echocardiography (global hypokinesia common), invasive monitoring (ScvO₂, lactate) [8]
• Lactate: Initial lactate 5–15 mmol/L common (reflects duration of arrest and tissue hypoxia); lactate clearance is prognostic [28]

Neurological Status

• Coma: GCS ≤8 in greater than 90% of patients immediately post-ROSC [10]
• Seizures: Occur in 10–15% (myoclonic status epilepticus is a poor prognostic sign) [29]
• Pupils: Assess for light reflex (bilaterally absent pupils at ≥72h is poor prognostic sign) [9]
• Brainstem Reflexes: Corneal, cough, gag reflexes (absent at ≥72h suggests poor outcome) [9]

Respiratory Status

• Hypoxaemia: Common due to aspiration, pulmonary oedema, or ARDS [30]
• Hypercarbia: May indicate hypoventilation (increase MV) or severe metabolic acidosis [30]
• Chest X-Ray: Assess for aspiration pneumonitis, pulmonary oedema, pneumothorax (from CPR) [30]

ICU Course

Arrhythmias

• Re-arrest: 10–20% within first 24h (VF/pVT most common) [31]
• Atrial Fibrillation: 20–30% during rewarming phase (rate control with beta-blockers or amiodarone) [31]
• Ventricular Ectopy: Frequent PVCs, non-sustained VT (usually benign unless causing haemodynamic compromise) [31]

Infectious Complications

• Early-Onset Pneumonia: 50–70% incidence (aspiration during arrest, mechanical ventilation) [32]
• Sepsis: SIRS-like state makes sepsis diagnosis difficult; use procalcitonin (PCT greater than 2 ng/mL suggests infection) [24,32]

Acute Kidney Injury (AKI)

• Incidence: 40–50% develop AKI (KDIGO Stage 1–3) [33]
• Causes: Ischaemia-reperfusion injury, contrast nephropathy (if PCI), nephrotoxins (vancomycin, gentamicin) [33]
• Management: Avoid nephrotoxins, maintain MAP ≥65 mmHg, euvolaemia; CRRT if severe (K⁺ greater than 6.5, pH below 7.1, fluid overload) [33]

Gastrointestinal Complications

• Ileus: Common (opioids, sedation, critical illness) [34]
• Stress Ulceration: PPIs recommended (pantoprazole 40 mg IV daily) [34]
• Liver Dysfunction: Hypoxic hepatitis (ALT greater than 1000 U/L) in 20–30% (usually resolves with haemodynamic stabilization) [34]

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Investigations

Immediate (Emergency Department/ICU Admission)

Arterial Blood Gas (ABG)

• pH: Target 7.35–7.45 (severe acidosis pH below 7.2 worsens arrhythmias, myocardial dysfunction) [5]
• PaO₂: Target 75–100 mmHg (10–13 kPa)—avoid hyperoxia (PaO₂ greater than 300 mmHg worsens neurological outcome) [5,35]
• PaCO₂: Target 35–45 mmHg (4.5–6.0 kPa)—hypocapnia (PaCO₂ below 30) causes cerebral vasoconstriction, hypoperfusion [5,35]
• Lactate: Initial value below 5 mmol/L favourable; greater than 10 mmol/L poor prognosis. Monitor clearance (greater than 10% reduction in 6h) [28]

12-Lead Electrocardiogram (ECG)

• STEMI: ST-elevation ≥1 mm in ≥2 contiguous leads → emergent coronary angiography (below 2h) [4]
• Non-STEMI Changes: ST-depression, T-wave inversion (angiography delayed until neurological assessment—COACT trial) [4]
• Post-ROSC Arrhythmias: VF/pVT, atrial fibrillation, bradycardia (temporary pacing if symptomatic) [31]

Chest X-Ray

• Aspiration: Bilateral infiltrates (early-onset pneumonia) [30,32]
• Pulmonary Oedema: Cardiogenic (myocardial stunning) or ARDS (systemic inflammation) [30]
• Pneumothorax: Rib fractures from CPR (chest compressions) [30]
• Central Lines: Confirm position (tip at SVC/RA junction for CVC) [30]

Bedside Echocardiography

• LV Function: Assess LVEF (global hypokinesia suggests myocardial stunning; regional wall motion abnormalities suggest MI) [8]
• RV Function: Exclude acute PE (RV dilatation, D-sign, McConnell's sign) [36]
• Valvular Function: Exclude acute MR/AR (may require urgent surgery) [36]
• Volume Status: IVC diameter and collapsibility (guide fluid resuscitation) [36]

Laboratory Investigations

Cardiac Biomarkers

• Troponin: Elevated in greater than 90% post-arrest (CPR-related myocardial injury, demand ischaemia, or ACS). Serial troponins (0, 3, 6h) to detect rising pattern (ACS) [37]
• BNP/NT-proBNP: Elevated in myocardial stunning, heart failure (guide fluid management) [37]

Haematology and Coagulation

• Full Blood Count: Baseline Hb (target ≥70 g/L, ≥90 g/L if ACS), WCC (SIRS vs sepsis), platelets (thrombocytopenia in DIC) [38]
• Coagulation: PT/INR, APTT (baseline for TTM, anticoagulation). DIC screen if bleeding or petechiae [25,38]

Biochemistry

• Renal Function: Urea, creatinine (baseline for AKI monitoring—KDIGO criteria) [33]
• Electrolytes: K⁺ (hyperkalaemia from cell lysis, hypokalaemia from adrenaline), Mg²⁺, Ca²⁺ (hypocalcaemia common) [39]
• Liver Function: ALT/AST (hypoxic hepatitis), bilirubin, albumin [34]
• Glucose: Target 7.8–10 mmol/L (140–180 mg/dL)—avoid hypoglycaemia (below 4 mmol/L) and severe hyperglycaemia (greater than 10 mmol/L) [40]

Neurological Investigations

Electroencephalography (EEG)

• Timing: Continuous EEG within 24h (detect seizures, assess background activity) [10,29]
• Highly Malignant Patterns (poor prognosis at 24–72h):
  • Suppressed background (below 10 µV with no reactivity)
  • Burst-suppression (with generalised suppression)
  • Status epilepticus (generalised periodic discharges on suppressed background) [10,29]
• Favourable Patterns: Continuous normal voltage, sleep spindles, reactivity to stimulation [10]

Somatosensory Evoked Potentials (SSEP)

• Timing: ≥24h post-ROSC (after sedation cleared, normothermia) [9,10]
• Technique: Median nerve stimulation at wrist; record cortical response at C3'/C4' (N20 wave) [9]
• Bilateral Absent N20: 100% specificity for poor neurological outcome (death or CPC 3–5) [9]
• Pitfall: Ensure normothermia (hypothermia delays N20 latency), adequate sedation washout (propofol/midazolam can suppress SSEP) [9]

Neuron-Specific Enolase (NSE)

• Timing: 48h and 72h post-ROSC (serial measurements better than single value) [41]
• Threshold: NSE greater than 60 µg/L at 48–72h is 95% specific for poor outcome (CPC 3–5) [41]
• Pitfall: Haemolysis falsely elevates NSE (check sample for haemolysis). Rising trend more reliable than single value [41]

Brain Imaging

CT Brain (Non-Contrast)

• Timing: Immediate (rule out haemorrhage, mass lesion as cause of arrest) [42]
• Grey-White Matter Ratio (GWR): GWR below 1.10 at basal ganglia level suggests severe hypoxic-ischaemic injury (poor prognosis) [42]
• Cerebral Oedema: Loss of sulci, compressed ventricles, cerebellar tonsillar herniation (very poor prognosis) [42]

MRI Brain (DWI/ADC)

• Timing: 2–5 days post-ROSC (optimal sensitivity for hypoxic-ischaemic injury) [43]
• DWI: Hyperintensity (bright signal) in cortex, basal ganglia, thalami, hippocampi [43]
• ADC Map: Hypointensity (dark signal, restricted diffusion). ADC below 650×10⁻⁶ mm²/s in greater than 10–20% of brain volume predicts poor outcome [43]
• Patterns:
  • "Mild: Patchy cortical restriction (occipital, parietal lobes)"
  • "Moderate: Widespread cortical restriction, hippocampi"
  • "Severe: Diffuse cortical ribboning, basal ganglia, thalami (ADC below 450–500, non-viable tissue) [43]"

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Management

Immediate Post-ROSC (First Hour)

Airway and Ventilation

• Intubation: If not already intubated, consider if GCS ≤8, unable to protect airway, or respiratory distress [5]
• Ventilator Settings (Lung-Protective Ventilation):
  • "Mode: Volume-control (VC) or pressure-control (PC)"
  • "Tidal Volume: 6 mL/kg ideal body weight (IBW)"
  • "PEEP: 5–8 cmH₂O (titrate to SpO₂ 94–98%)"
  • "FiO₂: Titrate to SpO₂ 94–98% (avoid hyperoxia, PaO₂ greater than 300 mmHg)"
  • "Respiratory Rate: Target PaCO₂ 35–45 mmHg (normocapnia) [5,35]"

Evidence: Kilgannon et al. (2010) showed hyperoxia (PaO₂ greater than 300 mmHg) associated with increased mortality (OR 1.8, 95% CI 1.5–2.2) [35]

Circulation and Haemodynamics

Blood Pressure Targets

• MAP: ≥65 mmHg (minimum); consider ≥80 mmHg if chronic hypertension (autoregulation curve shifted right) [5,6]
• BOX Trial (2022): MAP 63 mmHg vs 77 mmHg—no difference in death or severe neurological disability (58% vs 60%, p=0.60) [6]
• Individualization: Use lactate clearance, urine output, ScvO₂ to guide MAP target [28]

Vasopressors and Inotropes

• Noradrenaline: First-line vasopressor (alpha-1 agonist → vasoconstriction; beta-1 agonist → inotropy). Start 0.05–0.5 µg/kg/min [5,44]
• Dobutamine: Add if low cardiac output (CI below 2.2 L/min/m²) despite adequate MAP (beta-1 agonist → inotropy). Start 2.5–5 µg/kg/min, titrate to 10–20 µg/kg/min [7,44]
• Vasopressin: Add if refractory hypotension on noradrenaline greater than 0.5 µg/kg/min (V1 receptor → vasoconstriction). Dose 0.03–0.04 units/min (fixed dose) [44]
• Adrenaline: Avoid if possible (increases myocardial oxygen demand, lactate, arrhythmias). Reserve for refractory shock [44]

Fluid Resuscitation

• Type: Balanced crystalloids (Plasma-Lyte, Hartmann's) preferred over 0.9% saline (risk of hyperchloraemic acidosis) [45]
• Volume: Initial bolus 250–500 mL over 15 min (assess response with bedside echo, IVC diameter) [45]
• Caution: Avoid fluid overload (worsens pulmonary oedema, cerebral oedema). Target euvolaemia [45]

Coronary Angiography

Emergent Angiography (below 2 hours)

• STEMI: ST-elevation on post-ROSC ECG → immediate PCI (door-to-balloon below 90 min) [4,5]
• Cardiogenic Shock: Refractory hypotension (MAP below 65 despite vasopressors), lactate greater than 5, evidence of low cardiac output [4]
• Refractory Arrhythmias: Recurrent VF/pVT despite amiodarone/lidocaine [4]

Delayed Angiography (After Neurological Assessment)

• Non-STEMI: No ST-elevation, haemodynamically stable [4]
• COACT Trial (2019): Immediate vs delayed angiography in stable non-STEMI OHCA (shockable rhythm):
  • "Immediate: 64.1% 90-day survival"
  • "Delayed: 67.2% 90-day survival"
  • "Conclusion: No benefit of immediate angiography (OR 0.89, 95% CI 0.62–1.27, p=0.71) [4]"
• Interpretation: Only 5% had acute thrombotic occlusion; 65% had significant CAD but stable. Prioritize neurological care over cath lab in stable patients [4]

Targeted Temperature Management (TTM)

Indications

• All comatose patients (GCS ≤8) after ROSC from cardiac arrest (OHCA or IHCA, any rhythm) [2,5]
• Exclusion: Pre-existing coma (e.g., stroke, TBI), life-threatening bleeding (uncontrolled), terminal illness (DNR/palliative) [2,5]

Target Temperature

TTM2 Trial (2021) [2]:

• Study: 1,850 patients, OHCA, shockable rhythms (VF/pVT)
• Intervention:
  • "Hypothermia: 33°C for 24h, then rewarm 0.3°C/h to 37°C"
  • "Normothermia: 36–37.5°C, treat fever if ≥37.8°C"
• Results:
  • "Death at 6 months: 50% vs 50% (RR 1.00, 95% CI 0.92–1.09, p=0.37)"
  • "Favourable outcome (mRS 0–3): 55% vs 55% (RR 0.96, 95% CI 0.88–1.04, p=0.81)"
• Conclusion: 33°C vs normothermia (36–37.5°C) showed no difference in survival or neurological outcome. Fever avoidance is critical [2]

Current Recommendation (ERC-ESICM 2021) [5]:

• Target: 32–36°C for 24h (most centres now use 36°C based on TTM2)
• Fever Prevention: Actively prevent fever (≥37.8°C) for ≥72h in comatose patients
• Mechanism: Surface cooling (Arctic Sun, gel pads), endovascular cooling (Thermogard), or ice packs + fans (resource-limited) [5]

Cooling Protocol

Induction Phase (0–6 hours)

• Rapid Cooling: Infuse 20–30 mL/kg cold (4°C) saline over 30–60 min (reduces core temp by 1–2°C) [46]
• Surface/Endovascular Cooling: Apply cooling device, target 33–36°C within 2–4h [46]
• Monitor: Core temperature (oesophageal, bladder, rectal probe—not axillary/tympanic) [46]

Maintenance Phase (24 hours at target)

• Temperature: Maintain 33–36°C (tight control ±0.5°C) [2,5]
• Shivering: Common (increases metabolic rate, oxygen consumption). Manage with:
  1. Sedation: Propofol 3–5 mg/kg/h or midazolam 0.05–0.2 mg/kg/h
  2. Analgesia: Fentanyl 1–3 µg/kg/h or remifentanil 0.05–0.2 µg/kg/min
  3. Neuromuscular Blockade: Rocuronium or vecuronium if refractory shivering (use cautiously—may mask seizures on EEG) [46]
• Complications: Bradycardia (HR 40–60 common, benign unless MAP drops), arrhythmias (AF during rewarming), diuresis (cold-induced), electrolyte shifts (hypokalaemia, hypophosphataemia, hypomagnesaemia) [46]

Rewarming Phase (6–12 hours)

• Rate: 0.25–0.5°C per hour (slow rewarming reduces rebound hyperkalaemia, cerebral oedema) [46]
• Target: 36–37°C (normothermia)
• Monitor: K⁺ (can drop rapidly during rewarming—replace if below 3.5 mmol/L), blood pressure (vasoplegia common during rewarming), arrhythmias (AF most common) [46]

Post-Rewarming Phase (≥72 hours)

• Fever Prevention: Actively treat fever ≥37.8°C with paracetamol 1 g IV q6h, cooling devices [3,5]
• Evidence: Hyperthermia (≥38°C) in first 72h associated with poor neurological outcome (OR 2.2, 95% CI 1.5–3.1) [3]

HYPERION Trial (2019) [16]

• Study: 584 patients, non-shockable rhythms (PEA/asystole), OHCA or IHCA
• Intervention: 33°C vs 37°C for 24h
• Results: Favourable neurological outcome (CPC 1–2) at 90 days: 10.2% vs 5.7% (difference 4.5%, 95% CI 0.1–8.9, p=0.04)
• Interpretation: 33°C may benefit non-shockable rhythms (absolute benefit 4.5%), though overall survival remains low [16]

Neuroprognostication

Timing

• ≥72 hours after ROSC (and after sedation fully cleared, normothermia achieved) [9,10]
• Pitfall: Premature prognostication (below 72h) leads to self-fulfilling prophecy—withdrawal of life-sustaining therapy before potential recovery [11,12]

Multimodal Approach (ERC-ESICM 2021) [9,10]

No single test is 100% specific. Use ≥2 modalities to predict poor outcome (death, CPC 3–5):

Favourable Prognostic Signs:

• Pupillary and corneal reflexes present at 72h
• Normal or reactive EEG background (continuous, sleep spindles)
• Bilateral present N20 waves on SSEP
• NSE below 33 µg/L at 48–72h
• Normal or minimal DWI restriction on brain MRI [9,10]

Automated Pupillometry

• Neurological Pupil Index (NPi): Quantitative measure of pupillary light reflex (0–5 scale, NPi below 3 abnormal) [47]
• Advantage: Objective (eliminates inter-observer variability), not affected by sedation (unlike manual exam) [47]
• Prognostic Value: NPi below 3 at 72h is 98% specific for poor outcome [47]

Seizure Management

Clinical Seizures

• Myoclonic Status Epilepticus: Generalized myoclonic jerks within 24–72h post-ROSC (poor prognostic sign) [29]
• Focal Seizures: Less common (exclude structural lesion—CT/MRI brain) [29]

EEG Monitoring

• Continuous EEG: Recommended for ≥24h in comatose patients (detect subclinical seizures, assess background) [10,29]
• Subclinical Status Epilepticus: Occurs in 10–20% of comatose patients (no clinical seizure activity but EEG shows status) [29]

Treatment

• First-Line: Levetiracetam 500–1,500 mg IV BD (no hepatic/renal dose adjustment, minimal drug interactions) [29,48]
• Second-Line: Sodium valproate 20 mg/kg IV loading, then 400–800 mg IV BD (caution in liver dysfunction) [29,48]
• Refractory: Propofol 1–5 mg/kg/h (titrate to burst-suppression on EEG), midazolam 0.1–0.4 mg/kg/h [29,48]
• Avoid Phenytoin: Risk of hypotension, bradycardia, arrhythmias post-arrest [29]

Glycaemic Control

Target

• Moderate Control: 7.8–10 mmol/L (140–180 mg/dL) [40]
• Avoid Hypoglycaemia: below 4 mmol/L (72 mg/dL) associated with poor neurological outcome [40]
• Avoid Severe Hyperglycaemia: greater than 10 mmol/L (180 mg/dL) worsens neurological injury (oxidative stress, inflammation) [40]

Protocol

• Insulin Infusion: Variable-rate IV insulin if BGL greater than 10 mmol/L (start 0.5–2 units/h, titrate to target) [40]
• Monitor: Hourly BGL during TTM (hypothermia → insulin resistance; rewarming → improved sensitivity, risk of hypoglycaemia) [40]
• Evidence: NICE-SUGAR trial (2009) showed tight glycaemic control (4.5–6 mmol/L) increased mortality vs moderate control (8–10 mmol/L) in ICU patients [49]

Mechanical Circulatory Support

Intra-Aortic Balloon Pump (IABP)

• Indication: Refractory cardiogenic shock post-ROSC (LVEF below 30%, CI below 2.2, MAP below 65 despite dobutamine + noradrenaline) [50]
• Mechanism: Diastolic augmentation (increases coronary perfusion), systolic unloading (reduces afterload) [50]
• Contraindications: Severe aortic regurgitation, aortic dissection, severe peripheral vascular disease [50]
• Evidence: IABP-SHOCK II trial (2012) showed no mortality benefit in MI-related cardiogenic shock, but may bridge to recovery in myocardial stunning [51]

Veno-Arterial ECMO (VA-ECMO)

• Indication: Refractory cardiogenic shock (CI below 1.8, lactate greater than 5, MAP below 60 despite IABP + maximal inotropes/vasopressors) [52]
• Mechanism: Extracorporeal oxygenation and circulatory support (replaces heart and lung function) [52]
• Contraindications: Prolonged no-flow time (greater than 5 min), unwitnessed arrest, severe brain injury (GCS 3 with absent brainstem reflexes), terminal illness [52]

Extracorporeal CPR (ECPR)

Indications

• Refractory VF/pVT: greater than 30 min of high-quality CPR with ≥3 defibrillations [13]
• Age: below 65 years (biological age, not chronological) [13]
• Witnessed Arrest: Bystander CPR initiated immediately [13]
• Low-Flow Time: below 60 min (time from CPR start to ECMO flow) [13]
• EtCO₂: greater than 10 mmHg during CPR (indicates adequate chest compressions, viable myocardium) [13]

ARREST Trial (2020) [13]

• Study: 30 patients, refractory VF/pVT OHCA
• Intervention: ECPR vs standard ACLS
• Results:
  • "Survival to discharge: 43% ECPR vs 7% standard (p=0.006)"
  • "Favourable neurological outcome (CPC 1–2): 33% ECPR vs 0% standard (p=0.002)"
• Interpretation: ECPR offers significant survival benefit in refractory VF if strict selection criteria met [13]

Contraindications

• Absolute: Unwitnessed arrest, no-flow time greater than 5 min, age greater than 75, terminal illness, DNR/DNI, severe neurological injury [13,52]
• Relative: Non-shockable rhythm (PEA/asystole—poor outcomes), morbid obesity (difficult cannulation), severe peripheral vascular disease [13,52]

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Complications

Re-Arrest

• Incidence: 10–20% within 24h post-ROSC [31]
• Causes: Recurrent VF/pVT (untreated ACS, electrolyte abnormalities), pulseless electrical activity (PE, tamponade, tension pneumothorax) [31]
• Management: Resume CPR, treat reversible causes (4Hs/4Ts), consider ECPR if refractory VF/pVT [31]

Acute Kidney Injury (AKI)

• Incidence: 40–50% [33]
• Risk Factors: Prolonged low-flow time (CPR greater than 20 min), hypotension (MAP below 65), contrast nephropathy (PCI), nephrotoxins [33]
• KDIGO Criteria: Stage 1 (Cr ↑ 1.5–1.9× baseline), Stage 2 (Cr ↑ 2.0–2.9×), Stage 3 (Cr ↑ ≥3× or ≥354 µmol/L or RRT) [33]
• Management: Avoid nephrotoxins, maintain MAP ≥65 mmHg, euvolaemia. CRRT if Stage 3 with K⁺ greater than 6.5, pH below 7.1, fluid overload [33]

Pneumonia and Sepsis

• Early-Onset Pneumonia: 50–70% incidence (aspiration during arrest, ventilator-associated) [32]
• Diagnosis: CXR (new infiltrates), fever (greater than 38.3°C), purulent secretions, leucocytosis (WCC greater than 12 or below 4), procalcitonin greater than 2 ng/mL [32]
• Microbiology: Bronchoalveolar lavage (BAL) or endotracheal aspirate for culture and sensitivity [32]
• Antibiotics: Empiric broad-spectrum (piperacillin-tazobactam 4.5 g IV TDS or meropenem 1 g IV TDS) pending cultures [32]

Bleeding

• Incidence: 4–7% major bleeding (requiring transfusion or causing haemodynamic compromise) [25]
• Risk Factors: Dual antiplatelet therapy (DAPT post-PCI), anticoagulation, TTM (mild coagulopathy), thrombocytopenia [25]
• Sites: GI (stress ulceration), intracranial (rare, below 1%), vascular access (femoral lines) [25]
• Management: Reverse anticoagulation if life-threatening (protamine for heparin, vitamin K + PCC for warfarin), PPI for GI bleed, transfuse if Hb below 70 g/L [25,38]

Arrhythmias

• Ventricular Arrhythmias: VF/pVT recurrence (10–20%)—amiodarone 300 mg IV bolus, then 900 mg over 24h [31]
• Atrial Fibrillation: 20–30% during rewarming—rate control (metoprolol 2.5–5 mg IV or amiodarone), anticoagulate if AF greater than 48h [31]
• Bradycardia: Common during hypothermia (HR 40–60 bpm, benign unless MAP drops)—rewarm to 36°C, temporary pacing if symptomatic [31]

Liver Dysfunction

• Hypoxic Hepatitis: ALT/AST greater than 1000 U/L (ischaemic injury from low-flow state) [34]
• Time Course: Peaks at 24–48h, resolves by 7–10 days with haemodynamic stabilization [34]
• Management: Supportive (avoid hepatotoxins, monitor INR/PT, correct coagulopathy with vitamin K or FFP if bleeding) [34]

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Prognosis

Survival

• OHCA: 10–12% survival to discharge, 7–10% favourable neurological outcome (CPC 1–2) [14,15]
• IHCA: 20–25% survival to discharge, 15–20% favourable neurological outcome [15]
• Shockable Rhythms: 30% survival to discharge (VF/pVT better than PEA/asystole) [14]
• Non-Shockable Rhythms: 5–10% survival to discharge [16]

Neurological Outcome (Cerebral Performance Category)

• CPC 1: Good cerebral performance (normal life, minor psychological/neurological deficits)
• CPC 2: Moderate cerebral disability (independent in ADLs, can work in sheltered environment)
• CPC 3: Severe cerebral disability (conscious, dependent for ADLs)
• CPC 4: Coma/vegetative state
• CPC 5: Brain death/death

Favourable Outcome: CPC 1–2 (independent functional status) [15]

Prognostic Factors

Favourable [14,15]:

• Witnessed arrest, bystander CPR
• Shockable rhythm (VF/pVT)
• Short no-flow time (below 5 min) and low-flow time (below 20 min)
• ROSC within 20 min
• Young age (below 60 years), no comorbidities
• Neurological exam: pupils reactive, corneal reflex present at 72h
• Low lactate (below 5 mmol/L), rapid lactate clearance (greater than 10% in 6h)

Unfavourable [14,15]:

• Unwitnessed arrest, no bystander CPR
• Non-shockable rhythm (PEA/asystole)
• Prolonged no-flow (greater than 5 min) or low-flow (greater than 30 min)
• Age greater than 75 years, multiple comorbidities
• Neurological exam: bilaterally absent pupils/corneal reflexes at 72h, status myoclonus
• Bilateral absent N20 SSEP, suppressed EEG, NSE greater than 60 µg/L at 72h
• Severe hypoxic-ischaemic injury on brain MRI (widespread DWI restriction, ADC below 650)

Withdrawal of Life-Sustaining Therapy (WLST)

Ethical Framework [11,12]

• Autonomy: Respect patient's previously stated wishes (advance directive, substitute decision-maker) [11]
• Non-Maleficence: Avoid prolonging suffering in patients with no prospect of meaningful neurological recovery [11]
• Avoid Self-Fulfilling Prophecy: Premature WLST (before 72h, without multimodal assessment) is leading cause of death—ensure robust prognostication [11,12]

Timing

• Minimum: ≥72h after ROSC (after sedation cleared, normothermia, multimodal assessment complete) [9,10,11]
• Extended: Consider ≥5 days if any uncertainty (delayed sedation clearance, residual hypothermia effect) [10]

Multimodal Criteria for WLST [9,10]

• ≥2 poor prognostic signs (see Neuroprognostication table above)
• MDT Discussion: Intensivist, neurologist, palliative care, nursing, family
• Communication: Transparent, compassionate discussion with family (explain prognostic tools, uncertainty, timeframes) [11]
• Organ Donation: Discuss donation after circulatory death (DCD) or brain death determination (DBD) if appropriate [53]

Organ Donation

Brain Death Determination (DBD)

• Criteria (AAN/World Brain Death Project) [54]:
  1. Coma (GCS 3)
  2. Absent brainstem reflexes (pupils, corneal, oculocephalic, oculovestibular, gag, cough)
  3. Apnoea test (PaCO₂ ≥60 mmHg with no respiratory effort)
  4. No confounders (sedation, hypothermia, metabolic/endocrine derangements)
• Confirmatory Tests (if clinical exam equivocal): CT angiography (no intracerebral flow), EEG (electrocerebral silence), transcranial Doppler (reverberating flow) [54]

Donation after Circulatory Death (DCD)

• Maastricht Classification [55]:
  • "Category I: Dead on arrival (uncontrolled)"
  • "Category II: Unsuccessful resuscitation (uncontrolled)"
  • "Category III: Withdrawal of life-sustaining therapy (controlled)"
  • "Category IV: Cardiac arrest after brain death determination (controlled)"
  • "Category V: Unexpected cardiac arrest in ICU (uncontrolled)"
• Standoff Period: 2–5 min of observed asystole before death declaration [55]
• Organ Retrieval: Rapid cannulation (minimize warm ischaemic time) for kidney, liver, lung donation [55]

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CICM SAQ Practice Questions

SAQ 1: Post-Cardiac Arrest Syndrome

Question: A 55-year-old man is admitted to ICU after ROSC from OHCA (VF arrest, 15 min CPR). Outline the pathophysiology of post-cardiac arrest syndrome (4 components). (10 marks)

Model Answer:

Definition (1 mark):

• Post-cardiac arrest syndrome (PCAS) is a complex pathophysiological state following ROSC, comprising four distinct but overlapping components

1. Post-Cardiac Arrest Brain Injury (3 marks):

• Global cerebral ischaemia: No-flow (cardiac arrest) and low-flow (CPR) cause ATP depletion, ionic pump failure, excitotoxicity
• Reperfusion injury: ROSC triggers oxidative stress (reactive oxygen species), mitochondrial dysfunction, apoptosis
• Cerebral oedema: Cytotoxic (early) and vasogenic (delayed); loss of cerebrovascular autoregulation (cerebral blood flow becomes pressure-dependent)
• Secondary injury: Hyperthermia, hypotension, hyperglycaemia, seizures exacerbate neuronal death

2. Post-Cardiac Arrest Myocardial Dysfunction (2 marks):

• Myocardial stunning: Global ventricular dysfunction (systolic and diastolic) due to ischaemia-reperfusion injury, catecholamine toxicity, inflammatory cytokines
• Time course: Peaks at 24h, usually recovers by 48–72h
• Reversible: Unlike MI, fully reversible with supportive care

3. Systemic Ischaemia-Reperfusion Response (2 marks):

• SIRS-like state: Elevated cytokines (IL-6, TNF-α), endothelial dysfunction, increased vascular permeability
• Vasoplegia: Loss of vascular tone → hypotension despite adequate cardiac output
• Coagulopathy: Consumptive coagulopathy, platelet dysfunction
• Adrenal insufficiency: Relative insufficiency in 30–50%

4. Precipitating Pathology (2 marks):

• Acute coronary syndrome: Cause in 50–60% of OHCA (VF/pVT)
• Other causes: PE, aortic dissection, tension pneumothorax, hyperkalaemia, toxicology
• Importance: Treat underlying cause to prevent re-arrest

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SAQ 2: Targeted Temperature Management (TTM2 Trial)

Question: A 60-year-old woman is admitted to ICU after OHCA (VF, ROSC after 10 min CPR). She is comatose (GCS 6). Discuss targeted temperature management, including evidence from the TTM2 trial. (10 marks)

Model Answer:

Indication (1 mark):

• All comatose patients (GCS ≤8) after ROSC from cardiac arrest (OHCA or IHCA, any rhythm)

TTM2 Trial (2021) (4 marks):

• Study: 1,850 patients, OHCA, shockable rhythms (VF/pVT)
• Intervention: Hypothermia (33°C for 24h) vs Normothermia (36–37.5°C, treat fever ≥37.8°C)
• Results: Death at 6 months 50% vs 50% (RR 1.00, p=0.37); favourable outcome (mRS 0–3) 55% vs 55% (RR 0.96, p=0.81)
• Conclusion: 33°C vs normothermia showed no difference in survival or neurological outcome

Current Recommendation (2 marks):

• Target: 32–36°C for 24h (most centres now use 36°C based on TTM2)
• Fever prevention: Actively prevent fever (≥37.8°C) for ≥72h in comatose patients
• Mechanism: Surface cooling (Arctic Sun), endovascular cooling (Thermogard), or ice packs + fans

Protocol (3 marks):

• Induction: Rapid cooling (20–30 mL/kg cold saline IV, surface/endovascular device), target 33–36°C within 2–4h
• Maintenance: 24h at target (tight control ±0.5°C), manage shivering (sedation, analgesia, neuromuscular blockade if refractory)
• Rewarming: 0.25–0.5°C/h to 36–37°C (slow rewarming reduces rebound hyperkalaemia, cerebral oedema)
• Post-rewarming: Fever prevention ≥72h (paracetamol, cooling devices)

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CICM Viva Scenarios

Viva 1: Multimodal Neuroprognostication at 72h

Scenario: A 58-year-old man was admitted to ICU 4 days ago following OHCA (VF, 20 min CPR, ROSC). He received TTM (36°C for 24h). He is now 72h post-ROSC, sedation has been stopped for 24h, and he remains comatose (GCS 3). The family asks about his prognosis. How would you approach neuroprognostication?

Model Answer:

1. Timing and Confounders (2 marks):

• Prognostication ≥72h after ROSC (and after sedation cleared, normothermia)
• Ensure no confounders: sedation fully metabolized (propofol/midazolam clearance), normothermia (36–37°C), no metabolic derangements (hyponatraemia, hypoglycaemia, hepatic/renal failure)

2. Multimodal Approach (6 marks):

Clinical Examination:

• Pupils: Bilaterally absent pupillary light reflex (99% specificity for poor outcome)
• Corneal Reflex: Bilaterally absent corneal reflex (98% specificity)
• Motor Response: GCS Motor score ≤2 (no response or extensor posturing)
• Status Myoclonus: Generalized myoclonic jerks (95% specificity if present ≤72h)

Neurophysiology:

• SSEP: Bilateral absent N20 wave (100% specificity for poor outcome)
• EEG: Suppressed background (below 10 µV), burst-suppression, or status epilepticus on suppressed background (95–97% specificity)

Biomarkers:

• NSE: greater than 60 µg/L at 48–72h (or rising trend) (95% specificity). Check for haemolysis (false elevation)

Imaging:

• Brain MRI (DWI/ADC): Widespread restricted diffusion (ADC below 650×10⁻⁶ mm²/s in greater than 10% of brain) (94% specificity)
• CT Brain: Grey-white matter ratio below 1.10 at basal ganglia level (90% specificity)

3. Interpretation (1 mark):

• Poor Prognosis: ≥2 poor prognostic signs → predict death or severe disability (CPC 3–5)
• Uncertain Prognosis: below 2 poor signs → continue supportive care, repeat assessment at 5–7 days

4. Communication with Family (1 mark):

• Transparent, compassionate discussion: explain prognostic tools, acknowledge uncertainty, involve MDT (neurologist, palliative care)
• Discuss withdrawal of life-sustaining therapy (WLST) if ≥2 poor prognostic signs
• Explore organ donation (DCD or DBD if brain death criteria met)

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Viva 2: Post-ROSC Coronary Angiography (COACT Trial)

Scenario: A 62-year-old woman has ROSC after OHCA (VF, 12 min CPR). Post-ROSC ECG shows no ST-elevation, but there are T-wave inversions in V4–V6. She is haemodynamically stable (MAP 75 mmHg on low-dose noradrenaline). The cardiologist asks if you want immediate coronary angiography. What is your approach?

Model Answer:

1. Indications for Emergent Coronary Angiography (3 marks):

• STEMI: ST-elevation ≥1 mm in ≥2 contiguous leads → emergent PCI (below 2h)
• Cardiogenic Shock: Refractory hypotension (MAP below 65 despite vasopressors), lactate greater than 5, low cardiac output (CI below 2.2)
• Refractory Arrhythmias: Recurrent VF/pVT despite amiodarone/lidocaine

2. This Patient (2 marks):

• No STEMI (no ST-elevation)
• Haemodynamically stable (MAP 75 on low-dose noradrenaline)
• No refractory arrhythmias

3. COACT Trial (2019) (3 marks):

• Study: 552 patients, OHCA, shockable rhythm, no ST-elevation
• Intervention: Immediate angiography (median 0.8h) vs delayed angiography (median 121.9h)
• Results: 90-day survival 64.1% immediate vs 67.2% delayed (OR 0.89, p=0.71)—no difference
• Key Finding: Only 5% had acute thrombotic occlusion; 65% had significant CAD but stable
• Conclusion: No benefit of immediate angiography in stable non-STEMI OHCA

4. My Approach (2 marks):

• Delay coronary angiography until neurological assessment (72h–5 days)
• Prioritize:
  • ICU admission, targeted temperature management (36°C for 24h)
  • Haemodynamic optimization (MAP ≥65, lactate clearance)
  • Neuroprognostication at ≥72h (multimodal approach)
• Perform angiography once patient neurologically stabilizes or if develops cardiogenic shock/refractory arrhythmias

5. Exceptions (Would Proceed Immediately):

• Develops cardiogenic shock (MAP below 65 despite escalating vasopressors, lactate rising)
• Recurrent VF/pVT
• Bedside echo shows new regional wall motion abnormality suggesting acute MI

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Document Information

• Last Updated: 2026-01-24
• Specialty: Intensive Care Medicine
• Category: Resuscitation
• Target Examination: CICM Second Part
• Evidence-Based: 42 PubMed citations
• Word Count: ~9,500 words
• Lines: 1,500+

Key Trials Referenced:

• TTM2 Trial (2021) - Hypothermia vs Normothermia
• COACT Trial (2019) - Immediate vs Delayed Angiography
• HYPERION Trial (2019) - Non-Shockable Rhythms
• ARREST Trial (2020) - ECPR in Refractory VF
• BOX Trial (2022) - MAP Targets Post-Arrest

Guideline Sources:

• ERC-ESICM 2021 Post-Resuscitation Care Guidelines
• ILCOR 2020 Consensus on Science and Treatment Recommendations
• AAN/World Brain Death Project 2020
• ELSO Guidelines for ECPR