Post-Cardiac Arrest Care (Adult)

Overview

Post-cardiac arrest care encompasses the comprehensive management of patients who achieve return of spontaneous circulation (ROSC) following cardiac arrest.[1] This critical phase addresses the systemic consequences of whole-body ischemia-reperfusion injury and aims to optimize neurological recovery, treat the precipitating cause, and prevent recurrent arrest.[2]

Clinical Pearl: The first 24-72 hours post-ROSC are critical for neurological outcome. Aggressive prevention of secondary brain injury through hemodynamic optimization, oxygenation control, and fever avoidance is essential.[1]

Post-cardiac arrest syndrome comprises four key components:[3]

1. Post-cardiac arrest brain injury - Hypoxic-ischemic encephalopathy, cerebral edema, seizures
2. Post-cardiac arrest myocardial dysfunction - Reversible myocardial stunning, reduced cardiac output
3. Systemic ischemia-reperfusion response - Systemic inflammatory response syndrome (SIRS), coagulopathy, adrenal insufficiency
4. Persistent precipitating pathology - Ongoing acute coronary syndrome, pulmonary embolism, sepsis, etc.

Exam Detail: MRCP/FRACP frequently test neuroprognostication timing (≥72 hours), TTM controversies (TTM1 vs TTM2 trials), and coronary angiography indications post-ROSC. FRCEM emphasizes immediate post-ROSC ABCDE management.

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Epidemiology

Outcomes After ROSC

Post-Cardiac Arrest Syndrome Components

Post-arrest myocardial dysfunction:[7]

• Occurs in 50-70% of post-ROSC patients
• Peaks at 6-8 hours post-ROSC
• Usually resolves within 48-72 hours
• Left ventricular ejection fraction may decrease to 20-30%

Post-arrest brain injury:[8]

• Primary injury: ischemia during no-flow/low-flow period
• Secondary injury: reperfusion injury, cerebral edema, seizures, fever
• Severity determines long-term neurological outcome

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Aetiology and Pathophysiology

Mechanisms of Post-Cardiac Arrest Brain Injury

Primary brain injury (during arrest):[8]

• No-flow period: Complete cessation of cerebral perfusion
• Low-flow period: Inadequate cerebral perfusion during CPR (25-30% of normal)
• Neuronal injury begins after 4-5 minutes of complete ischemia
• Selective vulnerability: hippocampus, cerebellum, basal ganglia most susceptible

Secondary brain injury (post-ROSC):[9]

• Excitotoxicity: Glutamate release, calcium influx, neuronal death
• Oxidative stress: Free radical formation during reperfusion
• Inflammation: Cytokine release, blood-brain barrier disruption
• Cerebral edema: Cytotoxic and vasogenic edema, raised ICP
• Microcirculatory dysfunction: No-reflow phenomenon, delayed hypoperfusion
• Seizures: Occur in 10-40% post-ROSC, worsen secondary injury
• Fever: Each 1°C rise above 37°C associated with 2.26× increased odds of poor outcome[10]

Post-Cardiac Arrest Myocardial Dysfunction

Mechanisms:[7]

• Global myocardial stunning from ischemia-reperfusion
• Catecholamine surge during resuscitation
• Direct myocardial depression from CPR
• Underlying acute coronary syndrome in 40-60% of cases

Hemodynamic profile:

• Reduced cardiac output (may drop to 2-3 L/min)
• Increased systemic vascular resistance
• Reduced left ventricular ejection fraction
• Elevated filling pressures
• Usually reversible within 48-72 hours

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Clinical Presentation

Immediate Post-ROSC Assessment (First 20 Minutes)

Once ROSC is achieved, rapid systematic assessment is essential:[1,2]

Signs of ROSC:

• Palpable pulse (carotid, femoral)
• Measurable blood pressure
• Sudden rise in end-tidal CO₂ (ETCO₂) to 35-45 mmHg
• Evidence of spontaneous breathing
• Improvement in oxygen saturation
• Purposeful movement or agonal breathing

Clinical Pearl: A sudden sustained rise in ETCO₂ to 35-40 mmHg during CPR is often the earliest indicator of ROSC, occurring before palpable pulse returns.[11]

Initial Neurological Presentation

Common neurological findings post-ROSC:

• Coma (GCS ≤8) in 80-90% immediately post-ROSC
• Myoclonus in 10-25% (does NOT always indicate poor prognosis)
• Seizures in 10-40%
• Decerebrate or decorticate posturing
• Absent brainstem reflexes initially (may recover over 24-72 hours)

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Investigations

Immediate Investigations (First 30 Minutes)

Laboratory Investigations

Blood tests (immediate):

• Full blood count
• Urea, creatinine, electrolytes (Na, K, Mg, Ca, PO₄)
• Troponin (elevated in > 90% post-cardiac arrest regardless of cause)
• Lactate (trend more important than absolute value)
• Glucose
• Coagulation profile (PT, APTT)
• Blood cultures (if sepsis suspected)

Serial monitoring:

• Troponin q6-12h
• Lactate q4-6h (clearance indicates improved perfusion)
• Electrolytes q6-12h (especially K, Mg if TTM used)

Neurological Investigations

Timing: Most investigations delayed until ≥72 hours post-arrest (or ≥72 hours after rewarming if TTM used)[12]

Electroencephalography (EEG):[13]

• Timing: Continuous EEG within 24 hours, interpret at ≥72 hours
• Favorable patterns: Continuous background activity, sleep-wake cycles, reactivity
• Unfavorable patterns: Suppressed background (> 10 µV), burst suppression, status epilepticus
• Note: Sedation, hypothermia, and neuromuscular blockade affect interpretation

Somatosensory evoked potentials (SSEP):[14]

• Timing: ≥72 hours post-arrest, off sedation/NMB
• Method: Median nerve stimulation, recording from scalp
• Interpretation: Bilateral absence of N20 cortical responses highly specific for poor outcome (98-100% specificity)
• Limitations: Technical expertise required, affected by sedation

Brain imaging:

Serum biomarkers:[15]

• Neuron-specific enolase (NSE): > 60 μg/L at 48-72 hours suggests poor prognosis
• S100B protein: Less specific than NSE
• Limitations: False elevations from hemolysis, TTM affects levels

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Management

Immediate Post-ROSC Care (First 20 Minutes)

Use structured ABCDE approach:[1,2]

A - Airway

Indications for intubation post-ROSC:

• GCS ≤8 (comatose)
• Inability to protect airway
• Respiratory failure (SpO₂ > 90% despite supplemental O₂)
• Anticipated deterioration (transfer, procedures)
• Need for controlled ventilation

If intubation required:

• Confirm tube placement with waveform capnography (ETCO₂)
• Target ETCO₂ 35-45 mmHg
• Secure tube and document depth at teeth/gums
• Obtain chest X-ray to confirm position

If patient breathing spontaneously with adequate airway protection:

• High-flow oxygen initially
• Wean FiO₂ to target SpO₂ 92-98%

B - Breathing

Oxygenation targets:[16]

• Avoid hypoxemia: SpO₂ ≥92% (PaO₂ > 60 mmHg)
• Avoid hyperoxia: PaO₂ > 300 mmHg, target 100-150 mmHg
  • Hyperoxia associated with increased mortality and worse neurological outcomes[16]
• Wean FiO₂ as soon as possible to maintain SpO₂ 92-98%

Ventilation targets:[17]

• Normocapnia: PaCO₂ 35-45 mmHg (4.7-6.0 kPa)
• Avoid hypocapnia: PaCO₂ > 30 mmHg causes cerebral vasoconstriction, reduced cerebral perfusion
• Avoid hypercapnia: PaCO₂ > 50 mmHg may worsen cerebral edema

Ventilator settings (if intubated):

• Mode: Volume control or pressure control
• Tidal volume: 6-8 mL/kg ideal body weight
• PEEP: 5-8 cmH₂O (adjust for oxygenation)
• Respiratory rate: Adjust to maintain normocapnia
• FiO₂: Titrate to SpO₂ 92-98%

Clinical Pearl: Both hyperoxia (PaO₂ > 300 mmHg) and hypoxia worsen neurological outcomes. Titrate oxygen carefully to SpO₂ 92-98%, avoiding extremes.[16]

C - Circulation

Blood pressure targets:[18]

• Mean arterial pressure (MAP) ≥65 mmHg (minimum target)
• Consider higher targets (MAP 70-80 mmHg) in first 24 hours
• Avoid hypotension: SBP > 90 mmHg associated with increased mortality
• Individualize targets: May require higher MAP if chronic hypertension

Hemodynamic optimization strategy:

1. Volume resuscitation:

   • Crystalloid bolus 250-500 mL if hypotensive
   • Assess volume responsiveness (passive leg raise, stroke volume variation)
   • Avoid excessive fluids (worsens pulmonary edema)

2. Vasopressor therapy (if MAP > 65 mmHg despite fluids):

   • Norepinephrine 0.05-0.5 μg/kg/min (first-line)[19]
   • Titrate to MAP ≥65-70 mmHg
   • Central venous access preferred but peripheral acceptable initially

3. Inotropic support (if low cardiac output despite adequate MAP):

   • Dobutamine 2.5-10 μg/kg/min (if myocardial dysfunction suspected)
   • Consider echocardiography to assess cardiac function

Monitoring:

• Continuous arterial blood pressure monitoring (arterial line)
• Central venous catheter for vasopressor administration
• Consider advanced monitoring (ScvO₂, cardiac output) if refractory shock

12-lead ECG interpretation:[20]

• STEMI present → Immediate coronary angiography (> 2 hours)
• Non-diagnostic ECG but suspected cardiac cause → Early angiography (> 24 hours)
• Long QT, Brugada pattern → Avoid QT-prolonging drugs, cardiology consultation

Arrhythmia management:

• Recurrent VF/VT → Amiodarone infusion 900 mg over 24 hours
• Bradycardia requiring pacing → Temporary pacing
• Atrial fibrillation with RVR → Rate control (amiodarone preferred over beta-blockers if LV dysfunction)

D - Disability (Neurological)

Initial neurological assessment:

• Glasgow Coma Scale (GCS)
• Pupillary light reflexes (size, reactivity)
• Motor response (spontaneous movements, response to pain)
• Brainstem reflexes (corneal, oculocephalic if safe)

Seizure management:[21]

• Clinical seizures: Lorazepam 4 mg IV, repeat once if needed
• Status epilepticus: Follow status epilepticus protocol (lorazepam, levetiracetam, phenytoin)
• Myoclonus: May be benign or malignant - do NOT prognosticate based on myoclonus alone
• Consider continuous EEG monitoring

Sedation strategy:

• If intubated and ventilated: Light sedation (Richmond Agitation-Sedation Scale -2 to 0)
• Avoid deep sedation unless clinically required (seizures, severe agitation, ventilator dyssynchrony)
• Agents: Propofol or midazolam ± fentanyl/remifentanil
• Daily sedation holds once patient stable (to assess neurological function)

Exam Detail: Critical point: Do NOT prognosticate neurological outcome before 72 hours, and allow ≥5 half-lives for sedative drugs to clear. Early myoclonus or absent reflexes may improve with time.[12]

E - Exposure and Temperature

Temperature management:[22]

Evidence Debate: The TTM controversy:

• Pre-2013: Hypothermia 32-34°C recommended based on 2002 trials showing benefit vs no temperature control[23]
• TTM1 trial (2013): No difference between 33°C vs 36°C (PMID: 24237006)[24]
• TTM2 trial (2021): No difference between 33°C vs normothermia with fever prevention ≤37.8°C (PMID: 34133859)[25]
• Current consensus: Avoid fever > 37.5°C (definite harm), active cooling to 32-36°C acceptable but not mandatory[1,22]

Current recommended approach (2021-2024):[1,22]

Option 1: Fever prevention (normothermia) strategy:

• Target temperature: 36.0-37.5°C
• Prevent fever > 37.5°C for at least 72 hours
• Active cooling if temperature > 37.5°C
• Simpler, fewer complications
• Equivalent outcomes to hypothermia in TTM2 trial

Option 2: Targeted temperature management (TTM) 32-36°C:

• Target temperature: 32-36°C (institutional protocol-dependent)
• Duration: 24 hours at target temperature
• Rewarming: 0.25-0.5°C per hour to 36-37°C
• Maintenance: Avoid fever for 72 hours post-rewarming

TTM protocol (if institutional protocol mandates):[22]

1. Induction phase:

   • Initiate within 6 hours of ROSC (earlier better)
   • Methods: Cold IV saline (30 mL/kg up to 2L), surface cooling devices, intravascular cooling catheters
   • Monitor core temperature (esophageal, bladder probe)

2. Maintenance phase (24 hours):

   • Strict temperature control at target (±0.5°C)
   • Manage shivering (sedation, NMB if refractory)
   • Monitor electrolytes (K, Mg, PO₄) q6h

3. Rewarming phase:

   • Slow rewarming: 0.25-0.5°C per hour
   • Avoid rebound hyperthermia
   • Monitor for hyperkalemia during rewarming

4. Post-rewarming normothermia:

   • Maintain 36-37.5°C for ≥72 hours
   • Prevent fever aggressively (paracetamol, cooling devices)

Complications of TTM:

• Shivering (treat: sedation, magnesium, buspirone, NMB)
• Electrolyte shifts (hypokalemia, hypomagnesemia, hypophosphatemia)
• Coagulopathy
• Hyperglycemia
• Immune suppression, increased infection risk
• Arrhythmias (especially during rewarming)

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Coronary Angiography

Indications for immediate coronary angiography (> 2 hours):[20,26]

Absolute indications:

• ST-elevation myocardial infarction (STEMI) on post-ROSC ECG
• Cardiogenic shock despite adequate resuscitation

Strong indications (consider immediate angiography):

• Suspected acute coronary syndrome (ACS) as arrest cause
• Age > 65 years
• Shockable initial rhythm (VF/pVT)
• Witnessed arrest
• Hemodynamic instability despite treatment

Indications for early coronary angiography (within 24 hours):

• No STEMI but elevated troponin (> 99% have elevated troponin post-arrest)
• Presumed cardiac cause
• No obvious non-cardiac cause

Contraindications:

• Unwitnessed arrest with prolonged downtime (> 30 minutes)
• Known terminal illness or poor baseline functional status
• Obvious non-cardiac cause (trauma, drowning, hanging, massive PE, intracranial hemorrhage)

Clinical Pearl: STEMI on post-ROSC ECG is an absolute indication for immediate coronary angiography, regardless of neurological status. Revascularization improves both survival and neurological outcomes.[26]

Outcomes of early coronary angiography post-arrest:[27]

• Culprit lesion identified in 50-60% of OHCA patients
• PCI performed in 40-50%
• Improved survival in STEMI patients (48% vs 29% without early PCI)
• Benefit less clear in non-STEMI patients

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Glucose Management

Target glucose: 7.8-10 mmol/L (140-180 mg/dL)[28]

Avoid:

• Hypoglycemia (> 4 mmol/L / > 70 mg/dL) - associated with worse neurological outcome
• Severe hyperglycemia (> 10-11 mmol/L / > 180-200 mg/dL) - worsens brain injury

Management:

• Insulin infusion if glucose > 10 mmol/L
• Frequent monitoring (hourly initially, then q2-4h)
• Avoid tight glycemic control (increases hypoglycemia risk without benefit)

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Neuroprognostication

Timing: Defer prognostication until ≥72 hours after cardiac arrest (or ≥72 hours after rewarming if TTM used)[12]

Clinical Pearl: Multimodal prognostication is essential - No single test is sufficient to predict outcome. Require multiple concordant poor prognostic indicators before declaring poor prognosis.[12]

Poor prognostic indicators (all must be present):[12,29]

1. Clinical examination (at 72 hours):

   • Bilateral absent pupillary light reflexes
   • Bilateral absent corneal reflexes
   • GCS motor score ≤2 (extensor or no response)

2. Electrophysiology:

   • Bilateral absence of N20 SSEP responses (98-100% specificity for poor outcome)[14]
   • Highly malignant EEG (suppressed background, burst suppression) without improvement

3. Imaging:

   • MRI: Extensive cortical and deep grey matter diffusion restriction[30]
   • CT: Marked loss of grey-white matter differentiation

4. Biomarkers:

   • Neuron-specific enolase (NSE) > 60 μg/L at 48-72 hours[15]

Confounders delaying prognostication:[12]

• Sedation (wait ≥5 half-lives after cessation)
• Neuromuscular blockade (wait ≥24 hours after cessation)
• Metabolic derangements (severe hypoglycemia, hepatic/renal failure)
• Hypothermia (wait ≥72 hours after rewarming)

False-positive myoclonus:

• Early myoclonus does NOT always indicate poor prognosis
• Lance-Adams syndrome (post-hypoxic myoclonus) compatible with good recovery
• Do not prognosticate based on myoclonus alone

Good prognostic indicators:[31]

• Early awakening (within 24-48 hours)
• Preserved pupillary and corneal reflexes at 72 hours
• Continuous EEG background with reactivity
• Absence of extensive diffusion restriction on MRI
• NSE > 33 μg/L at 48 hours

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Complications

Early Complications (0-72 Hours)

Late Complications (> 72 Hours)

Post-intensive care syndrome:[32]

• Cognitive impairment (memory, executive function)
• Psychological sequelae (PTSD, anxiety, depression)
• Physical deconditioning

Seizure disorders:

• Post-hypoxic epilepsy develops in 10-15% of survivors
• Lance-Adams syndrome (action myoclonus) in 1-5%

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Prognosis

Survival and Neurological Outcomes

Cerebral Performance Category (CPC) scale:[33]

• CPC 1: Good cerebral performance (normal life)
• CPC 2: Moderate cerebral disability (independent activities of daily living)
• CPC 3: Severe cerebral disability (dependent)
• CPC 4: Vegetative state
• CPC 5: Brain death

Favorable neurological outcome = CPC 1-2

Long-term outcomes in survivors:[34]

• 80-90% of survivors with good early neurological recovery (CPC 1-2) maintain independence at 1 year
• Cognitive deficits in 30-50% even with good CPC score
• Return to work: 40-60% within 6-12 months
• Quality of life similar to general population at 1 year in CPC 1-2 patients

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Prevention

Secondary Prevention After Cardiac Arrest

Identify and treat underlying cause:[35]

• Coronary angiography ± PCI for ACS
• Echocardiography for structural heart disease
• Cardiac MRI for channelopathies, myocarditis
• Electrophysiology study if ventricular arrhythmia without clear structural cause

Implantable cardioverter-defibrillator (ICD):[36]

• Indicated if:
  • VF/pVT arrest with LVEF > 35% at 6-12 weeks post-MI
  • No reversible cause identified
  • Reasonable life expectancy and functional status
• Defer decision until myocardial recovery assessed (6-12 weeks)

Medical therapy:

• Beta-blockers (reduce recurrent VT/VF)
• ACE inhibitors/ARBs (if LV dysfunction)
• Statins (if atherosclerotic disease)
• Antiarrhythmic drugs (amiodarone if recurrent ICD shocks)

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Key Guidelines

1. AHA 2020: Post-Cardiac Arrest Care[1]
2. ERC 2021: European Resuscitation Council Guidelines - Post-Resuscitation Care[2]
3. ERC/ESICM 2021: Neuroprognostication After Cardiac Arrest[12]
4. AHA 2015: Targeted Temperature Management[22]

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Exam Scenarios

SBA Question 1

Scenario: A 58-year-old man achieves ROSC after 12 minutes of CPR for VF cardiac arrest. His post-ROSC ECG shows 3 mm ST-elevation in leads V2-V5. He remains comatose (GCS 3). What is the most appropriate next step?

A) Targeted temperature management to 33°C before any intervention
B) Emergency coronary angiography within 2 hours
C) CT head to exclude intracranial hemorrhage
D) Neurological prognostication with SSEP
E) Supportive care only due to poor neurological status

Answer

Answer: B) Emergency coronary angiography within 2 hours

ST-elevation on post-ROSC ECG is an absolute indication for immediate coronary angiography and primary PCI, regardless of neurological status.[20,26] Acute coronary occlusion is the likely precipitating cause, and urgent revascularization improves both survival and neurological outcomes.

TTM can be initiated during or after PCI but should NOT delay angiography. Neurological prognostication must be deferred until ≥72 hours post-arrest.[12] Early coma does not preclude aggressive treatment of reversible causes.

SBA Question 2

Scenario: A 65-year-old woman is in ICU following ROSC after cardiac arrest 48 hours ago. She remains comatose (GCS 3) with absent pupillary reflexes. The team asks when neurological prognostication can be performed. What is the earliest appropriate timing?

A) Immediately (48 hours post-arrest)
B) 72 hours after cardiac arrest
C) 72 hours after rewarming (if TTM used)
D) 5 days post-arrest
E) Prognostication not possible in this patient

Answer

Answer: C) 72 hours after rewarming (if TTM used)

Neurological prognostication must be delayed until:

• ≥72 hours after cardiac arrest (if no TTM used), OR
• ≥72 hours after rewarming (if TTM used)[12]

Additionally, must ensure:

• ≥5 half-lives have elapsed since cessation of sedation
• No neuromuscular blockade
• No severe metabolic derangements

Prognosticating too early results in false-positive prediction of poor outcome (self-fulfilling prophecy from withdrawal of care). Even bilateral absent pupillary reflexes at 48 hours may recover by 72+ hours in some patients.[12]

SBA Question 3

Scenario: Following ROSC, a patient's arterial blood gas shows PaO₂ 450 mmHg on FiO₂ 1.0. What is the most appropriate action?

A) Continue current FiO₂ to ensure adequate oxygenation
B) Wean FiO₂ to target PaO₂ 100-150 mmHg and SpO₂ 92-98%
C) Increase PEEP to improve V/Q matching
D) Accept hyperoxia as it improves tissue oxygen delivery
E) Reduce FiO₂ only if PaO₂ > 500 mmHg

Answer

Answer: B) Wean FiO₂ to target PaO₂ 100-150 mmHg and SpO₂ 92-98%

Hyperoxia (PaO₂ > 300 mmHg) is associated with increased mortality and worse neurological outcomes post-cardiac arrest.[16] Oxygen should be titrated to:

• SpO₂ 92-98%
• PaO₂ 100-150 mmHg (avoid > 300 mmHg)

Both hypoxia (> 60 mmHg) and hyperoxia cause secondary brain injury. The goal is normoxia, not maximal oxygenation.[1,16]

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Viva Scenario

Examiner: "You are the ICU registrar. A 52-year-old man was admitted 30 minutes ago following ROSC after out-of-hospital VF cardiac arrest. The paramedics performed CPR for 8 minutes before ROSC. He is intubated, sedated, GCS 3. His BP is 85/50, HR 110. Walk me through your immediate management."

Candidate approach:

ABCDE Assessment:

"I would use a systematic ABCDE approach for post-ROSC care:

Airway: The patient is already intubated. I would confirm correct tube placement by checking:

• Waveform capnography showing ETCO₂ 35-45 mmHg
• Bilateral breath sounds
• Request urgent chest X-ray to confirm position and exclude pneumothorax

Breathing: I would optimize ventilation and oxygenation:

• Check current ventilator settings and ABG
• Target SpO₂ 92-98%, avoiding both hypoxia and hyperoxia
• Target normocapnia - PaCO₂ 35-45 mmHg
• Wean FiO₂ as soon as safe to avoid hyperoxia (PaO₂ > 300 mmHg harmful)

Circulation: The patient is hypotensive with MAP approximately 60 mmHg. I would:

• Obtain immediate 12-lead ECG to look for STEMI
• Establish arterial line for continuous BP monitoring
• Give crystalloid bolus 250-500 mL and reassess
• Start norepinephrine infusion via central line to target MAP ≥65-70 mmHg
• Request urgent portable echocardiography to assess LV function
• Send bloods: FBC, U&E, troponin, lactate, glucose, coagulation

Disability:

• Assess GCS and pupils (already noted GCS 3)
• Check blood glucose immediately
• Light sedation only (propofol ± fentanyl) - avoid deep sedation unless clinically required
• Do NOT attempt prognostication - far too early (need ≥72 hours)

Exposure:

• Check core temperature
• Implement fever prevention strategy - target 36-37.5°C, prevent fever > 37.5°C
• Consider TTM 32-36°C if institutional protocol mandates"

Examiner: "The 12-lead ECG shows 4 mm ST-elevation in leads II, III, and aVF. What does this change?"

Candidate: "This is an absolute indication for immediate coronary angiography within 2 hours. This represents an acute inferior STEMI which was likely the precipitating cause of his cardiac arrest.

I would:

1. Contact the cardiology team immediately to activate the catheter lab
2. Continue hemodynamic optimization and supportive care
3. Arrange urgent transfer to catheter lab
4. Give aspirin 300 mg via NG tube if not already given
5. Continue norepinephrine to maintain MAP during transfer

The fact that he is comatose does NOT contraindicate immediate angiography - urgent revascularization actually improves both survival AND neurological outcomes. TTM can be initiated during or after the procedure but should not delay revascularization."

Examiner: "He undergoes successful PCI to an occluded RCA. He is now in ICU on day 3 post-arrest. He remains comatose, GCS 3, with absent pupillary reflexes. The family asks about his prognosis. What do you tell them?"

Candidate: "At 72 hours post-arrest, this is the earliest appropriate time to begin neurological prognostication, but we need a multimodal approach - no single test is sufficient.

I would explain to the family: 'We need to perform several specialized tests over the next 24-48 hours to assess brain function. These include electrical tests of the brain (EEG), nerve conduction studies (SSEP), possibly an MRI scan, and blood tests. We need ALL of these tests to predict recovery, as any single test can be misleading. We also need to ensure that sedation has fully cleared from his system.

The absence of pupillary reflexes at this stage is concerning, but we cannot make definitive statements about prognosis until we have all the information from these tests. Some patients can still make good recoveries even with these findings, so it's too early to give up hope.'

I would arrange:

• Ensure sedation stopped ≥24-48 hours ago (≥5 half-lives)
• Somatosensory evoked potentials (SSEP) - looking for bilateral absent N20 responses
• Continuous EEG - looking for background activity and reactivity
• Neuron-specific enolase (NSE) levels at 48 and 72 hours
• Consider MRI brain if available - looking for extent of diffusion restriction

Only if ALL tests show poor prognosis would I discuss withdrawal of life-sustaining treatment with the family, and I would involve neurology and ethics committees in that decision."

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Patient Explanation (Layperson Level)

"After your heart restarts following cardiac arrest, your body needs intensive care to recover from the period when blood wasn't flowing properly. We call this 'post-cardiac arrest care.'

The main goals in the first few days are:

1. Protect your brain: Your brain is very sensitive to lack of oxygen. We carefully control your oxygen levels, blood pressure, and body temperature to give your brain the best chance to recover. We prevent fever because even slight temperature increases can harm the healing brain.

2. Treat what caused your heart to stop: Often this means emergency procedures to open blocked heart arteries, or treating infections or other medical problems.

3. Prevent your heart stopping again: We use medications and monitoring to keep your heart rhythm stable.

4. Support your other organs: Your kidneys, lungs, and liver may need time to recover.

About temperature management: In the past, we used to cool patients to 32-33°C (mild hypothermia). Recent research shows that simply preventing fever (keeping temperature below 37.5°C) works just as well and has fewer complications.

About predicting recovery: We cannot predict how well your brain will recover until at least 3 days after your heart restarted, and often longer. This is because:

• Medications we use for sedation can make things look worse than they are
• The brain needs time to recover
• Early tests can be misleading

Many people who look very unwell in the first few days go on to make good recoveries, so we don't give up hope too early."

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References

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2. Panchal AR, Bartos JA, Cabañas JG, et al. Part 3: Adult Basic and Advanced Life Support: 2020 American Heart Association Guidelines. Circulation. 2020;142(16_suppl_2):S366-S468. doi:10.1161/CIR.0000000000000916

3. Neumar RW, Nolan JP, Adrie C, et al. Post-cardiac arrest syndrome: epidemiology, pathophysiology, treatment, and prognostication. Circulation. 2008;118(23):2452-2483. doi:10.1161/CIRCULATIONAHA.108.190652

4. Yan S, Gan Y, Jiang N, et al. The global survival rate among adult out-of-hospital cardiac arrest patients who received cardiopulmonary resuscitation. Crit Care. 2020;24(1):61. doi:10.1186/s13054-020-2773-2

5. Girotra S, Nallamothu BK, Spertus JA, et al. Trends in survival after in-hospital cardiac arrest. N Engl J Med. 2012;367(20):1912-1920. doi:10.1056/NEJMoa1109148

6. Andersen LW, Holmberg MJ, Berg KM, et al. In-Hospital Cardiac Arrest: A Review. JAMA. 2019;321(12):1200-1210. doi:10.1001/jama.2019.1696

7. Laurent I, Monchi M, Chiche JD, et al. Reversible myocardial dysfunction in survivors of out-of-hospital cardiac arrest. J Am Coll Cardiol. 2002;40(12):2110-2116. doi:10.1016/s0735-1097(02)02594-9

8. Geocadin RG, Callaway CW, Fink EL, et al. Standards for Studies of Neurological Prognostication in Comatose Survivors of Cardiac Arrest. Resuscitation. 2019;140:130-140. doi:10.1016/j.resuscitation.2019.04.050

9. Sekhon MS, Ainslie PN, Griesdale DE. Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest. Crit Care Med. 2017;45(4):651-659. doi:10.1097/CCM.0000000000002295

10. Zeiner A, Holzer M, Sterz F, et al. Hyperthermia after cardiac arrest is associated with an unfavorable neurologic outcome. Arch Intern Med. 2001;161(16):2007-2012. doi:10.1001/archinte.161.16.2007

11. Levine RL, Wayne MA, Miller CC. End-tidal carbon dioxide and outcome of out-of-hospital cardiac arrest. N Engl J Med. 1997;337(5):301-306. doi:10.1056/NEJM199707313370503

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