Post-Resuscitation Care

Quick Answer

Critical: Post-resuscitation care begins immediately after ROSC and focuses on preventing secondary brain injury through optimised oxygenation (SpO2 94-98%), normocapnia (PaCO2 35-45 mmHg), haemodynamic support (MAP ≥65 mmHg), temperature control (≤37.5°C), and urgent treatment of the precipitating cause including immediate coronary angiography for STEMI.

Post-resuscitation care is the critical phase between ROSC and definitive outcome, determining whether a patient survives with good neurological function [1]. The Post-Cardiac Arrest Syndrome (PCAS) comprises brain injury, myocardial dysfunction, systemic ischaemia-reperfusion response, and persistent precipitating pathology [2]. Australian data shows 25-40% of OHCA patients achieve ROSC, but only 11.7% survive to hospital discharge with 6-9% achieving favourable neurological outcome [3]. The first 72 hours are critical—aggressive prevention of secondary brain injury and early identification of treatable causes significantly improves outcomes. ANZCOR Guidelines 11.7 and 11.8 provide the evidence-based framework for post-resuscitation management in Australia and New Zealand [4,5].

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ACEM Exam Focus

Primary Exam Relevance

• Physiology: Cerebral autoregulation failure, ischaemia-reperfusion injury, mitochondrial dysfunction, excitotoxicity cascade, coronary perfusion pressure requirements, oxygen-haemoglobin dissociation curve, carbon dioxide and cerebral blood flow relationship
• Pharmacology: Catecholamine pharmacodynamics (noradrenaline alpha-1 effects, dobutamine beta-1 effects), amiodarone maintenance infusion, antiepileptic drug mechanisms (levetiracetam, valproate), sedative pharmacokinetics for neuroprognostication timing
• Anatomy: Selective brain vulnerability (hippocampus, basal ganglia, Purkinje cells), coronary anatomy for STEMI recognition, central line anatomy for vasopressor administration

Fellowship Exam Relevance

• Written SAQ Topics: Post-ROSC ABCDE priorities, oxygenation and ventilation targets (with evidence), temperature control controversies (TTM1 vs TTM2), neuroprognostication timing and multimodal approach, coronary angiography indications
• OSCE: Post-ROSC management station requiring systematic approach to comatose patient, communication station discussing prognosis with family (timing, uncertainty, multimodal approach)
• Key domains tested: Medical Expert (evidence-based targets), Leader (ICU team coordination), Communicator (sensitive family discussions about prognosis)

High-Yield Exam Points

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Key Points

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Epidemiology

Australian and New Zealand Data

Post-Cardiac Arrest Syndrome Components

Post-arrest myocardial dysfunction [17]:

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

Post-arrest brain injury [18]:

• Primary injury: ischaemia during no-flow/low-flow period
• Secondary injury: reperfusion injury, cerebral oedema, seizures, fever
• Severity determines long-term neurological outcome
• Selective vulnerability: hippocampus, basal ganglia, cerebellum

Systemic ischaemia-reperfusion response [2]:

• Systemic inflammatory response syndrome (SIRS)
• Coagulopathy (both pro-thrombotic and bleeding)
• Adrenal insufficiency (relative)
• Impaired vasoregulation
• Increased susceptibility to infection

Indigenous Health Disparities

Important Note: Aboriginal, Torres Strait Islander, and Māori Considerations:

Aboriginal and Torres Strait Islander Australians experience cardiac arrest at significantly younger ages with higher rates of underlying cardiovascular disease [19]:

• Earlier onset: Mean age of cardiac arrest 10-15 years younger than non-Indigenous Australians
• Higher risk factor prevalence: Smoking (41% vs 13%), diabetes (12% vs 5%), rheumatic heart disease (8-fold higher)
• Geographic barriers: Remote communities may have EMS response times over 60 minutes
• Lower bystander CPR rates: Due to geographic isolation and fewer trained community members
• Challenges in post-arrest care: Remote locations may delay access to coronary angiography and ICU
• Cultural considerations: Family-centred decision making, involvement of Aboriginal Health Workers in prognosis discussions
• Māori in New Zealand: Similar disparities with 2-3 times higher cardiovascular mortality, importance of whanau involvement

Implications for post-resuscitation care:

• Lower threshold for transfer to cardiac arrest centre
• Involve Aboriginal Health Workers/Māori Health Workers in family discussions
• Consider cultural beliefs about life support and prognostication
• Coordinate with retrieval services early (RFDS, helicopter services)

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Pathophysiology

Post-Cardiac Arrest Syndrome (PCAS)

The Post-Cardiac Arrest Syndrome describes the unique pathophysiological state following ROSC [2]. Understanding this syndrome is essential for rational post-resuscitation therapy.

Cardiac Arrest
     ↓
Global Ischaemia (No-flow)
     ↓
CPR (Low-flow: 25-30% normal cardiac output)
     ↓
ROSC
     ↓
Reperfusion Injury → POST-CARDIAC ARREST SYNDROME
     ↓
┌─────────────────────────────────────────────────────────────────┐
│  1. Brain Injury    │  2. Myocardial      │  3. Systemic     │
│     - Excitotoxicity│     Dysfunction     │     Response     │
│     - Free radicals │     - Stunning      │     - SIRS       │
│     - Oedema        │     - Low CO        │     - Coagulopathy│
│     - Seizures      │     - Arrhythmias   │     - Infection  │
└─────────────────────────────────────────────────────────────────┘
     ↓
4. Persistent Precipitating Pathology (ACS, PE, sepsis, toxins)

Mechanisms of Post-Cardiac Arrest Brain Injury

Primary brain injury (during arrest) [18,20]:

• No-flow period: Complete cessation of cerebral perfusion
• Low-flow period: CPR provides 25-30% of normal cerebral blood flow
• Neuronal injury begins after 4-5 minutes of complete ischaemia
• Selective vulnerability: hippocampus (memory), cerebellum, basal ganglia
• ATP depletion → failure of Na/K-ATPase → cellular swelling

Secondary brain injury (post-ROSC) [21,22]:

• Excitotoxicity: Glutamate release → NMDA receptor activation → calcium influx → neuronal death
• Oxidative stress: Free radical formation during reperfusion → lipid peroxidation, DNA damage
• Inflammation: Cytokine release (IL-6, TNF-α), blood-brain barrier disruption, microglial activation
• Cerebral oedema: Cytotoxic (cellular swelling) and vasogenic (BBB breakdown) → raised ICP
• Microcirculatory dysfunction: No-reflow phenomenon, endothelial dysfunction, microthrombi
• Seizures: Occur in 10-40% post-ROSC, worsen secondary injury through increased metabolic demand
• Fever: Each 1°C rise above 37°C associated with 2.26× increased odds of poor outcome [23]

Post-Cardiac Arrest Myocardial Dysfunction

Mechanisms [17,24]:

• Global myocardial stunning from ischaemia-reperfusion
• Catecholamine surge during resuscitation → myocardial injury
• Inflammatory mediators (IL-6, TNF-α) cause direct myocardial depression
• Underlying acute coronary syndrome in 40-60% of OHCA
• CPR-related myocardial contusion

Haemodynamic profile:

• Reduced cardiac output (may drop to 2-3 L/min)
• Increased systemic vascular resistance initially
• Reduced left ventricular ejection fraction (may fall to 20-30%)
• Elevated filling pressures
• Usually reversible within 48-72 hours with supportive care

Rationale for Therapeutic Targets

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Clinical Approach

Recognition of ROSC

Signs of ROSC [4]:

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

Immediate Post-ROSC Assessment (ABCDE)

Use a structured ABCDE approach immediately following ROSC [4]:

A - Airway

Indications for intubation post-ROSC:

• GCS ≤8 (comatose) - most common scenario
• Inability to protect airway (absent gag/cough reflexes)
• Respiratory failure despite supplemental oxygen
• Anticipated deterioration (transfer, procedures)
• Need for controlled ventilation

If intubation required:

• Use waveform capnography to confirm tube placement
• Target ETCO2 35-45 mmHg
• Secure tube and document depth at teeth/gums
• Chest X-ray to confirm position (2 cm above carina)

If patient breathing spontaneously with protected airway:

• High-flow oxygen initially
• Wean FiO2 to target SpO2 94-98% as soon as reliable monitoring available

B - Breathing

Oxygenation targets [6,7]:

• Avoid hypoxaemia: SpO2 ≥94%, PaO2 ≥60 mmHg
• Avoid hyperoxia: PaO2 below 300 mmHg, ideally 100-150 mmHg
• Rationale: Hyperoxia increases free radical formation during reperfusion
• Action: Wean FiO2 as soon as SpO2 monitoring reliable - target 94-98%

Ventilation targets [8]:

• Normocapnia: PaCO2 35-45 mmHg (4.7-6.0 kPa)
• Avoid hypocapnia: PaCO2 below 35 mmHg causes cerebral vasoconstriction
• Avoid hypercapnia: PaCO2 over 45 mmHg may worsen cerebral oedema
• Rationale: Impaired cerebral autoregulation means CO2 directly affects cerebral blood flow

Ventilator settings (if intubated):

• Mode: Volume control or pressure control
• Tidal volume: 6-8 mL/kg ideal body weight (lung-protective)
• PEEP: 5-8 cmH2O (adjust for oxygenation, monitor for hypotension)
• Respiratory rate: Adjust to maintain PaCO2 35-45 mmHg
• FiO2: Start at 1.0 then titrate down to SpO2 94-98%

C - Circulation

Blood pressure targets [4,26]:

• Mean arterial pressure (MAP) ≥65 mmHg - ANZCOR recommendation
• Consider higher targets (MAP 70-80 mmHg) if chronic hypertension
• Avoid hypotension: SBP below 100 mmHg associated with increased mortality
• Individualise targets based on premorbid blood pressure

Haemodynamic optimisation strategy:

Hypotension post-ROSC (MAP below 65 mmHg)
                ↓
1. Fluid bolus 250-500 mL crystalloid
   Assess volume responsiveness (PLR, SVV)
                ↓
2. If still hypotensive → Noradrenaline 0.05-0.5 μg/kg/min
   (First-line vasopressor per ANZCOR)
   Peripheral access acceptable initially
                ↓
3. If low cardiac output (cold peripheries, high lactate, low ScvO2)
   → Add Dobutamine 2.5-10 μg/kg/min
   → Consider bedside echocardiography
                ↓
4. Refractory shock → Advanced monitoring
   Arterial line, central line, consider cardiac output monitoring
   ICU consultation, consider mechanical circulatory support

Monitoring:

• Continuous arterial blood pressure monitoring (arterial line - ASAP)
• Central venous access for vasopressor administration
• Consider advanced monitoring (ScvO2, cardiac output) if refractory shock
• Serial lactate measurements (clearance indicates improved perfusion)

12-Lead ECG - CRITICAL [10,11]:

• Obtain immediately post-ROSC
• STEMI present → Immediate coronary angiography (within 2 hours)
• LBBB (new) → Treat as STEMI equivalent
• Non-diagnostic ECG but suspected cardiac cause → Early angiography (within 24 hours)
• Long QT, Brugada pattern → Avoid QT-prolonging drugs, cardiology consultation
• Coma is NOT a contraindication to angiography

Arrhythmia management:

• Recurrent VF/VT → Amiodarone infusion 0.6 mg/kg/hour (approximately 900 mg over 24 hours)
• Or lignocaine 2-4 mg/min infusion if amiodarone used during arrest
• Correct electrolytes (K+ 4.0-4.5 mmol/L, Mg2+ over 1.0 mmol/L)
• Bradycardia requiring treatment → Temporary pacing

D - Disability (Neurological)

Initial neurological assessment:

• Glasgow Coma Scale (GCS) - document fully (E_V_M_)
• Pupillary light reflexes (size, reactivity - both eyes)
• Motor response (spontaneous movements, response to pain)
• Brainstem reflexes (corneal, gag) if safe to assess

Neurological findings post-ROSC:

Seizure management [27]:

• Clinical seizures: Lorazepam 0.1 mg/kg (typically 4-8 mg) IV, repeat once if needed
• Status epilepticus: Follow status epilepticus protocol
  • Lorazepam → Levetiracetam 60 mg/kg (max 4.5g) OR Phenytoin 20 mg/kg
• Myoclonus: May be benign or malignant - do NOT prognosticate based on myoclonus alone
• Consider continuous EEG monitoring if available
• Seizure prophylaxis NOT recommended - treat seizures when they occur [4]

Sedation strategy:

• Light sedation only (RASS -2 to 0) unless clinically required
• Avoid deep sedation unless: seizures, severe agitation, ventilator dyssynchrony
• Agents: Propofol or midazolam ± fentanyl/remifentanil
• Daily sedation holds once stable to assess neurological function
• Document sedation doses for neuroprognostication timing

E - Exposure and Temperature

Temperature management [5,9]:

• Check core temperature immediately post-ROSC
• Target: ≤37.5°C (actively prevent fever)
• Duration: At least 72 hours

Current ANZCOR recommendations (post-TTM2):

Methods for temperature control:

• Paracetamol 1g IV/PO q6h (pharmacological)
• Surface cooling devices (cooling blankets, ice packs)
• Endovascular cooling catheters (most precise)
• Cold IV saline boluses (up to 30 mL/kg) for induction only

If institutional protocol mandates hypothermia (32-34°C):

1. Induction: Initiate within 6 hours of ROSC, cold saline, surface/endovascular cooling
2. Maintenance: 24 hours at target (±0.5°C), manage shivering
3. Rewarming: 0.25-0.5°C per hour, monitor for hyperkalaemia
4. Normothermia maintenance: Prevent fever for ≥72 hours post-rewarming

Shivering management:

• Magnesium sulphate 2g IV loading dose
• Adequate sedation (propofol, opioids)
• Buspirone 30 mg TDS via NG
• Neuromuscular blockade if refractory (risk: masks seizures)

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Investigations

Immediate Investigations (First 30 Minutes)

Laboratory Investigations

Blood tests (immediate):

• Full blood count (anaemia, infection)
• Urea, creatinine, eGFR (baseline renal function)
• Electrolytes: Na, K, Mg, Ca, PO4 (arrhythmia risk)
• Troponin (elevated in over 90% regardless of cause)
• Lactate (trend more important than absolute value)
• Glucose
• Coagulation profile (PT, APTT, INR)
• Blood cultures if sepsis suspected

Serial monitoring:

• Troponin q6-12h (peak identifies myocardial injury extent)
• Lactate q4-6h (clearance = improving perfusion)
• Electrolytes q6-12h (especially K, Mg during temperature control)
• ABG q4-6h initially (oxygenation, ventilation, pH)

Neurological Investigations

Timing: Most investigations delayed until ≥72 hours post-ROSC (or ≥72 hours after rewarming if hypothermia used) [12,13]

Electroencephalography (EEG) [29]:

Somatosensory Evoked Potentials (SSEP) [30]:

• Timing: ≥72 hours post-ROSC, off sedation/NMB
• Method: Median nerve stimulation, cortical recording
• Interpretation: Bilateral absent N20 responses = highly specific for poor outcome (98-100% specificity)
• Limitations: Requires technical expertise, affected by sedation

Brain imaging:

Serum biomarkers [31]:

• Neuron-specific enolase (NSE):
  • Normal NSE below 17 μg/L at 48-72 hours suggests better prognosis
  • greater than 60 μg/L at 48-72 hours associated with poor prognosis
  • "False elevations: haemolysis, neuroendocrine tumours"
• Neurofilament light chain (NfL): Research use, not yet recommended for clinical practice [4]

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Management

Immediate Post-ROSC Care Bundle (First Hour)

IMMEDIATE POST-ROSC PRIORITIES (First 60 Minutes)
┌─────────────────────────────────────────────────────────────────────┐
│ A - AIRWAY                                                          │
│   □ Intubate if GCS ≤8 or unable to protect airway                  │
│   □ Confirm ETT with waveform capnography                           │
│   □ CXR for tube position                                           │
├─────────────────────────────────────────────────────────────────────┤
│ B - BREATHING                                                       │
│   □ FiO2 1.0 initially, wean to SpO2 94-98%                         │
│   □ ABG within 10 minutes                                           │
│   □ Target PaCO2 35-45 mmHg (normocapnia)                           │
│   □ Avoid hyperoxia (PaO2 greater than 300 mmHg)                                │
├─────────────────────────────────────────────────────────────────────┤
│ C - CIRCULATION                                                     │
│   □ 12-lead ECG IMMEDIATELY - look for STEMI                        │
│   □ Arterial line for continuous BP monitoring                      │
│   □ Target MAP ≥65 mmHg (SBP greater than 100 mmHg)                             │
│   □ Noradrenaline if hypotensive despite fluid bolus                │
│   □ Bedside echo if available                                       │
│   □ STEMI → immediate coronary angiography                          │
├─────────────────────────────────────────────────────────────────────┤
│ D - DISABILITY                                                      │
│   □ Check glucose (treat hypo/hyperglycaemia)                       │
│   □ Document GCS, pupils, motor response                            │
│   □ Light sedation only unless clinically indicated                 │
│   □ Treat seizures (do not prophylax)                               │
│   □ DO NOT PROGNOSTICATE                                            │
├─────────────────────────────────────────────────────────────────────┤
│ E - EXPOSURE/ENVIRONMENT                                            │
│   □ Core temperature measurement                                     │
│   □ Initiate temperature control (target ≤37.5°C)                   │
│   □ Prevent fever for at least 72 hours                             │
│   □ Do NOT actively warm mild hypothermia                           │
└─────────────────────────────────────────────────────────────────────┘

Medications

Vasopressors and Inotropes

Antiarrhythmics

Sedation and Analgesia

Antiepileptic Drugs

Glucose Management

Coronary Angiography

Immediate coronary angiography (within 2 hours) [10,11]:

Absolute indications:

• STEMI on post-ROSC ECG
• New LBBB with suspected ACS
• Cardiogenic shock despite adequate resuscitation

Strong indications (consider immediate):

• Suspected ACS as arrest cause (chest pain pre-arrest, cardiac risk factors)
• Shockable initial rhythm (VF/pVT) without obvious non-cardiac cause
• Haemodynamic instability despite treatment

Early angiography (within 24 hours):

• No STEMI but elevated troponin (over 99th percentile)
• Presumed cardiac cause without alternative explanation
• No obvious non-cardiac cause identified

Relative contraindications:

• Unwitnessed arrest with prolonged downtime (over 30 minutes no-flow)
• Known terminal illness or poor baseline functional status
• Obvious non-cardiac cause (drowning, hanging, trauma, massive PE, ICH)

Temperature Control Protocol

ANZCOR-Recommended Approach (Post-TTM2) [5,9]:

TEMPERATURE CONTROL PROTOCOL
┌─────────────────────────────────────────────────────────────────────┐
│ RECOMMENDED: FEVER PREVENTION STRATEGY                              │
│                                                                     │
│ Target: ≤37.5°C                                                     │
│ Duration: At least 72 hours                                         │
│                                                                     │
│ Methods:                                                            │
│ • Paracetamol 1g IV/PO q6h                                          │
│ • Surface cooling (blankets, ice packs to axillae/groin)            │
│ • Cooling devices with feedback loop                                │
│ • Lower ambient temperature                                         │
│ • Avoid active warming of mild hypothermia                          │
│                                                                     │
│ Monitoring:                                                         │
│ • Core temperature (oesophageal, bladder, or rectal)                │
│ • Continuous or q1h during active cooling                           │
│                                                                     │
│ Management of fever episodes:                                        │
│ • Escalate cooling measures                                          │
│ • Investigate for infection if persistent                           │
│ • Continue for minimum 72 hours                                     │
└─────────────────────────────────────────────────────────────────────┘

If institutional protocol mandates hypothermia (32-34°C):

Complications of temperature control:

• Shivering (increases metabolic demand - treat aggressively)
• Electrolyte shifts (hypokalaemia during cooling, hyperkalaemia during rewarming)
• Coagulopathy (impaired platelet function, prolonged coagulation)
• Hyperglycaemia
• Immune suppression and infection risk
• Arrhythmias (QT prolongation, bradycardia)

Neuroprognostication

Timing and Approach [12,13]:

Multimodal Neuroprognostication Algorithm:

≥72 HOURS POST-ROSC (or post-rewarming)
         ↓
Confirm sedation cleared (≥5 half-lives)
         ↓
┌─────────────────────────────────────────────────────────────────────┐
│ CLINICAL EXAMINATION                                                │
│ • GCS motor score (≤2 vs greater than 3)                                        │
│ • Pupillary light reflex (bilateral absent = poor sign)             │
│ • Corneal reflex (bilateral absent = poor sign)                     │
│ • Myoclonus (requires EEG to characterise)                          │
└─────────────────────────────────────────────────────────────────────┘
         ↓
┌─────────────────────────────────────────────────────────────────────┐
│ ELECTROPHYSIOLOGY                                                   │
│ • EEG: Look for continuous background, reactivity (good)            │
│        Burst suppression, suppressed background (poor)              │
│ • SSEP: Bilateral absent N20 = highly specific for poor outcome     │
└─────────────────────────────────────────────────────────────────────┘
         ↓
┌─────────────────────────────────────────────────────────────────────┐
│ BIOMARKERS                                                          │
│ • NSE at 48-72 hours                                                │
│   - below 17 μg/L: suggests better prognosis                             │
│   - greater than 60 μg/L: associated with poor prognosis                        │
└─────────────────────────────────────────────────────────────────────┘
         ↓
┌─────────────────────────────────────────────────────────────────────┐
│ IMAGING                                                             │
│ • CT: Grey-white matter ratio at 24-48h                             │
│ • MRI DWI: Extensive diffusion restriction at 2-7 days              │
└─────────────────────────────────────────────────────────────────────┘
         ↓
MULTIDISCIPLINARY TEAM DISCUSSION
Only determine poor prognosis if MULTIPLE concordant poor prognostic indicators

Indicators of GOOD prognosis [4,12]:

• Early awakening (within 24-48 hours)
• GCS motor score over 3 within first 4 days
• Preserved pupillary and corneal reflexes at 72 hours
• Continuous/nearly continuous EEG background with reactivity
• Normal NSE (below 17 μg/L) at 48-72 hours
• Absence of diffusion restriction on MRI at 2-7 days

Indicators of POOR prognosis (need multiple) [4,12,13]:

• Bilateral absent pupillary light reflexes at ≥72 hours
• Bilateral absent corneal reflexes at ≥72 hours
• Bilateral absent N20 SSEP responses (most specific)
• Suppressed/burst suppression EEG pattern (off sedation)
• Extensive cortical diffusion restriction on MRI
• Marked reduced grey-white matter ratio on CT
• NSE over 60 μg/L at 48-72 hours

Common pitfalls:

• Prognosticating too early (before 72 hours)
• Relying on a single test
• Not accounting for sedation effects
• Assuming myoclonus = poor prognosis (it may be Lance-Adams syndrome)
• Self-fulfilling prophecy from early WLST

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Disposition

Admission Criteria

All patients with ROSC after cardiac arrest require admission to ICU or high-dependency unit with:

• Continuous cardiac monitoring
• Invasive blood pressure monitoring capability
• Temperature control capability
• Ventilator support if needed
• Access to emergency angiography

Transfer to Cardiac Arrest Centre

ANZCOR recommends transfer to a cardiac arrest centre where available [4]:

• 24/7 coronary angiography and PCI capability
• ICU with post-cardiac arrest care experience
• Targeted temperature management protocols
• Neuroprognostication expertise (EEG, SSEP, MRI)
• Neurointensive care capability

Consider retrieval/transfer if:

• Rural/regional hospital without coronary angiography
• Lack of TTM/temperature control capability
• Limited neurological prognostication resources
• Complex cases requiring specialist input

Remote/Rural Considerations

Important Note: Remote and Rural Emergency Medicine:

• Early retrieval activation: Contact retrieval services (RFDS, helicopter) immediately post-ROSC
• Telemedicine: Establish video link with receiving ICU/cardiac catheterisation lab
• Stabilisation priorities: ABCDE optimisation, temperature control initiation even in ED
• Limited resources: May need to prioritise targets (oxygenation, BP) with available monitoring
• Transfer logistics: Coordinate with retrieval team, anticipate flight/road times
• Communication: Early family discussion about need for transfer and prognosis uncertainty

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Pitfalls & Pearls

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Viva Practice

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OSCE Scenarios

Station 1: Post-ROSC Management

Format: Resuscitation leadership Time: 11 minutes Setting: ED resuscitation bay

Candidate Instructions:

A 60-year-old woman has just achieved ROSC after 10 minutes of CPR for VF cardiac arrest. She is intubated and sedated. An IV cannula and arterial line are in place. You are the team leader. Manage the immediate post-ROSC period.

Examiner Instructions:

• Patient is intubated, GCS 3T
• Initial vitals: BP 95/60, HR 105 sinus rhythm, SpO2 96% on FiO2 1.0
• Provide 12-lead ECG when requested showing 3mm ST elevation in II, III, aVF (inferior STEMI)
• Have nursing staff available to follow instructions

Expected Actions:

1. Confirm ROSC - check pulse, BP, ETCO2
2. Systematic ABCDE assessment
3. Request immediate 12-lead ECG
4. Recognise STEMI and call for urgent coronary angiography
5. Optimise oxygenation (wean FiO2 to SpO2 94-98%)
6. Target MAP ≥65 mmHg with vasopressors if needed
7. Initiate temperature control
8. NOT prognosticate - too early
9. Communicate with team using closed-loop communication

Marking Criteria:

Expected Standard:

• Pass: ≥6/11
• Key discriminators: Recognition of STEMI and appropriate action, avoidance of hyperoxia

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Station 2: Family Communication - Prognosis Discussion

Format: Communication Time: 11 minutes Setting: ICU relatives room

Candidate Instructions:

You are the ICU registrar. Mr Thompson (68 years) was admitted 4 days ago following ROSC from out-of-hospital cardiac arrest. He underwent TTM at 33°C for 24 hours. He remains comatose (GCS 3). His wife is asking about his prognosis. The results show: bilateral absent pupillary reflexes, bilateral absent N20 on SSEP, burst suppression on EEG, NSE 85 μg/L, and extensive cortical diffusion restriction on MRI. The team has discussed and feels the prognosis is poor. Discuss with Mrs Thompson.

Actor Brief (Mrs Thompson):

• 65-year-old wife, been at bedside continuously
• Anxious, tearful, wants honest information
• Will ask: "Will he wake up?"
  • "Should we stop treatment?"
  • "Did we do everything?"
• If approached sensitively, will express understanding
• If approached poorly, will become defensive or distressed

Marking Criteria:

Expected Standard:

• Pass: ≥6/11
• Key discriminators: Empathy while delivering difficult news, explaining multimodal approach, allowing time for questions

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SAQ Practice

Question 1 (8 marks)

Stem: A 55-year-old man achieves ROSC after 15 minutes of CPR for out-of-hospital VF cardiac arrest. He is intubated and transferred to your ED. His initial arterial blood gas on FiO2 1.0 shows: pH 7.18, PaO2 485 mmHg, PaCO2 28 mmHg, lactate 9 mmol/L.

Question: Outline your management priorities and physiological targets in the first 60 minutes post-ROSC. (8 marks)

Model Answer:

• Airway/Breathing (2 marks):

  • Wean FiO2 to target SpO2 94-98% (1 mark) - PaO2 485 mmHg is hyperoxic, associated with worse neurological outcomes
  • Increase respiratory rate to target PaCO2 35-45 mmHg (1 mark) - current PaCO2 28 mmHg is hypocapnic, causes cerebral vasoconstriction

• Circulation (2 marks):

  • Immediate 12-lead ECG to identify STEMI (1 mark) - if STEMI present, immediate coronary angiography
  • Target MAP ≥65 mmHg using vasopressors if needed (1 mark) - noradrenaline first-line

• Disability (2 marks):

  • Check blood glucose and treat hypo/hyperglycaemia (1 mark) - target 7.8-10 mmol/L
  • Document GCS, pupils, motor response (1 mark) - light sedation only, do NOT prognosticate early

• Temperature control (2 marks):

  • Measure core temperature and initiate fever prevention (1 mark) - target ≤37.5°C
  • Continue fever prevention for at least 72 hours (1 mark)

Examiner Notes:

• Accept: Mention of ANZCOR guidelines, specific drug names for vasopressors
• Do not accept: TTM 32-34°C as mandatory (uncertain benefit post-TTM2), aggressive hyperventilation

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Question 2 (6 marks)

Stem: A 62-year-old woman is day 4 post-cardiac arrest. She remains comatose (GCS 3) with absent pupillary light reflexes bilaterally. The family asks about prognosis.

Question: List the components of a multimodal neuroprognostication assessment according to current guidelines. (6 marks)

Model Answer:

• Clinical examination (1 mark): Pupillary light reflex, corneal reflex, GCS motor score, myoclonus assessment at ≥72 hours post-ROSC
• Electrophysiology - SSEP (1 mark): Bilateral absent N20 cortical responses highly specific for poor outcome
• Electrophysiology - EEG (1 mark): Continuous background (good) vs burst suppression/suppressed background (poor)
• Biomarkers (1 mark): Neuron-specific enolase (NSE) at 48-72 hours - over 60 μg/L associated with poor prognosis
• Imaging (1 mark): CT (grey-white matter ratio at 24-48h), MRI DWI (diffusion restriction at 2-7 days)
• Timing/confounders (1 mark): Assessment at ≥72 hours post-ROSC, ensure sedation cleared (≥5 half-lives)

Examiner Notes:

• Accept: Mention of multimodal approach, need for multiple concordant findings
• Do not accept: Single test as sufficient, prognostication before 72 hours

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Question 3 (6 marks)

Stem: A 50-year-old man achieves ROSC after VF cardiac arrest. His post-ROSC 12-lead ECG shows 4mm ST elevation in leads V1-V4.

Question: Outline the indications for immediate coronary angiography in this patient and the key points regarding timing and TTM interaction. (6 marks)

Model Answer:

• Indication in this patient (2 marks): STEMI (anterior) on post-ROSC ECG is an absolute indication for immediate coronary angiography (within 2 hours) regardless of neurological status or coma

• Coma is NOT a contraindication (1 mark): Revascularisation improves both survival and neurological outcomes - do not delay for neurological assessment

• Other indications (2 marks):

  • New LBBB with suspected ACS
  • Cardiogenic shock despite adequate resuscitation
  • Strong suspicion of ACS as arrest cause (shockable rhythm, cardiac risk factors)
  • Non-STEMI with elevated troponin - early angiography within 24 hours reasonable

• TTM interaction (1 mark): PCI during temperature control is feasible and safe - TTM should not delay coronary angiography for STEMI

Examiner Notes:

• Accept: Reference to TOMAHAWK/COACT trials for non-STEMI
• Do not accept: Delaying angiography for TTM initiation or neurological assessment in STEMI

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Australian/ANZCOR Guidelines Summary

ANZCOR Guideline 11.7 - Post-resuscitation Therapy [4]

Haemodynamics:

• Target MAP ≥60-65 mmHg initially (may need higher for chronic hypertensives)
• Vasopressors and fluids as part of post-resuscitation care bundle
• No specific BP target proven superior

Oxygenation/Ventilation:

• Use 100% O2 initially until SpO2 reliably monitored
• Then titrate to SpO2 94-98% (avoid hypoxaemia and hyperoxia)
• Target normocapnia (PaCO2 35-45 mmHg)

Glucose:

• Monitor frequently, treat hyperglycaemia over 10 mmol/L
• Avoid hypoglycaemia

Seizures:

• Do NOT give seizure prophylaxis
• DO treat seizures when they occur

Coronary angiography:

• STEMI: immediate coronary angiography
• No STEMI: early (2-6 hours) or delayed (within 24 hours) both reasonable

Neuroprognostication:

• Multimodal approach mandatory
• ≥72 hours post-ROSC (or post-rewarming)
• No single test sufficient

ANZCOR Guideline 11.8 - Temperature Control [5]

Recommended approach (post-TTM2):

• Actively prevent fever by targeting temperature ≤37.5°C
• Duration: at least 72 hours in comatose patients
• Uncertain if hypothermia (32-34°C) benefits subpopulations

Methods:

• Surface or endovascular cooling techniques
• Cooling devices with feedback system preferred
• Cold IV saline (up to 30 mL/kg) for induction only - not maintenance

Pre-hospital cooling:

• NOT recommended (increased re-arrest and pulmonary oedema)

Mild hypothermia after ROSC:

• Do NOT actively warm to normothermia

Key Differences from AHA/ERC

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Remote/Rural Considerations

Pre-Hospital and Retrieval

Rural/remote challenges:

• Prolonged transport times to definitive care
• Limited monitoring capabilities
• Variable access to coronary angiography
• Delayed access to neurological prognostication tools

Stabilisation priorities before retrieval:

• Confirm airway secure with capnography
• Optimise oxygenation and ventilation (portable ABG if available)
• Establish haemodynamic stability (noradrenaline infusion if needed)
• Initiate temperature control (ice packs, paracetamol)
• Obtain and transmit 12-lead ECG to receiving centre

Retrieval considerations:

• Early activation of retrieval services (RFDS, helicopter)
• Establish telemedicine link with receiving ICU/cardiac catheter lab
• Prepare for in-flight complications (arrhythmias, hypotension)
• Document all interventions and findings for handover

Telemedicine Support

• Video link to specialist for ECG interpretation
• Remote guidance for post-ROSC management
• Assistance with family communication regarding prognosis
• Coordination of transfer timing and destination

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Additional Viva Scenarios

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Additional OSCE Station

Station 3: Post-ROSC ABG Interpretation and Management

Format: Clinical reasoning/data interpretation Time: 11 minutes Setting: ED resuscitation bay

Candidate Instructions:

A 55-year-old man achieved ROSC 20 minutes ago after 14 minutes of CPR for VF cardiac arrest. He is intubated and ventilated on the following settings: FiO2 1.0, TV 500 mL, RR 16, PEEP 5 cmH2O. His arterial blood gas shows:

• pH 7.12
• PaO2 520 mmHg
• PaCO2 28 mmHg
• HCO3 11 mmol/L
• Lactate 12 mmol/L
• K+ 5.8 mmol/L
• Glucose 14 mmol/L

Interpret this ABG and outline your immediate management priorities.

Expected Answer Structure:

1. ABG interpretation:

   • Severe metabolic acidosis (low pH, low HCO3, elevated lactate)
   • Respiratory alkalosis (low PaCO2) - patient is being over-ventilated
   • Hyperoxia (PaO2 520 mmHg on FiO2 1.0) - excessive oxygen administration
   • Hyperkalaemia (K+ 5.8) - risk of arrhythmias
   • Hyperglycaemia (glucose 14) - requires treatment

2. Management priorities:

   • Reduce FiO2: Wean to achieve SpO2 94-98%, avoid hyperoxia
   • Reduce respiratory rate: Target normocapnia (PaCO2 35-45 mmHg)
   • Treat hyperkalaemia: Calcium gluconate 10 mL of 10% IV, insulin/dextrose if persistent
   • Treat hyperglycaemia: Insulin infusion if glucose greater than 10 mmol/L
   • Monitor lactate trend: Indicates perfusion status
   • Do NOT over-correct acidosis: Will improve with perfusion

Marking Criteria:

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Additional SAQ Practice

Question 4 (6 marks)

Stem: A 70-year-old man with no significant past history achieves ROSC after 8 minutes of CPR for witnessed VF arrest at a shopping centre. He is intubated, sedated with propofol, and transferred to your ED. He remains comatose (GCS 3T).

Question: Describe the key components of the ANZCOR-recommended temperature control strategy for this patient. (6 marks)

Model Answer:

• Target temperature: ≤37.5°C (actively prevent fever) (1 mark)
• Duration: Maintain for at least 72 hours while patient remains comatose (1 mark)
• Methods: Surface cooling devices, endovascular cooling catheters, paracetamol, environmental cooling - devices with feedback systems preferred (1 mark)
• Avoid pre-hospital cold IV fluids: Associated with increased re-arrest and pulmonary oedema (1 mark)
• Mild spontaneous hypothermia: Do NOT actively warm to normothermia (1 mark)
• Monitoring: Core temperature measurement (oesophageal, bladder, or rectal probe), continuous or hourly during active cooling (1 mark)

Examiner Notes:

• Accept: Mention of TTM2 trial influencing current practice
• Accept: Noting uncertainty about hypothermia 32-34°C for subpopulations
• Do not accept: Mandating hypothermia 32-34°C as standard of care

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Question 5 (8 marks)

Stem: A 58-year-old woman is day 5 post-cardiac arrest. She received TTM at 33°C for 24 hours and has been normothermic for 4 days. She remains comatose with the following findings:

• GCS 3 (no eye opening, no verbal, no motor response to pain)
• Bilateral absent pupillary light reflexes
• Bilateral absent corneal reflexes
• SSEP: Bilateral absent N20 cortical responses
• EEG: Suppressed background, no reactivity
• MRI: Extensive cortical and deep grey matter diffusion restriction
• NSE at 72 hours: 95 μg/L

Question: Discuss how you would use this information to prognosticate and what you would tell the family. (8 marks)

Model Answer:

• Multimodal approach (2 marks): Multiple concordant poor prognostic indicators are present - this satisfies the requirement for multimodal assessment before determining poor prognosis
• Timing appropriateness (1 mark): Day 5 post-arrest (and over 72 hours post-rewarming) is appropriate for prognostication. Sedation has cleared (propofol half-life allows clearance by this time)
• Clinical findings (1 mark): Bilateral absent pupillary and corneal reflexes at ≥72 hours are poor prognostic signs (high specificity for poor outcome)
• SSEP findings (1 mark): Bilateral absent N20 is the most specific test (98-100% specificity) for poor neurological outcome
• EEG findings (1 mark): Suppressed background without reactivity, when combined with other tests, supports poor prognosis
• Imaging and biomarkers (1 mark): Extensive diffusion restriction on MRI and NSE over 60 μg/L both support poor prognosis
• Family communication (1 mark): Would explain that multiple independent tests all point to the same conclusion - that meaningful recovery is very unlikely. Would offer MDT meeting, give time for other family members to arrive, discuss withdrawal of life-sustaining treatment when family ready

Examiner Notes:

• Accept: Emphasis on involving neurology, palliative care, ethics if needed
• Accept: Discussion of organ donation if appropriate
• Do not accept: Prognostication based on single test alone

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Long-Term Outcomes and Rehabilitation

Survival and Functional Outcomes

Cerebral Performance Category (CPC) Scale [37]:

Favourable neurological outcome = CPC 1-2

Long-Term Survivor Outcomes

Physical function:

• 60-80% of CPC 1-2 survivors return to pre-arrest physical function within 6-12 months
• Fatigue is common, affecting 50-70% of survivors
• Cardiac rehabilitation improves exercise capacity and quality of life

Cognitive function [37]:

• 30-50% of survivors with good CPC have measurable cognitive deficits
• Memory impairment most common (hippocampal vulnerability)
• Executive dysfunction affects work and complex tasks
• May improve over 6-12 months but some deficits persist

Psychological outcomes:

• Anxiety: 25-40% of survivors
• Depression: 15-30% of survivors
• PTSD: 15-25% of survivors
• Screen all survivors using validated tools (PHQ-9, GAD-7, PCL-5)

Return to work:

• 40-60% of survivors return to work within 6-12 months
• May require modified duties or reduced hours initially
• Neuropsychological assessment helpful for workplace planning

Follow-Up Care

Recommended follow-up structure:

Cardiac secondary prevention:

• ICD assessment (if VF/VT without reversible cause, LVEF ≤35%)
• Optimisation of cardiac risk factors
• Cardiac rehabilitation program
• Review of medications (beta-blockers, ACE inhibitors, statins)

Driving restrictions (Australian guidelines):

• Private vehicle: Typically 6 months minimum post-arrest
• Commercial vehicle: Usually permanent restriction
• Individual assessment by cardiologist/neurologist required
• Must be seizure-free and cognitively competent

Quality of Life

Factors associated with better quality of life:

• Shorter downtime
• VF/VT as initial rhythm
• Early ROSC
• Younger age
• Good cognitive recovery
• Strong social support

Survivor support:

• Cardiac arrest survivor support groups
• Peer mentoring programs
• Psychological therapy (CBT, trauma-focused therapy)
• Family/carer support and education

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Complications

Early Complications (0-72 Hours)

Late Complications (greater than 72 Hours)

Post-intensive care syndrome:

• Cognitive impairment persisting after discharge
• Psychological sequelae (anxiety, depression, PTSD)
• Physical weakness and deconditioning
• Sleep disturbance

Seizure disorders:

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

Cardiac complications:

• Heart failure (from underlying disease or post-arrest cardiomyopathy)
• Recurrent arrhythmias
• May require ICD implantation

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References

ARC/ANZCOR Guidelines

1. ANZCOR. Guideline 11.7 – Post-resuscitation Therapy in Adult Advanced Life Support. 2024. Available from: https://anzcor.org
2. Neumar RW, Nolan JP, Adrie C, et al. Post-cardiac arrest syndrome: epidemiology, pathophysiology, treatment, and prognostication. Circulation. 2008;118(23):2452-2483. PMID: 19004177
3. Bray JE, Stub D, Bernard S, Smith K. Exploring variations in outcomes in the Australian Resuscitation Outcomes Consortium Epistry. Resuscitation. 2019;135:156-161. PMID: 30590128
4. ANZCOR. Guideline 11.7 – Post-resuscitation Therapy in Adult Advanced Life Support. 2024. Available from: https://anzcor.org
5. ANZCOR. Guideline 11.8 – Temperature Control after Cardiac Arrest. 2024. Available from: https://anzcor.org

Key Evidence - Oxygenation and Ventilation

6. Kilgannon JH, Jones AE, Shapiro NI, et al. Association between arterial hyperoxia following resuscitation from cardiac arrest and in-hospital mortality. JAMA. 2010;303(21):2165-2171. PMID: 20516417
7. Roberts BW, Kilgannon JH, Hunter BR, et al. Association between early hyperoxia exposure after resuscitation from cardiac arrest and neurological disability. Circulation. 2018;137(20):2114-2124. PMID: 29700121
8. Roberts BW, Kilgannon JH, Chansky ME, et al. Association between postresuscitation partial pressure of arterial carbon dioxide and neurological outcome. Circulation. 2013;127(21):2107-2113. PMID: 23613256

Key Evidence - Temperature Management

9. Dankiewicz J, Cronberg T, Lilja G, et al. Hypothermia versus Normothermia after Out-of-Hospital Cardiac Arrest. N Engl J Med. 2021;384(24):2283-2294. PMID: 34133859
10. Lemkes JS, Janssens GN, van der Hoeven NW, et al. Coronary Angiography after Cardiac Arrest without ST-Segment Elevation. N Engl J Med. 2019;380(15):1397-1407. PMID: 30883057
11. Desch S, Freund A, Akin I, et al. Angiography after Out-of-Hospital Cardiac Arrest without ST-Segment Elevation. N Engl J Med. 2021;385(27):2544-2553. PMID: 34459570

Key Evidence - Neuroprognostication

12. Nolan JP, Sandroni C, Böttiger BW, et al. European Resuscitation Council and European Society of Intensive Care Medicine guidelines 2021: post-resuscitation care. Intensive Care Med. 2021;47(4):369-421. PMID: 33765189
13. Sandroni C, Cariou A, Cavallaro F, et al. Prognostication in comatose survivors of cardiac arrest: an advisory statement. Resuscitation. 2014;85(12):1779-1789. PMID: 25447032
14. Dicker B, Davey P, Todd VF, et al. Out-of-hospital cardiac arrest registry methodology and results for a New Zealand regional database. Resuscitation. 2019;140:159-166. PMID: 31096029

Epidemiology and Outcomes

15. 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. PMID: 23150959
16. Andersen LW, Holmberg MJ, Berg KM, et al. In-Hospital Cardiac Arrest: A Review. JAMA. 2019;321(12):1200-1210. PMID: 30912843
17. 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. PMID: 12505221
18. Sekhon MS, Ainslie PN, Griesdale DE. Clinical pathophysiology of hypoxic ischemic brain injury after cardiac arrest. Crit Care Med. 2017;45(4):651-659. PMID: 28350643

Indigenous Health

19. Brown A, Walsh W, Wheatley V, Jerrgensen M. Cardiovascular disease in Indigenous Australians. Aust Health Rev. 2018;42(5):473-475. PMID: 30208824

Pathophysiology

20. 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. PMID: 31075369
21. Elmer J, Torres C, Guyette FX, et al. Association of early withdrawal of life-sustaining therapy for perceived neurological prognosis with mortality after cardiac arrest. Resuscitation. 2016;102:127-135. PMID: 27068662
22. Adrie C, Adib-Conquy M, Laurent I, et al. Successful cardiopulmonary resuscitation after cardiac arrest as a "sepsis-like" syndrome. Circulation. 2002;106(5):562-568. PMID: 12147537
23. 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. PMID: 11525703
24. Kern KB, Hilwig RW, Rhee KH, et al. Myocardial dysfunction after resuscitation from cardiac arrest: an example of global myocardial stunning. J Am Coll Cardiol. 1996;28(1):232-240. PMID: 8752819

ROSC Recognition and Monitoring

25. 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. PMID: 9233867
26. Ameloot K, De Deyne C, Eertmans W, et al. Early goal-directed haemodynamic optimization of cerebral oxygenation in comatose survivors after cardiac arrest. Resuscitation. 2019;135:145-152. PMID: 30576777

Seizures

27. Rossetti AO, Rabinstein AA, Oddo M. Neurological prognostication of outcome in patients in coma after cardiac arrest. Lancet Neurol. 2016;15(6):597-609. PMID: 27017070

Pre-Hospital Cooling

28. Kim F, Nichol G, Maynard C, et al. Effect of prehospital induction of mild hypothermia on survival and neurological status among adults with cardiac arrest. JAMA. 2014;311(1):45-52. PMID: 24240712

Electrophysiology

29. Westhall E, Rossetti AO, van Rootselaar AF, et al. Standardized EEG interpretation accurately predicts prognosis after cardiac arrest. Neurology. 2016;86(16):1482-1490. PMID: 27009259
30. Zandbergen EG, Hijdra A, Koelman JH, et al. Prediction of poor outcome within the first 3 days of postanoxic coma. Neurology. 2006;66(1):62-68. PMID: 16401847

Biomarkers

31. Stammet P, Collignon O, Hassager C, et al. Neuron-Specific Enolase as a Predictor of Death or Poor Neurological Outcome After Out-of-Hospital Cardiac Arrest. Circulation. 2015;131(5):427-435. PMID: 25472913

Coronary Angiography Trials

32. Desch S, Freund A, Akin I, et al. Angiography after Out-of-Hospital Cardiac Arrest without ST-Segment Elevation (TOMAHAWK). N Engl J Med. 2021;385(27):2544-2553. PMID: 34459570

TTM Trials

33. Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med. 2002;346(8):549-556. PMID: 11856793
34. Nielsen N, Wetterslev J, Cronberg T, et al. Targeted temperature management at 33°C versus 36°C after cardiac arrest. N Engl J Med. 2013;369(23):2197-2206. PMID: 24237006

Imaging

35. Wijman CA, Mlynash M, Caulfield AF, et al. Prognostic value of brain diffusion-weighted imaging after cardiac arrest. Ann Neurol. 2009;65(4):394-402. PMID: 19399889

Quality and Outcomes

36. Cronberg T, Rundgren M, Westhall E, et al. Neuron-specific enolase correlates with other prognostic markers after cardiac arrest. Neurology. 2011;77(7):623-630. PMID: 21775732
37. Moulaert VR, Verbunt JA, van Heugten CM, et al. Cognitive impairments in survivors of out-of-hospital cardiac arrest. Resuscitation. 2009;80(3):297-305. PMID: 19131171

Additional ILCOR Evidence

38. Soar J, Berg KM, Andersen LW, et al. Adult Advanced Life Support: 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Resuscitation. 2020;156:A80-A119. PMID: 33098917
39. Berg KM, Bray JE, Ng KC, et al. 2023 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Resuscitation. 2023;194:109992. PMID: 37963835
40. Granfeldt A, Holmberg MJ, Nolan JP, et al. Targeted Temperature Management in Adult Cardiac Arrest: Systematic Review and Meta-Analysis. Resuscitation. 2021;167:160-172. PMID: 34508820

Australian Data

41. Aus-ROC Steering Committee. Australian Resuscitation Outcomes Consortium (Aus-ROC) Epistry Annual Report 2022. Melbourne: Aus-ROC; 2023.
42. Straney LD, Bray JE, Beck B, et al. Regions of high out-of-hospital cardiac arrest incidence and low bystander CPR rates in Victoria, Australia. PLoS One. 2015;10(11):e0139776. PMID: 26523747