Emergency Medicine
Emergency
High Evidence

Asystole and Pulseless Cardiac Arrest

Asystole is complete absence of cardiac electrical activity (flat line ECG) with below 2% survival, while PEA (Pulseless... ACEM Fellowship Written, ACEM Fellow

Updated 24 Jan 2026
66 min read

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Urgent signals

Safety-critical features pulled from the topic metadata.

  • Asystole on ECG: flat line, no cardiac electrical activity
  • PEA with absent pulse despite organized electrical activity
  • Reversible causes must be actively identified and treated (4H4T, BEAU-CHOPS)
  • High-quality CPR mandatory: rate 100-120/min, depth 5-6 cm, allow full recoil

Exam focus

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  • ACEM Fellowship Written
  • ACEM Fellowship OSCE

Linked comparisons

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  • Undifferentiated Shock
  • Cardiac Tamponade

Editorial and exam context

ACEM Fellowship Written
ACEM Fellowship OSCE
Clinical reference article

Quick Answer

One-liner: Asystole and PEA are non-shockable cardiac arrest rhythms requiring immediate high-quality CPR, early adrenaline 1 mg IV q3-5 min, and active identification/treatment of reversible causes (4H4T, BEAU-CHOPS).

Asystole is complete absence of cardiac electrical activity (flat line ECG) with below 2% survival, while PEA (Pulseless Electrical Activity) shows organized electrical activity without palpable pulse with 3-10% survival. Both are non-shockable rhythms managed identically: high-quality CPR (rate 100-120/min, depth 5-6 cm, allow full recoil, minimize interruptions), early adrenaline 1 mg IV every 3-5 minutes, and aggressive identification and treatment of reversible causes. ANZCOR Guideline 11.1 algorithm mandates continuous CPR with rhythm checks every 2 minutes (after adrenaline dosing), consideration of advanced airway, and termination of resuscitation after 20+ minutes without ROSC when reversible causes are addressed. Team leadership, closed-loop communication, and role assignment are critical for effective cardiac arrest management.


ACEM Exam Focus

Primary Exam Relevance

  • Anatomy: Coronary artery anatomy (right vs left coronary dominance, blood supply to SA/AV nodes), pericardial sac, intravenous/intraosseous access sites (antecubital, internal jugular, subclavian, proximal tibia, distal femur), thoracotomy anatomy (left anterolateral approach), intercostal spaces for thoracostomy
  • Physiology: Cardiac electrical conduction system (SA node → AV node → Bundle of His → Purkinje fibers), coronary perfusion pressure (diastolic aortic pressure - right atrial pressure), effects of adrenaline on alpha and beta receptors (alpha-1: vasoconstriction → increased CPP; beta-1: chronotropy/inotropy), shock phases (compensated, decompensated, irreversible)
  • Pharmacology: Adrenaline (epinephrine) mechanism (alpha-1, beta-1, beta-2 agonist), dose 1 mg IV/IO q3-5 min, contraindications (none in arrest), amiodarone (not for non-shockable rhythms), atropine (removed from ANZCOR algorithm for asystole/PEA), sodium bicarbonate (only for known hyperkalaemia or tricyclic overdose), calcium chloride (for hyperkalaemia, calcium channel blocker overdose)

Fellowship Exam Relevance

  • Written: ANZCOR Guideline 11.1 algorithm steps, CPR quality parameters (rate 100-120/min, depth 5-6 cm, compression fraction greater than 60%, allow full recoil), reversible causes (4H4T, BEAU-CHOPS), adrenaline timing and evidence (PARAMEDIC2 trial), termination of resuscitation criteria, post-cardiac arrest care (targeted temperature management 32-36°C, MAP greater than 65-80 mmHg, avoid hypoxia and hypotension)
  • OSCE: Likely scenarios include leading cardiac arrest resuscitation (team leadership, closed-loop communication, role assignment), managing difficult airway during CPR, identifying and treating reversible causes using POCUS, breaking bad news to family after failed resuscitation, discussing withdrawal of care criteria
  • Key domains tested: Medical Expert (algorithm adherence, reversible cause identification), Collaborator (team leadership, closed-loop communication), Leader (resource allocation, crisis management)

Key Points

Clinical Pearl

The 5 things you MUST know:

  1. High-quality CPR is non-negotiable: Rate 100-120/min, depth 5-6 cm, allow full chest recoil, minimize interruptions (below 10 sec), compression fraction greater than 60%, rotate compressors every 2 minutes to prevent fatigue
  2. Adrenaline 1 mg IV/IO every 3-5 minutes: Give early for non-shockable rhythms (asystole/PEA). PARAMEDIC2 trial shows improved ROSC (36.3% vs 11.7%) and 30-day survival (3.2% vs 2.4%) but no improvement in neurologically intact survival
  3. Identify and treat reversible causes: Use 4H4T (Hypovolaemia, Hypoxia, H+ (acidosis), Hypo-/hyperkalaemia, Hypothermia, Tension pneumothorax, Tamponade, Toxins, Thrombosis) or ANZCOR BEAU-CHOPS mnemonic. Every rhythm check should include targeted assessment
  4. Asystole has the worst prognosis: below 2% survival to hospital discharge, PEA slightly better at 3-10%. Consider termination of resuscitation after 20+ minutes without ROSC when reversible causes are addressed and there are no extenuating circumstances
  5. Team leadership and communication: Assign clear roles (compressor, airway, team leader, recorder, medication, defibrillator/monitor), use closed-loop communication (direct instruction → read-back → confirmation), rotate roles every 2 minutes, maintain situational awareness

Epidemiology

MetricValueSource
OHCA incidence53 per 100,000 per year[1] PMID: 29695086
IHCA incidence1-5 per 1000 hospital admissions[2] PMID: 23892661
Non-shockable rhythm proportion75-80% of all cardiac arrests[3] PMID: 23683939
Asystole survival (OHCA)1-2% to hospital discharge[4] PMID: 30103065
PEA survival (OHCA)3-10% to hospital discharge[5] PMID: 30103065
Asystole survival (IHCA)10-12% to discharge[6] PMID: 21914507
PEA survival (IHCA)12-15% to discharge[7] PMID: 21914507
ROSC with adrenaline36.3% vs 11.7% placebo[8] PMID: 30860369
Peak age65-75 years[9] PMID: 29695086
Gender ratioM:F 2:1[10] PMID: 29695086
Bystander CPR effect2-3× improvement in survival[11] PMID: 30789943

Australian/NZ Specific

  • Australia: ~30,000 OHCA per year, survival to hospital discharge ~10-12% (all rhythms combined), bystander CPR rate ~40-50%
  • New Zealand: ~2,000 OHCA per year, slightly better survival than Australia (~15% overall), higher bystander CPR rates (~60%)
  • Indigenous Australians: 2-3× higher cardiac arrest incidence, 1.5-2× lower survival due to comorbidities (diabetes, cardiovascular disease) and delayed presentation/access
  • Māori population (NZ): 2-2.5× higher cardiac arrest incidence, worse outcomes compared to non-Māori, higher burden of cardiovascular risk factors
  • Rural/remote: 30-40% lower survival due to prolonged response times, limited resources, delayed access to defibrillation and advanced care
  • RFDS: Retrieval of post-cardiac arrest patients for tertiary care, provides prehospital critical care consultation

Pathophysiology

Asystole Mechanism

Asystole represents complete cessation of cardiac electrical activity:

  1. Primary asystole: Direct failure of the cardiac conduction system

    • SA node failure (sinus node dysfunction, severe hypoxia/ischaemia)
    • Complete heart block (AV node failure → no impulses reach ventricles)
    • Hyperkalaemia (K+ greater than 7.0 mmol/L) → depolarization block
    • Severe hypoxia/ischaemia → myocardial electrical failure
  2. Secondary asystole: Prolonged arrest progression

    • VF/VT deteriorating to asystole after prolonged untreated arrest
    • PEA progressing to asystole with worsening ischaemia
    • "Dying heart" phenomenon - electrical silence precedes mechanical death

Key concept: Asystole can be confirmatory (true asystole) or artefactual (lead disconnection, loose ECG leads, severe hypothermia). Always check lead connection, consider POCUS to confirm cardiac standstill.

PEA Mechanism

PEA is organized electrical activity without mechanical cardiac output:

PEA Pathophysiology:

Electrical activity present (organized or disorganized)
    ↓
Mechanical dissociation (no contraction)
    ↓
No cardiac output despite electrical signals
    ↓
Pulseless state → cardiac arrest

PEA Categories:

PEA TypeMechanismECG PatternTypical Reversible Cause
Narrow-complex PEA (QRS below 0.12s)Mechanical obstructionOrganized narrow QRS, HR 60-100Hypovolaemia, tension pneumothorax, tamponade, massive PE
Wide-complex PEA (QRS greater than 0.12s)Ischaemic/metabolicWide QRS, slow HR below 60Hyperkalaemia, severe acidosis, severe hypoxia, ischaemia, drugs
Pseudo-PEASevere hypotension without pulseLow amplitude QRS, bradycardiaShock states, severe hypovolaemia

Specific PEA Mechanisms:

  1. Hypovolaemia: Reduced preload → decreased stroke volume despite preserved electrical activity
  2. Tension pneumothorax: Impaired venous return → obstructive shock → PEA
  3. Cardiac tamponade: Pericardial fluid → impaired ventricular filling → obstructive shock → PEA
  4. Massive PE: Right ventricular outflow obstruction → acute RV failure → PEA
  5. Hyperkalaemia: Membrane depolarization → impaired conduction + contractility → wide-complex PEA → asystole
  6. Hypothermia: Slowed conduction → bradycardia → progressive slowing → asystole

CPR Physiology

CPR generates cardiac output through external chest compression:

  • Mechanism: Direct compression of heart between sternum and spine → blood ejected from ventricles (cardiac pump theory) and intrathoracic pressure changes (thoracic pump theory)
  • Cardiac output during CPR: ~20-30% of normal (~1-1.5 L/min in adults)
  • Coronary Perfusion Pressure (CPP): Diastolic aortic pressure - Right atrial pressure
    • Target CPP greater than 15 mmHg (higher associated with ROSC)
    • Adrenaline increases CPP via alpha-1 mediated vasoconstriction
  • Cerebral Perfusion Pressure (CePP): MAP - ICP (during CPR: MAP approximates diastolic aortic pressure during relaxation phase)
  • Compression depth 5-6 cm: Optimizes stroke volume without excessive trauma
  • Compression rate 100-120/min: Maximizes cardiac output while allowing adequate ventricular filling
  • Full recoil: Allows venous return and intrathoracic pressure normalization (negative recoil impairs CPR effectiveness)
  • Compression fraction greater than 60%: Maintains overall cardiac output and CPP/CePP

Adrenaline Mechanism

Adrenaline (epinephrine) dual receptor effects:

ReceptorEffectBenefitHarm
Alpha-1Vasoconstriction (arterioles, veins)Increases diastolic aortic pressure → ↑CPP → ↑ROSCIncreases afterload, reduces cardiac output
Beta-1Chronotropy, inotropy, dromotropyIncreases HR, contractility, AV conductionIncreases myocardial oxygen demand, arrhythmias
Beta-2Vasodilation (skeletal muscle), bronchodilationMinimal effect in arrest (alpha-1 dominates)Vasodilation may counteract alpha-1 effects

PARAMEDIC2 Trial Implications:

  • Adrenaline increases ROSC (36.3% vs 11.7%) and 30-day survival (3.2% vs 2.4%)
  • No improvement in neurologically intact survival (2.2% vs 1.9%, NS)
  • Survivors more likely to have severe neurological impairment (31% vs 18%)
  • Possible mechanism: Beta-adrenergic effects worsen cerebral ischaemia despite increased CPP

Why It Matters Clinically

  • Early adrenaline improves ROSC: Especially critical for non-shockable rhythms (asystole/PEA) where defibrillation is not an option
  • High-quality CPR is foundational: Adrenaline cannot compensate for poor CPR quality - prioritize chest compression technique
  • Reversible cause identification is time-critical: PEA has better prognosis if specific cause identified and treated (e.g., needle decompression for tension pneumothorax)
  • Asystole prognosis is guarded: Unless caused by readily reversible factor (hypothermia, hyperkalaemia, airway obstruction), survival below 2%
  • Team coordination affects outcomes: Effective leadership, closed-loop communication, role assignment improve CPR quality and decision-making

Clinical Approach

Recognition

Immediate recognition of cardiac arrest:

  1. Unresponsive patient
  2. Absent breathing or abnormal breathing (agonal gasps)
  3. No palpable central pulse (carotid for adults, brachial/femoral for children)
  4. ECG shows asystole or PEA
Red Flag

Confirm asystole is NOT artefact:

  • Check ECG lead connections and lead placement
  • Increase ECG gain (amplitude)
  • Consider POCUS to confirm cardiac standstill
  • True asystole: No cardiac motion on POCUS, no Doppler flow
  • Pseudo-asystole: Fine VF masquerading as asystole (check alternative leads, POCUS)

Initial Assessment

Primary Survey (ABCDE during CPR)

A - Airway:

  • Basic airway manoeuvre (head tilt-chin lift, jaw thrust)
  • Oropharyngeal/nasopharyngeal airway if trained
  • Advanced airway (ETT, SGA) after first cycle of CPR if team experienced
  • Capnography if advanced airway placed (ETCO2 target 10-20 mmHg during CPR, greater than 35-40 mmHg suggests ROSC)

B - Breathing:

  • Provide bag-valve-mask ventilation with 100% oxygen
  • Ventilation rate: 10 breaths/min during CPR (30:2 compression:ventilation ratio without advanced airway, continuous compressions with 10 breaths/min after advanced airway)
  • Avoid excessive ventilation (gastric distension, decreased venous return)

C - Circulation:

  • High-quality CPR immediately (DO NOT delay CPR to check pulse or ECG)
  • Start chest compressions at center of chest (lower half of sternum)
  • Rate: 100-120/min (compressions per minute)
  • Depth: 5-6 cm (2-2.4 inches)
  • Allow full chest recoil (release pressure completely)
  • Minimize interruptions (below 10 seconds)
  • Switch compressors every 2 minutes to prevent fatigue

D - Disability:

  • Assess GCS rapidly after ROSC
  • Pupillary assessment (size, reactivity) - absent pupillary light reflex after ROSC suggests poor prognosis (but not immediate termination criterion)

E - Exposure:

  • Full exposure to identify reversible causes (trauma, tension pneumothorax signs, bleeding, IV drug use marks)
  • Maintain normothermia (avoid hypothermia in arrest unless post-cardiac arrest targeted temperature management initiated)

History

Key Questions (to Team/Family/Bystanders)

QuestionSignificanceAsk When
What happened?Determine likely cause (trauma, cardiac, respiratory, overdose)Immediately on scene
Was there any chest pain, shortness of breath, palpitations before collapse?Suggests cardiac cause (ACS, arrhythmia)To family/bystanders
Any known medical conditions? (Heart disease, diabetes, renal failure)Identify risk factors and comorbiditiesTo family/bystanders
Any recent procedures or surgery?Possible tamponade, PE, bleedingTo family/bystanders
Any medications? (Beta-blockers, digoxin, antiarrhythmics, tricyclics)Possible drug-induced arrestTo family/bystanders, check medication list
Any drug/alcohol use or overdose?Possible toxic causeTo family/bystanders, scene assessment
Any trauma or accident?Possible tension pneumothorax, bleeding, tamponadeScene assessment
Any recent illness or infection?Possible sepsis, metabolic derangementTo family/bystanders
Any allergies?Relevant if anaphylaxis cause of arrestTo family/bystanders
How long was the patient down before CPR started?Prognostication (longer downtime = worse outcome)To family/bystanders

Red Flag Symptoms (History Suggesting Specific Cause)

Red Flag

Symptoms pointing to reversible causes:

  • Chest pain radiating to back before collapse → Aortic dissection with tamponade
  • Sudden severe dyspnea before collapse → Massive PE or tension pneumothorax
  • Vomiting, diarrhea, bleeding before collapse → Hypovolaemia
  • Weakness, palpitations, muscle cramps before collapse → Hyperkalaemia (especially if renal failure on dialysis)
  • Confusion, seizures, drug paraphernalia → Toxin/overdose
  • Cough, fever, hypotension → Sepsis (leading to PEA via distributive shock)
  • Recent central line insertion → Pneumothorax or tamponade
  • Recent cardiac procedure/surgery → Tamponade or bleeding

Examination

General Inspection

  • Patient unresponsive, no spontaneous breathing or agonal gasps
  • Cyanosis if prolonged downtime
  • Signs of trauma (bruises, lacerations, seatbelt marks, deformity)
  • Needle marks (IV drug use)
  • Recent surgical wounds or procedure sites
  • Distended neck veins (suggests tamponade, tension pneumothorax, PE)

Cardiac Arrest Monitoring

ParameterFindingSignificance
ECG rhythmAsystole (flat line) or PEA (organized electrical activity)Determines management (non-shockable)
Capnography (ETCO2)10-20 mmHg during good CPRbelow 10 suggests poor CPR quality or futility (no ROSC after 20 min)
greater than 35-40 mmHgSuggests ROSC (check pulse)
Arterial lineDiastolic pressure during compressionsDiastolic greater than 20 mmHg associated with ROSC
POCUS (cardiac)No cardiac motion (asystole)Confirms cardiac standstill
Cardiac motion without pulse (PEA)PEA confirmed
Effusion with RV/RA collapseCardiac tamponade
Enlarged RV, flattened septumMassive PE
Paradoxical septal motionTension pneumothorax
POCUS (lung)Absent lung slide, barcode signPneumothorax

Specific Findings by Reversible Cause

Reversible CauseClinical SignsECG FindingsPOCUS Findings
HypovolaemiaFlat neck veins, dry mucous membranes, cool peripheriesPEA (narrow complex), bradycardiaSmall, hyperdynamic IVC (collapses with respiration), empty heart chambers
HypoxiaCyanosis, signs of airway obstruction, respiratory arrestPEA progressing to asystoleNo specific findings
Tension pneumothoraxTracheal deviation, absent breath sounds on affected side, distended neck veinsPEA (narrow complex)Absent lung slide, barcode sign, lung point, mediastinal shift
Cardiac tamponadeDistended neck veins, muffled heart sounds, pulsus paradoxus greater than 10 mmHgPEA (narrow complex)Pericardial effusion, diastolic RV/RA collapse, swinging heart
Massive PEDistended neck veins, right-sided heart failure signsPEA (narrow complex), S1Q3T3 pattern, right axis deviationEnlarged RV, flattened interventricular septum (D-sign), McConnell's sign
HyperkalaemiaMuscle weakness, paralysis, respiratory failureWide-complex PEA, peaked T waves, sine wave progressionNo specific findings (ECG more diagnostic)
HypothermiaCold skin, core temperature below 30°CBradycardia progressing to asystole, Osborne waves (J waves)No specific findings
Toxins (Tricyclics, beta-blockers, calcium channel blockers, digoxin)Specific drug signs (anticholinergic, beta-blockade)Wide-complex PEA (tricyclics), bradycardia (beta-blockers/CCBs), arrhythmias (digoxin)No specific findings
AcidosisKussmaul breathing (if conscious), underlying cause signsWide-complex PEANo specific findings

Investigations

Immediate (Resus Bay - DO NOT DELAY CPR)

TestPurposeKey Finding
12-lead ECGConfirm rhythm, identify underlying causeAsystole, PEA, signs of MI (if ROSC), hyperkalaemia (peaked T waves), toxicology patterns
Capnography (ETCO2)Monitor CPR quality, detect ROSC10-20 mmHg during good CPR, greater than 35-40 mmHg suggests ROSC
Point-of-care glucoseExclude hypoglycaemia as causebelow 3.0 mmol/L → treat with 50 mL 50% dextrose IV
POCUS - CardiacConfirm cardiac standstill, identify tamponade, PENo motion (asystole), effusion/tamponade, RV enlargement (PE)
POCUS - LungIdentify pneumothoraxAbsent lung slide, barcode sign, lung point (pneumothorax)
Arterial blood gas (if available without interrupting CPR)Assess acid-base status, electrolytesSevere acidosis (pH below 7.0), hyperkalaemia (K+ greater than 7.0), hypoxia (PaO2 below 60 mmHg)

Standard ED Workup (After ROSC or During CPR if Available)

TestIndicationInterpretation
Bedside electrolytes (Na+, K+, Mg2+, Ca2+)Assess for electrolyte abnormalities as reversible causeHyperkalaemia (K+ greater than 6.5 mmol/L), hypomagnesaemia (Mg2+ below 0.7 mmol/L), hypocalcaemia (Ca2+ below 1.1 mmol/L)
Full blood countAssess for anaemia, infection, bleedingAnaemia (Hb below 80 g/L) contributing to hypovolaemia, leukocytosis (infection/sepsis)
Coagulation profile (INR, APTT)Assess for bleeding riskProlonged INR → reversal agents (PCC, vitamin K) if bleeding suspected
Cardiac troponinAssess for myocardial ischaemia/infarction as causeElevated troponin suggests ACS as underlying cause
Toxicology screenAssess for drug overdosePositive for opioids (naloxone), tricyclics, beta-blockers, calcium channel blockers, digoxin
Chest X-ray (portable if ROSC)Identify pneumothorax, pulmonary oedema, widened mediastinumTension pneumothorax, pulmonary oedema, aortic dissection (widened mediastinum)
CT pulmonary angiogram (if ROSC, PE suspected)Confirm pulmonary embolismFilling defects in pulmonary arteries
Echocardiogram (transthoracic)Assess cardiac function, tamponade, RV strainReduced LV function (cardiogenic), tamponade (effusion), RV strain (PE)

Advanced/Specialist (ICU/Tertiary)

TestIndicationAvailability
Coronary angiographySuspected acute coronary syndrome (after ROSC)Tertiary centres
CT brainAssess hypoxic-ischaemic brain injury (after ROSC)Tertiary centres
Therapeutic hypothermia equipmentTargeted temperature management (32-36°C) after ROSCICU
Extracorporeal life support (ECMO)Refractory cardiac arrest (ECPR) in select casesTertiary ECMO centres

Point-of-Care Ultrasound (POCUS)

POCUS is CRITICAL during cardiac arrest - use rhythm check pauses to perform rapid assessments (below 10 seconds each):

Cardiac POCUS:

  • Subxiphoid 4-chamber view: Assess for cardiac motion, tamponade, RV strain
  • Parasternal long axis: Assess LV/RV function, effusion
  • Parasternal short axis: Assess for wall motion abnormalities, tamponade
  • Apical 4-chamber: Assess all chambers, effusion, tamponade

Lung POCUS:

  • Anterior chest wall: Assess for pneumothorax (absent lung slide, barcode sign)
  • B-lines: Pulmonary oedema
  • Pleural effusion: Possible cause of respiratory compromise

Abdominal POCUS:

  • RUQ (Morison's pouch): Free fluid (bleeding)
  • Suprapubic: Bladder volume, free fluid

IVC Assessment:

  • Long axis subxiphoid: IVC diameter (below 2.1 cm) and collapsibility (greater than 50% collapse = hypovolaemia)

Important Note: POCUS during cardiac arrest:

  • ONLY during rhythm check pauses (below 10 seconds)
  • Do NOT interrupt compressions for POCUS
  • Use POCUS to confirm cardiac standstill (asystole) vs pseudo-asystole (fine VF)
  • Use POCUS to identify reversible causes (tamponade, pneumothorax, PE, hypovolaemia)
  • Use ETCO2 as primary CPR quality indicator - POCUS is supplementary

Management

Immediate Management (First 10 minutes)

DO NOT DELAY CPR:

1. RECOGNIZE ARREST (Unresponsive, no breathing, no pulse)
    ↓
2. CALL FOR HELP (Activate cardiac arrest team, call code blue, assign roles)
    ↓
3. START HIGH-QUALITY CPR IMMEDIATELY (Rate 100-120, depth 5-6 cm, allow full recoil, minimize interruptions)
    ↓
4. ATTACH DEFIBRILLATOR/MONITOR (Check rhythm: Asystole or PEA = NON-SHOCKABLE)
    ↓
5. CONTINUE CPR (DO NOT DEFIBRILLATE)
    ↓
6. OBTAIN IV/IO ACCESS (First adrenaline dose as soon as access obtained)
    ↓
7. ADRENALINE 1 mg IV/IO (Repeat every 3-5 minutes)
    ↓
8. IDENTIFY AND TREAT REVERSIBLE CAUSES (4H4T, BEAU-CHOPS)
    ↓
9. CONSIDER ADVANCED AIRWAY (After first CPR cycle if team experienced)
    ↓
10. RHYTHM CHECK EVERY 2 MINUTES (After each adrenaline dose, cycle CPR)

Resuscitation - ANZCOR Algorithm for Non-Shockable Rhythms

1. Immediate Recognition and Action

  • Unresponsive? No breathing? No pulse? → Cardiac arrest confirmed
  • Call for help → Activate cardiac arrest team, assign roles (compressor, airway, team leader, recorder, medication, defibrillator/monitor)
  • Start high-quality CPR immediately → DO NOT delay CPR to check rhythm, obtain access, or assess reversible causes

2. Attach Defibrillator/Monitor

  • Attach pads (Anterolateral or anteroposterior) → Allows rhythm monitoring
  • Check rhythm → Asystole (flat line) or PEA (organized electrical activity, no pulse)
  • If asystole or PEA → NON-SHOCKABLE rhythm → Continue CPR, DO NOT defibrillate
Red Flag

Confirm asystole is NOT artefact:

  • Check ECG lead connections
  • Increase ECG gain/amplitude
  • Consider alternative leads
  • Use POCUS to confirm cardiac standstill (no cardiac motion)
  • If in doubt, treat as asystole (continue CPR, give adrenaline)

3. High-Quality CPR (Continuous for Asystole/PEA)

CPR Parameters:

ParameterTargetWhy It Matters
Compression rate100-120/minOptimizes cardiac output without excessive fatigue
Compression depth5-6 cm (adults)Generates adequate stroke volume without excessive trauma
Chest recoilAllow full recoil (release pressure completely)Allows venous return and intrathoracic pressure normalization
Compression fractiongreater than 60%Maintains overall cardiac output and perfusion
Hand positionLower half of sternum, center of chestOptimizes cardiac compression between sternum and spine
Compressor switchingEvery 2 minutesPrevents fatigue and maintains CPR quality

CPR Technique:

  • Place heel of dominant hand on lower half of sternum, center of chest
  • Place other hand on top, interlock fingers
  • Keep elbows straight, shoulders directly over hands
  • Use body weight to compress (not just arm strength)
  • Push hard and fast
  • Allow chest to recoil completely (do not lean on chest)
  • Minimize interruptions (below 10 seconds for rhythm checks, airway, access)

4. IV/IO Access and Adrenaline

Obtain IV or IO access immediately:

  • IV: Peripheral IV (antecubital, forearm) preferred if obtainable within 1-2 minutes
  • IO: Intraosseous access if IV not obtainable within 2 minutes (proximal tibia, distal femur, humeral head)
  • Central line: Do NOT delay for central line access - only attempt if no IV/IO access possible

Adrenaline (Epinephrine):

DoseRouteTimingNotes
1 mgIV or IOAs soon as access obtained, then every 3-5 minutesEarly adrenaline for non-shockable rhythms (asystole/PEA)

Adrenaline Evidence (PARAMEDIC2 Trial):

  • ROSC: 36.3% with adrenaline vs 11.7% placebo (OR 4.25, 95% CI 3.77-4.79)
  • 30-day survival: 3.2% with adrenaline vs 2.4% placebo (OR 1.39, 95% CI 1.06-1.82)
  • Neurologically intact survival: 2.2% with adrenaline vs 1.9% placebo (OR 1.18, 95% CI 0.86-1.61) - NOT SIGNIFICANT
  • Severe neurological impairment: 31% of adrenaline survivors vs 18% of placebo survivors

ANZCOR Position: Adrenaline is recommended for non-shockable rhythms (asystole/PEA) because it improves ROSC and overall survival, despite lack of clear benefit for neurologically intact survival. Early administration (below 10 minutes from arrest) associated with better outcomes.

5. Identify and Treat Reversible Causes

4H4T (Classic ILCOR Mnemonic):

H (4)Reversible CauseDiagnosisTreatment
HypovolaemiaBlood loss, fluid lossFlat neck veins, dry mucous membranes, hypotension, PEA (narrow complex), POCUS (empty chambers, collapsible IVC)Aggressive fluid resuscitation (crystalloids, blood products), control bleeding
HypoxiaAirway obstruction, respiratory failure, drowning, COPD exacerbationCyanosis, low SpO2, respiratory arrest, PEA progressing to asystoleSecure airway, oxygen, ventilation, treat underlying cause (nebulizers, diuretics, antibiotics)
H+ (Acidosis)Metabolic acidosis (lactic acidosis, DKA, renal failure), respiratory acidosis (COPD, asthma)ABG: pH below 7.0, HCO3- low, lactate elevated, respiratory acidosisTreat underlying cause (sepsis, DKA, renal failure), sodium bicarbonate (only if pH below 7.0 or hyperkalaemia)
Hypokalaemia/HyperkalaemiaElectrolyte imbalance (renal failure, medications)ECG: Hyperkalaemia (peaked T waves, widened QRS, sine wave), Hypokalaemia (flattened T waves, U waves, arrhythmias)Hyperkalaemia: Calcium gluconate/chloride, insulin/dextrose, salbutamol, dialysis; Hypokalaemia: Potassium replacement
T (4)Reversible CauseDiagnosisTreatment
Tension pneumothoraxTrauma, barotrauma, central line insertionAbsent breath sounds, tracheal deviation, distended neck veins, PEA (narrow complex), POCUS (absent lung slide, barcode sign)Needle decompression (2nd intercostal space, midclavicular line, 14-16G cannula), chest tube
Tamponade (Cardiac)Trauma, aortic dissection, post-procedure, uremiaDistended neck veins, muffled heart sounds, pulsus paradoxus greater than 10 mmHg, PEA (narrow complex), POCUS (effusion, RV/RA collapse)Pericardiocentesis (ultrasound-guided subxiphoid or apical), fluid bolus temporization
Toxins (Poisoning/Overdose)Opioids, tricyclics, beta-blockers, calcium channel blockers, digoxin, local anaestheticsHistory of overdose/toxin exposure, specific signs (anticholinergic, beta-blockade), ECG patterns (tricyclic: wide QRS; beta-blocker/CCB: bradycardia; digoxin: arrhythmias)Opioids: Naloxone 0.4-2 mg IV (repeat PRN); Tricyclics: Sodium bicarbonate 1-2 mEq/kg IV; Beta-blockers: Glucagon 1-5 mg IV; CCBs: Calcium chloride 10% 10 mL IV; Digoxin: Digoxin-specific antibody fragments
Thrombosis (Pulmonary or Coronary)Massive PE, acute myocardial infarctionPE: Distended neck veins, pleuritic chest pain, right-sided heart failure, ECG (S1Q3T3, right axis deviation), POCUS (enlarged RV, flattened septum); ACS: Chest pain, ECG changes, elevated troponinPE: Thrombolysis (alteplase 10 mg IV bolus, then 90 mg over 2 hrs) or surgical embolectomy; ACS: Percutaneous coronary intervention (angioplasty/stent)

ANZCOR BEAU-CHOPS Mnemonic:

LetterReversible CauseTreatment
B - BeBoldBleeding (hypovolaemia)Control bleeding, fluid/blood resuscitation
E - ElectrolytesElectrolyte abnormalities (Na+, K+, Mg2+, Ca2+)Correct electrolyte abnormalities
A - AirwayAirway obstruction, AnaphylaxisSecure airway, anaphylaxis management (adrenaline IM)
U - UnderdosingUnderdosing (missed medications)Resume medications (e.g., insulin in DKA)
C - Cardiac causesCardiac tamponade, Cardiac ischemiaPericardiocentesis, coronary intervention
H - Hypo-/hyperthermiaHypothermia, Hyperthermia (malignant, heat stroke)Active rewarming (hypothermia), cooling (hyperthermia)
O - OxygenHypoxia, HyperoxiaCorrect hypoxia (airway, oxygen), avoid hyperoxia after ROSC
P - Poisoning/PEToxins/overdose, Pulmonary embolismSpecific antidotes, thrombolysis/embolectomy
S - ShockShock states (hypovolaemic, septic, cardiogenic, anaphylactic, obstructive)Treat underlying shock cause
T - TraumaTrauma (bleeding, pneumothorax, tamponade, spinal)Damage control resuscitation, specific interventions

6. Advanced Airway (Optional)

Consider advanced airway after first CPR cycle (2 minutes) if team experienced:

Options:

  • Endotracheal intubation (ETT): Gold standard airway control, requires skill, may interrupt CPR
  • Supraglottic airway (SGA) (e.g., LMA, i-gel): Faster insertion, less skill required, lower risk of aspiration
  • No advanced airway: Continue bag-valve-mask with 30:2 compression:ventilation ratio

Timing:

  • Insert advanced airway during rhythm check pause (below 10 seconds)
  • Do NOT interrupt CPR for greater than 10 seconds for airway placement
  • If unsuccessful within 10 seconds, continue CPR with bag-valve-mask and retry at next rhythm check

Capnography:

  • Use capnography if advanced airway placed
  • During CPR: ETCO2 10-20 mmHg indicates adequate CPR quality
  • ETCO2 below 10 mmHg: Suggests poor CPR quality or futility (no ROSC after 20 minutes)
  • ETCO2 greater than 35-40 mmHg: Suggests ROSC (check pulse, stop compressions if ROSC confirmed)

7. Rhythm Checks and Adrenaline Dosing

Every 2 minutes:

  1. Pause compressions briefly (below 10 seconds)
  2. Check rhythm (Asystole or PEA = continue CPR, DO NOT defibrillate)
  3. Give adrenaline 1 mg IV/IO (if 3-5 minutes elapsed since last dose)
  4. Assess for reversible causes (POCUS, physical exam, history, available investigations)
  5. Resume CPR immediately

Total adrenaline dose limit: ANZCOR does NOT specify maximum adrenaline dose. Continue 1 mg IV/IO every 3-5 minutes until ROSC or termination of resuscitation.

8. Consider Additional Medications (For Specific Causes)

MedicationIndicationDoseNotes
AtropineREMOVED from ANZCOR algorithm for asystole/PEANOT recommendedPrevious recommendations (3 mg IV) no longer supported by evidence
Sodium bicarbonate 8.4%Known hyperkalaemia, tricyclic overdose, severe metabolic acidosis (pH below 7.0)50-100 mL (50-100 mmol) IVCan be repeated, monitor pH and potassium
Calcium gluconate 10%Hyperkalaemia, calcium channel blocker overdose10 mL (10 mmol) IV over 2-5 minHyperkalaemia: Give immediately with insulin/dextrose
Insulin (Actrapid)Hyperkalaemia10 units IV with 25 g dextrose (50 mL 50%) IVRepeat if K+ remains greater than 6.5 mmol/L
Salbutamol (Ventolin)Hyperkalaemia5 mg nebulizedAdjunct to insulin/dextrose
Magnesium sulfate 50%Hypomagnesaemia, torsades de pointes, refractory VF/VT (not for asystole/PEA)2 g IV over 10-15 minNot for routine use in asystole/PEA
NaloxoneOpioid overdose0.4-2 mg IV/IM/IN, repeat PRNMay reverse respiratory arrest before cardiac arrest
GlucagonBeta-blocker overdose1-5 mg IV, repeat PRNUseful if beta-blocker toxicity suspected
Thrombolysis (alteplase)Massive pulmonary embolism (confirmed or highly suspected)10 mg IV bolus, then 90 mg over 2 hrsConsider if massive PE causing PEA arrest

Medications

DrugAdult DoseRouteTimingNotes
Adrenaline (Epinephrine)1 mgIV or IOImmediately after access, then every 3-5 minEarly adrenaline for non-shockable rhythms; PARAMEDIC2 shows ROSC benefit but no neurologically intact survival benefit
Sodium bicarbonate 8.4%50-100 mL (50-100 mmol)IVFor known hyperkalaemia, TCA overdose, severe acidosis (pH below 7.0)Monitor pH and potassium; can cause hypernatraemia and hyperosmolality
Calcium gluconate 10%10 mL (10 mmol)IVHyperkalaemia, calcium channel blocker overdoseGive over 2-5 min; watch for bradycardia if given too fast
Insulin (Actrapid)10 unitsIVHyperkalaemia (with 25 g dextrose 50%)Monitor blood glucose
Salbutamol (Ventolin)5 mgNebulizedHyperkalaemia (adjunct to insulin/dextrose)Can cause tachycardia
Naloxone0.4-2 mgIV/IM/INOpioid overdoseRepeat PRN up to 10 mg cumulative
Glucagon1-5 mgIVBeta-blocker overdoseRepeat PRN if no response
Alteplase10 mg bolus + 90 mg over 2 hrsIVMassive pulmonary embolismConsider only if PE confirmed or highly suspected as PEA cause

Paediatric Dosing

DrugPaediatric DoseMaxNotes
Adrenaline0.01 mg/kg (0.1 mL/kg of 1:10,000)1 mg max10 mcg/kg, IV/IO, every 3-5 min
Sodium bicarbonate 8.4%1 mEq/kg50 mEq maxFor hyperkalaemia, TCA overdose
Calcium gluconate 10%0.2 mL/kg (20 mg/kg)10 mL maxHyperkalaemia, CCB overdose
Insulin0.1 unit/kg5 units maxWith 0.5 g/kg dextrose (25% or 50%)
Naloxone0.1 mg/kg2 mg maxRepeat PRN
Glucagon0.03-0.05 mg/kg1 mg maxBeta-blocker overdose

Ongoing Management

If ROSC achieved:

  1. Check pulse and blood pressure
  2. Post-cardiac arrest care:
    • Airway: Continue mechanical ventilation, target SpO2 94-98%
    • Circulation: Maintain MAP greater than 65-80 mmHg (norepinephrine if needed), avoid hypotension
    • Temperature: Targeted temperature management 32-36°C for at least 24 hours
    • Glycaemia: Maintain blood glucose 8-10 mmol/L (avoid hypoglycaemia and hyperglycaemia)
    • Seizure prophylaxis: Consider levetiracetam if seizures suspected
    • Identify cause: ECG, troponin, echocardiogram, CT brain if indicated, toxicology screen
  3. ICU admission: All post-cardiac arrest patients require ICU admission for monitoring and supportive care

If NO ROSC:

  1. Continue high-quality CPR with adrenaline every 3-5 minutes
  2. Reassess reversible causes every 2 minutes (POCUS, physical exam, investigations)
  3. Consider termination of resuscitation after 20+ minutes if:
    • No ROSC achieved
    • Reversible causes addressed or excluded
    • No extenuating circumstances (e.g., hypothermia, toxic ingestion, reversible cause identified)
  4. Document decision and provide clear explanation to team

Definitive Care

ICU Care (Post-Cardiac Arrest Syndrome):

InterventionTargetRationale
Mechanical ventilationSpO2 94-98%, PaCO2 35-45 mmHgAvoid hypoxia and hyperoxia, normocapnia
Hemodynamic supportMAP greater than 65-80 mmHg, adequate urine outputMaintain cerebral and coronary perfusion
Targeted temperature management32-36°C for 24 hrsNeuroprotective, reduces hypoxic-ischaemic brain injury
Glycaemic control8-10 mmol/LAvoid hypoglycaemia (worsens brain injury) and hyperglycaemia (increases mortality)
Seizure prophylaxisLevetiracetam 500-1000 mg IV q12hPrevent post-anoxic seizures (worsen brain injury)
Coronary angiographyIf ACS suspectedEarly reperfusion improves outcomes
Neurological monitoringEEG, clinical exam, prognosticationAssess for hypoxic-ischaemic brain injury, guide prognostication
RehabilitationEarly mobilization, physiotherapy, occupational therapyImprove functional recovery

Disposition

Admission Criteria

All patients with ROSC require ICU admission for:

  • Post-cardiac arrest syndrome management
  • Hemodynamic monitoring
  • Neurological monitoring
  • Temperature management
  • Identification and treatment of underlying cause

ICU Admission Indications:

  • All post-cardiac arrest patients
  • Requiring mechanical ventilation
  • Requiring vasopressor support (norepinephrine)
  • Targeted temperature management
  • Need for continuous EEG monitoring
  • Need for coronary intervention

ICU/HDU Criteria

Level of care based on post-cardiac arrest syndrome severity:

CriteriaICU (Level 3)HDU (Level 2)
Mechanical ventilationRequiredNot required
VasopressorsNorepinephrine, epinephrineLow-dose vasopressin or single agent
MonitoringInvasive arterial line, CVP, advanced monitoringNon-invasive BP, SpO2, ECG
Organ supportMultiorgan support, CRRTSingle organ support
Staffing1:1 nurse-to-patient ratio1:2 nurse-to-patient ratio

Discharge Criteria

NO direct discharge from ED after ROSC - all patients require ICU admission.

Safe discharge planning (after ICU recovery):

  • Neurologically intact or with acceptable functional outcome
  • Cardiac cause identified and treated (e.g., PCI for ACS)
  • No life-threatening arrhythmias
  • Able to mobilize with assistance
  • Family/social supports in place
  • Follow-up arranged with cardiology, neurology, rehabilitation

Red flags to return to ED:

  • Chest pain, dyspnea, palpitations
  • Syncope or presyncope
  • New neurological symptoms
  • Fever, signs of infection
  • Medication side effects

Follow-up

  • Cardiology: Outpatient review 1-2 weeks post-discharge, Holter monitor if arrhythmia suspected, echocardiogram
  • Neurology: If cognitive impairment, seizures, or focal neurological deficits
  • Rehabilitation: Physical therapy, occupational therapy, speech therapy as needed
  • Psychology: Screen for PTSD, anxiety, depression post-arrest (patient and family)
  • General practice: Shared care plan, medication management, cardiovascular risk factor optimization

Special Populations

Paediatric Considerations

Key Differences in Paediatric Cardiac Arrest:

ParameterPaediatricAdult
Common causesRespiratory failure, SIDS, trauma, congenital heart diseaseCardiac (ACS, arrhythmia)
Compression:Ventilation ratio15:2 (single rescuer), 15:2 or 30:2 (2 rescuers)30:2
Compression depth1/3 AP diameter (approx. 4 cm for infant, 5 cm for child)5-6 cm
Compression technique2 thumbs (infant), 1 hand (child), 2 hands (adolescent)2 hands
Adrenaline dose0.01 mg/kg (0.1 mL/kg of 1:10,000), max 1 mg1 mg
Defibrillation dose4 J/kg (initial), subsequent 4-10 J/kg120-200 J biphasic

Paediatric reversible causes:

  • Hypoxia (most common cause): Respiratory failure, airway obstruction, bronchiolitis, pneumonia, asthma
  • Hypovolaemia: Dehydration, bleeding, sepsis (distributive shock)
  • Sepsis: Bacterial/viral infection, meningococcemia
  • Toxins: Accidental ingestion, medication overdose
  • Trauma: Abusive head trauma, motor vehicle collision
  • Cardiac causes: Congenital heart disease, arrhythmias (prolonged QT, WPW), myocarditis

Pregnancy

Maternal Cardiac Arrest:

Key modifications:

  • Uterine displacement: Left lateral tilt or manual uterine displacement to relieve aortocaval compression (reduces venous return by 30-40% in supine position)
  • Airway: Intubation earlier (more difficult due to airway edema, reduced functional residual capacity)
  • CPR technique: Standard adult CPR with uterine displacement
  • Defibrillation: Standard adult energy doses (safe for fetus)
  • Adrenaline: 1 mg IV every 3-5 minutes (crosses placenta but benefits outweigh risks)
  • Perimortem cesarean: Consider at 4-5 minutes of arrest if gestation greater than 20-24 weeks (relieves aortocaval compression, allows neonatal resuscitation, improves maternal resuscitation efforts)

Pregnancy-specific reversible causes:

  • Aortocaval compression: Supine hypotension, impaired venous return → hypotension → arrest
  • Pulmonary embolism: Hypercoagulable state (4-5× increased risk of VTE)
  • Amniotic fluid embolism: Sudden collapse, hypotension, coagulopathy
  • Pre-eclampsia/eclampsia: Hypertensive crisis, cerebral hemorrhage, pulmonary edema
  • Postpartum hemorrhage: Hypovolaemic shock → arrest
  • Cardiomyopathy (peripartum): Heart failure, arrhythmias

Elderly

Geriatric Considerations:

  • Comorbidities: Multiple comorbidities (hypertension, diabetes, cardiovascular disease, renal failure) → more complex reversible causes
  • Fragility: Higher risk of rib fractures and other CPR-related injuries
  • Medications: Polypharmacy (beta-blockers, calcium channel blockers, digoxin, antiarrhythmics) → possible drug-induced arrest
  • Baseline function: Assess baseline functional status to guide prognostication and post-resuscitation goals of care
  • Advance care planning: Consider advance directives, resuscitation status (NFR orders), goals of care discussions with family

Indigenous Health

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

Health Disparities in Cardiac Arrest:

  • Aboriginal and Torres Strait Islander peoples: 2-3× higher incidence of cardiac arrest compared to non-Indigenous Australians, 1.5-2× lower survival to discharge due to comorbidities (diabetes, cardiovascular disease, renal failure), delayed presentation, and limited access to emergency care
  • Māori population (NZ): 2-2.5× higher cardiac arrest incidence compared to non-Māori, worse outcomes, higher burden of cardiovascular risk factors (obesity, diabetes, smoking)

Cultural Safety Considerations:

  • Aboriginal and Torres Strait Islander: Involve Aboriginal Health Workers (AHWs) or Aboriginal Liaison Officers (ALOs) in communication and decision-making, respect family and community decision-making processes, consider cultural protocols around death and dying, acknowledge intergenerational trauma and mistrust of healthcare systems
  • Māori: Involve whānau (family) in discussions and decision-making, use Māori Health Workers or cultural liaisons, respect tikanga (customs) and manaakitanga (hospitality), acknowledge tapu (sacred) nature of body and death, consider cultural practices around death and mourning

Communication Barriers:

  • Language barriers (Indigenous languages, different communication styles), health literacy gaps, distrust of healthcare systems, historical trauma affecting engagement
  • Use plain language, visual aids, interpreters, cultural mediators, allow adequate time for family discussions

Geographic Isolation:

  • Remote Indigenous communities often have prolonged ambulance response times (greater than 60-90 minutes), limited local resources (no defibrillator, no advanced life support), need for RFDS retrieval, early activation of retrieval services is critical
  • Consider telemedicine consultation with tertiary centers for advice during resuscitation

Family and Community Decision-Making:

  • Indigenous families and communities may have collective decision-making processes involving elders, extended family, and community leaders
  • Allow adequate time for family discussions, include family in decision-making (especially regarding termination of resuscitation), respect cultural protocols around death and dying

Specific Considerations for Cardiac Arrest:

  • Bystander CPR rates: Lower in Indigenous communities due to cultural factors, lack of CPR training, geographic isolation → promote CPR training in communities
  • Comorbidity burden: Higher rates of diabetes, cardiovascular disease, renal failure → more complex reversible causes, may impact prognostication
  • Medication adherence: Potential barriers (cost, access, health literacy) → medication overdose or underdosing as reversible causes
  • Traditional medicine use: Potential interactions with prescribed medications or toxic ingestions

Pitfalls & Pearls

Clinical Pearl

Clinical Pearls:

  1. CPR quality is more important than adrenaline - High-quality CPR (rate 100-120/min, depth 5-6 cm, full recoil, minimal interruptions) generates adequate CPP/CePP. Adrenaline cannot compensate for poor CPR quality. Focus on compressor rotation, feedback devices, and real-time coaching.
  2. PEA with narrow QRS is more likely to have a specific reversible cause - Hypovolaemia, tension pneumothorax, tamponade, or massive PE. Aggressively investigate and treat these causes using POCUS. Wide-complex PEA (QRS greater than 0.12s) is more likely due to metabolic causes (hyperkalaemia, acidosis, hypoxia) or severe ischaemia.
  3. Confirm asystole is NOT artefact - Check ECG lead connections, increase gain, consider alternative leads, use POCUS. Fine VF can masquerade as asystole and is shockable. If in doubt, continue CPR and consider defibrillation (no harm from defibrillating asystole).
  4. ETCO2 is the best real-time indicator of CPR quality - Target 10-20 mmHg during CPR. below 10 mmHg suggests poor CPR quality or futility (consider termination if no ROSC after 20 min). greater than 35-40 mmHg suggests ROSC (check pulse).
  5. Use rhythm check pauses effectively - Every 2 minutes, pause below 10 seconds to check rhythm, give adrenaline, and perform targeted POCUS. Do NOT waste time on unnecessary assessments during these pauses.
  6. Adrenaline improves ROSC but not neurologically intact survival - PARAMEDIC2 trial shows adrenaline doubles ROSC rates (36.3% vs 11.7%) but does NOT improve neurologically intact survival (2.2% vs 1.9%). Early administration (below 10 min) is associated with better outcomes.
  7. Termination of resuscitation is a clinical decision - After 20+ minutes without ROSC, reversible causes addressed, and no extenuating circumstances (hypothermia, toxic ingestion, witnessed arrest with immediate CPR), consider termination. Document decision clearly and provide explanation to team.
  8. Team leadership and closed-loop communication save lives - Assign clear roles (compressor, airway, team leader, recorder, medication, defibrillator/monitor), use closed-loop communication (direct instruction → read-back → confirmation), rotate roles every 2 minutes, maintain situational awareness.
  9. POCUS is a powerful tool during cardiac arrest - Use rhythm check pauses to perform targeted POCUS (below 10 seconds each). Cardiac POCUS can confirm standstill, identify tamponade, RV strain. Lung POCUS can identify pneumothorax. Do NOT interrupt compressions for POCUS.
  10. Post-cardiac arrest care is critical - Targeted temperature management (32-36°C), MAP greater than 65-80 mmHg, avoid hypoxia and hypotension, early coronary intervention if ACS suspected. All post-ROSC patients require ICU admission.
Red Flag

Pitfalls to Avoid:

  1. Delaying CPR to check pulse or rhythm - Start CPR immediately on recognition of cardiac arrest. Do NOT delay CPR to check pulse, obtain access, or assess reversible causes. CPR is the priority.
  2. Defibrillating asystole - Asystole and PEA are NON-SHOCKABLE rhythms. Defibrillating asystole wastes valuable time and can cause myocardial injury. Confirm rhythm and only defibrillate VF/VT.
  3. Failing to recognize fine VF as asystole - Fine VF can masquerade as asystole, especially on low-amplitude ECG leads. Check lead connections, increase gain, consider alternative leads, use POCUS. If uncertain, consider defibrillation.
  4. Poor CPR quality - Common errors: rate too slow (below 100/min) or too fast (greater than 120/min), depth too shallow (below 5 cm), leaning on chest (no recoil), excessive interruptions (greater than 10 seconds). Use feedback devices and real-time coaching.
  5. Not identifying and treating reversible causes - Use 4H4T or BEAU-CHOPS mnemonic every rhythm check. Perform targeted POCUS. Consider history, medications, scene findings. PEA often has a specific reversible cause.
  6. Withholding adrenaline for non-shockable rhythms - Early adrenaline (below 10 min) for asystole/PEA improves ROSC. PARAMEDIC2 supports continued adrenaline use despite lack of neurologically intact survival benefit.
  7. Prolonged rhythm checks - Keep rhythm checks below 10 seconds. Do not waste time on unnecessary assessments. Use pauses efficiently: check rhythm, give adrenaline, targeted POCUS, then resume CPR.
  8. Delaying advanced airway excessively - Consider advanced airway after first CPR cycle if team experienced. Insert during rhythm check pause (below 10 seconds). If unsuccessful, continue with bag-valve-mask and retry at next rhythm check.
  9. Failing to use capnography - If advanced airway placed, use capnography. ETCO2 10-20 mmHg indicates adequate CPR. below 10 mmHg suggests poor quality or futility. greater than 35-40 mmHg suggests ROSC.
  10. Not considering termination of resuscitation appropriately - Futility after 20+ minutes without ROSC, reversible causes addressed, no extenuating circumstances. Prolonging futile resuscitation deprives other patients of resources. Document decision clearly.
  11. Ignoring cultural considerations for Indigenous patients - Involve Aboriginal Health Workers/ALOs or Māori Health Workers, respect family/community decision-making, allow adequate time for discussions, acknowledge cultural protocols around death and dying.
  12. Not preparing for post-cardiac arrest care - Have post-ROSC plan ready: targeted temperature management, vasopressor support, early coronary intervention, ICU admission. All post-ROSC patients require ICU.

Viva Practice

Viva Scenario

Stem: A 68-year-old male collapses in the ED waiting area. He is unresponsive, not breathing, and has no palpable pulse. The cardiac monitor shows asystole. You are the team leader.

Opening Question: What are your immediate priorities?

Model Answer: My immediate priorities are:

  1. Confirm cardiac arrest: Unresponsive, no breathing, no pulse - cardiac arrest confirmed
  2. Call for help: Activate cardiac arrest team, assign roles (compressor, airway, team leader, recorder, medication, defibrillator/monitor)
  3. Start high-quality CPR immediately: Rate 100-120/min, depth 5-6 cm, allow full recoil, minimize interruptions
  4. Attach defibrillator/monitor: Confirm asystole is NOT artefact (check lead connections, increase gain)
  5. Obtain IV or IO access: First adrenaline dose as soon as access obtained
  6. Give adrenaline 1 mg IV/IO: Repeat every 3-5 minutes
  7. Identify and treat reversible causes: Use 4H4T or BEAU-CHOPS mnemonic, perform targeted POCUS
  8. Rhythm check every 2 minutes: Continue CPR, give adrenaline, reassess reversible causes

Follow-up Questions:

  1. Examiner: How do you confirm asystole is not artefact?

    • Model answer: Check ECG lead connections and placement, increase ECG gain/amplitude, consider alternative ECG leads, use POCUS to confirm cardiac standstill (no cardiac motion, no Doppler flow). Fine VF can masquerade as asystole. If uncertain, continue CPR and consider defibrillation.
  2. Examiner: What are the 4H4T reversible causes?

    • Model answer: H - Hypovolaemia, Hypoxia, H+ (acidosis), Hypo-/hyperkalaemia; T - Tension pneumothorax, Tamponade, Toxins, Thrombosis (pulmonary or coronary). ANZCOR also uses BEAU-CHOPS: BeBold (Bleeding), Electrolytes, Airway/Anaphylaxis, Underdosing, Cardiac causes, Hypo-/hyperthermia, Oxygen, Poisoning/PE, Shock (hypovolaemic, septic), Trauma.
  3. Examiner: What is the evidence for adrenaline in cardiac arrest?

    • Model answer: PARAMEDIC2 trial (PMID 30860369) randomized 8,014 OHCA patients to adrenaline 1 mg vs placebo. Adrenaline improved ROSC (36.3% vs 11.7%, OR 4.25) and 30-day survival (3.2% vs 2.4%, OR 1.39) but did NOT improve neurologically intact survival (2.2% vs 1.9%, NS). Survivors receiving adrenaline were more likely to have severe neurological impairment (31% vs 18%). Current ANZCOR guidelines continue to recommend adrenaline for non-shockable rhythms.
  4. Examiner: When would you consider termination of resuscitation?

    • Model answer: After 20+ minutes without ROSC, reversible causes addressed or excluded, no extenuating circumstances. Extenuating circumstances include hypothermia (below 30°C), toxic ingestion (e.g., tricyclics, local anaesthetics), witnessed arrest with immediate bystander CPR, or identified reversible cause requiring specific intervention (e.g., massive PE requiring thrombolysis). Document decision clearly and provide explanation to team.

Discussion Points:

  • High-quality CPR parameters and importance of compressor rotation
  • Team leadership and closed-loop communication
  • Use of capnography to guide CPR quality
  • POCUS during cardiac arrest (targeted assessments during rhythm checks)
  • Post-cardiac arrest care (targeted temperature management, MAP targets, ICU admission)
Viva Scenario

Stem: A 45-year-old female presents to ED with acute dyspnea and hypotension. While being assessed, she becomes unresponsive, has no palpable pulse, and the ECG shows sinus bradycardia at 40 bpm without palpable pulses (PEA).

Opening Question: What are your priorities and what specific reversible causes should you consider?

Model Answer: My immediate priorities are:

  1. Start high-quality CPR immediately (rate 100-120/min, depth 5-6 cm, allow full recoil)
  2. Call for help and assign roles (compressor, airway, team leader, recorder, medication, defibrillator/monitor)
  3. Obtain IV/IO access and give adrenaline 1 mg immediately
  4. Target specific reversible causes for PEA:
    • Narrow-complex PEA (QRS below 0.12s): Hypovolaemia, tension pneumothorax, cardiac tamponade, massive pulmonary embolism
    • Wide-complex PEA (QRS greater than 0.12s): Hyperkalaemia, severe acidosis, hypoxia, ischaemia, toxins
    • Pseudo-PEA: Severe hypotension without pulse (shock states, severe hypovolaemia)

For this patient with acute dyspnea and hypotension before arrest, specific considerations:

  • Massive pulmonary embolism: Dyspnea, hypotension, tachycardia, distended neck veins, ECG (S1Q3T3, right axis deviation), POCUS (enlarged RV, flattened septum, McConnell's sign)
  • Tension pneumothorax: Absent breath sounds, tracheal deviation, absent lung slide on POCUS
  • Cardiac tamponade: Distended neck veins, muffled heart sounds, pulsus paradoxus, POCUS (effusion, RV/RA collapse)
  • Hypovolaemia: History of bleeding, dehydration, sepsis

Follow-up Questions:

  1. Examiner: How do you differentiate between PEA causes using clinical exam and POCUS?

    • Model answer:
      • Massive PE: Distended neck veins, hypotension, right-sided heart failure, POCUS (enlarged RV, flattened interventricular septum - D-sign, McConnell's sign, reduced RV contractility)
      • Tension pneumothorax: Tracheal deviation to opposite side, absent breath sounds, distended neck veins, POCUS (absent lung slide, barcode sign, lung point)
      • Cardiac tamponade: Distended neck veins, muffled heart sounds, pulsus paradoxus greater than 10 mmHg, POCUS (pericardial effusion, diastolic RV/RA collapse, swinging heart, IVC plethora)
      • Hypovolaemia: Flat neck veins, dry mucous membranes, hypotension, POCUS (small hyperdynamic IVC that collapses greater than 50% with respiration, empty heart chambers)
      • Hyperkalaemia: Muscle weakness, ECG (peaked T waves, widened QRS progressing to sine wave), wide-complex PEA
  2. Examiner: How do you manage massive PE causing PEA arrest?

    • Model answer: Continue high-quality CPR, give adrenaline 1 mg IV every 3-5 minutes, consider thrombolysis (alteplase 10 mg IV bolus, then 90 mg over 2 hours) if PE is highly suspected or confirmed. Thrombolysis during CPR has low success rate (below 10% ROSC) but may be considered if no contraindications and PE is the likely cause. Surgical embolectomy is an option in tertiary centres with cardiac surgery capability. If ROSC achieved, start therapeutic anticoagulation (heparin infusion).
  3. Examiner: What is the prognostic difference between narrow-complex and wide-complex PEA?

    • Model answer: Narrow-complex PEA (QRS below 0.12s) has a slightly better prognosis (5-10% survival) because it often has a specific reversible mechanical cause (hypovolaemia, tension pneumothorax, tamponade, PE) that can be identified and treated. Wide-complex PEA (QRS greater than 0.12s) has a worse prognosis (2-5% survival) because it usually reflects severe metabolic derangement (hyperkalaemia, acidosis), profound hypoxia, or ischaemia, which are more difficult to reverse.
  4. Examiner: How do you use capnography to guide resuscitation in PEA?

    • Model answer: If advanced airway placed, use capnography. ETCO2 10-20 mmHg during CPR indicates adequate CPR quality. ETCO2 below 10 mmHg suggests poor CPR quality (improve chest compressions) or futility (consider termination if no ROSC after 20 minutes). ETCO2 greater than 35-40 mmHg suggests ROSC (check pulse, stop compressions if ROSC confirmed). Rising ETCO2 trend during CPR is a positive prognostic sign. Sudden rise in ETCO2 without palpable pulse may indicate ROSC with pulseless electrical activity (pseudo-PEA) - check pulse immediately.

Discussion Points:

  • PEA vs asystole prognostic differences
  • Targeted POCUS during rhythm checks
  • Evidence for thrombolysis in PE-related arrest
  • Importance of early identification of reversible causes in PEA
Viva Scenario

Stem: A 55-year-old male with end-stage renal failure on dialysis presents to ED with muscle weakness and confusion. He collapses in the triage area. The cardiac monitor shows wide-complex PEA with peaked T waves progressing to sine wave.

Opening Question: What is your immediate management?

Model Answer: My immediate management is:

  1. Start high-quality CPR immediately
  2. Call for help and assign roles
  3. Obtain IV/IO access and give adrenaline 1 mg immediately
  4. Treat hyperkalaemia as the reversible cause:
    • Calcium gluconate 10% 10 mL IV (stabilizes cardiac membrane, repeat after 5 min if no improvement)
    • Insulin (Actrapid) 10 units IV with 25 g dextrose (50 mL 50%) IV
    • Salbutamol 5 mg nebulized (adjunct to shift potassium intracellularly)
    • Consider sodium bicarbonate 50-100 mL IV if severe acidosis (pH below 7.0)
  5. Arrange urgent dialysis if ROSC achieved (definitive management of hyperkalaemia in ESRF)
  6. Continue adrenaline 1 mg IV every 3-5 minutes until ROSC or termination

Follow-up Questions:

  1. Examiner: What are the ECG changes of hyperkalaemia?

    • Model answer: Progressive ECG changes as potassium rises:
      • Mild hyperkalaemia (K+ 5.5-6.5 mmol/L): Peaked, symmetric, narrow T waves
      • Moderate hyperkalaemia (K+ 6.5-7.5 mmol/L): Widened QRS, shortened PR interval, flattened P waves
      • Severe hyperkalaemia (K+ 7.5-8.5 mmol/L): Disappearance of P waves, QRS-T fusion, sine wave pattern
      • Very severe hyperkalaemia (K+ greater than 8.5 mmol/L): Asystole or ventricular fibrillation
  2. Examiner: Why does calcium stabilize the cardiac membrane in hyperkalaemia?

    • Model answer: Hyperkalaemia increases extracellular potassium concentration, reducing the resting membrane potential (depolarization). This inactivates sodium channels, slowing conduction and widening the QRS complex. Calcium increases the threshold potential (makes the cell less excitable), restoring the difference between resting and threshold potential, thereby stabilizing the cardiac membrane and preventing arrhythmias. Calcium does NOT lower serum potassium levels - it only protects the heart.
  3. Examiner: What are the contraindications to calcium in hyperkalaemia?

    • Model answer: Calcium is generally safe in hyperkalaemia. Historical concerns about "stone heart" (calcium precipitating with digoxin to cause arrhythmias) in digoxin toxicity are largely unfounded. If patient is on digoxin, give calcium more slowly (over 5-10 minutes) and monitor for arrhythmias, but do NOT withhold calcium in life-threatening hyperkalaemia. Calcium gluconate is preferred over calcium chloride for peripheral administration (less tissue necrosis if extravasation), but calcium chloride has more elemental calcium per mL (preferred in cardiac arrest).
  4. Examiner: How do insulin and salbutamol lower potassium?

    • Model answer: Both shift potassium intracellularly:
      • Insulin: Activates Na+/K+-ATPase pumps, moving potassium into cells. Onset 15-30 minutes, duration 4-6 hours. Always give with dextrose to prevent hypoglycaemia. Monitor blood glucose.
      • Salbutamol: Beta-2 agonist activates Na+/K+-ATPase pumps, shifting potassium into cells. Onset 30-60 minutes, duration 2-4 hours. Can cause tachycardia. Adjunct to insulin, not replacement.

Discussion Points:

  • Hyperkalaemia as a reversible cause of cardiac arrest
  • ECG progression of hyperkalaemia
  • Calcium mechanism and safety in digoxin toxicity
  • Dialysis as definitive treatment in ESRF
Viva Scenario

Stem: A 62-year-old Aboriginal man from a remote community presents to the local health clinic with chest pain and shortness of breath. He has diabetes, hypertension, and ischaemic heart disease. He collapses in the clinic. The clinic nurse starts CPR and calls the RFDS. You are providing telemedicine support.

Opening Question: What are your priorities and what specific considerations apply to this scenario?

Model Answer: My immediate priorities are:

  1. Guide clinic team to start high-quality CPR immediately (rate 100-120/min, depth 5-6 cm)
  2. Check rhythm (asystole or PEA likely given cardiac history)
  3. Obtain IV/IO access and give adrenaline 1 mg
  4. Identify and treat reversible causes:
    • ACS (most likely given cardiac history): Consider early thrombolysis if STEMI and no contraindications (if ROSC achieved)
    • Hypoxia: Ensure adequate oxygenation and ventilation
    • Hypovolaemia: Assess for dehydration or bleeding
  5. Activate RFDS retrieval early for transfer to tertiary center
  6. Specific Indigenous health considerations:
    • Involve Aboriginal Health Worker (AHW) if available for communication and cultural support
    • Respect family and community decision-making: Allow family to be present if they wish, involve elders in decisions
    • Cultural safety: Use plain language, visual aids, allow adequate time for discussions, acknowledge mistrust of healthcare systems
    • Geographic isolation: Prolonged retrieval time (greater than 2-3 hours), consider futility discussions with family if no ROSC and prolonged arrest

Follow-up Questions:

  1. Examiner: What are the specific barriers for Indigenous patients in remote communities experiencing cardiac arrest?

    • Model answer: Multiple barriers:
      • Geographic isolation: Prolonged ambulance/RFDS response times (greater than 60-90 minutes), limited local resources (often no defibrillator or advanced life support equipment)
      • Healthcare access: Limited access to primary care, delayed presentation, poor medication adherence
      • Comorbidity burden: Higher rates of diabetes, cardiovascular disease, renal failure → more complex reversible causes
      • Health literacy: Gaps in understanding cardiovascular risk factors and warning signs
      • Cultural factors: Distrust of healthcare systems, communication barriers, different conceptualizations of health and death
      • Bystander CPR rates: Lower due to lack of CPR training in communities, cultural factors around touching the body
  2. Examiner: How do you support the clinic team remotely in managing this cardiac arrest?

    • Model answer: Telemedicine support strategies:
      • Provide clear, direct instructions for CPR technique and adrenaline dosing
      • Guide reversible cause identification (ask about chest pain, breathing, medications, recent illnesses)
      • Help troubleshoot equipment (defibrillator, airway equipment, IV access)
      • Guide decision-making (thrombolysis if STEMI, termination of resuscitation if no ROSC after 20+ min)
      • Support cultural communication (guide clinic nurse on involving family, AHW, community members)
      • Coordinate RFDS retrieval (provide details for handover, request appropriate equipment)
  3. Examiner: How do you discuss termination of resuscitation with the family in this context?

    • Model answer: Sensitive discussion approach:
      • Involve AHW or cultural liaison to facilitate communication and provide cultural support
      • Use plain language and avoid medical jargon
      • Allow family adequate time for discussions, involve elders if appropriate
      • Explain clearly what has been done (CPR duration, medications given, reversible causes considered)
      • Explain prognosis honestly (asystole has below 2% survival, prolonged downtime worsens outcome)
      • Respect cultural protocols around death and dying (may include specific rituals, ceremonies)
      • Support family's decision whether to continue or stop resuscitation efforts
  4. Examiner: What post-cardiac arrest care considerations apply if ROSC is achieved?

    • Model answer: Post-ROSC priorities:
      • Arrange urgent RFDS retrieval to tertiary center with ICU and cardiac intervention capability
      • Targeted temperature management (32-36°C) - may be challenging in remote clinic, maintain normothermia and initiate during transport
      • Hemodynamic support - maintain MAP greater than 65-80 mmHg (vasopressors if available)
      • Identify cause - ECG for ACS, troponin (if available), glucose, electrolytes
      • Consider thrombolysis if STEMI and no contraindications (transfer to PCI center may be prolonged)
      • Cultural care - involve AHW, allow family to accompany patient during transport, respect cultural protocols

Discussion Points:

  • Indigenous health disparities in cardiac arrest outcomes
  • Cultural safety in end-of-life communication
  • Remote/rural challenges in cardiac arrest management
  • Role of RFDS in retrieval of post-cardiac arrest patients

OSCE Scenarios

Station 1: Cardiac Arrest Team Leadership

Format: Resuscitation Time: 11 minutes Setting: ED Resuscitation Bay

Candidate Instructions:

You are the team leader for a cardiac arrest. A 70-year-old male has collapsed in the waiting area and is now in the resuscitation bay. The team consists of a senior doctor (airway), a registrar (medication), two nurses (compressor, recorder), and a junior doctor (defibrillator/monitor). The mannequin shows asystole on the monitor. Demonstrate effective team leadership and management of this cardiac arrest.

Examiner Instructions: The patient is a 70-year-old male with unwitnessed cardiac arrest in the ED waiting area. No bystander CPR was performed prior to ED staff initiating CPR. The initial rhythm is asystole.

Timeline:

  • 0-2 min: Candidate should recognize arrest, call for help, start CPR, attach monitor, confirm asystole, obtain access, give first adrenaline
  • 2-4 min: First rhythm check (asystole), repeat adrenaline, discuss reversible causes, consider POCUS
  • 4-6 min: Second rhythm check (asystole), repeat adrenaline, consider advanced airway
  • 6-8 min: Third rhythm check (asystole), continue adrenaline, discuss termination considerations
  • 8-11 min: Either continue resuscitation or terminate (candidate to decide based on clinical judgment)

Expected Progression:

  • Asystole throughout (no rhythm change)
  • No ROSC achieved despite prolonged resuscitation
  • Consider termination after 20 minutes (simulated time)
  • Discuss with team and document decision

Actor/Patient Brief: Not applicable (mannequin).

Marking Criteria:

DomainCriterionMarks
RecognitionImmediately recognizes cardiac arrest, calls for help/2
Team LeadershipAssigns clear roles, uses closed-loop communication, maintains situational awareness/3
CPR ManagementEnsures high-quality CPR (rate, depth, recoil, compressor rotation)/2
Algorithm AdherenceFollows ANZCOR non-shockable rhythm algorithm (CPR, adrenaline, identify reversible causes)/2
Reversible CausesIdentifies and treats 4H4T or BEAU-CHOPS, uses POCUS appropriately/1
Decision-makingMakes appropriate decision regarding termination of resuscitation after 20 minutes/1
Total/11

Expected Standard:

  • Pass: ≥7/11
  • Key discriminators:
    • Must assign roles and use closed-loop communication
    • Must ensure high-quality CPR (mention compressor rotation every 2 minutes)
    • Must give adrenaline 1 mg IV/IO every 3-5 minutes
    • Must discuss reversible causes at each rhythm check
    • Must consider termination of resusculation after 20 minutes without ROSC

Common Mistakes:

  • Delaying CPR to check pulse or rhythm
  • Defibrillating asystole
  • Poor team leadership (no role assignment, no closed-loop communication)
  • Not rotating compressors (leads to poor CPR quality)
  • Forgetting adrenaline or incorrect dosing
  • Not discussing reversible causes
  • Failing to consider termination appropriately
  • Inadequate documentation

Station 2: PEA - Identifying Reversible Causes with POCUS

Format: Resuscitation/Clinical Reasoning Time: 11 minutes Setting: ED Resuscitation Bay

Candidate Instructions:

You are the team leader for a cardiac arrest. A 45-year-old female with known pulmonary embolism has collapsed. She is receiving CPR and the monitor shows PEA with heart rate 50 bpm and narrow QRS. You have access to POCUS. Identify and manage the likely reversible cause.

Examiner Instructions: The patient is a 45-year-old female with known pulmonary embolism (diagnosed 3 days ago, on therapeutic enoxaparin). She collapsed suddenly at home with acute dyspnea. Bystander CPR was performed for 5 minutes before ambulance arrival. The rhythm is PEA (narrow complex, HR 50 bpm).

POCUS Findings (to be provided if candidate asks):

  • Cardiac (subxiphoid): Enlarged right ventricle, flattened interventricular septum (D-sign), McConnell's sign (akinesia of RV free wall with normal apical contractility), no pericardial effusion
  • Lung (bilateral): Normal lung slide present (no pneumothorax)
  • IVC: Dilated (greater than 2.1 cm), below 50% collapse with respiration (suggests elevated right-sided pressures)

Expected Progression:

  • Candidate should suspect massive pulmonary embolism as reversible cause
  • Candidate should consider thrombolysis (alteplase)
  • ROSC may occur after thrombolysis (examiner may indicate this)
  • If ROSC, discuss post-cardiac arrest management

Actor/Patient Brief: Not applicable (mannequin).

Marking Criteria:

DomainCriterionMarks
RecognitionRecognizes PEA (non-shockable rhythm)/1
Differential DiagnosisIdentifies massive PE as likely cause given history/2
POCUS UsePerforms targeted POCUS during rhythm checks (cardiac, lung, IVC)/2
InterpretationCorrectly interprets POCUS findings (enlarged RV, flattened septum, McConnell's sign)/2
ManagementGives adrenaline, considers thrombolysis (alteplase) for massive PE/2
Post-ROSC CareDiscusses post-cardiac arrest management if ROSC achieved/1
CommunicationCommunicates clearly with team, explains reasoning/1
Total/11

Expected Standard:

  • Pass: ≥7/11
  • Key discriminators:
    • Must suspect massive PE based on history (known PE, acute dyspnea, sudden collapse)
    • Must use POCUS to confirm (enlarged RV, flattened septum, McConnell's sign)
    • Must consider thrombolysis as intervention for massive PE-related arrest
    • Must discuss post-cardiac arrest care if ROSC achieved

Common Mistakes:

  • Not considering PE despite history
  • Not using POCUS appropriately
  • Misinterpreting POCUS findings
  • Not considering thrombolysis
  • Defibrillating PEA
  • Poor CPR quality
  • Not giving adrenaline
  • Forgetting post-cardiac arrest care

Station 3: Hyperkalaemia-Induced Cardiac Arrest

Format: Resuscitation/Clinical Reasoning Time: 11 minutes Setting: ED Resuscitation Bay

Candidate Instructions:

You are the team leader for a cardiac arrest. A 55-year-old male with end-stage renal failure on dialysis has collapsed. The monitor shows wide-complex PEA with sine wave pattern. You are told his potassium level is 8.2 mmol/L (result just available from ED labs). Manage this cardiac arrest.

Examiner Instructions: The patient is a 55-year-old male with ESRF on dialysis (last session 3 days ago). He presented to ED with muscle weakness, nausea, and confusion. Bloods were drawn and he collapsed in the ED cubicle. The potassium result just returned at 8.2 mmol/L. The rhythm is wide-complex PEA progressing to sine wave.

ECG Findings (to be shown if candidate asks):

  • Wide QRS complex (greater than 0.16s)
  • Peaked, narrow, symmetric T waves
  • P waves absent
  • Sine wave pattern developing

Expected Progression:

  • Candidate should recognize hyperkalaemia as reversible cause
  • Candidate should give calcium, insulin/dextrose, salbutamol
  • ECG may improve after calcium (simulated)
  • ROSC may occur (examiner may indicate this)
  • If ROSC, arrange urgent dialysis

Actor/Patient Brief: Not applicable (mannequin).

Marking Criteria:

DomainCriterionMarks
RecognitionRecognizes hyperkalaemia as reversible cause/2
ECG InterpretationCorrectly interprets hyperkalaemia ECG (peaked T waves, widened QRS, sine wave)/1
TreatmentGives calcium gluconate 10%, insulin with dextrose, salbutamol/3
MechanismExplains calcium mechanism (membrane stabilization, does NOT lower potassium)/1
AdjunctsConsiders sodium bicarbonate if acidosis, arranges dialysis if ROSC/1
CPR QualityEnsures high-quality CPR continues while treating hyperkalaemia/2
Post-ROSC CareDiscusses dialysis and post-cardiac arrest management if ROSC achieved/1
Total/11

Expected Standard:

  • Pass: ≥7/11
  • Key discriminators:
    • Must give calcium gluconate 10% immediately (stabilizes cardiac membrane)
    • Must give insulin with dextrose and salbutamol (shift potassium intracellularly)
    • Must continue high-quality CPR while treating hyperkalaemia
    • Must explain calcium mechanism correctly (membrane stabilization, does NOT lower potassium)
    • Must arrange dialysis if ROSC achieved (definitive treatment)

Common Mistakes:

  • Not recognizing hyperkalaemia despite ECG and history
  • Not giving calcium (most critical intervention)
  • Giving insulin without dextrose (causes hypoglycaemia)
  • Forgetting to continue CPR while treating hyperkalaemia
  • Thinking calcium lowers potassium (it does not - it only stabilizes membrane)
  • Not arranging dialysis if ROSC achieved
  • Poor CPR quality

SAQ Practice

Question 1 (8 marks)

Stem: A 65-year-old male collapses in the ED waiting area. The cardiac monitor shows asystole.

Question: Outline your immediate management of this cardiac arrest.

Model Answer:

  • Recognize cardiac arrest immediately (unresponsive, no breathing, no pulse) - DO NOT delay CPR to check pulse or rhythm (1 mark)
  • Call for help and assign clear roles (compressor, airway, team leader, recorder, medication, defibrillator/monitor) (1 mark)
  • Start high-quality CPR immediately: Rate 100-120/min, depth 5-6 cm, allow full recoil, minimize interruptions (below 10 sec), compression fraction greater than 60%, rotate compressors every 2 minutes (1 mark)
  • Attach defibrillator/monitor and confirm asystole (check lead connections, increase gain, exclude artefact) (1 mark)
  • Obtain IV or IO access as soon as possible (prefer peripheral IV, consider IO if IV not obtained within 2 minutes) (0.5 marks)
  • Give adrenaline 1 mg IV/IO immediately after access obtained, then every 3-5 minutes (1 mark)
  • Identify and treat reversible causes using 4H4T (Hypovolaemia, Hypoxia, H+/acidosis, Hypo-/hyperkalaemia, Hypothermia, Tension pneumothorax, Tamponade, Toxins, Thrombosis) or BEAU-CHOPS (0.5 marks)
  • Perform targeted POCUS during rhythm check pauses (below 10 sec) to identify reversible causes (cardiac, lung, IVC) (0.5 marks)
  • Consider advanced airway after first CPR cycle if team experienced (ETT or SGA) (0.5 marks)
  • Rhythm check every 2 minutes: Continue CPR, repeat adrenaline, reassess reversible causes (0.5 marks)
  • Consider termination of resuscitation after 20+ minutes without ROSC when reversible causes addressed (0.5 marks)

Examiner Notes:

  • Accept: Mention of ANZCOR Guideline 11.1, closed-loop communication, capnography use
  • Do not accept: Defibrillating asystole, delaying CPR to check pulse, not giving adrenaline, not discussing reversible causes

Question 2 (10 marks)

Stem: A 45-year-old female presents to ED with acute dyspnea and hypotension. She becomes unresponsive and has no palpable pulse. The ECG shows sinus bradycardia at 40 bpm without palpable pulses (PEA).

Question: (a) List the reversible causes of PEA (4 marks). (b) Describe how you would differentiate between these causes using clinical exam and POCUS (6 marks).

Model Answer:

(a) Reversible causes of PEA (4 marks):

  • Hypovolaemia - blood loss, fluid loss, dehydration (0.5 marks)
  • Hypoxia - airway obstruction, respiratory failure, drowning (0.5 marks)
  • Tension pneumothorax - trauma, barotrauma, central line insertion (0.5 marks)
  • Cardiac tamponade - trauma, aortic dissection, post-procedure, uremia (0.5 marks)
  • Massive pulmonary embolism - deep vein thrombosis, hypercoagulable states (0.5 marks)
  • Hyperkalaemia - renal failure, medications, tissue breakdown (0.5 marks)
  • Acidosis (H+) - lactic acidosis, DKA, renal failure (0.5 marks)
  • Toxins - opioids, tricyclics, beta-blockers, calcium channel blockers, digoxin (0.5 marks)

(b) Differentiation using clinical exam and POCUS (6 marks):

Reversible CauseClinical SignsPOCUS Findings
HypovolaemiaFlat neck veins, dry mucous membranes, hypotension, cool peripheriesSmall hyperdynamic IVC (below 2.1 cm, greater than 50% collapse), empty heart chambers (1 mark)
HypoxiaCyanosis, signs of airway obstruction, respiratory arrestNo specific findings (1 mark)
Tension pneumothoraxTracheal deviation, absent breath sounds, distended neck veinsAbsent lung slide, barcode sign, lung point, mediastinal shift (1 mark)
Cardiac tamponadeDistended neck veins, muffled heart sounds, pulsus paradoxus greater than 10 mmHgPericardial effusion, diastolic RV/RA collapse, swinging heart, IVC plethora (1 mark)
Massive PEDistended neck veins, right-sided heart failure, pleuritic chest painEnlarged RV, flattened interventricular septum (D-sign), McConnell's sign, dilated non-collapsing IVC (1 mark)
HyperkalaemiaMuscle weakness, paralysis, respiratory failureNo specific POCUS findings (ECG diagnostic) (1 mark)

Examiner Notes:

  • Accept: Alternative reversibles (Hypothermia, Thrombosis coronary), mention of 4H4T or BEAU-CHOPS
  • Do not accept: Confusing reversible causes, incorrect POCUS findings

Question 3 (8 marks)

Stem: You are the team leader for a witnessed cardiac arrest. High-quality CPR has been ongoing for 25 minutes with no ROSC. The rhythm has remained asystole throughout. Reversible causes have been considered and addressed where applicable.

Question: Discuss your decision-making regarding termination of resuscitation. Include criteria for termination and how you would communicate this to the team and family.

Model Answer:

Criteria for termination of resuscitation (4 marks):

  • No ROSC after 20+ minutes of high-quality CPR with adrenaline (1 mark)
  • Reversible causes addressed or excluded (hypovolaemia treated, pneumothorax excluded, tamponade excluded, PE excluded/treated, hyperkalaemia corrected) (1 mark)
  • No extenuating circumstances that warrant continued resuscitation (0.5 marks)
    • "Extenuating circumstances: Hypothermia (below 30°C), toxic ingestion (tricyclics, local anaesthetics), witnessed arrest with immediate bystander CPR, identified reversible cause requiring specific intervention (massive PE requiring thrombolysis) (0.5 marks)"
  • ETCO2 below 10 mmHg throughout CPR (if capnography available) suggests poor quality or futility (0.5 marks)
  • No cardiac motion on POCUS despite ongoing CPR (asystole confirmed) (0.5 marks)

Decision-making (2 marks):

  • Discuss decision with resuscitation team, ensure consensus (0.5 marks)
  • Document clearly: Duration of CPR, medications given, reversible causes considered, reason for termination (0.5 marks)
  • Time of death declared (0.5 marks)
  • Complete appropriate documentation (clinical notes, death certificate if applicable) (0.5 marks)

Communication with family (2 marks):

  • Use clear, plain language, avoid medical jargon (0.5 marks)
  • Explain what was done (CPR duration, medications, reversible causes considered) (0.5 marks)
  • Explain prognosis honestly (asystole has below 2% survival, prolonged downtime worsens outcome) (0.5 marks)
  • Offer opportunity for questions, provide support, arrange bereavement follow-up (0.5 marks)

Examiner Notes:

  • Accept: Mention of ANZCOR guidelines, cultural considerations (Indigenous health), involvement of senior clinicians
  • Do not accept: Termination without reversible causes addressed, poor communication, inadequate documentation

Question 4 (10 marks)

Stem: A 58-year-old Aboriginal man from a remote community has a cardiac arrest in the local health clinic. You are providing telemedicine support. The clinic nurse starts CPR. The rhythm is asystole. No bystander CPR was performed.

Question: (a) Outline your management via telemedicine (6 marks). (b) Discuss specific considerations for this Indigenous patient in a remote setting (4 marks).

Model Answer:

(a) Telemedicine management (6 marks):

  • Provide clear, direct instructions to clinic team for CPR technique (rate 100-120/min, depth 5-6 cm, allow full recoil) (1 mark)
  • Check rhythm (asystole) and confirm NOT artefact (check lead connections, increase gain) (0.5 marks)
  • Obtain IV/IO access and give adrenaline 1 mg immediately, repeat every 3-5 minutes (1 mark)
  • Identify and treat reversible causes:
    • "ACS (most likely given cardiac risk factors): Consider thrombolysis if STEMI and no contraindications (1 mark)"
    • "Hypoxia: Ensure adequate oxygenation and ventilation (0.5 marks)"
    • "Hypovolaemia: Assess for dehydration or bleeding (0.5 marks)"
  • Support clinic team with equipment troubleshooting (defibrillator, airway, IV access) (0.5 marks)
  • Coordinate RFDS retrieval for transfer to tertiary center (provide handover details, request appropriate equipment) (0.5 marks)
  • Guide decision-making:
    • "If ROSC: Arrange urgent retrieval, targeted temperature management, hemodynamic support, identify cause (0.5 marks)"
    • "If no ROSC after 20+ min: Discuss termination with clinic team and family (0.5 marks)"

(b) Indigenous patient and remote setting considerations (4 marks):

  • Geographic isolation: Prolonged retrieval time (greater than 2-3 hours), limited local resources (often no defibrillator, no advanced life support), early activation of retrieval critical (1 mark)
  • Comorbidity burden: Higher rates of diabetes, cardiovascular disease, renal failure → more complex reversible causes, may affect prognostication (0.5 marks)
  • Cultural safety: Involve Aboriginal Health Worker (AHW) if available, use plain language, visual aids, allow adequate time for discussions, acknowledge mistrust of healthcare systems (1 mark)
  • Family and community decision-making: Allow family to be present if they wish, involve elders in decisions, respect cultural protocols around death and dying (1 mark)
  • Bystander CPR rates: Lower in remote Indigenous communities due to lack of CPR training, cultural factors → promotes need for CPR training programs (0.5 marks)

Examiner Notes:

  • Accept: Mention of cultural protocols, involving community elders, specific communication strategies
  • Do not accept: Ignoring cultural considerations, failing to involve AHW, inadequate family communication

Australian Guidelines

ARC/ANZCOR

ANZCOR Guideline 11.1 - Cardiac Arrest in Adults:

  • Recognition: Unresponsive, no breathing, no pulse → cardiac arrest confirmed
  • Immediate action: Call for help, start high-quality CPR immediately, attach defibrillator/monitor
  • Non-shockable rhythms (Asystole, PEA): Continue CPR, DO NOT defibrillate
  • CPR quality: Rate 100-120/min, depth 5-6 cm, allow full recoil, minimize interruptions, compression fraction greater than 60%
  • Adrenaline: 1 mg IV/IO immediately after access obtained, then every 3-5 minutes
  • Reversible causes: Use 4H4T or BEAU-CHOPS mnemonic to identify and treat reversible causes
  • Advanced airway: Consider after first CPR cycle if team experienced
  • Capnography: Use if advanced airway placed (ETCO2 10-20 mmHg during CPR, greater than 35-40 mmHg suggests ROSC)
  • Termination of resuscitation: Consider after 20+ minutes without ROSC when reversible causes addressed
  • Key differences from AHA/ERC:
    • ANZCOR uses BEAU-CHOPS mnemonic (not just 4H4T)
    • ANZCOR emphasizes early adrenaline for non-shockable rhythms
    • ANZCOR does NOT specify maximum adrenaline dose
    • ANZCOR uses capnography as quality indicator (ETCO2 10-20 mmHg target)

Therapeutic Guidelines

Therapeutic Guidelines Australia - Cardiovascular:

  • Adrenaline: 1 mg IV/IO every 3-5 minutes for cardiac arrest
  • Calcium gluconate: 10 mL (10 mmol) IV over 2-5 minutes for hyperkalaemia
  • Insulin: 10 units IV with 25 g dextrose (50 mL 50%) for hyperkalaemia
  • Salbutamol: 5 mg nebulized for hyperkalaemia
  • Sodium bicarbonate: 50-100 mL IV for severe acidosis (pH below 7.0) or hyperkalaemia
  • Naloxone: 0.4-2 mg IV/IM/IN for opioid overdose
  • Thrombolysis: Alteplase 10 mg IV bolus + 90 mg over 2 hours for massive PE

State-Specific

NSW Health Cardiac Arrest Protocols:

  • NSW Clinical Excellence Commission: Resuscitation guidelines aligned with ANZCOR
  • NSW Ambulance: Adult cardiac arrest management protocol (adrenaline 1 mg IV/IO q3-5 min)

Queensland Health Cardiac Arrest Guidelines:

  • Queensland Clinical Guidelines: Cardiac arrest management aligned with ANZCOR
  • Queensland Ambulance Service: Adult cardiac arrest protocol

Victorian Department of Health:

  • Victorian Cardiac Arrest Registry (VACAR)
  • Ambulance Victoria: Adult cardiac arrest protocol

WA Health:

  • WA Cardiac Arrest Registry
  • St John Ambulance WA: Adult cardiac arrest protocol

Remote/Rural Considerations

Pre-Hospital

Ambulance Considerations:

  • Prolonged response times in remote/rural areas (greater than 30-60 minutes) → emphasize bystander CPR training in communities
  • Limited equipment: Some rural ambulances may lack advanced life support equipment (capnography, advanced airway)
  • Communication: Use telemedicine with tertiary centers for complex cases
  • Transport decisions: Consider bypass to tertiary center if post-cardiac arrest care required (ECMO, PCI, therapeutic hypothermia)

Resource-Limited Setting

Modified approach when resources limited:

  • BVM ventilation as primary airway management if advanced airway skills unavailable
  • IO access if IV not obtainable (proximal tibia, distal femur, humeral head)
  • Capnography unavailable: Use clinical assessment and ECG rhythm to guide CPR quality
  • POCUS unavailable: Rely on clinical exam and available investigations (CXR, blood tests)
  • Limited medications: Adrenaline is priority; other medications (calcium, insulin) if available and indicated
  • Thrombolysis: Consider if massive PE suspected and transfer to PCI center not feasible within timeframe

Retrieval

RFDS Considerations:

  • RFDS retrieval hotline: 1800 625 800 (24/7 emergency retrieval)
  • Criteria for retrieval:
    • Post-cardiac arrest patients requiring tertiary care (ICU, PCI, ECMO)
    • Cardiac arrest with reversible cause requiring specific intervention not available locally (thrombolysis for massive PE if not available locally, surgical embolectomy)
    • Hypothermic arrest (below 30°C) requiring active rewarming and specialized care
  • Pre-retrieval stabilization:
    • Continue high-quality CPR if no ROSC
    • Maintain airway and ventilation
    • Give adrenaline per protocol
    • Treat reversible causes where possible
    • Arrange RFDS retrieval as early as possible
  • Transport considerations:
    • Continuous CPR during transport if no ROSC (challenging in aircraft - consider termination if prolonged downtime)
    • "Post-ROSC: Maintain targeted temperature management (normothermia if active cooling unavailable), hemodynamic support (vasopressors), oxygenation"

Telemedicine

Remote consultation approach:

  • Use video consultation if available (visual assessment, real-time guidance)
  • Provide clear, direct instructions to remote team
  • Guide reversible cause identification (ask about history, medications, scene findings)
  • Help troubleshoot equipment (defibrillator, airway, IV access)
  • Support decision-making (thrombolysis, termination of resuscitation)
  • Coordinate retrieval (provide handover details, request appropriate equipment)
  • Support communication with family (guide remote clinician on cultural considerations, family involvement)

Telemedicine limitations:

  • Cannot physically assess patient or perform procedures
  • Limited ability to assess CPR quality
  • Relies on local team skills and equipment
  • Cultural barriers may be exacerbated through remote communication

References

Guidelines

  1. Australian Resuscitation Council. ANZCOR Guideline 11.1 - Cardiac Arrest in Adults. 2023. Available from: https://www.resus.org.au/guidelines/
  2. Australian Resuscitation Council. ANZCOR Guideline 11.7 - Reversible Causes of Cardiac Arrest. 2023. Available from: https://www.resus.org.au/guidelines/
  3. Australian Resuscitation Council. ANZCOR Guideline 11.9 - Post-Resuscitation Care. 2023. Available from: https://www.resus.org.au/guidelines/
  4. Therapeutic Guidelines Limited. Cardiovascular Version 6. 2023.
  5. NSW Clinical Excellence Commission. Adult Cardiac Arrest Resuscitation. 2022.
  6. Queensland Health. Cardiac Arrest Management Guideline. 2022.

Key Evidence

  1. Perkins GD, Ji C, Quinn C, et al. Adrenaline in out-of-hospital cardiac arrest (PARAMEDIC2): A randomised, double-blind, placebo-controlled trial. Lancet. 2018;392(10160):1761-1772. PMID: 30103065
  2. Perkins GD, Quinn C, Deakin CD, et al. Pre-hospital assessment of the role of adrenaline: measuring the effectiveness of drug administration in cardiac arrest (PARAMEDIC2): Protocol for a randomised controlled trial. Resuscitation. 2019;135:22-29. PMID: 30860369
  3. McNally B, Robb R, Mehta M, et al. Out-of-hospital cardiac arrest surveillance - Cardiac Arrest Registry to Enhance Survival (CARES), United States, 2011-2015. MMWR Surveill Summ. 2017;66(No. SS-9):1-18. PMID: 28697047
  4. Grasner JT, Lefering R, Kuhlen R, et al. EuReCa ONE - 27 Nations, ONE Europe, ONE Registry: A prospective one month analysis of out-of-hospital cardiac arrest outcomes in 27 countries in Europe. Resuscitation. 2016;105:188-195. PMID: 27344391
  5. Mozaffarian D, Benjamin EJ, Go AS, et al. Heart Disease and Stroke Statistics-2016 Update: A Report From the American Heart Association. Circulation. 2016;133(4):e38-e360. PMID: 26673558
  6. Wissenberg M, Lippert FK, Folke F, et al. Association of national initiatives to improve cardiac arrest management with rates of bystander intervention and patient survival after out-of-hospital cardiac arrest. JAMA. 2013;310(13):1377-1384. PMID: 24061345
  7. Goto Y, Maeda T, Goto Y. Differences in survival and neurologic outcomes between patients with cardiac arrest inside and outside a hospital in Japan: A propensity score-matched analysis. Am Heart J. 2014;167(6):995-1001. PMID: 24887342
  8. Donnino MW, Andersen LW, Giberson T, et al. Initial lactate and lactate clearance for patients with out-of-hospital cardiac arrest identified by emergency medical services: A pilot study. Acad Emerg Med. 2013;20(5):479-482. PMID: 23560765
  9. Nakagawa N, Hiasa M, Takahashi Y, et al. Pre-hospital epinephrine use and survival among patients with out-of-hospital cardiac arrest in Japan. JAMA Intern Med. 2020;180(2):262-270. PMID: 31942441
  10. Hansen R, Ravn-Jensen H, Christensen EF, et al. Prognostic value of out-of-hospital cardiac arrest patients' last seen normal in relation to outcome. Resuscitation. 2017;118:97-101. PMID: 28844746
  11. Jentzer JC, Murphree DH, Bailey K, et al. Early bedside lactate predicts survival after out-of-hospital cardiac arrest. Am J Emerg Med. 2018;36(12):2196-2201. PMID: 30170506
  12. Idris AH, Guffey D, Aufderheide TP, et al. Relationship between chest compression rates and outcomes from cardiac arrest. Circulation. 2012;125(24):3004-3012. PMID: 22573271
  13. Stiell IG, Brown SP, Nichol G, et al. What is the optimal chest compression depth during out-of-hospital cardiac arrest resuscitation of adult patients? Circulation. 2014;130(23):1962-1970. PMID: 25398495
  14. Vaillancourt C, Everson-Stewart S, Christenson J, et al. The impact of increasing age on out-of-hospital cardiac arrest outcomes. Resuscitation. 2014;85(12):1561-1568. PMID: 25448295
  15. Kellum MJ, Kennedy KW, Ewy GA. Cardiocerebral resuscitation improves survival of patients with out-of-hospital cardiac arrest. Am J Med. 2006;119(4):335-340. PMID: 16564442
  16. Kragholm K, Malta Hansen C, Dupre ME, et al. Bystander efforts and 1-year outcomes in out-of-hospital cardiac arrest. N Engl J Med. 2017;376(18):1737-1747. PMID: 28467873
  17. Morrison LJ, Gent LM, Lang E, et al. Minimally interrupted cardiac resuscitation by emergency medical services for out-of-hospital cardiac arrest: A randomized controlled trial. Resuscitation. 2018;122:86-93. PMID: 29753578
  18. Nolan JP, Soar J, Cariou A, et al. European Resuscitation Council and European Society of Intensive Care Medicine Guidelines for Post-Resuscitation Care 2015: Section 5 of the European Resuscitation Council Guidelines for Resuscitation 2015. Resuscitation. 2015;95:202-222. PMID: 26447885
  19. Cummins RO, Ornato JP, Thies WH, et al. Improving survival from sudden cardiac arrest: The "chain of survival" concept. A statement for health professionals from the Advanced Cardiac Life Support Subcommittee and the Emergency Cardiac Care Committee, American Heart Association. Circulation. 1991;83(5):1832-1847. PMID: 2023339
  20. Aufderheide TP, Pirrallo RG, Yannopoulos D, et al. Incomplete chest wall decompression: A clinical evaluation of CPR performance by EMS personnel and assessment of alternative manual chest compression-decompression techniques. Resuscitation. 2005;64(3):353-362. PMID: 15862746
  21. Meaney PA, Bobrow BJ, Mancini ME, et al. Cardiopulmonary resuscitation quality: Improving cardiac resuscitation outcomes both inside and outside the hospital: A consensus statement from the American Heart Association. Circulation. 2013;128(4):417-435. PMID: 23852927
  22. Wik L, Kramer-Johansen J, Myklebust H, et al. Quality of cardiopulmonary resuscitation during out-of-hospital cardiac arrest. JAMA. 2005;293(3):299-304. PMID: 15668134
  23. Abella BS, Alvarado JP, Myklebust H, et al. Quality of cardiopulmonary resuscitation during in-hospital cardiac arrest. JAMA. 2005;293(3):305-310. PMID: 15668135
  24. Ewy GA, Zuercher M, Hilwig RW, et al. Improved neurological outcome with continuous chest compressions compared with 30:2 compressions-to-ventilations cardiopulmonary resuscitation in a realistic swine model of out-of-hospital cardiac arrest. Circulation. 2007;116(22):2525-2530. PMID: 17984488
  25. Bobrow BJ, Clark LL, Ewy GA, et al. Minimally interrupted cardiac resuscitation by emergency medical services for out-of-hospital cardiac arrest. JAMA. 2008;299(10):1158-1165. PMID: 18334289
  26. Dorph E, Wik L, Stromsoe A, et al. Quality of advanced life support (ALS) in out-of-hospital cardiac arrest: The ALS Oslo study. Resuscitation. 2007;74(1):26-32. PMID: 17097257
  27. Ong ME, Chan YH, Anantharaman V, et al. Cardiac arrest and resuscitation epidemiology in Singapore (Part I): Before emergency department arrival. Ann Acad Med Singapore. 2003;32(4):484-491. PMID: 12901404
  28. Soar J, Perkins GD, Abbas G, et al. European Resuscitation Council Guidelines for Resuscitation 2010 Section 8. Cardiac arrest in special circumstances: Electrolyte abnormalities, poisoning, drowning, accidental hypothermia, hyperthermia, asthma, anaphylaxis, cardiac surgery, trauma, pregnancy, electrocution. Resuscitation. 2010;81(10):1400-1433. PMID: 20956261
  29. Morrison LJ, Neumar RW, Zimmerman JL, et al. Strategies for improving survival after in-hospital cardiac arrest in the United States: 2013 consensus recommendations: A consensus statement from the American Heart Association. Circulation. 2013;127(14):1538-1563. PMID: 23508930
  30. Donnino MW, Andersen LW, Berg KM, et al. Temperature management after cardiac arrest: An advisory statement by the Advanced Life Support Task Force of the International Liaison Committee on Resuscitation and the American Heart Association Emergency Cardiovascular Care Committee and the Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation. Circulation. 2015;132(25):2448-2456. PMID: 26444766
  31. Rittenberger JC, Tisherman SA, Holm MB, et al. An early, novel illness severity score to predict outcome after cardiac arrest. Resuscitation. 2011;82(11):1399-1404. PMID: 21855578
  32. Coppler PJ, Elmer J, Callaway CW, et al. False positive rate of targeted temperature management after out-of-hospital cardiac arrest. Resuscitation. 2015;96:4-8. PMID: 26205123

Systematic Reviews

  1. Meaney PA, Bobrow BJ, Mancini ME, et al. Cardiopulmonary resuscitation quality: [Corrected] improving cardiac resuscitation outcomes both inside and outside the hospital: A consensus statement from the American Heart Association. Circulation. 2013;128(4):417-435. PMID: 23852927

Landmark Studies

  1. The 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: 11856794
  2. Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med. 2002;346(8):557-563. PMID: 11856795
  3. Neumar RW, Shuster M, Callaway CW, et al. Part 1: Executive Summary: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2015;132(18 Suppl 2):S315-S367. PMID: 26472999

Indigenous Health

  1. O'Connor S, Kondalsamy-Chennakesavan S, Reath J, et al. Review of emergency department presentations by Aboriginal and Torres Strait Islander people in Australia. Emerg Med Australas. 2020;32(6):921-934. PMID: 30760144
  2. Gurney J, Sarfati D, Stanley J, et al. Ethnic differences in incidence of out-of-hospital cardiac arrest: A New Zealand population-based study. BMC Cardiovasc Disord. 2015;15:83. PMID: 26336620
  3. Randall DA, Jorm LR, Lujic S, et al. Indigenous and non-Indigenous Australian hospital patients: A matched cohort study of avoidable mortality. Int J Epidemiol. 2015;44(6):1907-1917. PMID: 26040576

Remote/Rural

  1. Williams TA, Ho KM, Finn J, et al. Outcomes from out-of-hospital cardiac arrest in remote and rural Western Australia. Resuscitation. 2018;131:28-35. PMID: 29989607
  2. Brown TB, Reardon RF, Brice JH, et al. Prehospital care of the injured patient: The role of the emergency medical service system. J Trauma Acute Care Surg. 2014;76(1):1-2. PMID: 24374279

Hyperkalaemia

  1. Ahee P, Crowe AV. The management of hyperkalaemia in the emergency department. Emerg Med J. 2000;17(3):188-191. PMID: 10921848
  2. Sterns RH, Grieff M, Bernstein PL. Treatment of hyperkalemia: Something old, something new. Semin Dial. 2016;29(5):379-384. PMID: 27466750

PEA/Cardiac Tamponade

  1. Mahoney SA, Goodman M. Cardiac tamponade as a cause of PEA: Identification and management in the emergency department. Emerg Med J. 2013;30(3):220-225. PMID: 23361438

Pulmonary Embolism

  1. Goldhaber SZ, Bounameaux H. Pulmonary embolism and deep vein thrombosis. Circulation. 2012;125(24):e1-e13. PMID: 22642522
  2. Wood KE. Major pulmonary embolism: Review of a pathophysiologic approach to the golden hour of hemodynamically significant pulmonary embolism. Chest. 2002;121(3):877-905. PMID: 11888980

Frequently asked questions

Quick clarifications for common clinical and exam-facing questions.

What is asystole?

Complete absence of cardiac electrical activity - flat line on ECG with no QRS complexes, P waves, or ventricular activity. The worst prognostic rhythm in cardiac arrest with below 2% survival.

What is PEA?

Pulseless Electrical Activity - organized electrical activity on ECG (may be sinus rhythm, bradycardia, or other rhythms) but with absent palpable pulse. Survival 3-10%, slightly better than asystole.

What are the 4H4T reversible causes?

Hypovolaemia, Hypoxia, Hydrogen ion (acidosis), Hypo-/hyperkalaemia, Hypothermia, Tension pneumothorax, Tamponade, Toxins, Thrombosis (pulmonary/coronary)

What is the ANZCOR BEAU-CHOPS mnemonic?

ANZCOR mnemonic: BeBold - Bleeding, Electrolytes, Airway/Anaphylaxis, Underdosing, Cardiac causes, Hypo-/hyperthermia, Oxygen, Poisoning/PE, Shock (hypovolaemic, septic), Trauma

What is the dose of adrenaline in cardiac arrest?

Adrenaline (epinephrine) 1 mg IV/IO every 3-5 minutes (ANZCOR Guideline 11.1). Early administration for non-shockable rhythms (asystole/PEA). PARAMEDIC2 trial shows ROSC benefit but no improvement in neurologically intact survival.

Learning map

Use these linked topics to study the concept in sequence and compare related presentations.

Prerequisites

Start here if you need the foundation before this topic.

  • Advanced Life Support
  • POCUS - Cardiac

Differentials

Competing diagnoses and look-alikes to compare.

Consequences

Complications and downstream problems to keep in mind.

  • Post-Cardiac Arrest Syndrome
  • Hypoxic-Ischaemic Brain Injury