Perioperative Cardiac Arrest

Quick Answer

Perioperative cardiac arrest occurs in 5-10 cases per 10,000 anaesthetics, with mortality ranging from 25-50% depending on aetiology and response time. The most common causes are hypoxaemia (25-30%), hypovolaemia (20-25%), and drug toxicity (15-20%). Immediate management follows ARC/ANZCOR Advanced Life Support (ALS) guidelines with modifications for perioperative context. The "4 Hs and 4 Ts" framework (Hypoxia, Hypovolaemia, Hydrogen ion [acidosis], Hyper/Hypokalaemia, Hypothermia, Tension pneumothorax, Tamponade, Toxins/Thromboembolism) guides diagnosis and treatment. Management priorities: (1) Recognize cardiac arrest (loss of pulse, unresponsiveness, apnoea), (2) Call for help and activate emergency response, (3) Begin high-quality CPR immediately (30:2 compressions:ventilations, rate 100-120/min, depth 5-6 cm), (4) Attach defibrillator pads immediately, (5) Analyze rhythm and deliver shocks if VF/pulseless VT (200J biphasic, repeated if needed). Perioperative modifications: (1) Remove causative drugs immediately, (2) Reversal agents for neuromuscular blockade (sugammadex 2-4 mg/kg for rocuronium/vecuronium), (3) Treat specific aetiologies (epinephrine for anaphylaxis, lipid emulsion for LAST), (4) Consider early ECMO in refractory cases, (5) Prolonged resuscitation if reversible cause present. Post-arrest care includes targeted temperature management (32-36°C for 24 hours), invasive monitoring, echocardiography, and treatment of underlying cause. Indigenous patients may have higher baseline cardiovascular risk and reduced access to post-arrest critical care, requiring culturally safe communication and planning for transfer if needed. [1-10]

Pathophysiology

Aetiology of Perioperative Cardiac Arrest

Perioperative cardiac arrest differs from out-of-hospital cardiac arrest in several important ways: it occurs in a monitored environment with immediate access to equipment, often has identifiable precipitating causes, and frequently has reversible aetiologies. Understanding these aetiologies is critical for effective management.

Primary Causes (Categories by Frequency):

1. Hypoxaemia (25-30% of cases):

Inadequate airway: Difficult intubation, CICV scenario, airway obstruction
Ventilation failure: Equipment malfunction, circuit disconnection, esophageal intubation
Pulmonary pathology: Pneumothorax, pulmonary embolism, aspiration
Drug-induced respiratory depression: Excessive opioids, muscle relaxants, residual anaesthesia

2. Hypovolaemia (20-25% of cases):

Surgical bleeding: Major vessel injury, coagulopathy, anastomotic leak
Non-surgical bleeding: Trauma, gastrointestinal hemorrhage, ruptured aneurysm
Fluid redistribution: Vasodilation from spinal/epidural anaesthesia, sepsis
Third-spacing: Burns, pancreatitis, abdominal compartment syndrome

3. Drug Toxicity (15-20% of cases):

Local anaesthetic systemic toxicity (LAST): Accidental intravascular injection
Anaphylaxis: Antibiotics, NMBA, latex, chlorhexidine
Drug interactions: MAOI inhibitors, pethidine + MAOI, beta-blockers + hypoglycaemia treatment
Overdose: Excessive anaesthetic agents, opioids, benzodiazepines

4. Cardiovascular Causes (10-15% of cases):

Myocardial ischaemia/infarction: Coronary artery disease, demand ischaemia
Arrhythmias: New-onset atrial fibrillation, ventricular tachycardia
Valve dysfunction: Critical aortic stenosis, mitral regurgitation
Cardiac tamponade: Surgical injury, pericardial effusion

5. Electrolyte and Acid-Base Disorders (5-10% of cases):

Hyperkalaemia: Renal failure, massive transfusion, succinylcholine
Hypokalaemia: Diuretic use, malnutrition, alkalosis
Hypocalcaemia: Massive transfusion, citrate accumulation
Metabolic acidosis: Severe sepsis, shock, cardiac arrest itself

6. Tension Pneumothorax (2-5% of cases):

Iatrogenic: Central venous catheter insertion, nerve blocks, laparoscopic surgery
Spontaneous: Underlying lung disease (COPD)
Traumatic: Rib fractures, thoracic surgery

7. Pulmonary Embolism (1-2% of cases):

Deep vein thrombosis: PE in high-risk surgical patients
Fat embolism: Orthopaedic surgery, long bone fractures
Air embolism: Hysteroscopy, sitting position, CVC insertion

8. Hypothermia (1-2% of cases):

Cold environment: Operating theatre temperature
Redistribution: Anesthesia-induced vasodilation
Massive transfusion: Cold blood products
Burns or extensive exposure

Secondary Risk Factors:

Patient-Specific Factors:

Cardiovascular disease: Ischaemic heart disease, heart failure, valvular disease
Respiratory disease: COPD, asthma, restrictive lung disease
Renal disease: Chronic kidney disease, dialysis dependence
Diabetes mellitus: Autonomic neuropathy, coronary artery disease
Obesity: Reduced FRC, difficult airway, cardiovascular strain
Age >65 years: Reduced physiological reserve
Emergency surgery: Limited preparation time, unstable patients

Procedure-Specific Factors:

Cardiac surgery: Cardiac manipulation, bypass, reperfusion injury
Vascular surgery: Major vessel manipulation, embolism risk
Thoracic surgery: One-lung ventilation, pulmonary injury risk
Major abdominal surgery: Fluid shifts, third-spacing
Orthopaedic surgery: Fat embolism risk, blood loss
Obstetric surgery: Amniotic fluid embolism, haemorrhage

Anaesthetic-Specific Factors:

Deep neuromuscular blockade: Respiratory depression
High-dose opioids: Apnoea, respiratory depression
Regional anaesthesia: Sympathectomy-induced hypotension
General anaesthesia: Myocardial depression, vasodilation

Mechanisms of Cardiac Arrest by Aetiology

Hypoxaemia-Induced Arrest:

Pathophysiology:

Arterial oxygen desaturation → myocardial oxygen delivery ↓
Myocardial hypoxia → impaired contractility and electrical instability
Cellular anaerobic metabolism → acidosis
Progressive deterioration → arrhythmias → asystole

Clinical Course:

Initial bradycardia (hypoxia-induced vagal stimulation)
Progression to ventricular arrhythmias
Final progression to asystole
Rapid progression if hypoxaemia severe

Hypovolaemia-Induced Arrest:

Pathophysiology:

Reduced intravascular volume → preload ↓
Reduced stroke volume → cardiac output ↓
Compensatory tachycardia → increased myocardial oxygen demand
Coronary perfusion pressure falls → myocardial ischaemia
Ventricular failure → pump failure → asystole

Clinical Course:

Tachycardia with narrow pulse pressure
Progressively falling blood pressure
Loss of palpable pulse
May progress to PEA initially, then asystole

Anaphylaxis-Induced Arrest:

Pathophysiology:

Mast cell degranulation → massive histamine, tryptase release
Profound vasodilation → distributive shock
Increased capillary permeability → capillary leak, hypovolaemia
Myocardial depression → direct negative inotropy
Bronchospasm → hypoxaemia
Combined effects → cardiovascular collapse

Clinical Course:

Rapid hypotension refractory to vasopressors
Bronchospasm with high airway pressures
Cardiovascular collapse within seconds to minutes
May present as PEA or asystole

LAST-Induced Arrest:

Pathophysiology:

Sodium channel blockade → impaired cardiac conduction
QRS widening → intraventricular conduction delay
Negative inotropy → calcium channel inhibition
Mitochondrial dysfunction → impaired energy metabolism
Arrhythmias → VT/VF refractory to defibrillation

Clinical Course:

May be first sign without CNS warning (especially bupivacaine)
Wide complex arrhythmias
Refractory to standard defibrillation
"Stone heart" (intractable VF/asystole)

Tamponade-Induced Arrest:

Pathophysiology:

Pericardial fluid accumulation → increased pericardial pressure
Equalized diastolic pressures → restricted ventricular filling
Reduced stroke volume → cardiac output ↓
Compensatory tachycardia → ultimately fails
Cardiogenic shock → arrest

Clinical Course:

Beck's triad: hypotension, JVD, muffled heart sounds
Pulsus paradoxus
Progressive cardiovascular collapse
Often PEA rather than VF/asystole

Tension Pneumothorax-Induced Arrest:

Pathophysiology:

Intrapleural air accumulation → mediastinal shift
Contralateral lung compression → hypoxaemia
Impaired venous return → preload ↓
Reduced cardiac output → cardiovascular collapse

Clinical Course:

Unilateral absent breath sounds
Tracheal deviation away from affected side
Sudden hypotension and desaturation
May progress to arrest if not relieved

Clinical Presentation

Recognition of Cardiac Arrest

Diagnostic Criteria:

Cardiac arrest is confirmed when all three of the following are present:

Unresponsiveness: No response to verbal or painful stimuli
Absence of palpable central pulse: No carotid or femoral pulse palpable for ≥10 seconds
Absence of breathing: Apnoea or agonal breathing

ECG Findings:

Cardiac arrest rhythm categories:

Shockable Rhythms (Amenable to Defibrillation):

Ventricular Fibrillation (VF): Chaotic, disorganized electrical activity without distinct QRS complexes
Pulseless Ventricular Tachycardia (VT): Organized rapid rhythm (≥150 bpm) without pulse

Non-Shockable Rhythms:

Pulseless Electrical Activity (PEA): Organized electrical activity without mechanical cardiac output
Asystole: No electrical activity, flat line (or occasional P waves only)

Perioperative Warning Signs:

Pre-Arrest Indicators (Call for help):

Haemodynamic:

Sudden severe hypotension: SBP <60 mmHg or >30% drop from baseline
Refractory hypotension: No response to atropine, ephedrine, or phenylephrine
Bradycardia: HR <40 bpm or sudden drop from baseline
Tachycardia: HR >120 bpm with hypotension

Respiratory:

Loss of end-tidal CO₂ waveform: Sudden disappearance
Rapid desaturation: SpO₂ <90% despite 100% O₂
High airway pressures: >30 cm H₂O suggesting bronchospasm or obstruction
Apnoea: No spontaneous respirations

ECG Changes:

ST elevation/depression: Ischaemic changes
New arrhythmias: Atrial fibrillation, VT
QRS widening: Suggests hyperkalaemia, sodium channel blockade
Peaked T waves: Hyperkalaemia

Other Signs:

Loss of consciousness: Sudden unresponsiveness
Cyanosis: Central cyanosis
Dilated pupils: May appear in cardiac arrest
Skin changes: Urticaria, erythema (anaphylaxis)
Bleeding: Sudden major surgical bleeding

Immediate Actions on Recognition:

The "CODE" Response:

Call for help loudly — "Cardiac arrest, help!"
Confirm arrest — check central pulse for ≤10 seconds
Begin CPR immediately — do not delay for confirmation
Attach defibrillator/monitor — analyze rhythm ASAP
Follow ALS algorithm — rhythm-specific treatment

Time-Critical Nature:

Survival decreases rapidly with time:

Best outcomes: CPR started within 4-6 minutes
Neurological injury: Likely after 6-8 minutes without CPR
Poor prognosis: >10 minutes without CPR/defibrillation

Perioperative advantage:

Immediate recognition (monitored patient)
Equipment readily available
Team already present
Earlier recognition and response compared to out-of-hospital arrest

Management

Immediate Management: Advanced Life Support (ALS)

ARC/ANZCOR ALS Guidelines with Perioperative Modifications:

Phase 1: Immediate Resuscitation (0-60 seconds)

1. Confirm Cardiac Arrest and Call for Help [10 seconds]

Assess unresponsiveness
Check central pulse (carotid or femoral) for ≤10 seconds
Simultaneously call for help loudly
Activate emergency response system
Note the time of arrest

2. Begin High-Quality CPR [Start Immediately]

CPR Parameters:

Compression depth: 5-6 cm (adults)
Compression rate: 100-120 compressions per minute
Compression:ventilation ratio: 30:2 (or continuous compressions with advanced airway)
Compression fraction: ≥60% (maximizing chest compressions)
Allow full chest recoil after each compression
Minimize interruptions (<10 seconds for rhythm check/pulse check)

Chest Compression Technique:

Hard and fast
Place heel of hand on lower half of sternum
Interlock fingers, arms straight, shoulders over hands
Full recoil after each compression

Ventilation:

100% oxygen
Rate: 8-10 breaths/minute (with advanced airway)
Volume: 6-7 mL/kg (500-600 mL for adult)
Observe chest rise
Avoid hyperventilation

3. Attach Defibrillator/Monitor [20-30 seconds]

Actions:

Attach defibrillator pads (anterior-lateral or anterior-posterior)
Rapidly assess rhythm (minimize CPR interruption)
Do not interrupt CPR for >10 seconds to check rhythm

4. Identify Rhythm and Deliver Shocks if Indicated

VF/pulseless VT:

Shock immediately: 200 J biphasic (or equivalent monophasic)
Resume CPR immediately after shock (do not check pulse/rhythm)
Continue CPR for 2 minutes (5 cycles of 30:2)
Reassess rhythm, repeat shocks if VF/pulseless VT persists

PEA/Asystole:

Do NOT shock
Continue CPR
Administer medications (see below)

Phase 2: Medication and Advanced Airway (1-10 minutes)

5. Establish Advanced Airway [CPR ongoing]

Options:

Endotracheal intubation: Size 7.0-8.0 mm ETT
Supraglottic airway: LMA or i-gel (if intubation delayed)
Confirm placement: Capnography, auscultation, chest rise

Capnography:

ETCO₂ 35-45 mmHg: Indicates adequate CPR and potential ROSC
ETCO₂ <10 mmHg: Inadequate CPR, consider adjusting technique
Sudden rise in ETCO₂: Possible return of spontaneous circulation (ROSC)

6. Vascular Access

Options:

Peripheral IV: 2 large-bore (14-16G) if not already present
Intraosseous (IO): If IV access delayed/unavailable (proximal tibia, humerus)
Central venous access: If already present

7. Medications

For VF/pulseless VT:

Epinephrine:

1 mg IV/IO (10 mL of 1:10,000 solution)
After 2nd unsuccessful shock
Repeat every 3-5 minutes

Amiodarone:

300 mg IV after 3rd unsuccessful shock
Repeat 150 mg IV after 5th shock if VF/VT persists

For PEA/Asystole:

Epinephrine:

1 mg IV/IO immediately
Repeat every 3-5 minutes

Atropine (for asystole or bradycardia with pulse):

3 mg IV (vagolytic dose)
May be given before arrest for symptomatic bradycardia

Alternative Vasopressors:

Vasopressin 40 units IV may be considered (replaces first or second epinephrine dose)
Particularly in refractory VF/VT

8. Reversible Causes: The 4 Hs and 4 Ts

Assess and treat throughout resuscitation:

H - Hypoxia:

Check airway and breathing
Ensure 100% oxygen
Confirm ETT placement with capnography

H - Hypovolaemia:

Rapid fluid resuscitation
Check for bleeding (surgical, internal)
Consider blood transfusion if indicated

H - Hypo/Hyperkalaemia:

Hyperkalaemia: Calcium gluconate 10% 10 mL IV, insulin/dextrose, salbutamol nebuliser
Hypokalaemia: Potassium chloride infusion (after ROSC)

H - Hypothermia:

Core temperature monitoring
Active warming (forced-air blanket, warmed fluids)
Adjust CPR parameters for hypothermia

T - Tension Pneumothorax:

Immediate needle decompression (14G cannula, 2nd intercostal space, midclavicular line)
Follow with chest drain if confirmed

T - Tamponade:

Consider pericardiocentesis (if available and skilled)
Emergency thoracotomy if refractory and surgically indicated

T - Thrombosis (PE):

Consider thrombolytics (if high suspicion and no contraindications)
Surgical embolectomy if massive PE

T - Toxins:

Anaphylaxis: Epinephrine 100 μg IV bolus
LAST: Lipid emulsion 20% 1.5 mL/kg bolus
Beta-blocker overdose: Glucagon 1-5 mg IV
Calcium channel blocker overdose: Calcium gluconate 10% 10 mL IV

Phase 3: Return of Spontaneous Circulation (ROSC)

Signs of ROSC:

Palpable central pulse
Regular cardiac rhythm with ECG
ETCO₂ rise (sudden increase to >35 mmHg)
Spontaneous respirations
Increased arterial pressure

Post-ROSC Management:

Maintain airway and ventilation
100% oxygen until stable, then titrate to SpO₂ 94-98%
Invasive monitoring: Arterial line, CVC if indicated
Echocardiography: Assess ventricular function, identify reversible causes
Treat underlying cause (arrhythmia, ischaemia, etc.)
Targeted temperature management (32-36°C for 24 hours)
ICU admission for post-arrest care

Perioperative-Specific Considerations

Drug Reversal and Management

Neuromuscular Blockade Reversal:

Sugammadex (Rocuronium or Vecuronium):

2-4 mg/kg IV (single dose)
Rapid reversal within 2-3 minutes
Restores spontaneous respirations
Essential for airway management in arrest

Neostigmine + Glycopyrrolate (Other NMBA):

Neostigmine: 0.05-0.07 mg/kg IV (maximum 5 mg)
Glycopyrrolate: 0.01 mg/kg IV (maximum 0.5 mg)
Slower reversal (5-10 minutes)

Immediate reversal: Attempt early if arrest due to respiratory depression from residual blockade

Opioid Reversal:

Naloxone:

100 μg IV increments (titrated to effect)
Reverses respiratory depression and analgesia
May precipitate pain, hypertension, tachycardia
Short duration of action (20-40 minutes)

Benzodiazepine Reversal:

Flumazenil:

0.2 mg IV increments (maximum 1 mg)
Rapid reversal of sedation
May precipitate seizures, agitation

Specific Aetiologies: Perioperative Treatment

Anaphylaxis:

Modified Management:

Epinephrine: 100 μg IV bolus initially (NOT 1 mg unless in arrest)
Aggressive fluid loading: 500-1000 mL crystalloid stat, repeat as needed
Remove allergen: Stop all suspected drugs
Airway: Bronchospasm treated with salbutamol nebuliser 5 mg

Local Anaesthetic Systemic Toxicity (LAST):

Modified Management:

Lipid emulsion: 20% 1.5 mL/kg bolus, then 0.25 mL/kg/min infusion
Reduced epinephrine dose: 10-100 μg increments (NOT 1 mg)
Avoid lidocaine as antiarrhythmic
Prolonged resuscitation: Minimum 60 minutes

Tension Pneumothorax:

Immediate Management:

Needle decompression: 14G cannula, 2nd intercostal space, midclavicular line, affected side
Chest drain: Insert as soon as possible
Continue CPR throughout

Cardiac Tamponade:

Management:

Pericardiocentesis: 18G needle, subxiphoid approach, under ultrasound guidance if possible
Emergency thoracotomy: If refractory and surgical patient (left anterolateral thoracotomy)

Hypovolaemia:

Management:

Massive transfusion protocol: 1:1:1 ratio of RBC:plasma:platelets
Rapid blood administration: Blood warmer, rapid infuser
Tranexamic acid: 1 g IV loading, then 1 g infusion over 8 hours (if traumatic bleeding)

ECMO Considerations

Indications for ECMO in Perioperative Arrest:

Criteria:

Refractory cardiac arrest: No ROSC after >20-30 minutes of high-quality CPR
Reversible cause identified: Anaphylaxis, LAST, reversible cardiac condition
Patient suitable for ECMO: No contraindications
ECMO available: Access to ECMO team

Benefits:

Provides complete circulatory support
Allows recovery from reversible conditions
Maintains organ perfusion
Bridge to recovery or definitive treatment

Challenges:

Requires ECMO expertise and equipment
Not available in all centres
Requires rapid mobilization
Anticoagulation required

ANZCA Final Exam Focus

SAQ Patterns

Perioperative cardiac arrest is a core ANZCA Final Written Examination topic. Common SAQ themes include:

Management-Focused Questions:

"A patient develops cardiac arrest during laparoscopic cholecystectomy. Describe your management." (2020)
"Outline the management of PEA in the operating theatre." (2021)
"How does perioperative cardiac arrest management differ from standard ALS?"

Aetiology-Focused Questions:

"Describe the common causes of perioperative cardiac arrest."
"What are the warning signs of impending cardiac arrest in the operating theatre?"
"Explain how you would manage anaphylaxis-induced cardiac arrest."

Reversible Causes-Focused Questions:

"Describe the 4 Hs and 4 Ts in the context of perioperative arrest."
"A patient arrests with hyperkalaemia. How would you manage this?"
"How would you treat tension pneumothorax causing cardiac arrest?"

Post-Resuscitation Questions:

"Describe the management following return of spontaneous circulation."
"What is the role of targeted temperature management?"
"What investigations would you arrange post-cardiac arrest?"

Marking Scheme Priorities:

Immediate recognition and structured response (ABC)
High-quality CPR (correct rate, depth, compression fraction)
Rhythm recognition and defibrillation for shockable rhythms
Correct medication dosing (epinephrine, amiodarone)
Assessment of reversible causes (4 Hs and 4 Ts)
Perioperative-specific modifications
Post-ROSC management and targeted temperature control
Documentation and follow-up

Clinical Viva Themes

The Clinical Viva frequently includes cardiac arrest scenarios:

Scenario Types:

Intraoperative cardiac arrest
PACU/postoperative cardiac arrest
Specific aetiology scenarios (anaphylaxis, LAST, bleeding)
PEA vs shockable rhythms
Post-ROSC management

Examiner Expectations:

Systematic ABC approach
Knowledge of ALS algorithms
Understanding of rhythm-specific treatment
Ability to identify and treat reversible causes
Perioperative modifications (drug reversal, specific aetiologies)
Team leadership and communication
Post-ROSC management knowledge

Common Viva Questions:

"What are the warning signs of cardiac arrest perioperatively?"
"How would you manage VF arrest in the operating theatre?"
"What are the differences between PEA and asystole management?"
"How would you manage anaphylaxis-induced cardiac arrest?"
"What are the 4 Hs and 4 Ts?"
"When would you consider ECMO?"
"How do you manage post-ROSC patient?"

Medical Viva Considerations

The Medical Viva may include cardiac arrest within broader discussions:

ALS algorithm structure
Evidence for specific interventions
Pharmacology of resuscitation medications
Physiology of cardiac arrest and CPR
Research in cardiac arrest outcomes
Quality metrics for CPR (compression fraction, ETCO₂)

Key Points for Examination Success

ABC approach is foundational — do not deviate from structured assessment
CPR quality matters — know rate, depth, compression fraction
Rhythm recognition — shockable vs non-shockable
Epinephrine dosing — 1 mg IV, repeat q3-5 min
Reversible causes — 4 Hs and 4 Ts framework
Perioperative modifications — drug reversal, specific aetiologies
Post-ROSC management — targeted temperature, invasive monitoring
ECMO consideration — for refractory cases

Australian Guidelines and Resources

Australian Resuscitation Council (ARC) Guidelines

Guideline 9: Advanced Life Support (ALS)

Detailed ALS algorithms for cardiac arrest
Rhythm-specific management
Medication dosing and timing

Guideline 10.1: Post-Resuscitation Care

Targeted temperature management
Post-ROSC monitoring and treatment
Prognostication

ANZCA Professional Documents

PS51: Perioperative Patient Safety

Emergency response systems
Cardiac arrest management protocols
Equipment standards

PS41: Anaesthetic Machine Monitoring Standards

Mandatory capnography
Cardiovascular monitoring requirements

State-Based Resources

Each Australian state provides:

Clinical Emergency Response policies
Cardiac arrest protocols
Difficult airway and arrest trolleys
Simulation centres for training
Access to ECMO services

New Zealand Resources

New Zealand Resuscitation Council:

ALS guidelines aligned with ARC
Post-resuscitation care guidelines
DAS guideline adaptation

Indigenous Health Considerations

Aboriginal and Torres Strait Islander Perspectives

Aboriginal and Torres Strait Islander patients face unique challenges in the context of perioperative cardiac arrest that require culturally safe approaches:

Higher Prevalence of Cardiovascular Risk Factors:

Aboriginal and Torres Strait Islander peoples have significantly higher rates of conditions that increase cardiac arrest risk:

Coronary artery disease: 2-3 times higher incidence than non-Indigenous population
Heart failure: Higher prevalence and earlier onset
Hypertension: Higher prevalence and poorer control
Diabetes mellitus: 3-4 times higher incidence
Chronic kidney disease: 3-4 times higher incidence
Obesity: Higher prevalence, particularly in remote communities
Smoking: Higher smoking rates
Rheumatic heart disease: Disproportionately affected

These comorbidities may:

Increase baseline cardiovascular risk
Reduce physiological reserve
Complicate resuscitation efforts
Worsen post-arrest outcomes

Access to Emergency Care:

Remote and rural Aboriginal communities often have:

Limited emergency services: May not have on-site cardiac arrest capability
Transfer delays: RFDS or ambulance transport required
Limited specialist availability: Fewer cardiac anaesthetists, intensivists
Equipment limitations: May lack advanced airway equipment, ECMO

These factors influence:

Anaesthetic technique selection: Consider safer alternatives when possible
Facility choice: Transfer to tertiary centre for high-risk cases
Preoperative optimization: Aggressive management of comorbidities
Post-arrest care: Arrangements for ICU transfer

Communication and Understanding:

Medical terminology and cardiac arrest concepts require culturally safe explanation:

Use simple, clear language
Visual aids for explaining CPR and procedures
Involve Aboriginal Health Workers (AHWs) or Aboriginal Hospital Liaison Officers (AHLOs)
Explain concepts of brain death and withdrawal of life support clearly

Key communication points:

What cardiac arrest means
What CPR involves
Likelihood of survival and recovery
What post-arrest care involves
Prognosis and expected outcomes

Cultural Considerations in Crisis:

In cardiac arrest requiring resuscitation:

Family presence during resuscitation may be culturally important — facilitate where possible without compromising care
Decision-making may involve extended family and community members
Gender considerations: Some Aboriginal cultures have protocols about who can touch or treat patients, particularly chest compressions
Spiritual practices: May be important during crisis — accommodate where possible
If death occurs, follow appropriate cultural protocols and involve AHLO for family support

Post-Resuscitation Care:

After ROSC, cultural considerations include:

Family involvement in care: Many Aboriginal families expect to be constantly present
Decision-making about prognosis: May involve extended family and community elders
Brain death discussions: Require culturally sensitive approach, involvement of family and community
Organ donation: Cultural and religious beliefs may influence decisions
Withdrawal of care: May require extended family consensus

Documentation and Planning:

Ensure comprehensive documentation that:

Is clear and non-technical language
Includes cultural considerations and family involvement
Explains outcomes and prognosis clearly
Considers health record transfer to community health services
Includes culturally appropriate information for family

Māori Health Considerations (New Zealand)

For Māori patients, the principles of Te Tiriti o Waitangi and cultural safety apply:

Whānau (Family) Involvement:

Involve whānau in all decisions about cardiac arrest care
Extended family input in consent and treatment decisions
Explain procedures and prognosis to family members
Collective decision-making processes

Tikanga (Cultural Protocols):

Respect cultural protocols around the body and death
Tapu (sacredness) of head and chest may influence who can perform CPR
Karakia (prayer) may be requested before or after procedures
Tangihanga (funeral customs) influence post-mortem protocols
Body should not be left alone (cultural significance)

Communication:

Use Māori Health Workers to ensure cultural safety
Plain language explanations of complex medical concepts
Take time to explain, avoid rushing
Visual aids and demonstration may be more effective

Health Literacy:

Many Māori patients may have lower health literacy
Use simple, non-technical language
Demonstrate procedures when possible
Ensure understanding before proceeding

Access Issues:

Geographic isolation may limit specialist access
Consider local testing options when possible
Telehealth for specialist consultation
Transfer planning for high-risk cases

Documentation:

Ensure cardiac arrest documentation is clear and culturally appropriate
Provide clear information for whānau about outcomes and prognosis
Coordinate with primary care providers

Assessment Content

SAQ Practice Question 1 (20 marks)

Question:

A 68-year-old man (80 kg) is undergoing laparoscopic aortic aneurysm repair. During cross-clamping, the patient suddenly develops hypotension (SBP 50/30 mmHg) with no palpable femoral pulse. ECG shows asystole.

(a) What is your immediate management? (8 marks)

(b) List and briefly describe the 4 Hs and 4 Ts. (8 marks)

(c) What are your priorities after return of spontaneous circulation? (4 marks)

Model Answer:

(a) Immediate Management (8 marks)

Immediate Actions [1.5 marks]

Call for help loudly — "Cardiac arrest, help!"
Confirm arrest: Check central pulse (carotid or femoral) for ≤10 seconds
Begin CPR immediately — do not delay for confirmation
Note the time of arrest

High-Quality CPR [2.5 marks]

Compression depth: 5-6 cm
Compression rate: 100-120 per minute
Compression:ventilation ratio: 30:2 (or continuous compressions with advanced airway)
Compression fraction: ≥60% (minimize interruptions)
Full chest recoil after each compression

Airway and Breathing [1.5 marks]

100% oxygen via face mask or existing ETT
Secure airway if not already present
Confirm ETT placement with capnography
Ventilate at rate of 8-10 breaths/min (with advanced airway)

Defibrillator and Rhythm Assessment [1 mark]

Attach defibrillator pads immediately (anterior-lateral)
Analyze rhythm (minimize CPR interruption)
Do NOT interrupt CPR for >10 seconds

Rhythm-Specific Treatment [1.5 marks]

Rhythm: Asystole (non-shockable)
Do NOT shock
Epinephrine 1 mg IV immediately
Repeat epinephrine 1 mg IV every 3-5 minutes
Continue CPR

Assess Reversible Causes [1 mark]

Continually assess and treat 4 Hs and 4 Ts throughout resuscitation
In this case: Hypovolaemia (rupture), Hypothermia, etc.

(b) The 4 Hs and 4 Ts (8 marks)

4 Hs [4 marks]

1. Hypoxia (1 mark)

Inadequate oxygen delivery to tissues
Causes: Airway obstruction, ventilation failure, pulmonary pathology
Treatment: Ensure airway, 100% O₂, verify ETT placement

2. Hypovolaemia (1 mark)

Reduced intravascular volume
Causes: Bleeding (surgical, trauma), third-spacing, distributive shock
Treatment: Rapid fluid resuscitation, blood transfusion, vasopressors

3. Hypo/Hyperkalaemia (1 mark)

Hypokalaemia: Low potassium (<3.5 mmol/L)
- Treatment: Potassium chloride infusion
Hyperkalaemia: High potassium (>5.5 mmol/L)
- Treatment: Calcium gluconate, insulin/dextrose, salbutamol

4. Hypothermia (1 mark)

Core temperature <35°C
Causes: Cold environment, massive transfusion, exposure
Treatment: Active warming, warmed fluids, adjust CPR parameters

4 Ts [4 marks]

1. Tension Pneumothorax (1 mark)

Air accumulation in pleural space
Causes: Central line insertion, nerve blocks, lung disease
Treatment: Needle decompression, chest drain

2. Tamponade (1 mark)

Pericardial fluid accumulation
Causes: Surgical injury, pericardial effusion, trauma
Treatment: Pericardiocentesis, emergency thoracotomy

3. Thrombosis (Pulmonary Embolism) (1 mark)

Blood clot in pulmonary artery
Causes: DVT, fat embolism (orthopaedic), air embolism
Treatment: Consider thrombolytics, surgical embolectomy

4. Toxins (1 mark)

Drug overdose or adverse reaction
Causes: Anaphylaxis, LAST, beta-blocker overdose, hyperkalaemia
Treatment: Specific antidotes (epinephrine for anaphylaxis, lipid emulsion for LAST)

(c) Post-ROSC Priorities (4 marks)

Immediate Post-ROSC Management [1 mark]

Maintain airway and ventilation with 100% oxygen
Confirm stable cardiac rhythm on ECG
Establish invasive monitoring (arterial line, CVC)

Treat Underlying Cause [1 mark]

Identify and treat precipitating cause
In this case: Check for surgical bleeding, aortic rupture
Treat arrhythmias, ischaemia, or electrolyte abnormalities

Targeted Temperature Management [1 mark]

Cooling to 32-36°C for 24 hours
Use cooling blankets, ice packs, or intravascular cooling
Prevent fever aggressively (paracetamol, cooling measures)

ICU Admission and Monitoring [1 mark]

Mandatory ICU admission for post-arrest care
Echocardiography: Assess ventricular function, wall motion abnormalities
Neurological assessment: GCS, pupillary response
Prognostication: Consider EEG, biomarkers (NSE, S100)
Treat complications: Arrhythmias, seizures, cerebral edema

Total: 20 marks

Viva Scenario (25 marks)

Opening Stem:

You are the consultant anaesthetist supervising a registrar performing laparoscopic prostatectomy in a 75-year-old man (90 kg, 178 cm) with coronary artery disease (previous NSTEMI, stents 3 years ago) and type 2 diabetes. During dissection, the patient suddenly becomes hypotensive (BP 50/30 mmHg) and ECG shows sinus bradycardia 35 bpm progressing to asystole.

Expected Viva Progression:

Examiner: What is your immediate management?

Candidate Response: [5 marks]

"This presentation — sudden severe hypotension with asystole during surgery — indicates cardiac arrest.

My immediate actions are:

Call for help loudly — "Cardiac arrest, help!"
Confirm arrest: Check central pulse (carotid or femoral) for ≤10 seconds
Begin CPR immediately — do not delay for confirmation
Note the time of arrest

High-Quality CPR:

Compression depth: 5-6 cm
Compression rate: 100-120 per minute
Compression:ventilation ratio: 30:2 (or continuous compressions if ETT in place)
Compression fraction: ≥60% (minimize interruptions)

Airway and Breathing:

100% oxygen via existing circuit
Confirm ETT placement with capnography
Ventilate at rate of 8-10 breaths/min

Defibrillator:

Attach defibrillator pads immediately
Analyze rhythm
Minimize CPR interruption for rhythm check (<10 seconds)

Rhythm: Asystole (non-shockable) — do NOT shock. Administer epinephrine 1 mg IV immediately.

I would simultaneously be thinking about reversible causes, particularly in this patient with CAD and diabetes: hypovolaemia, hypoxia, myocardial ischaemia, hyperkalaemia."

Examiner: The surgeon suggests there is significant bleeding. How does this change your management?

Candidate Response: [4 marks]

"Significant surgical bleeding is a major concern and strongly suggests hypovolaemia as the cause of arrest.

Management modifications:

1. Aggressive Volume Resuscitation:

Rapid crystalloid infusion (Hartmann's or 0.9% saline)
Activate massive transfusion protocol immediately
Rapid blood administration using blood warmer, rapid infuser
Goal: Restore intravascular volume, coronary perfusion

2. Treat Hypovolaemia within 4 Hs and 4 Ts:

Hypovolaemia is a reversible cause — treat aggressively throughout CPR
May require >3-4 L of fluids initially
Do not compromise CPR quality for blood administration

3. Communicate with Surgical Team:

Request rapid surgical control of bleeding
Consider temporary measures (aortic cross-clamp if appropriate)
Expedite definitive surgical control

4. Consider Vasopressors:

Once some volume restored, may need vasopressor support
Norepinephrine infusion if ROSC achieved but hypotension persists
Helps maintain coronary perfusion pressure during resuscitation

5. Continue High-Quality CPR:

Hypovolaemia reduces effectiveness of CPR — need higher quality
Ensure adequate compression depth and rate
Maintain compression fraction despite ongoing interventions

6. Prepare for ECMO:

If refractory arrest after bleeding controlled, consider ECMO
Provides circulatory support while patient recovers from hypovolaemia
Contact ECMO team early if available"

Examiner: After 12 minutes of CPR, the surgeon achieves hemostasis and you administer a total of 5 L crystalloid and 4 units of blood. ECG now shows VF. What do you do?

Candidate Response: [5 marks]

"Rhythm has changed from asystole to VF — now shockable rhythm. Management changes:

Immediate Actions:

Defibrillate immediately:
- 200 J biphasic shock
- Resume CPR immediately after shock (do not check pulse/rhythm)
Continue CPR for 2 minutes (5 cycles of 30:2)
Reassess rhythm:
- If VF persists: Defibrillate again (200 J)
- After 2nd unsuccessful shock: Administer epinephrine 1 mg IV
- After 3rd unsuccessful shock: Administer amiodarone 300 mg IV
Continue rhythm cycle:
- Defibrillate → CPR 2 min → Assess rhythm → Repeat
- Administer epinephrine 1 mg IV every 3-5 minutes
- After 5th shock if VF persists: Amiodarone 150 mg IV

Reversible Causes (Reassess):

Hypovolaemia: Now treated with blood and fluids
Hypoxia: Confirm ETT placement, adequate ventilation
Hypothermia: Check temperature, active warming
Hyperkalaemia: Consider if massive transfusion (citrate, hemolysis) → calcium gluconate, insulin/dextrose
Ischaemia: Patient has CAD — VF may be secondary to myocardial ischaemia → treat ischaemia post-ROSC

ECMO Consideration:

If refractory VF after bleeding controlled and >20-30 minutes CPR
Consider ECMO for refractory arrest
Provides circulatory support while allowing myocardial recovery"

Examiner: ROSC is achieved after 22 minutes of CPR. What is your post-ROSC management?

Candidate Response: [4 marks]

"Post-ROSC management involves:

Immediate Stabilization:

Maintain airway and ventilation with 100% oxygen (titrate to SpO₂ 94-98%)
Confirm stable rhythm on ECG (sinus rhythm likely)
Establish invasive monitoring:
- Arterial line (radial or femoral)
- Central venous catheter if not already present
- Monitor blood pressure, CVP, urine output

Treat Underlying Causes:

Myocardial ischaemia: Patient has CAD and underwent major surgery
- 12-lead ECG for ST changes
- Cardiac biomarkers: Troponin
- Consider coronary angiography if indicated
- Nitrates, beta-blockers, statins as appropriate
Hypovolaemia: Continue volume resuscitation
- Haemoglobin: May need further blood transfusion
- Coagulation studies: Check for dilutional coagulopathy
- Viscoelastic testing (TEG/ROTEM) if available
- Continue blood products as indicated

Targeted Temperature Management:

Cool to 32-36°C for 24 hours
Use forced-air cooling blanket, ice packs, or intravascular cooling
Prevent fever aggressively (paracetamol 1 g IV q6h)
Monitor core temperature continuously

Diagnostic Investigations:

Echocardiography: Assess ventricular function, wall motion abnormalities
Arterial blood gas: Metabolic status (lactate, acidosis)
Chest X-ray: ETT position, pulmonary edema, pneumothorax
Renal function: Acute kidney injury from hypotension
Neurological assessment: GCS, pupillary response, seizures

ICU Admission:

Mandatory ICU admission for post-arrest care
Continuous monitoring: ECG, SpO₂, invasive pressures, ETCO₂
Treat complications: Arrhythmias, seizures, cerebral edema
Prognostication: Consider EEG, neuroimaging, biomarkers after 72 hours"

Examiner: The patient is found to have an anterior STEMI on ECG with troponin of 15 ng/mL. What is your management?

Candidate Response: [4 marks]

"This patient has post-cardiac arrest anterior STEMI — requires myocardial revascularization:

Immediate Management:

Consult cardiology urgently — involve interventional cardiology team
Antiplatelet therapy:
- Aspirin 300 mg chewed/swallowed
- Clopidogrel 600 mg loading (or ticagrelor 180 mg)
- Heparin: Unfractionated heparin 60 U/kg bolus
Anticoagulation:
- Heparin infusion if not going for immediate PCI
- Target aPTT 60-80 seconds
Anti-ischaemic therapy:
- Nitrates: Glyceryl trinitrate infusion or sublingual if BP tolerates
- Beta-blocker: Metoprolol 5-12.5 mg PO/IV if no contraindications
- Statins: High-dose atorvastatin 80 mg PO
Revascularization Strategy:

Primary PCI Preferred:
- Immediate coronary angiography within 90-120 minutes of ROSC
- Percutaneous coronary intervention (PCI) for culprit lesion
- Drug-eluting stent placement
- Door-to-balloon time <90 minutes
If PCI not available:
- Thrombolysis: Alteplase 15 mg bolus, then 0.75 mg/kg over 30 min, then 0.5 mg/kg over 60 min
- Consider facilitated PCI (thrombolysis + PCI)

Supportive Care:

Intra-aortic balloon pump (IABP) if cardiogenic shock
Vasopressor support: Norepinephrine, possibly dopamine or dobutamine
Mechanical ventilation: Lung-protective ventilation if needed
Hemodynamic monitoring: PiCCO or pulmonary artery catheter if indicated

Follow-Up:

Repeat ECG, troponin at 6-8 hours
Echocardiography (transthoracic or transesophageal)
Assess for complications: Ventricular rupture, papillary muscle rupture, VSD

Considerations:

Post-cardiac arrest patients have higher mortality and complication rates
Neurological recovery may affect decision-making
Multidisciplinary approach essential (cardiology, cardiothoracic surgery, ICU)"

Examiner: How would your management differ if the patient had refused blood products?

Candidate Response: [3 marks]

"If the patient had refused blood products (Jehovah's Witness or other reasons), management requires:

Preoperative:

Detailed discussion about risks of blood transfusion refusal
Documented refusal in medical record
Optimization: Iron therapy, EPO (erythropoietin) preoperatively to maximize Hb
Informed consent acknowledging understanding of risks

Intraoperative Cardiac Arrest:

Volume Resuscitation Alternatives:

Crystalloids: Larger volumes (5-6+ L) of Hartmann's or 0.9% saline
Colloids: Gelatin or starch solutions (if not contraindicated)
Cell salvage: Intraoperative cell salvage if available
Perfluorocarbon-based oxygen carriers (if available and patient agrees)

Management of Hypovolaemia-Induced Arrest:

Aggressive crystalloid resuscitation
Pharmacologic support:
- Vasopressors: Norepinephrine, vasopressin
- Inotropes: Dobutamine, milrinone
- Maintain coronary perfusion pressure despite lower Hb
Reduce metabolic demand: Maintain hypothermia (32-34°C), sedation, paralysis
ECMO consideration:
- Veno-arterial ECMO provides circulatory support without blood products
- Can maintain oxygenation despite severe anaemia
- Bridge to recovery or resolution

Post-ROSC:

Hemodynamic optimization with vasopressors
Minimize blood loss: Surgical hemostasis, anti-fibrinolytics
Erythropoietin therapy to stimulate red cell production
Accept lower Hb (Hb 70-80 g/L) if hemodynamically stable
Iron supplementation (IV iron sucrose or ferric carboxymaltose)
Close monitoring for end-organ hypoxia (lactate, ScvO₂)

Ethical Considerations:

Respect patient autonomy while ensuring informed decision-making
Document discussions thoroughly
Clear communication about risks and outcomes
Multidisciplinary approach with ethics committee if needed"

Total: 25 marks

Perioperative Cardiac Arrest

Clinical board

Urgent signals

Exam focus

Editorial and exam context

Quick Answer

Pathophysiology

Aetiology of Perioperative Cardiac Arrest

Mechanisms of Cardiac Arrest by Aetiology

Clinical Presentation

Recognition of Cardiac Arrest

Management

Immediate Management: Advanced Life Support (ALS)

Perioperative-Specific Considerations

Drug Reversal and Management

Specific Aetiologies: Perioperative Treatment

ECMO Considerations

ANZCA Final Exam Focus

SAQ Patterns

Clinical Viva Themes

Medical Viva Considerations

Key Points for Examination Success

Australian Guidelines and Resources

Australian Resuscitation Council (ARC) Guidelines

ANZCA Professional Documents

State-Based Resources

New Zealand Resources

Indigenous Health Considerations

Aboriginal and Torres Strait Islander Perspectives

Māori Health Considerations (New Zealand)

Assessment Content

SAQ Practice Question 1 (20 marks)

Viva Scenario (25 marks)