What is the difference between VF and pulseless VT?

VF shows chaotic, irregular waveforms with no identifiable QRS complexes. Pulseless VT shows organised, regular wide-complex rhythm at rate greater than 150 bpm but with no palpable pulse

When should adrenaline be given in shockable rhythms?

According to ARC/ANZCOR Guideline 11, adrenaline 1mg IV should be given after the 3rd shock, then every 3-5 minutes

What is the biphasic defibrillation energy for VF/pVT?

150-200J for biphasic defibrillators (manufacturer-specific) or 360J for monophasic defibrillators

What is double sequential defibrillation?

The near-simultaneous delivery of two defibrillation shocks using two separate defibrillators, sometimes used for refractory VF. Evidence is limited but may be considered after standard measures fail

Shockable Rhythms - Ventricular Fibrillation and Pulseless Ventricular Tachycardia

Quick Answer

Critical: VF and pulseless VT are shockable rhythms requiring immediate defibrillation. Every minute of delay reduces survival by 7-10%. Survival is 2-3 times higher than non-shockable rhythms when defibrillation is delivered early.

Ventricular fibrillation (VF) and pulseless ventricular tachycardia (pVT) represent the most treatable causes of cardiac arrest. VF is characterised by chaotic electrical activity with no organised cardiac output, appearing as irregular, chaotic waveforms without identifiable QRS complexes. Pulseless VT shows organised wide-complex tachycardia (greater than 150 bpm) but without effective cardiac contraction. Management follows ARC/ANZCOR Guideline 11: immediate defibrillation (biphasic 150-200J), continuous high-quality CPR, adrenaline 1mg after the 3rd shock, and amiodarone 300mg after the 3rd shock. Refractory VF may require double sequential defibrillation, alternative pad positioning, or ECMO consideration.

ACEM Exam Focus

Primary Exam Relevance

Physiology (High Yield)

Cardiac action potential: Phase 0-4, ionic currents (Na+, K+, Ca2+)
Re-entry mechanism: Requirements (unidirectional block, slow conduction, recovery of excitability)
Automaticity: Enhanced vs triggered activity
Defibrillation physiology: Critical mass theory, upper limit of vulnerability
Myocardial oxygen consumption: Determinants during VF vs CPR

Pharmacology (High Yield)

Adrenaline: Alpha-1 effects on coronary perfusion pressure, beta effects, timing rationale
Amiodarone: Class III antiarrhythmic, mechanism in VF, adverse effects
Lignocaine: Historical use, when to consider as alternative
Magnesium: Role in hypomagnesaemia and torsades de pointes

Anatomy (Medium Yield)

Cardiac conduction system: SA node, AV node, bundle branches, Purkinje fibres
Coronary anatomy: LAD territory and VF risk
Chest wall anatomy: Optimal pad placement, transthoracic impedance

Fellowship Exam Relevance

Written Exam

Algorithm knowledge with ARC-specific timing
Drug doses, routes, and timing
Reversible causes identification
Refractory VF management options
Post-resuscitation care priorities

OSCE

Resuscitation station: High-probability scenario - VF arrest leadership
Key competencies: Team leadership, closed-loop communication, ARC algorithm adherence
Discrimination points: Correct shock energy, drug timing, pad placement

Key Domains Tested

Medical Expert: Algorithm knowledge, pharmacology
Leader: Team coordination, decision-making under pressure
Communicator: Closed-loop communication, debriefing

Key Points

Clinical Pearl

The 10 things you MUST know:

Recognition: VF = chaotic, irregular, no QRS; pVT = broad complex, regular, rate greater than 150 bpm
Immediate action: Defibrillation is the definitive treatment - do not delay
Energy: Biphasic 150-200J (manufacturer-specific), monophasic 360J
CPR timing: Immediately resume CPR after shock, minimise interruptions to under 10 seconds
Adrenaline timing (ARC): After the 3rd shock, then every 3-5 minutes
Amiodarone: 300mg after 3rd shock, 150mg after 5th shock
Rhythm check: Every 2 minutes during CPR cycle
Fine VF: Check two leads, increase gain - may mimic asystole
Reversible causes: Always consider 4Hs and 4Ts
Refractory VF: Consider pad position change, double sequential defibrillation, ECMO

Red Flag

Fine VF misinterpreted as asystole → Missed shockable rhythm
Delayed defibrillation for IV access → Every minute counts
Wrong AHA timing → ARC gives adrenaline after 3rd shock, not 2nd
Prolonged rhythm checks → Interrupt CPR for under 10 seconds only
Hyperventilation → Decreases venous return and coronary perfusion

Epidemiology

Incidence and Prevalence

Metric	Value	Source
VF/pVT as initial rhythm (OHCA)	20-25%	[1]
VF/pVT as initial rhythm (IHCA)	15-20%	[2]
OHCA incidence (Australia)	55-113 per 100,000/year	[3]
Survival to discharge (shockable)	25-30%	[4]
Survival to discharge (non-shockable)	8-10%	[5]
Favourable neurological outcome (shockable)	20-25%	[6]
Witnessed VF with bystander CPR + AED	50-70% survival	[7]

Temporal Trends

Period	Finding	Implication
1990s-2000s	Declining proportion of VF as initial rhythm	More PEA arrests, earlier bystander intervention
2000s-2020s	Increasing survival from VF arrests	PAD programs, CPR training
2020-present	COVID-19 impact on OHCA outcomes	Delayed response, PPE requirements

Australian/NZ Specific Data

Metric	Australia	New Zealand
Bystander CPR rate	40-60%	50-65%
Public AED use	5-10% of OHCA	8-12%
EMS response time (urban)	8-12 min	8-10 min
EMS response time (rural)	15-30+ min	15-25+ min

Risk Factors for VF Arrest

Category	Specific Risk Factors
Cardiac	Ischaemic heart disease, prior MI, cardiomyopathy, heart failure, LV hypertrophy
Electrolyte	Hypokalaemia, hyperkalaemia, hypomagnesaemia, hypocalcaemia
Drugs/Toxins	Digoxin, tricyclic antidepressants, cocaine, amphetamines, organophosphates
Congenital	Long QT syndrome, Brugada syndrome, catecholaminergic polymorphic VT, ARVC
Other	Electrocution, drowning (secondary), hypothermia, commotio cordis

Pathophysiology

Mechanisms of Ventricular Arrhythmias

Three primary mechanisms underlie VF and VT:

1. Re-entry (Most Common - 90% of VF)

Definition: Continuous circular propagation of electrical impulse around a fixed or functional obstacle.

Requirements for Re-entry (All Must Be Present):

Unidirectional block: Impulse blocked in one direction but not the other
Slow conduction pathway: Alternative route with delayed conduction
Recovery of excitability: Previously blocked tissue recovers in time for next impulse

Anatomical Re-entry:

Fixed anatomical circuit (e.g., scar from prior MI)
Pathway around non-conducting tissue
Stable circuit = monomorphic VT

Functional Re-entry:

No fixed anatomical obstacle
Created by varying refractory periods in adjacent tissue
Multiple wavelet re-entry = VF

Clinical Correlates:

Substrate	Mechanism	Rhythm
Post-MI scar	Border zone re-entry	Monomorphic VT
Acute ischaemia	Functional re-entry	VF
Dilated cardiomyopathy	Scar-mediated	VT → VF

2. Automaticity

Definition: Spontaneous depolarisation of myocardial cells that normally lack pacemaker activity.

Enhanced Normal Automaticity:

Increased slope of phase 4 depolarisation
Causes: Catecholamines, ischaemia, electrolyte disturbance

Abnormal Automaticity:

Cells depolarise from abnormally low resting membrane potential
Causes: Ischaemia, digoxin toxicity, hypokalaemia

Clinical Correlates:

Idiopathic VT from RVOT or LVOT
Accelerated idioventricular rhythm
Digoxin-induced ventricular ectopy

3. Triggered Activity

Definition: Abnormal depolarisations that depend on a preceding action potential.

Early Afterdepolarisations (EADs):

Occur during phase 2 or 3 of action potential
Prolonged repolarisation required
Causes: Long QT syndrome, hypokalaemia, hypomagnesaemia, drugs
Result: Torsades de pointes → VF

Delayed Afterdepolarisations (DADs):

Occur after complete repolarisation (phase 4)
Calcium overload in cell
Causes: Digoxin toxicity, catecholamine excess, ischaemia
Result: VT

Why VF Causes Cardiac Arrest

Electrophysiology:

Multiple simultaneous re-entrant wavefronts (4-12 at any time)
No coordinated ventricular depolarisation
No organised ventricular contraction
Cardiac output = zero

Haemodynamic Consequences:

Time	Effect
0-10 sec	Loss of consciousness (cerebral hypoxia)
10-60 sec	Myocardial ATP depletion begins
1-4 min	Reversible cellular injury, coarse VF → fine VF
4-10 min	Irreversible neuronal injury begins
over 10 min	Multi-organ ischaemia, fine VF → asystole

VF Waveform Characteristics

Feature	Coarse VF	Fine VF
Amplitude	Above 0.5 mV	Below 0.5 mV
Frequency	Higher	Lower
Energy state	Better myocardial energy stores	Depleted energy stores
Defibrillation success	Higher	Lower
Duration of arrest	Earlier	Later

Clinical Implication: Coarse VF is more responsive to defibrillation. Fine VF may benefit from CPR before shock to restore myocardial energy stores (though immediate defibrillation remains standard of care).

Defibrillation Physiology

How Defibrillation Works:

Critical Mass Theory: Defibrillation must depolarise a "critical mass" (≥75%) of myocardium simultaneously to terminate VF
Upper Limit of Vulnerability: Successful defibrillation requires energy above the defibrillation threshold but below the upper limit that could re-induce VF
Mechanism:
- Simultaneously depolarises all excitable myocardium
- Terminates all re-entrant circuits
- Allows normal pacemaker (SA node) to resume control
- Creates a "fresh start" for coordinated rhythm

Factors Affecting Defibrillation Success:

Factor	Effect	Optimisation
Transthoracic impedance	Higher = less current delivery	Shave chest hair, good electrode contact
Electrode position	Affects current pathway	AP positioning for refractory VF
Energy level	Too low = failure, too high = myocardial damage	Manufacturer recommendations
VF duration	Longer = worse success	Minimise pre-shock pause
CPR quality	Better coronary perfusion = better success	High-quality compressions
Myocardial metabolic state	Acidosis, hypoxia reduce success	CPR before shock if prolonged arrest

Rhythm Recognition

Ventricular Fibrillation (VF)

Clinical Pearl

ECG Characteristics of VF:

Rate: Cannot be determined (no organised rhythm)
Rhythm: Chaotic, completely irregular
P waves: None identifiable
QRS: No identifiable QRS complexes
Appearance: Irregular, chaotic waveforms of varying amplitude and frequency
Baseline: Undulating, no isoelectric line

VF Subtypes

Type	Amplitude	Frequency	Appearance	Prognosis
Coarse VF	Above 0.5 mV	Above 150/min	Large, chaotic waves	Better shock response
Fine VF	Below 0.5 mV	Below 150/min	Small, low-amplitude	Worse, may mimic asystole

Key Recognition Points

Feature	Description
Chaos	No regular pattern, completely disorganised
No QRS	Cannot identify discrete QRS complexes
Variable amplitude	Waveform height varies throughout
No isoelectric baseline	Continuous undulating pattern

Red Flag

Fine VF may be misdiagnosed as asystole!

Check two perpendicular leads (fine VF may be isoelectric in one lead)
Increase monitor gain
Check electrode connections
If in doubt, treat as asystole (do NOT shock flat line)
CPR may convert fine VF to coarse VF

Pulseless Ventricular Tachycardia (pVT)

Clinical Pearl

ECG Characteristics of pVT:

Rate: over 150 bpm (typically 150-250 bpm)
Rhythm: Regular (or nearly regular)
P waves: Usually not visible (AV dissociation may be present)
QRS: Wide greater than 120 ms (usually over 140 ms)
Axis: Often extreme axis deviation
Morphology: Consistent beat-to-beat (monomorphic) or varying (polymorphic)

Monomorphic vs Polymorphic VT

Feature	Monomorphic VT	Polymorphic VT
QRS morphology	Same beat-to-beat	Varies beat-to-beat
QRS axis	Constant	Rotates
Common causes	Scar-related, structural heart disease	Ischaemia, long QT, electrolytes
Specific type	-	Torsades de pointes (twisting)
Management	Standard ALS + antiarrhythmics	Defibrillation + treat cause (Mg for torsades)

VT vs SVT with Aberrancy

Feature	Favours VT	Favours SVT with Aberrancy
AV dissociation	Yes	No
Fusion/capture beats	Yes	No
QRS width	Above 140 ms	Usually below 140 ms
Extreme axis deviation	Yes	No
Positive/negative concordance (V1-V6)	Yes	No
History of heart disease	Yes	Less likely
Brugada criteria	Positive	Negative

Clinical Rule: In cardiac arrest with wide-complex tachycardia, TREAT AS VT. Do not waste time differentiating.

ECG Artefacts That Mimic VF

Artefact	Cause	Differentiation
Motion artefact	Patient movement, tremor	Check patient, regular pattern
Electrical interference	50 Hz (Australia)	Very regular frequency
Loose electrodes	Poor contact	Variable baseline, check leads
CPR artefact	Compressions	Correlates with compression rate

Management Algorithm

ARC/ANZCOR Guideline 11: Shockable Rhythm Pathway

┌─────────────────────────────────────────────────────────────────────┐
│                     CARDIAC ARREST CONFIRMED                         │
│            (Unresponsive, not breathing, no pulse)                  │
└─────────────────────────────────────────────────────────────────────┘
                                  │
                                  ▼
┌─────────────────────────────────────────────────────────────────────┐
│                        CALL FOR HELP                                 │
│              Activate resuscitation team / Call 000                  │
│                     Request defibrillator                            │
└─────────────────────────────────────────────────────────────────────┘
                                  │
                                  ▼
┌─────────────────────────────────────────────────────────────────────┐
│                   START HIGH-QUALITY CPR                             │
│         30:2 ratio | Rate 100-120/min | Depth 5-6 cm                │
│              Minimise interruptions throughout                       │
└─────────────────────────────────────────────────────────────────────┘
                                  │
                                  ▼
┌─────────────────────────────────────────────────────────────────────┐
│                      ATTACH DEFIBRILLATOR                            │
│                       ANALYSE RHYTHM                                 │
│                         ┌────────┐                                   │
│                         │VF/pVT? │                                   │
│                         └───┬────┘                                   │
│                    YES ◄────┴────► NO                                │
│                     │              │                                 │
│                     ▼              ▼                                 │
│              SHOCKABLE       NON-SHOCKABLE                          │
│             (This pathway)    (See PEA/Asystole)                    │
└─────────────────────────────────────────────────────────────────────┘
                                  │
         ┌────────────────────────┘ (SHOCKABLE)
         │
         ▼
┌─────────────────────────────────────────────────────────────────────┐
│                          SHOCK 1                                     │
│         Biphasic: 150-200J (manufacturer specific)                  │
│                   Monophasic: 360J                                   │
│              ⚠️ Clear - Shock - Immediate CPR                       │
└─────────────────────────────────────────────────────────────────────┘
                                  │
                                  ▼
┌─────────────────────────────────────────────────────────────────────┐
│                   CPR FOR 2 MINUTES                                  │
│                • Establish IV/IO access                              │
│                • Consider airway management                          │
│                • Consider reversible causes                          │
└─────────────────────────────────────────────────────────────────────┘
                                  │
                                  ▼
┌─────────────────────────────────────────────────────────────────────┐
│              RHYTHM CHECK (minimise pause below 10 sec)                   │
│                      Still VF/pVT?                                   │
│                    YES │        │ NO                                 │
└─────────────────────────┼────────┼──────────────────────────────────┘
                          │        │
                          ▼        ▼
                    SHOCK 2    Check pulse/
                          │    assess rhythm
                          ▼
┌─────────────────────────────────────────────────────────────────────┐
│                   CPR FOR 2 MINUTES                                  │
│                   (Continue access, airway)                          │
└─────────────────────────────────────────────────────────────────────┘
                                  │
                                  ▼
┌─────────────────────────────────────────────────────────────────────┐
│              RHYTHM CHECK - Still VF/pVT?                            │
│                    YES │        │ NO                                 │
└─────────────────────────┼────────┼──────────────────────────────────┘
                          │        │
                          ▼        ▼
                    SHOCK 3    Check pulse
                          │
                          ▼
┌─────────────────────────────────────────────────────────────────────┐
│                   ⚡ AFTER 3RD SHOCK ⚡                               │
│                                                                      │
│              💉 ADRENALINE 1mg IV/IO                                 │
│              💊 AMIODARONE 300mg IV/IO                               │
│                                                                      │
│                   Then resume CPR 2 min                              │
└─────────────────────────────────────────────────────────────────────┘
                                  │
                                  ▼
┌─────────────────────────────────────────────────────────────────────┐
│                      CONTINUE CYCLE                                  │
│                                                                      │
│   • Shock every 2 min if persistent VF/pVT                          │
│   • Adrenaline 1mg every 3-5 minutes                                │
│   • Amiodarone 150mg after 5th shock                                │
│   • Consider reversible causes throughout                           │
│   • Consider advanced airway if not interrupting CPR                │
└─────────────────────────────────────────────────────────────────────┘
                                  │
                                  ▼
┌─────────────────────────────────────────────────────────────────────┐
│                  IF PERSISTENT VF (REFRACTORY)                       │
│                                                                      │
│   Consider:                                                          │
│   • Change pad position (anterior-posterior)                        │
│   • Double sequential defibrillation                                │
│   • Check and treat reversible causes aggressively                  │
│   • ECMO (if available and appropriate)                             │
│   • Alternative antiarrhythmics                                     │
└─────────────────────────────────────────────────────────────────────┘
                                  │
                                  ▼
┌─────────────────────────────────────────────────────────────────────┐
│                         IF ROSC                                      │
│                                                                      │
│   • Optimise oxygenation (SpO2 94-98%)                              │
│   • Maintain normocapnia (PaCO2 35-45 mmHg)                         │
│   • 12-lead ECG - STEMI = emergent PCI                              │
│   • Haemodynamic support (MAP greater than 65-70 mmHg)                          │
│   • TTM consideration                                               │
│   • ICU admission                                                   │
└─────────────────────────────────────────────────────────────────────┘

Key ARC/ANZCOR Timing Points

Action	ARC/ANZCOR Timing	AHA Timing	Difference
Adrenaline (shockable)	After 3rd shock	After 2nd shock	ARC delays by 1 cycle
Amiodarone	After 3rd shock	After 3rd shock	Same
Subsequent adrenaline	Every 3-5 min	Every 3-5 min	Same
Amiodarone 2nd dose	After 5th shock	After 5th shock	Same

Airway Management During Arrest

Priority	Action	Notes
1	BVM ventilation	Do not interrupt CPR for intubation
2	Supraglottic airway	LMA/i-gel if BVM inadequate
3	Endotracheal intubation	Only by experienced provider, under 10 sec interruption
4	Continuous compressions	Once advanced airway placed, ventilate 10/min

Defibrillation

Energy Selection

Device Type	First Shock	Subsequent Shocks	Notes
Biphasic truncated exponential	150-200J	Same or escalating	Follow manufacturer guidance
Biphasic rectilinear	120-200J	Same or escalating	ZOLL typically 120J
Monophasic	360J	360J	No escalation

Defibrillator Pad Placement

Standard Anterolateral Position

Pad	Location
Sternal (Right)	Right of sternum, below clavicle
Apical (Left)	Left mid-axillary line, V6 electrode level

Alternative Positions

Position	Indication	Placement
Anterior-Posterior	Refractory VF, obese patients, pacemaker	Anterior: Left precordium / Posterior: Left infrascapular
Biaxillary	Alternative for refractory VF	Both mid-axillary lines

Clinical Pearl

Pad Placement Tips:

Avoid placing directly over pacemaker/ICD (minimum 8 cm distance)
Avoid placing over medication patches (remove first)
Shave excessive chest hair if time permits and causes poor contact
Use anterior-posterior position for refractory VF or very obese patients
Ensure good electrode contact - check for gaps/air

Defibrillation Technique

Step	Action	Rationale
1	Charge during CPR	Minimise pre-shock pause
2	Clear command	"Stand clear, I'm going to shock"
3	Visual check	Ensure all hands off patient
4	Deliver shock	Press shock button firmly
5	Immediate CPR	Resume without rhythm check

Minimising Peri-Shock Pause

Component	Target	How to Achieve
Pre-shock pause	Under 5 seconds	Charge during CPR, hands-off only at shock
Post-shock pause	0 seconds	Immediate CPR without rhythm check
Total peri-shock pause	Under 10 seconds	Practice, choreography

Biphasic vs Monophasic Defibrillation

Parameter	Biphasic	Monophasic
Current direction	Reverses mid-shock	One direction
Energy required	Lower (150-200J)	Higher (360J)
First shock success	90%+	70-80%
Myocardial injury	Less	More
Availability	Current standard	Older devices

Double Sequential Defibrillation (DSD)

Definition: Near-simultaneous delivery of two defibrillation shocks using two separate defibrillators.

Indication: Refractory VF (failing standard defibrillation after multiple shocks)

Technique:

Apply two sets of pads (anterior-posterior and anterolateral)
Charge both defibrillators simultaneously
Deliver shocks sequentially (within 1 second of each other)

Evidence: Limited evidence (case series, observational studies). ILCOR does not recommend routine use but notes it may be considered in refractory VF when standard measures fail. [8,9]

Important Note: DSD Considerations:

Not standard of care - consider after multiple failed standard shocks
Requires two defibrillators and two sets of pads
Theoretical risk of increased myocardial injury
May be bridge to ECMO
Document use and rationale clearly

Paediatric Defibrillation

Age Group	Energy	Notes
Infant (under 1 year)	4 J/kg	Use paediatric pads/AED pads
Child (1-8 years)	4 J/kg	Paediatric pads if available
Over 8 years or over 25 kg	Adult energy	Adult pads acceptable

Medications

Adrenaline (Epinephrine)

Parameter	Adult	Paediatric
Dose	1 mg	10 mcg/kg (0.01 mg/kg)
Concentration	1:10,000 (0.1 mg/mL) or 1:1,000 (1 mg/mL)	1:10,000
Route	IV or IO	IV or IO
Timing (shockable)	After 3rd shock	After 3rd shock
Timing (non-shockable)	Immediately	Immediately
Repeat interval	Every 3-5 minutes	Every 3-5 minutes
Maximum single dose	1 mg	1 mg

Mechanism of Action:

Alpha-1: Vasoconstriction → increased coronary and cerebral perfusion pressure
Beta-1: Increased myocardial contractility (post-ROSC)
Beta-2: Bronchodilation (minimal effect during arrest)

Clinical Pearl

ARC vs AHA Adrenaline Timing:

ARC (Australia): Adrenaline after 3rd shock for shockable rhythms
AHA (USA): Adrenaline after 2nd shock for shockable rhythms
Rationale: ARC prioritises early defibrillation without drug delays

Amiodarone

Parameter	Adult	Paediatric
First dose	300 mg IV/IO	5 mg/kg
Second dose	150 mg IV/IO	5 mg/kg
Timing (1st)	After 3rd shock	After 3rd shock
Timing (2nd)	After 5th shock	After 5th shock
Route	IV or IO (can be given undiluted)	IV or IO
Maximum total	450 mg (arrest)	15 mg/kg

Mechanism: Class III antiarrhythmic - blocks potassium channels, prolongs action potential duration, increases refractory period

Evidence: ALPS trial showed amiodarone and lignocaine both improved survival to hospital admission vs placebo in OHCA, but no difference in survival to discharge or neurological outcomes. [10]

Lignocaine (Alternative)

Parameter	Adult
Dose	1-1.5 mg/kg IV/IO
Repeat	0.5-0.75 mg/kg every 5-10 min
Maximum	3 mg/kg
Indication	Alternative if amiodarone unavailable

Magnesium

Parameter	Adult	Paediatric
Dose	2 g (8 mmol) IV	25-50 mg/kg (0.1-0.2 mmol/kg)
Indication	Torsades de pointes, hypomagnesaemia	Same
Route	IV over 1-2 min	IV over 2-5 min
Maximum	2 g	2 g

Other Medications

Drug	Dose	Indication	Notes
Calcium chloride 10%	10 mL (6.8 mmol Ca2+)	Hyperkalaemia, Ca-blocker OD, hypocalcaemia	Slow IV push
Calcium gluconate 10%	30 mL (6.8 mmol Ca2+)	Same as above	Preferred via peripheral IV
Sodium bicarbonate	1 mmol/kg (50-100 mL 8.4%)	Severe acidosis (pH below 7.1), hyperkalaemia, TCA OD	Not routine
Atropine	NOT recommended	-	No longer used in cardiac arrest
Thrombolytics	tPA 50 mg	Suspected PE causing arrest	Consider empirical if high suspicion

Medication Delivery

Route	Access Time	Notes
Peripheral IV	If already in place	First choice if accessible
Intraosseous	Under 60 seconds	Preferred if no IV, tibial or humeral
Central line	Minutes	Only if other routes fail
ETT	-	NOT recommended (unreliable absorption)

Reversible Causes (4Hs and 4Ts)

The 4 Hs

Cause	Recognition	Treatment	VF/pVT Specific
Hypoxia	History, cyanosis, pulse oximetry	Secure airway, oxygenation	Less common cause of shockable rhythm
Hypovolaemia	Trauma, bleeding, dehydration history	IV fluids, blood products, surgery	Rarely causes VF (usually PEA)
Hypo/Hyperkalaemia	ECG changes, renal history, dialysis patient	Calcium, insulin/dextrose, dialysis	Hyperkalaemia can cause VF
Hypothermia	Core temperature below 30°C, exposure history	Rewarming, continue CPR until warm	VF refractory until rewarmed

The 4 Ts

Cause	Recognition	Treatment	VF/pVT Specific
Tension pneumothorax	Absent BS, tracheal deviation, trauma	Finger/needle thoracostomy	Rarely primary cause of VF
Tamponade	Muffled HS, raised JVP, PEA pattern	Pericardiocentesis, thoracotomy	Usually causes PEA
Toxins	History, toxidrome, medication list	Specific antidotes	Digoxin, TCAs, organophosphates, cocaine
Thrombosis	History, ECG changes, risk factors	Thrombolysis, PCI, ECMO	MOST COMMON reversible cause of VF

Toxins Causing VF/pVT

Toxin	Mechanism	Specific Treatment
Digoxin	Increased automaticity, DADs	Digoxin-specific Fab antibodies
Tricyclic antidepressants	Na channel block, prolonged QT	Sodium bicarbonate, lipid emulsion
Cocaine	Catecholamine excess, Na channel block	Benzodiazepines, avoid beta-blockers
Amphetamines	Catecholamine excess	Benzodiazepines, cooling
Organophosphates	Cholinergic excess, hypoxia	Atropine (high dose), pralidoxime
Local anaesthetics	Na channel block	Lipid emulsion 20%
Potassium (overdose)	Membrane potential alteration	Calcium, insulin/dextrose

Electrolyte Derangements and ECG Changes

Electrolyte	ECG Finding	Risk of VF
Hypokalaemia	U waves, T wave flattening, prolonged QT	High (via torsades)
Hyperkalaemia	Peaked T waves → widened QRS → sine wave → VF	Very high
Hypomagnesaemia	Prolonged QT, torsades de pointes	High
Hypocalcaemia	Prolonged QT	Moderate

Special Circumstances

Witnessed VF Arrest with AED

Confirm cardiac arrest
Send for help and request AED
Start CPR immediately
Apply AED as soon as available
Follow AED prompts
Shock if advised
Resume CPR immediately after shock
Continue until EMS arrives or patient recovers

Cardiac Catheterisation Lab Arrest

Immediate defibrillation (pads should already be on)
Continue PCI if technically feasible
Mechanical CPR allows ongoing angiography
Consider ECMO if refractory

Post-Cardiac Surgery Arrest

Consider emergency resternotomy (within 10 days of surgery)
Internal defibrillation (10-20J)
May need internal cardiac massage
Early consideration of tamponade, haemorrhage

Pregnancy

Modification	Rationale
Left lateral tilt (15-30°) or manual uterine displacement	Relieve aortocaval compression
Higher hand position for compressions	Elevated diaphragm
Perimortem caesarean by 5 minutes	Improve maternal resuscitation
Consider magnesium toxicity	If receiving MgSO4 for pre-eclampsia

Implantable Cardioverter-Defibrillator (ICD)

ICDs may deliver shocks during VF
If ICD fails to terminate VF, external defibrillation required
Place pads ≥8 cm from ICD generator
Avoid AP positioning if posterior generator
Magnet application inhibits ICD therapies (if malfunctioning)

Hypothermic Arrest

Temperature	Management
Above 30°C	Standard ALS with rewarming
28-30°C	May attempt 3 shocks, then defer further shocks until warmer
Below 28°C	CPR, single shock attempt, defer medications, continue to rewarm
Rewarming	ECMO preferred if available; otherwise aggressive active rewarming

Post-Resuscitation Care

Immediate Post-ROSC Management

Domain	Target	Intervention
Airway	Secure, verified position	Confirm ETT with waveform capnography
Breathing	SpO2 94-98%, normocapnia	Titrate FiO2, avoid hyperventilation
Circulation	MAP above 65-70 mmHg, HR below 100	Vasopressors (noradrenaline), fluids
Disability	Avoid hyperthermia	Active fever prevention
Exposure	12-lead ECG	STEMI = emergent angiography

Oxygenation Post-ROSC

Parameter	Target	Evidence
SpO2	94-98%	Hyperoxia associated with worse outcomes [11]
PaO2	Above 60 mmHg, below 300 mmHg	Titrate FiO2 to avoid extremes
PaCO2	35-45 mmHg (4.7-6.0 kPa)	Hypo/hypercapnia both harmful [12]

Haemodynamic Targets

Parameter	Target	Notes
MAP	Above 65-70 mmHg	May need higher in chronic hypertensives
Heart rate	Below 100 bpm	Beta-blocker if persistent tachycardia
Lactate	Trending down	Serial measurements
Urine output	Above 0.5 mL/kg/hr	Marker of perfusion

Coronary Angiography

Finding	Timing	Recommendation
ST-elevation	Immediate	Emergent PCI within 2 hours
No ST-elevation	Early (within 24h)	Consider angiography in comatose survivors
Non-cardiac cause	As indicated	Treat underlying cause

Targeted Temperature Management (TTM)

Parameter	Recommendation	Evidence
Target temperature	32-36°C	TTM2 trial showed no difference between 33°C and normothermia [13]
Duration	At least 24 hours	Minimum duration
Avoid fever	For 72 hours post-arrest	Fever associated with worse outcomes
Rewarming rate	0.25-0.5°C per hour	Slow rewarming

Prognostication

Important Note: Multimodal prognostication at ≥72 hours after normothermia:

Clinical examination (pupillary reflexes, corneal reflexes, motor response)
EEG (unreactive background, status epilepticus)
SSEP (bilateral absent N20)
CT/MRI (diffuse anoxic injury)
Biomarkers (NSE above 60 µg/L at 48-72h)

No single test is 100% specific - use multimodal approach

Indigenous Health Considerations

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

Epidemiology:

Higher rates of cardiovascular disease at younger ages (10-20 years earlier)
Increased prevalence of risk factors: diabetes, hypertension, smoking, obesity
Higher OHCA incidence in Indigenous communities
Reduced access to timely emergency care in remote areas

Cultural Safety:

Involve family in resuscitation decisions when possible
Aboriginal liaison officers for family support
Respect for cultural practices around death and dying
"Sorry business" may affect family engagement
Gender considerations for some procedures

Systemic Barriers:

Remote community access to defibrillators and CPR-trained personnel
Delayed EMS response times in remote areas
Limited access to cardiac catheterisation and ECMO services
Retrieval challenges (RFDS, helicopter availability)

Opportunities:

Community CPR and AED training programs
Telehealth-supported resuscitation
First responder programs in remote communities
Closing the Gap initiatives for cardiovascular health

New Zealand Specific (Māori):

Te Whare Tapa Whā model of health
Whānau (family) involvement in decisions
Cultural liaison and interpreter services
Recognition of health inequities

Remote and Rural Considerations

Pre-Hospital Challenges

Challenge	Impact	Mitigation
Prolonged response times	Worse outcomes for shockable rhythms	Public AED programs, community CPR training
Limited resources	No ECMO, delayed PCI	Thrombolysis protocols, retrieval coordination
Single provider response	Fatigue, limited skills	Mechanical CPR devices, telemedicine
Transport distances	Prolonged resuscitation	Mechanical CPR, early retrieval activation

RFDS/Retrieval Considerations

Activate retrieval early if ROSC anticipated
Mechanical CPR allows safer transport
Pre-notify receiving facility
Helicopter vs fixed-wing decision based on distance and weather
Telemedicine support available 24/7

Resource-Limited Resuscitation

Scenario	Adaptation
No defibrillator	Precordial thump (very limited evidence), await AED
No IV access	IO access, continue CPR
Single rescuer	Call for help, CPR, AED when available
No advanced airway	BVM adequate, supraglottic airway

Pitfalls and Pearls

Clinical Pearl

Clinical Pearls - VF/pVT:

EtCO2 monitoring: Value below 10 mmHg suggests poor CPR quality or poor prognosis; sudden rise may indicate ROSC before pulse return
Rhythm check timing: Limit to under 10 seconds; charge defibrillator during compressions to minimise pre-shock pause
Fine VF: Always check two leads before calling asystole; increase gain settings
Coarse → Fine VF transition: Indicates prolonged arrest, depleted energy stores, worse prognosis
Pad position change: Consider anterior-posterior positioning for refractory VF - changes current vector
Mechanical CPR: Allows transport, angiography, and consistent quality during prolonged resuscitation
Magnesium: Give early if torsades de pointes or suspected hypomagnesaemia (often co-exists with hypokalaemia)
Post-shock rhythm: Don't check immediately - resume CPR and check at 2 minutes
Recurrent VF: If VF recurs after ROSC, underlying cause not treated; consider ischaemia, electrolytes, drugs
ECMO consideration: Early contact with ECMO centre for refractory VF in young patients with reversible cause

Red Flag

Pitfalls to Avoid:

Delayed defibrillation for IV access: Shock first, IV during CPR - defibrillation is definitive treatment
Wrong adrenaline timing: ARC = after 3rd shock (not 2nd like AHA)
Prolonged rhythm checks: Over 10 seconds interruption significantly worsens outcomes
Hyperventilation: Causes decreased venous return, decreased coronary perfusion, increased intrathoracic pressure
Fine VF called as asystole: Check two leads, increase gain - missed shockable rhythm
Forgetting reversible causes: Especially in refractory VF - electrolytes, coronary thrombosis, toxins
Early termination: VF has best prognosis - persist with resuscitation longer than non-shockable rhythms
Using AHA algorithms in Australia: Different adrenaline timing, use ARC/ANZCOR
Not changing pad position: For refractory VF, try AP positioning
Hyperoxia post-ROSC: Titrate FiO2 to SpO2 94-98%, not 100%

Viva Practice

Viva Scenario

Stem: You are called to the resuscitation bay. A 58-year-old male collapsed at the shopping centre. Bystander CPR was commenced within 2 minutes. Paramedics shocked him twice en route for VF. He is still in VF on arrival. You are the team leader.

Opening Question: Talk me through your approach.

Model Answer: I would assume the team leader role and confirm the arrest by checking for responsiveness and pulse. I would ensure high-quality CPR is ongoing with minimal interruptions - rate 100-120/min, depth 5-6 cm, full chest recoil.

The patient has already received two shocks from paramedics. As he remains in VF, I would charge the defibrillator to 200J biphasic and deliver a third shock after ensuring everyone is clear. Immediately after the shock, I would resume CPR for 2 minutes.

Since this is the third shock, I would now give:

Adrenaline 1mg IV
Amiodarone 300mg IV

During the 2-minute CPR cycle, I would ensure IV or IO access is established if not already done, consider an advanced airway without interrupting CPR, and begin considering reversible causes.

After 2 minutes, I would briefly pause for rhythm check. If still VF, I would shock again, resume CPR, and continue adrenaline every 3-5 minutes. Amiodarone 150mg would be given after the 5th shock.

Throughout, I would consider the 4Hs and 4Ts, particularly coronary thrombosis given his age and presentation.

Follow-up Questions:

What are your specific considerations for reversible causes in this patient?

Model answer: Given the setting (shopping centre collapse in a 58-year-old male), acute coronary syndrome is the most likely cause. I would obtain a 12-lead ECG as soon as possible after ROSC to look for STEMI. Other considerations include hypokalaemia (especially if on diuretics), toxins, or less likely tension pneumothorax or tamponade. I would review any available history from paramedics or bystanders.
After 6 shocks, he remains in refractory VF. What additional measures would you consider?

Model answer: For refractory VF, I would:
- Change defibrillator pad position to anterior-posterior
- Consider double sequential defibrillation if available
- Ensure all reversible causes are addressed (check VBG for K+, consider empirical calcium)
- Consider lignocaine 1-1.5 mg/kg if amiodarone has failed
- Early contact with cardiac catheterisation lab or ECMO centre
- Consider thrombolysis if high suspicion for PE or STEMI without PCI access
- Ensure CPR quality is optimal with EtCO2 monitoring
He achieves ROSC after 8 shocks. What are your immediate priorities?

Model answer: Post-ROSC priorities:
- Confirm ROSC: check pulse, waveform capnography, blood pressure
- Optimise oxygenation: target SpO2 94-98%, avoid hyperoxia
- Maintain normocapnia: PaCO2 35-45 mmHg
- 12-lead ECG: if STEMI, emergent angiography within 2 hours
- Haemodynamic support: target MAP greater than 65-70 mmHg, consider vasopressors
- Targeted temperature management consideration
- ICU admission and neuroprotective care
- Avoid hyperthermia
The 12-lead ECG shows ST elevation in leads V1-V4. What do you do?

Model answer: This represents an anterior STEMI, likely from LAD occlusion. I would immediately contact the cardiac catheterisation lab and arrange emergent PCI within 2 hours. I would give dual antiplatelet therapy (aspirin 300mg if not already given, P2Y12 inhibitor as per local protocol), anticoagulation (heparin), and arrange mechanical CPR for transport if needed. The patient should go directly to the cath lab.

Viva Scenario

Stem: A 45-year-old female on haemodialysis presents in cardiac arrest. She missed her dialysis session yesterday. Initial rhythm is VF. Despite 4 shocks and standard ALS, she remains in VF.

Opening Question: What specific reversible cause are you most concerned about, and how would you address it?

Model Answer: In a dialysis patient who missed a session presenting with refractory VF, hyperkalaemia is my primary concern. Potassium accumulation causes progressive ECG changes and can lead to VF that is refractory to defibrillation until the electrolyte abnormality is corrected.

I would:

Immediately give calcium chloride 10% 10mL IV or calcium gluconate 30mL to stabilise the cardiac membrane
Give insulin 10 units IV with 50mL 50% dextrose to shift potassium intracellularly
Give sodium bicarbonate 50-100mL 8.4% if severe acidosis suspected
Obtain urgent VBG to confirm potassium level
Contact nephrology/ICU for emergent dialysis once ROSC achieved
Continue standard VF management with defibrillation and drugs

Follow-up Questions:

What ECG changes would you expect with hyperkalaemia?

Model answer: Progressive ECG changes with increasing potassium:
- K+ 5.5-6.5: Peaked, tented T waves
- K+ 6.5-7.5: PR prolongation, P wave flattening, QRS widening
- K+ 7.5-8.5: Loss of P waves, further QRS widening
- K+ greater than 8.5: Sine wave pattern, VF, asystole
Would you withhold defibrillation until electrolytes are corrected?

Model answer: No. I would continue defibrillation attempts alongside electrolyte correction. Defibrillation may be less effective in severe hyperkalaemia, but should still be attempted. Calcium administration may improve defibrillation success. The priority is simultaneous treatment of the rhythm and the underlying cause.
She achieves ROSC. What dialysis modality would you request?

Model answer: Emergent haemodialysis, ideally continuous renal replacement therapy (CRRT) in ICU for haemodynamic stability post-arrest. Intermittent haemodialysis may cause hypotension. I would target normal potassium with ongoing monitoring. If dialysis not immediately available, continue medical management of hyperkalaemia.

Viva Scenario

Stem: A 22-year-old male collapses during a football match. Bystanders start CPR immediately. An AED delivers one shock for VF. When you arrive, he is in sinus rhythm with a pulse but GCS 6 (E1V2M3).

Opening Question: What specific aetiologies are you considering in this young patient?

Model Answer: In a young person with witnessed VF during exertion, I would consider:

Structural causes:

Hypertrophic cardiomyopathy (most common cause of SCD in young athletes)
Arrhythmogenic right ventricular cardiomyopathy (ARVC)
Anomalous coronary arteries
Myocarditis

Electrical causes:

Long QT syndrome
Brugada syndrome
Catecholaminergic polymorphic VT (CPVT)
Wolff-Parkinson-White syndrome

Other causes:

Commotio cordis (blow to chest during vulnerable period)
Drug-induced (stimulants, energy drinks, anabolic steroids)
Hyperthermia/heat stroke
Electrolyte abnormality

Follow-up Questions:

What investigations would you prioritise?

Model answer:
- 12-lead ECG: Looking for long QT, Brugada pattern, WPW, epsilon waves (ARVC)
- Echocardiography: Structural abnormalities, LV hypertrophy, RV abnormalities
- Troponin: Myocardial injury, myocarditis
- Electrolytes, glucose, toxicology screen
- Consider cardiac MRI once stable
- Coronary angiography to exclude anomalous coronaries
- Genetic testing if channelopathy suspected
What is commotio cordis?

Model answer: Commotio cordis is VF induced by a blunt, non-penetrating blow to the chest during the vulnerable phase of the cardiac cycle (20-30ms before the T-wave peak). It occurs without structural heart disease. Risk factors include: projectile impact to precordium (baseball, hockey puck), timing within vulnerable window, and chest wall compliance (more common in children). Treatment is immediate defibrillation.
He recovers neurologically. What prevention measures would you discuss?

Model answer:
- ICD implantation for secondary prevention (survived VF arrest)
- Genetic counselling and family screening
- Activity restrictions based on underlying diagnosis
- Sports cardiology review for return-to-play decisions
- First-degree relatives should be screened (ECG, echo, consider genetic testing)
- Discussion of driving restrictions

Viva Scenario

Stem: You are asked about the electrophysiology of ventricular fibrillation.

Opening Question: Explain the mechanism of re-entry as it relates to ventricular fibrillation.

Model Answer: Re-entry is the most common mechanism of VF. It occurs when an electrical impulse continuously propagates around a circuit rather than terminating after activating the myocardium.

Three requirements must be met for re-entry:

Unidirectional block: The impulse is blocked in one direction (due to refractory tissue) but can conduct in the other direction
Slow conduction pathway: An alternative pathway with delayed conduction exists, allowing the impulse to travel around the blocked area
Recovery of excitability: By the time the impulse returns to the originally blocked tissue, that tissue has recovered and can be re-activated

In VF, multiple re-entrant wavefronts (4-12 simultaneously) exist, creating chaotic, disorganised electrical activity. This can be:

Functional re-entry: No fixed anatomical obstacle; created by varying refractory periods
Anatomical re-entry: Fixed circuit around scar tissue (e.g., post-MI)

Acute ischaemia promotes functional re-entry by:

Creating areas of slow conduction
Creating heterogeneous refractory periods
Causing action potential duration dispersion

Follow-up Questions:

How does defibrillation terminate VF?

Model answer: Defibrillation works by the critical mass theory. A successful shock must simultaneously depolarise a critical mass of myocardium (approximately 75% or more). This terminates all re-entrant wavefronts simultaneously by making all tissue refractory at the same time. With no excitable tissue to propagate re-entry, the arrhythmia terminates and the dominant pacemaker (SA node) can resume control.
What is the upper limit of vulnerability?

Model answer: The upper limit of vulnerability is the concept that shock energy must be above the defibrillation threshold to terminate VF, but must also be below a certain level that could itself induce VF. For clinical defibrillators, we operate well within the therapeutic window, but this concept explains why sometimes shocks can be pro-arrhythmic. The vulnerable period is during the relative refractory period (approximately 30ms before T-wave peak).
Explain the difference between enhanced automaticity and triggered activity.

Model answer:
- Enhanced automaticity: Increased rate of spontaneous phase 4 depolarisation in cells that normally have pacemaker activity, or development of pacemaker activity in cells that don't normally have it. Caused by catecholamines, ischaemia, electrolyte disturbance.
- Triggered activity: Abnormal depolarisations that depend on a preceding action potential. Two types:
  - Early afterdepolarisations (EADs): During phase 2-3, caused by prolonged repolarisation (long QT), leads to torsades de pointes
  - Delayed afterdepolarisations (DADs): After complete repolarisation (phase 4), caused by calcium overload (digoxin toxicity)

OSCE Scenarios

Station 1: VF Cardiac Arrest - Resuscitation Leadership

Format: Resuscitation leadership Time: 11 minutes Setting: ED resuscitation bay ACEM Domain: Medical Expert, Leader, Communicator

Candidate Instructions:

You are the Emergency Registrar. A 62-year-old male has been brought in by ambulance in cardiac arrest. Paramedics have been performing CPR and have delivered one shock for VF. The rhythm remains VF. You are now the team leader.

Lead the resuscitation.

Resources Available:

2 nurses (one experienced, one junior)
1 intern
Full resuscitation equipment
Defibrillator with pads attached
Drugs drawn up: Adrenaline 1mg, Amiodarone 300mg

Examiner Instructions:

Initial rhythm: VF
After shock 2: Remains VF
After shock 3: Remains VF
After shock 4: Converts to sinus rhythm, ROSC achieved
Post-ROSC: BP 85/50, HR 110, SpO2 94% on 100% O2
12-lead ECG shows inferior STEMI (II, III, aVF)

Expected Actions:

Assume team leader role with clear verbal statement
Allocate roles to team members
Confirm cardiac arrest (rhythm check)
Ensure high-quality CPR continues
Deliver defibrillation at appropriate energy
Resume CPR immediately after each shock
Give adrenaline 1mg and amiodarone 300mg after 3rd shock
Consider reversible causes throughout
Recognise ROSC and transition to post-resuscitation care
Identify STEMI and activate cath lab
Demonstrate closed-loop communication

Marking Criteria:

Domain	Criterion	Marks
Leadership	Assumes team leader role clearly	/1
Leadership	Allocates roles appropriately	/1
Algorithm	Follows ARC ALS algorithm (shockable pathway)	/2
Defibrillation	Correct energy selection and delivery	/1
CPR Quality	Ensures/verifies quality metrics	/1
Drugs	Correct drugs, doses, and ARC timing (after 3rd shock)	/2
Reversible causes	Considers/verbalises 4Hs and 4Ts	/1
Communication	Closed-loop communication throughout	/1
Post-ROSC	Appropriate immediate management	/1
STEMI	Recognises STEMI and activates cath lab	/1
Total		/12

Pass Standard: ≥7/12 Key Discriminators: ARC algorithm adherence (adrenaline after 3rd shock), team leadership, closed-loop communication

Station 2: Defibrillation Technique and Troubleshooting

Format: Procedural skills with structured questions Time: 8 minutes Setting: Skills laboratory ACEM Domain: Medical Expert

Candidate Instructions:

A manikin represents a patient in ventricular fibrillation. Demonstrate safe defibrillation technique. The examiner will then ask you some questions.

Equipment Available:

Adult manikin
Defibrillator with self-adhesive pads
Monitor showing VF

Expected Actions:

Confirm rhythm is VF
Apply pads correctly (anterolateral position)
Charge defibrillator to appropriate energy (150-200J biphasic)
Clear the patient (verbal and visual check)
Deliver shock safely
Immediately commence/direct CPR

Structured Questions:

Question	Model Answer	Marks
What is the correct pad placement for anterolateral position?	Right pad: right of sternum, below clavicle. Left pad: left mid-axillary line, V6 level	/1
What energy would you select for this biphasic defibrillator?	150-200J (manufacturer specific) for first shock	/1
When would you consider changing pad position?	Refractory VF, obese patient, pacemaker in path	/1
What is the anterior-posterior pad position?	Anterior: left precordium. Posterior: left infrascapular area	/1
What is double sequential defibrillation?	Near-simultaneous delivery of two shocks from two defibrillators	/1
What are contraindications to defibrillation?	None in VF arrest. Relative: wet patient (dry first), metal contact	/1

Marking Criteria:

Domain	Criterion	Marks
Recognition	Correctly identifies VF	/1
Pad placement	Correct anterolateral position	/1
Energy selection	Appropriate for device	/1
Safety	Clears patient verbally and visually	/1
Technique	Smooth delivery, immediate CPR	/1
Knowledge	Answers structured questions	/6
Total		/11

Station 3: Breaking Bad News - Unsuccessful Resuscitation

Format: Communication station Time: 8 minutes Setting: ED relatives room ACEM Domain: Communicator, Professional

Candidate Instructions:

A 55-year-old male presented in VF cardiac arrest. Despite 45 minutes of resuscitation including 8 shocks, adrenaline, and amiodarone, he did not achieve ROSC and resuscitation was ceased.

His wife is waiting in the relatives room. She witnessed the collapse at home and called 000. She performed CPR until paramedics arrived.

Break the news of her husband's death to her.

Actor Briefing (Wife):

Anxious, knows something is wrong
Will ask "Is he going to be okay?"
May become tearful, then angry ("Why couldn't you save him?")
Will ask about what happened and whether she did CPR correctly
May ask to see him

Expected Actions:

Introduce yourself, confirm identity
Establish understanding ("Tell me what you know so far")
Deliver news clearly using word "died" or "dead"
Allow silence for reaction
Respond empathetically to emotions
Acknowledge her CPR efforts positively
Answer questions honestly and simply
Offer to see her husband
Discuss support services
Arrange follow-up

Marking Criteria:

Domain	Criterion	Marks
Introduction	Appropriate introduction, privacy ensured	/1
Preparation	Establishes current understanding	/1
Delivery	Clear, unambiguous language ("died"/"dead")	/2
Empathy	Allows silence, empathetic response to emotion	/2
CPR acknowledgment	Acknowledges wife's CPR efforts positively	/1
Questions	Answers questions honestly, simply	/1
Viewing	Offers opportunity to see husband	/1
Support	Offers support services, pastoral care	/1
Closure	Appropriate closure, follow-up arranged	/1
Total		/11

SAQ Practice

Question 1 (6 marks)

Stem: A 60-year-old male is in cardiac arrest with ventricular fibrillation on the monitor.

Question: According to ARC/ANZCOR Guideline 11, list 6 key differences in managing a shockable rhythm (VF/pVT) compared to a non-shockable rhythm (PEA/Asystole).

Time allocation: 6 minutes

Model Answer:

Shockable (VF/pVT)	Non-Shockable (PEA/Asystole)	Mark
Defibrillation is indicated	Defibrillation is NOT indicated	(1)
Adrenaline given after 3rd shock	Adrenaline given immediately	(1)
Amiodarone 300mg after 3rd shock	Amiodarone not routinely indicated	(1)
Energy 150-200J biphasic	No shock delivered	(1)
Higher survival rate (25-30%)	Lower survival rate (8-10%)	(1)
Consider double sequential defibrillation if refractory	Not applicable	(1)

Examiner Notes:

Award full marks for 6 correct differences
Accept other valid differences (e.g., more aggressive resuscitation for VF, consider ECMO earlier)

Question 2 (8 marks)

Stem: A 50-year-old female has been in refractory ventricular fibrillation for 30 minutes despite 8 defibrillation shocks, adrenaline, and amiodarone.

Question: (a) List 4 potentially reversible causes you should actively exclude or treat in this scenario (2 marks) (b) Describe 4 additional strategies for managing refractory VF beyond standard ALS (4 marks) (c) List 2 criteria that would support consideration of ECMO (2 marks)

Time allocation: 8 minutes

Model Answer:

(a) Reversible causes (0.5 each, max 2 marks):

Hypokalaemia or hyperkalaemia (check VBG urgently)
Coronary thrombosis (likely, consider empirical thrombolysis)
Toxins (drug history, toxidrome)
Hypomagnesaemia (give empirical magnesium)
Hypoxia (check airway, ventilation)
Hypothermia (check core temperature)

(b) Additional strategies for refractory VF (1 each, max 4 marks):

Change pad position to anterior-posterior placement
Double sequential defibrillation (two defibrillators, two pad sets)
Lignocaine 1-1.5 mg/kg IV if amiodarone failed
Empirical calcium chloride 10mL for possible hyperkalaemia
Thrombolysis (tPA 50mg) if PE or STEMI suspected
ECMO/ECPR if available and patient appropriate
Ensure optimal CPR quality (EtCO2 monitoring)
Beta-blocker (esmolol) in catecholamine storm

(c) Criteria supporting ECMO consideration (1 each, max 2 marks):

Witnessed arrest with good-quality bystander CPR
Initial shockable rhythm
Age under 65-70 years
Suspected reversible cause (e.g., MI, PE, hypothermia)
No-flow time under 5 minutes
EtCO2 above 10 mmHg during CPR
Absence of terminal illness or significant comorbidities

Question 3 (6 marks)

Stem: You are the team leader during a VF cardiac arrest.

Question: Describe 6 specific actions you would take to optimise defibrillation success in a patient with refractory VF.

Time allocation: 6 minutes

Model Answer:

Action	Rationale	Mark
Minimise pre-shock pause (under 5 seconds)	Reduces hands-off time, maintains coronary perfusion	(1)
Charge during CPR	Reduces pre-shock pause	(1)
Change pad position to anterior-posterior	Alters defibrillation vector, may capture more myocardium	(1)
Ensure good electrode contact (shave chest hair if needed)	Reduces transthoracic impedance	(1)
Consider double sequential defibrillation	May terminate refractory VF when single shock fails	(1)
Treat reversible causes (especially electrolytes)	Hypokalaemia/hypomagnesaemia reduce defibrillation success	(1)

Examiner Notes:

Accept other valid actions: ensure defibrillator is functioning correctly, use maximum energy, apply firm pressure to pads, dry wet skin

Question 4 (8 marks)

Stem: You are teaching junior doctors about the management of ventricular arrhythmias.

Question: (a) Describe the mechanism of re-entry that underlies most cases of VF (3 marks) (b) Explain how defibrillation terminates VF (2 marks) (c) List 3 factors that affect defibrillation success (3 marks)

Time allocation: 8 minutes

Model Answer:

(a) Re-entry mechanism (1 each, max 3 marks):

Unidirectional block: impulse blocked in one direction but conducts in the other
Slow conduction pathway: alternative route with delayed conduction around blocked area
Recovery of excitability: originally blocked tissue recovers in time to be re-activated

(b) Defibrillation mechanism (1 each, max 2 marks):

Critical mass depolarisation: shock simultaneously depolarises ≥75% of myocardium
Terminates all re-entrant wavefronts by making all tissue refractory simultaneously
Allows dominant pacemaker (SA node) to resume control

(c) Factors affecting defibrillation success (1 each, max 3 marks):

Transthoracic impedance (lower = better current delivery)
Duration of VF (shorter = better, coarse VF more responsive than fine)
Pad position (affects current pathway through heart)
Energy level delivered
CPR quality (better coronary perfusion improves success)
Metabolic state of myocardium (acidosis, hypoxia reduce success)

Australian Guidelines Summary

ANZCOR Guideline 11: Adult Advanced Life Support

Element	ANZCOR Recommendation
Shockable rhythm	Immediate defibrillation, then CPR 2 min
Biphasic energy	150-200J (manufacturer specific)
Monophasic energy	360J
Adrenaline timing (VF/pVT)	After 3rd shock, then every 3-5 min
Adrenaline timing (PEA/asystole)	Immediately, then every 3-5 min
Amiodarone 1st dose	300mg after 3rd shock (VF/pVT)
Amiodarone 2nd dose	150mg after 5th shock
CPR rate	100-120 compressions/min
CPR depth	5-6 cm (adult)
Compression:ventilation ratio	30:2
Rhythm check interval	Every 2 minutes

Key Differences from AHA Guidelines

Element	ARC/ANZCOR	AHA	Clinical Implication
Adrenaline timing (shockable)	After 3rd shock	After 2nd shock	ARC delays by one cycle
Shock-first vs CPR-first	Either acceptable	Shock-first for witnessed	Minimal practical difference
Emergency number	000 (Aus) / 111 (NZ)	911	Local knowledge essential
Compression-only CPR	Acceptable for untrained rescuers	Emphasised	Both support
Amiodarone vs lidocaine	Amiodarone preferred	Either acceptable	Evidence similar

Quality Improvement

CPR Quality Metrics

Metric	Target	How to Monitor
Compression rate	100-120/min	Metronome, feedback device
Compression depth	5-6 cm	Feedback device, accelerometer
Chest recoil	Complete	Visual assessment, feedback device
Compression fraction	Above 80%	Minimise interruptions
Ventilation rate	10/min (with advanced airway)	Count, capnography
Pre-shock pause	Under 5 seconds	Timer, practice
EtCO2 during CPR	Above 10 mmHg	Waveform capnography

Debriefing After Resuscitation

Component	Content
Hot debrief	Immediate, brief, emotional support
Cold debrief	Later, structured, educational
What went well	Positive reinforcement
What could improve	Constructive feedback, systems issues
Action items	Specific changes for next time
Staff wellbeing	Check in on team, offer support

References

Guidelines

Australian Resuscitation Council. ANZCOR Guideline 11: Adult Advanced Life Support. 2023. https://resus.org.au
Australian Resuscitation Council. ANZCOR Guideline 11.2: Shockable Rhythms. 2023.
Australian Resuscitation Council. ANZCOR Guideline 11.4: Electrical Therapy. 2023.
Soar J, et al. European Resuscitation Council Guidelines 2021: Adult advanced life support. Resuscitation. 2021;161:115-151. PMID: 33773825
Panchal AR, et al. Part 3: Adult Basic and Advanced Life Support. Circulation. 2020;142:S366-S468. PMID: 33081529

Epidemiology and Outcomes

Bray JE, et al. Temporal trends in the utilisation of defibrillators for out-of-hospital cardiac arrest in Australia. Resuscitation. 2021;160:1-7. PMID: 33515614
Nehme Z, et al. Outcomes from out-of-hospital cardiac arrest in Australia. Heart Lung Circ. 2020;29:673-682. PMID: 31677982
Sasson C, et al. Predictors of survival from out-of-hospital cardiac arrest. Circ Cardiovasc Qual Outcomes. 2010;3:63-81. PMID: 20123673
Beck B, et al. Regional variation in the characteristics, incidence and outcomes of out-of-hospital cardiac arrest in Australia and New Zealand. Resuscitation. 2018;126:49-57. PMID: 29477393
Girotra S, et al. Trends in survival after in-hospital cardiac arrest. N Engl J Med. 2012;367:1912-1920. PMID: 23150959

Defibrillation

Link MS, et al. Part 7: Adult Advanced Cardiovascular Life Support. Circulation. 2015;132:S444-S464. PMID: 26472995
Cheskes S, et al. The association between chest compression release velocity and outcomes from out-of-hospital cardiac arrest. Resuscitation. 2019;139:245-251. PMID: 31034968
Stiell IG, et al. Early versus later rhythm analysis in patients with out-of-hospital cardiac arrest. N Engl J Med. 2011;365:787-797. PMID: 21879896
Deakin CD, et al. A comparison of the initial success rates of defibrillation using manual defibrillators versus automated external defibrillators. Resuscitation. 2010;81:158-162. PMID: 19926189

Double Sequential Defibrillation

Cheskes S, et al. Double sequential external defibrillation for refractory ventricular fibrillation. Resuscitation. 2019;139:371-377. PMID: 31028821
Ross EM, et al. Time to first shock and survival from out-of-hospital cardiac arrest with double sequential defibrillation. Prehosp Emerg Care. 2016;20:137-142. PMID: 26274095

Medications

Kudenchuk PJ, et al. Amiodarone, lidocaine, or placebo in out-of-hospital cardiac arrest (ALPS). N Engl J Med. 2016;374:1711-1722. PMID: 27043165
Perkins GD, et al. A randomized trial of epinephrine in out-of-hospital cardiac arrest (PARAMEDIC2). N Engl J Med. 2018;379:711-721. PMID: 30021076
Jacobs IG, et al. Effect of adrenaline on survival in out-of-hospital cardiac arrest. Resuscitation. 2011;82:1138-1143. PMID: 21745533

Pathophysiology

Weiss JN, et al. Ventricular fibrillation: how do we stop the waves from breaking? Circ Res. 2000;87:1103-1107. PMID: 11110766
Jalife J. Ventricular fibrillation: mechanisms of initiation and maintenance. Annu Rev Physiol. 2000;62:25-50. PMID: 10845083
Zipes DP, et al. Mechanisms of sudden cardiac death. Circulation. 1998;98:2334-2351. PMID: 9826323

Post-Resuscitation Care

Nolan JP, et al. Post-resuscitation care. Resuscitation. 2022;161:A220-A269. PMID: 33773825
Dankiewicz J, et al. Hypothermia versus normothermia after out-of-hospital cardiac arrest (TTM2). N Engl J Med. 2021;384:2283-2294. PMID: 34133859
Sandroni C, et al. Prognostication after cardiac arrest. Crit Care. 2018;22:150. PMID: 29871657
Donnino MW, et al. Temperature management after cardiac arrest: an advisory statement. Circulation. 2015;132:2448-2456. PMID: 26434495

Special Circumstances

Jeejeebhoy FM, et al. Cardiac arrest in pregnancy. Circulation. 2015;132:1747-1773. PMID: 26475871
Brown DJ, et al. Hypothermic cardiac arrest. N Engl J Med. 2012;367:1930-1938. PMID: 23150960
Maron BJ, et al. Clinical profile and spectrum of commotio cordis. JAMA. 2002;287:1142-1146. PMID: 11879111

CPR Quality

Meaney PA, et al. Cardiopulmonary resuscitation quality: improving cardiac resuscitation outcomes both inside and outside the hospital. Circulation. 2013;128:417-435. PMID: 23801105
Stiell IG, et al. What is the role of chest compression depth during out-of-hospital cardiac arrest resuscitation? Crit Care Med. 2012;40:1192-1198. PMID: 22202708
Idris AH, et al. Chest compression rates and survival following out-of-hospital cardiac arrest. Crit Care Med. 2015;43:840-848. PMID: 25565457

ECMO and Advanced Therapies

Yannopoulos D, et al. ECMO for refractory out-of-hospital cardiac arrest (ARREST). Lancet. 2020;396:1807-1816. PMID: 33197396
Belohlavek J, et al. ECMO for cardiac arrest due to ventricular fibrillation (Prague OHCA). N Engl J Med. 2022;387:e12. PMID: 36027564
Stub D, et al. ECMO for out-of-hospital cardiac arrest. Resuscitation. 2015;92:82-87. PMID: 25956937

Indigenous Health

Brown A, et al. Cardiovascular health in Indigenous Australians. Heart Lung Circ. 2010;19:327-331. PMID: 20185369
Katzenellenbogen JM, et al. Epidemiology of heart failure in Australia. Int J Cardiol. 2020;299:211-216. PMID: 31296424

Prognostication

Nolan JP, et al. European Resuscitation Council and European Society of Intensive Care Medicine guidelines 2021: post-resuscitation care. Resuscitation. 2021;161:220-269. PMID: 33773827

Clinical board

Urgent signals

Exam focus

Linked comparisons

Editorial and exam context

Quick Answer

ACEM Exam Focus

Primary Exam Relevance

Physiology (High Yield)

Pharmacology (High Yield)

Anatomy (Medium Yield)

Fellowship Exam Relevance

Written Exam

OSCE

Key Domains Tested

Key Points

Epidemiology

Incidence and Prevalence

Temporal Trends

Australian/NZ Specific Data

Risk Factors for VF Arrest

Pathophysiology

Mechanisms of Ventricular Arrhythmias

1. Re-entry (Most Common - 90% of VF)

2. Automaticity

3. Triggered Activity

Why VF Causes Cardiac Arrest

VF Waveform Characteristics

Defibrillation Physiology

Rhythm Recognition

Ventricular Fibrillation (VF)

VF Subtypes

Key Recognition Points

Pulseless Ventricular Tachycardia (pVT)

Monomorphic vs Polymorphic VT

VT vs SVT with Aberrancy

ECG Artefacts That Mimic VF

Management Algorithm

ARC/ANZCOR Guideline 11: Shockable Rhythm Pathway

Key ARC/ANZCOR Timing Points

Airway Management During Arrest

Defibrillation

Energy Selection

Defibrillator Pad Placement

Standard Anterolateral Position

Alternative Positions

Defibrillation Technique

Minimising Peri-Shock Pause

Biphasic vs Monophasic Defibrillation

Double Sequential Defibrillation (DSD)

Paediatric Defibrillation

Medications

Adrenaline (Epinephrine)

Amiodarone

Lignocaine (Alternative)

Magnesium

Other Medications

Medication Delivery

Reversible Causes (4Hs and 4Ts)

The 4 Hs

The 4 Ts

Toxins Causing VF/pVT

Electrolyte Derangements and ECG Changes

Special Circumstances

Witnessed VF Arrest with AED

Cardiac Catheterisation Lab Arrest

Post-Cardiac Surgery Arrest

Pregnancy

Implantable Cardioverter-Defibrillator (ICD)

Hypothermic Arrest

Post-Resuscitation Care

Immediate Post-ROSC Management

Oxygenation Post-ROSC

Haemodynamic Targets

Coronary Angiography

Targeted Temperature Management (TTM)

Prognostication

Indigenous Health Considerations

Remote and Rural Considerations

Pre-Hospital Challenges