Broad-Complex Tachycardia

Quick Answer

One-liner: Broad-complex tachycardia (QRS ≥120ms, rate greater than 100/min) is VT until proven otherwise; haemodynamic instability mandates immediate synchronized cardioversion, while stable patients require systematic ECG analysis (Brugada criteria) and VT-first pharmacotherapy.

Broad-complex tachycardia accounts for 20-30% of ED tachyarrhythmias. Approximately 80% are VT, rising to 95% in patients with structural heart disease or prior MI. Misdiagnosis is life-threatening: treating VT as SVT with AV nodal blockers (adenosine, verapamil) can precipitate cardiovascular collapse. ANZCOR Guideline 11.8 mandates immediate synchronized cardioversion for unstable patients; stable patients receive amiodarone 300 mg IV or procainamide, NOT adenosine. Special care is required for polymorphic VT (suggests ischaemia or long QT) and pre-excited AF (WPW), where inappropriate drug selection can trigger ventricular fibrillation.

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ACEM Exam Focus

Primary Exam Relevance

• Anatomy: Conduction system (SA node, AV node, His-Purkinje), accessory pathways (Bundle of Kent in WPW), coronary artery supply to conduction tissue
• Physiology: Cardiac action potential (Phase 0-4), refractory periods, automaticity vs re-entry mechanisms, AV nodal conduction delay
• Pharmacology: Class I antiarrhythmics (procainamide - Na⁺ channel block), Class III (amiodarone - K⁺ channel block), magnesium (membrane stabilization)

Fellowship Exam Relevance

• Written: Differentiation VT vs SVT-aberrancy (Brugada criteria), ANZCOR tachycardia algorithm, drug selection, WPW management, polymorphic VT/torsades
• OSCE: High-yield resuscitation station (unstable VT → cardioversion), ECG interpretation station (apply Brugada algorithm), communication (consent for cardioversion, discussing ICD)
• Key domains tested: Medical Expert (ECG interpretation, drug choice), Communicator (informed consent under time pressure), Leader (resuscitation team coordination)

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Key Points

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Epidemiology

Australian/NZ Specific

• Aus-ROC data: Tachyarrhythmia accounts for 8-12% of prehospital cardiac arrest conversions
• Indigenous populations: Aboriginal and Torres Strait Islander adults have 2-3× higher rates of ischaemic heart disease (major VT substrate)
• Rural/remote: 40% of VT presentations in remote settings are initially misdiagnosed as SVT due to limited ECG interpretation experience

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Pathophysiology

Mechanism

Ventricular Tachycardia (VT)

Re-entry (90%): Most common mechanism. Requires anatomical substrate (scar from prior MI, cardiomyopathy) creating areas of slow conduction and unidirectional block. Impulse circulates around scar tissue, generating wide-complex beats.

Automaticity (10%): Enhanced automaticity of ventricular pacemaker cells. Seen in:

• Triggered activity: Early or delayed afterdepolarizations (torsades de pointes)
• Catecholamine-induced: Exercise-induced VT, arrhythmogenic right ventricular cardiomyopathy (ARVC)

SVT with Aberrancy

Bundle branch block: Supraventricular impulse (e.g., AF, AVNRT) conducted to ventricles but one bundle branch is refractory → aberrant (wide) conduction.

Pre-excitation (WPW): Accessory pathway (Bundle of Kent) bypasses AV node → early ventricular activation → delta wave (narrow complex sinus rhythm). During AF, rapid atrial impulses conduct down accessory pathway → irregular broad-complex tachycardia (can degenerate to VF if drugs block AV node and divert ALL impulses down pathway).

Pathological Progression

Substrate (MI scar/cardiomyopathy) → Trigger (PVC) → Re-entry circuit → Sustained VT
   ↓
Haemodynamic compromise (↓ CO, ↓ coronary perfusion) → Ischaemia → Degeneration to VF

Why It Matters Clinically

• VT reduces cardiac output by 30-50% (loss of atrial kick, rapid rate, dyssynchrony) → hypotension, pulmonary oedema
• Coronary perfusion pressure falls → myocardial ischaemia → electrical instability → VF
• Misdiagnosis kills: Adenosine/verapamil in VT causes vasodilation + negative inotropy → cardiovascular collapse
• WPW + AF + AV blocker = VF: Blocking AV node diverts all atrial impulses down fast accessory pathway → extremely rapid ventricular rate (greater than 300/min) → VF

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Clinical Approach

Recognition

Triggers for Suspicion

• Palpitations with rate greater than 100/min
• Syncope or pre-syncope (suggests haemodynamic compromise)
• Chest pain (ischaemia or high rate)
• Dyspnoea (acute heart failure)
• Cardiac arrest survivor (presenting rhythm may be VT)

Initial Assessment

Primary Survey

• A: Airway patent? (Conscious level may be impaired if severe hypoperfusion)
• B: Respiratory rate, SpO₂ (pulmonary oedema from acute LV failure?), signs of distress
• C: CRITICAL - Haemodynamic status determines immediate management
  • "Blood pressure: SBP below 90 mmHg suggests shock"
  • "Heart rate: Usually 120-250/min (VT typically 120-180/min; pre-excited AF greater than 200/min)"
  • "Peripheral perfusion: Cold, clammy, mottled = poor perfusion"
  • "JVP: Cannon A waves suggest AV dissociation (VT)"
• D: GCS, confusion, altered mental status (cerebral hypoperfusion)
• E: Sweating, pallor; ICD present? (suggests prior VT/VF)

History

Key Questions

Red Flag Symptoms

Examination

General Inspection

• Appearance: Distressed, sweating, pale, clammy (shock)
• Conscious level: Alert vs confused vs obtunded
• Work of breathing: Tachypnoea, use of accessory muscles (pulmonary oedema)
• Devices: ICD scar (left infraclavicular), pacemaker

Specific Findings

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Investigations

Immediate (Resus Bay)

Standard ED Workup

Advanced/Specialist

Point-of-Care Ultrasound

ED POCUS applications:

1. Parasternal long axis: LV systolic function (severe LV dysfunction supports VT diagnosis)
2. Apical 4-chamber: Wall motion abnormalities (prior MI → scar → VT substrate)
3. IVC: Volume status (if hypotensive, is it from VT alone or concurrent hypovolaemia?)

POCUS pearls:

• Severe LV dysfunction (LVEF below 30%) makes VT diagnosis greater than 95% likely
• Normal LV function does NOT rule out VT (can occur in ARVC, channelopathies)

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ECG Differentiation: VT vs SVT with Aberrancy

The Brugada Criteria (1991)

Apply sequentially. If ANY step is positive → VT.

If ALL four steps are negative → SVT with aberrancy

Step 4: Morphology Criteria

If V1 Positive (RBBB-like Pattern)

VT if:

• Monophasic R wave in V1
• QR pattern in V1
• R/S ratio below 1 in V6 (dominant S wave)

If V1 Negative (LBBB-like Pattern)

VT if:

• R wave greater than 30ms (greater than 0.75 small squares) in V1 or V2
• Notched S wave downstroke in V1 or V2
• Any Q wave in V6

Alternative: The aVR Algorithm (Vereckei 2008)

Faster, uses only lead aVR. VT if ANY of:

1. Initial R wave present in aVR
2. Initial r or q wave greater than 40ms in aVR
3. Notch on descending limb of negative QRS in aVR
4. Ventricular activation-velocity ratio (Vi/Vt) ≤1 in aVR

R-Wave Peak Time (RWPT) in Lead II (Pava 2010)

• Measure: Time from QRS onset to peak of R wave in lead II
• VT if: RWPT ≥50ms
• Advantage: Very simple, single measurement

Clinical Clues (Do NOT Rely on These Alone)

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Management

ANZCOR Guideline 11.8: Tachycardia Algorithm

┌─────────────────────────────────────────────────────────┐
│     TACHYCARDIA (Rate greater than 100/min, QRS ≥120ms)            │
└─────────────────────────────────────────────────────────┘
                        ↓
┌─────────────────────────────────────────────────────────┐
│         ASSESS HAEMODYNAMIC STATUS                      │
│  • Hypotension (SBP below 90)                                │
│  • Altered mental status                                │
│  • Chest pain (ischaemia)                               │
│  • Acute heart failure                                  │
└─────────────────────────────────────────────────────────┘
                        ↓
            ┌───────────┴───────────┐
            │                       │
         UNSTABLE               STABLE
            │                       │
            ↓                       ↓
 ┌──────────────────────┐  ┌──────────────────────┐
 │ IMMEDIATE SYNC DC    │  │ IDENTIFY RHYTHM      │
 │ CARDIOVERSION        │  │ • 12-lead ECG        │
 │                      │  │ • Rhythm strip       │
 │ 120-200J biphasic    │  │ • Apply Brugada      │
 │ (Sedate if possible) │  └──────────────────────┘
 └──────────────────────┘           ↓
                              ┌─────┴─────┐
                              │           │
                          REGULAR    IRREGULAR
                              │           │
                              ↓           ↓
                    ┌──────────────┐  ┌──────────────┐
                    │ Monomorphic  │  │ AF with      │
                    │ VT           │  │ aberrancy OR │
                    │ or           │  │ pre-excited  │
                    │ SVT-aberrant │  │ AF (WPW)     │
                    └──────────────┘  └──────────────┘
                          ↓                 ↓
              ┌──────────────────┐  ┌──────────────────┐
              │ ASSUME VT        │  │ If WPW: AVOID    │
              │                  │  │ adenosine, vera, │
              │ AMIODARONE 300mg │  │ diltiazem        │
              │ IV over 20-60min │  │                  │
              │                  │  │ Give amiodarone  │
              │ or               │  │ or cardiovert    │
              │                  │  └──────────────────┘
              │ PROCAINAMIDE     │
              │ 10mg/kg over     │
              │ 30-60 min        │
              └──────────────────┘
                      ↓
         ┌────────────────────────┐
         │ If refractory:         │
         │ SYNCHRONIZED CARDIOVERT│
         │ 120-200J               │
         └────────────────────────┘

Immediate Management (First 10 minutes)

UNSTABLE Broad-Complex Tachycardia (SBP below 90, altered mental status, chest pain, acute HF)

1. CALL FOR HELP - activate resus team
2. Oxygen: Apply high-flow if hypoxic (target SpO₂ 94-98%)
3. IV access x2 (large bore)
4. Attach defibrillator pads - SYNCHRONIZED MODE
5. SEDATION if conscious:
   - Midazolam 2-5 mg IV OR
   - Fentanyl 50-100 mcg IV OR
   - Ketamine 0.5-1 mg/kg IV (if available, maintains BP)
6. SYNCHRONIZED CARDIOVERSION:
   - 120-200J biphasic (or 200J monophasic)
   - Ensure SYNC button activated (marker on R waves)
   - "Clear, all clear, shocking" → deliver shock
7. Check pulse and rhythm
8. If unsuccessful: Repeat at higher energy (200J, then 360J)
9. Post-cardioversion: 12-lead ECG, check BP, continue monitoring
10. Identify and treat underlying cause

STABLE Broad-Complex Tachycardia

1. Continuous telemetry monitoring
2. Oxygen if hypoxic (SpO₂ below 94%)
3. IV access x2
4. 12-lead ECG + rhythm strip
5. Bloods: FBC, UEC, Mg²⁺, Ca²⁺, troponin, (digoxin level if applicable)
6. Apply Brugada criteria (assume VT if uncertain)
7. PHARMACOTHERAPY (see below)
8. If refractory or deteriorates → cardioversion

Pharmacotherapy (Stable VT or Uncertain Diagnosis)

First-Line: Amiodarone (ANZCOR Guideline 11.8)

Alternative: Procainamide

Synchronized Cardioversion Technique

Preparation

1. Consent (if time permits): "You have a dangerous heart rhythm. I need to give you an electric shock to reset it. I'll give you sedation first."
2. Fasting status: Not relevant in emergency (aspiration risk is outweighed by arrhythmia risk)
3. Sedation: Midazolam 2-5 mg IV (titrate) ± fentanyl 50-100 mcg (or ketamine 0.5-1 mg/kg if BP low)
4. Team briefing: "This is synchronized cardioversion for VT. Pads on, sync mode, 200J, charging now."

Procedure

1. Apply defibrillator pads (anterolateral or anteroposterior)
2. CRITICAL: Activate SYNC button (should see markers on R waves; if unsure, switch leads)
3. Select energy: 120-200J biphasic (or 200J monophasic)
4. Charge defibrillator
5. Safety check: "I'm clear, you're clear, everyone clear" (visual check)
6. Press and HOLD shock button (delay while device waits for next R wave, then delivers)
7. Check pulse and rhythm immediately
8. If unsuccessful: Increase to 200J, then 360J

Post-Cardioversion

• 12-lead ECG (check for STEMI, QT prolongation)
• Continuous telemetry x24h minimum
• Troponin (cardioversion causes minor rise; significant rise suggests ischaemia)
• Treat underlying cause
• Cardiology referral for risk stratification, consideration of ICD

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Special Scenarios

Polymorphic VT (Torsades de Pointes)

Recognition: Broad-complex tachycardia with continuously varying QRS morphology ("twisting of the points")

Causes:

1. Long QT syndrome (congenital or acquired - drugs, hypokalaemia, hypomagnesaemia)
2. Acute ischaemia (STEMI, Wellens' syndrome)

Management:

Pre-Excited Atrial Fibrillation (WPW)

Recognition:

• Irregular broad-complex tachycardia
• Very rapid (often greater than 200/min)
• History of WPW or known delta waves on prior ECG

Pathophysiology: AF impulses conduct down accessory pathway (bypasses AV node) → extremely rapid ventricular rate → risk of degeneration to VF

Management:

VT Storm (≥3 Episodes in 24 Hours)

Definition: Recurrent VT requiring multiple cardioversions or antiarrhythmic interventions

Causes:

• Acute MI / unstable angina
• Electrolyte derangement (K⁺, Mg²⁺)
• Drug toxicity (digoxin, proarrhythmic from antiarrhythmics)
• Decompensated heart failure

Management:

1. Urgent cardiology/EP consult
2. Amiodarone loading: 300 mg IV, then 900 mg/24h infusion
3. Beta-blocker (if ischaemic, once haemodynamically stable): Metoprolol 25-50 mg PO q6h
4. Electrolyte repletion: K⁺ greater than 4.5, Mg²⁺ greater than 1.0 mmol/L
5. Sedation: Reduce sympathetic drive (midazolam, propofol infusion)
6. Urgent coronary angiography if ischaemic VT
7. EP lab referral: For catheter ablation if refractory

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Disposition

Admission Criteria

ALL patients with broad-complex tachycardia require admission (minimum telemetry ward, often CCU)

ICU/CCU Criteria

Discharge Criteria

Broad-complex tachycardia is NOT suitable for ED discharge. Even if rhythm converts, risk of recurrence and need for investigation mandates admission.

Possible exceptions (senior consultant decision only):

• Young patient, structurally normal heart, proven SVT with aberrancy (confirmed on prior ECG), rapid return to sinus with adenosine, normal troponin, cardiology follow-up in 1-2 weeks

Follow-up

All VT patients require:

1. Cardiology outpatient within 1-2 weeks (or sooner if high-risk)
2. Echocardiography (if not done inpatient)
3. Exercise stress test or angiography (assess ischaemic substrate)
4. Electrophysiology referral if:
   • Recurrent VT
   • LVEF below 35%
   • Cardiac arrest survivor
   • Structural heart disease
5. ICD consideration if:
   • LVEF ≤35% (primary prevention)
   • Cardiac arrest survivor (VT/VF)
   • Recurrent VT despite medical therapy

GP letter must include:

• Diagnosis (VT vs SVT-aberrancy, if determined)
• Precipitant (ischaemia, electrolytes, drugs)
• Medications commenced (amiodarone, beta-blocker)
• Follow-up arranged (cardiology, echo, angiography)

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Special Populations

Paediatric Considerations

Different etiologies:

• Structural heart disease: Post-surgical (TOF, TGA repair), cardiomyopathy
• Channelopathies: Long QT syndrome, catecholaminergic polymorphic VT (CPVT)
• Myocarditis

Drug dosing:

Paediatric cardiology consult mandatory for all paediatric VT.

Pregnancy

Physiological changes:

• Increased blood volume → increased preload → may unmask cardiomyopathy
• Peripartum cardiomyopathy (last month pregnancy to 5 months postpartum)

Management principles:

• Cardioversion is safe in all trimesters (no fetal harm; prioritize maternal resuscitation)
• Amiodarone: Category D (fetal thyroid toxicity) - use if life-saving, inform obstetrics
• Procainamide: Category C (safer)
• Position: Left lateral tilt (after 20 weeks) to relieve aortocaval compression

Elderly

Considerations:

• Polypharmacy: QT-prolonging drugs (antipsychotics, SSRIs, macrolides) + diuretics → hypokalaemia → torsades
• Renal impairment: Reduce procainamide dose if eGFR below 30
• Frailty: Higher risk of falls post-cardioversion sedation; higher bleeding risk if anticoagulation needed for AF

Indigenous Health

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

Health disparities:

• Aboriginal and Torres Strait Islander Australians: 2-3× higher rates of ischaemic heart disease, heart failure, diabetes (all VT substrates)
• Māori: 1.5-2× higher CVD mortality, often presenting at younger age (below 50 years)
• Rheumatic heart disease: Higher prevalence in Indigenous populations (may have AF with aberrancy)

Cultural safety:

• Family involvement: Whānau (Māori) or extended family often central to decision-making; include in consent for cardioversion, ICD discussions
• Interpreter services: Arrange Aboriginal Health Liaison or Māori Health Worker if language/cultural barrier
• Traditional medicine: Ask about concurrent use; some traditional remedies may interact with antiarrhythmics
• Historical trauma: Mistrust of healthcare system; build rapport, explain clearly, avoid paternalism

Remote/rural access:

• 40% of Indigenous Australians live in regional/remote areas with limited cardiology access
• VT may be mismanaged initially due to lack of ECG interpretation expertise
• RFDS retrieval: Essential for transfer to PCI-capable centre; delays of 4-8 hours common
• Telehealth: Use for remote ECG interpretation (connect with metro EP/cardiology)

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Pitfalls & Pearls

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Viva Practice

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OSCE Scenarios

Station 1: Resuscitation - Unstable VT

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

Candidate Instructions:

A 60-year-old male has just arrived by ambulance with palpitations and chest pain. The paramedics report BP 80/50, HR 170. He is confused and diaphoretic. You are the team leader. Lead the resuscitation.

Examiner Instructions:

• Patient is on monitor showing regular broad-complex tachycardia, HR 170, QRS 150ms
• BP 80/50 (measured by nurse at 0min)
• GCS 13 (E3V4M6) - confused, responds to voice
• SpO₂ 92% on room air
• IV access x1 (20G left ACF)
• Defibrillator available, pads not yet applied

Scenario Progression:

• If candidate applies oxygen: "SpO₂ improves to 96%"
• If candidate applies defibrillator pads: "Rhythm confirmed - regular broad-complex tachycardia, 170/min"
• If candidate requests sedation: "Midazolam available - how much?"
  • Appropriate dose (2-5mg): "Patient sedated, eyes closed, still has purposeful movement to voice"
• If candidate performs synchronized cardioversion:
  • "SYNC button on?"
• Yes/No determines success
  • Appropriate energy (120-200J): "Shock delivered. Rhythm now sinus, rate 85. BP 105/65. Patient opening eyes."
  • If unsynchronized mode used for organized rhythm: Examiner says "Patient develops VF. What now?" → Test CPR/defibrillation skills
• If candidate delays cardioversion for amiodarone: "While you're drawing up amiodarone, patient becomes unresponsive. No pulse. Monitor shows VF."

Actor/Patient Brief:

• You are confused, sweating, short of breath
• If asked "How are you feeling?": "Dizzy... heart racing..."
• Do not volunteer information
• After cardioversion (if appropriate): Wake up gradually, ask "What happened?"

Marking Criteria:

Expected Standard:

• Pass (≥6/11): Recognizes unstable patient, performs synchronized cardioversion with appropriate sedation and energy, reassesses post-shock
• Fail (below 6/11): Delays cardioversion for pharmacotherapy, uses unsynchronized mode for organized rhythm, fails to recognize instability
• Key discriminator: Immediate cardioversion vs delayed pharmacotherapy (ANZCOR mandates immediate cardioversion for unstable patients)

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Station 2: ECG Interpretation - Apply Brugada Criteria

Format: ECG interpretation and discussion Time: 11 minutes Setting: ED clinical area

Candidate Instructions:

You are shown an ECG from a 58-year-old man with palpitations. HR 155, BP 115/70, alert. Interpret the ECG and explain your management approach to the examiner.

Examiner Instructions:

• Provide ECG showing regular broad-complex tachycardia (rate 155, QRS 160ms)
• Features: LBBB-like pattern (V1 negative), R wave 40ms in V1, notched S wave, Q wave in V6, no clear P waves
• Correct interpretation: VT (Brugada criteria positive - Step 4 morphology)

ECG provided: [Regular BCT, LBBB-like, VT morphology features]

Expected Discussion:

1. Systematic approach:
   • "This is a 12-lead ECG showing regular broad-complex tachycardia, rate ~155/min, QRS duration ~160ms"
2. Apply Brugada criteria:
   • Step 1: Absence of RS in all precordial leads? "No - there are RS complexes in V4-V6"
   • Step 2: RS interval greater than 100ms? "Let me measure... V4 shows RS interval ~90ms, V5 ~95ms - all below 100ms"
   • Step 3: AV dissociation? "I don't see clear P waves marching through, no obvious capture or fusion beats - Step 3 negative"
   • Step 4: Morphology criteria. "V1 is negative, so this is LBBB-like. VT criteria are: R greater than 30ms in V1, notched S downstroke, or Q wave in V6. Looking at V1, the R wave is approximately 40ms (1 small square = 40ms) - this meets VT criteria. Also, there's a small Q wave in V6. This is VT."
3. Management:
   • "Patient is stable (BP 115/70, alert) so immediate cardioversion not required"
   • "I would manage this as VT: continuous telemetry, defibrillator pads applied, IV access x2, oxygen if hypoxic"
   • "Bloods: FBC, UEC, Mg²⁺, troponin (ischaemic trigger?)"
   • "Pharmacotherapy: Amiodarone 300mg IV over 20-60 minutes per ANZCOR Guideline 11.8"
   • "If refractory or deteriorates: synchronized cardioversion 120-200J"
   • "All VT patients require admission, telemetry, echo, cardiology consult"

Marking Criteria:

Expected Standard:

• Pass (≥6/11): Systematic ECG interpretation, applies Brugada criteria (even if imperfectly), correct diagnosis of VT, appropriate management (amiodarone, not adenosine)
• Fail (below 6/11): Does not apply Brugada criteria, misdiagnoses as SVT, suggests adenosine
• Key discriminator: Ability to apply morphology criteria (Step 4 - most complex step, highest yield)

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Station 3: Communication - Consent for Cardioversion

Format: Communication/consent discussion Time: 11 minutes Setting: ED cubicle

Candidate Instructions:

You are managing a 52-year-old man with broad-complex tachycardia. He is stable (BP 110/70, alert) but VT has persisted despite amiodarone. You need to obtain consent for elective synchronized cardioversion.

Examiner Instructions:

• Patient is alert, anxious, never had cardioversion before
• Wife is present (if candidate asks)
• Patient will ask: "Is this dangerous? Will it hurt? What if it doesn't work?"

Actor/Patient Brief:

• You are anxious about the shock
• Ask questions: "Why do I need this? Can't we just wait? Is there another medication?"
• If candidate explains clearly and empathetically, you agree
• If candidate is rushed or doesn't address concerns, you hesitate

Expected Approach:

1. Introduction and establish rapport:

   • "Mr Smith, I'm Dr [name]. I've been looking after you today. How are you feeling right now?"
   • "I know this must be very worrying for you. Can I take a few minutes to explain what's happening and what we recommend?"

2. Explain the problem:

   • "Your heart is in an abnormal rhythm called ventricular tachycardia, or VT. It's beating too fast and not as effectively as it should."
   • "We've tried medication - the amiodarone drip - but your heart is still in this rhythm. If we leave it, there's a risk it could get worse or make you very unwell."

3. Explain the procedure:

   • "The treatment we recommend is called cardioversion. It's a controlled electric shock to reset your heart rhythm back to normal."
   • "Here's what will happen:"
     • "We'll give you medication through the drip to make you sleepy - you won't feel anything during the procedure"
     • "Once you're asleep, we'll place pads on your chest and deliver a very brief electric shock"
     • "The shock resets the electrical system of your heart, like rebooting a computer"
     • "You'll wake up a few minutes later, and hopefully your heart will be back in a normal rhythm"

4. Address risks and benefits:

   • "Benefits: Very effective - about 85-90% chance of success in getting your heart back to normal rhythm"
   • "Risks:"
     • "The sedation can make you feel drowsy for 1-2 hours afterward"
     • "There's a small risk (1-2%) the rhythm could change to a more dangerous rhythm, but we're fully equipped to manage that"
     • "Very rarely, the shock can cause skin burns (we use gel pads to prevent this)"
     • "There's a small chance it doesn't work, and we'd need to try again or use different medication"

5. Invite questions:

   • "What questions do you have?"
   • If asked "Will it hurt?": "No - we'll make sure you're fully asleep before the shock. You won't feel anything. Some people have mild chest soreness afterward, like a bruise, which settles in a day or two."
   • If asked "What if it doesn't work?": "If the first shock doesn't work, we can try again at a higher energy level. If it still doesn't work, we'd consider other medications or discuss the plan with our heart specialists."
   • If asked "Is there another option?": "We could try another medication, but cardioversion is more effective and faster. Given your heart has already not responded to the first medication, I think cardioversion gives you the best chance of getting your rhythm back to normal quickly."

6. Confirm understanding and consent:

   • "Does that make sense? Do you have any other questions?"
   • "Are you happy for us to proceed with the cardioversion?"
   • [If yes]: "Great. I'll organize the sedation and we'll get you sorted. Your wife can stay with you until we're ready to start, and we'll come and get her as soon as you're awake."

Marking Criteria:

Expected Standard:

• Pass (≥6/11): Clear explanation of VT and cardioversion, addresses risks, empathetic communication, obtains consent
• Fail (below 6/11): Uses jargon without explanation, doesn't address patient concerns, rushed or dismissive
• Key discriminator: Ability to explain complex procedure in layman's terms and address anxiety

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SAQ Practice

Question 1 (6 marks)

Stem: A 65-year-old man with a history of previous myocardial infarction presents with palpitations. His ECG shows a regular broad-complex tachycardia at 160 beats per minute. He is alert, with a blood pressure of 105/70 mmHg.

Question: List the 4 steps of the Brugada criteria used to differentiate ventricular tachycardia from supraventricular tachycardia with aberrancy. (4 marks)

Model Answer:

1. Absence of RS complex in all precordial leads (V1-V6) - If there is no lead with both an R and S wave, this indicates VT (1 mark)
2. RS interval greater than 100 ms in any precordial lead - Measured from the start of R to the nadir of S; if greater than 100ms (2.5 small squares), this indicates VT (1 mark)
3. Atrioventricular dissociation - P waves marching through QRS at a different rate, or presence of capture/fusion beats, indicates VT (1 mark)
4. Morphology criteria present in V1-2 AND V6 - Specific QRS morphology patterns:
   • If V1 positive (RBBB-like): monophasic R, QR, or R/S below 1 in V6 suggests VT
   • If V1 negative (LBBB-like): R greater than 30ms, notched S downstroke, or Q wave in V6 suggests VT (1 mark)

Examiner Notes:

• Accept: Descriptions that capture the essence (e.g., "P waves independent of QRS" for AV dissociation)
• Do not accept: Vague answers like "ECG morphology" without specifics
• Bonus: If candidate states "Apply sequentially - if ANY step positive, diagnosis is VT" → examiner's discretion (+0.5)

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Question 2 (8 marks)

Stem: A 55-year-old woman presents with broad-complex tachycardia. She is hypotensive (BP 75/50 mmHg) and confused.

Question: Outline the immediate management of this patient according to ANZCOR guidelines. (8 marks)

Model Answer:

1. Call for help - Activate resuscitation team (1 mark)
2. Oxygen - High-flow oxygen via non-rebreather mask if hypoxic (target SpO₂ 94-98%) (0.5 marks)
3. Monitoring - Attach continuous telemetry, pulse oximetry, blood pressure monitoring (0.5 marks)
4. IV access - Establish two large-bore peripheral IV cannulas (0.5 marks)
5. Defibrillator pads - Apply pads in preparation for cardioversion (0.5 marks)
6. Sedation - Midazolam 2-5 mg IV (or ketamine 0.5-1 mg/kg IV) if patient is conscious; do NOT delay cardioversion if unconscious or peri-arrest (1 mark)
7. Synchronized cardioversion - Immediate synchronized DC cardioversion at 120-200 J biphasic (1 mark)
   • Must activate SYNC mode (0.5 marks)
   • Safety check ("I'm clear, you're clear, everyone clear") (0.5 marks)
8. Reassess - Check pulse, rhythm, and blood pressure after cardioversion (0.5 marks)
9. Post-cardioversion management - 12-lead ECG, treat underlying cause, continuous monitoring (0.5 marks)
10. If unsuccessful - Repeat cardioversion at higher energy (200J, then 360J) (0.5 marks)

Examiner Notes:

• Critical: Must include immediate synchronized cardioversion (2 marks for this alone if detailed)
• Accept: "Electricity" or "shock" instead of "cardioversion" if context clear
• Do not accept: Amiodarone as first-line (this is UNSTABLE - cardiovert first, not medication)
• Partial marks: Can allocate 0.5 marks for each key component if answer incomplete

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Question 3 (6 marks)

Stem: A 28-year-old male with known Wolff-Parkinson-White (WPW) syndrome presents with an irregular broad-complex tachycardia at a rate of 220 beats per minute. He is alert and his blood pressure is 110/65 mmHg.

Question: List 3 medications that are contraindicated in this patient and explain why. (6 marks - 2 marks each)

Model Answer:

1. Adenosine (or accept: "AV nodal blockers")

   • Contraindicated because it blocks the AV node, which diverts all atrial impulses down the accessory pathway (Bundle of Kent)
   • This results in extremely rapid ventricular rate (greater than 300/min) and risk of degeneration to ventricular fibrillation (2 marks)

2. Verapamil (or accept: "Calcium channel blockers"

• diltiazem)
  • Blocks AV node, same mechanism as adenosine - diverts impulses down accessory pathway
  • Causes severe hypotension (negative inotrope) and risk of VF (2 marks)

3. Digoxin
   • Blocks AV node AND shortens the refractory period of the accessory pathway
   • Increases conduction velocity down accessory pathway → very rapid ventricular rate → VF risk (2 marks)

Alternative acceptable answer (instead of #3):

• Beta-blockers (e.g., metoprolol, atenolol) - Slow AV node conduction, same diversion mechanism (partial credit 1.5/2 - less absolute contraindication than adenosine/CCBs/digoxin, but still avoided in acute pre-excited AF)

Examiner Notes:

• Must include mechanism (not just list the drug) to get full 2 marks per drug
• Accept: "Diverts to accessory pathway" or "all impulses go down Bundle of Kent" or "bypasses AV node rate control"
• Do not accept: "Causes arrhythmia" without specifying mechanism

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Question 4 (8 marks)

Stem: A 70-year-old woman on haloperidol and furosemide develops polymorphic ventricular tachycardia (torsades de pointes). She is successfully defibrillated and is now in sinus rhythm with a QTc of 580 ms. Her potassium is 2.8 mmol/L.

Question: Outline the management to prevent recurrence of torsades de pointes. (8 marks)

Model Answer:

1. Magnesium sulfate - 2 g IV over 1-2 minutes, can repeat if torsades recurs (even if serum Mg²⁺ normal) (1.5 marks)
2. Potassium repletion - Urgent correction to target K⁺ greater than 4.5 mmol/L:
   • Give 20-40 mmol KCl IV over 1-3 hours via central line (or 20 mmol peripherally, repeated) (1.5 marks)
3. Stop QT-prolonging drugs - Cease haloperidol immediately (0.5 marks)
4. Reduce/cease furosemide - Causes ongoing potassium loss, contributing to hypokalaemia (0.5 marks)
5. Magnesium repletion - Target Mg²⁺ greater than 1.0 mmol/L (if low) (0.5 marks)
6. Increase heart rate (if bradycardic or pause-dependent torsades):
   • Isoprenaline infusion 2-10 mcg/min IV OR temporary pacing at 90-110/min (1 mark)
   • Rationale: Higher heart rate shortens QT interval and prevents post-ectopic pauses that trigger torsades (0.5 marks)
7. Continuous telemetry monitoring - ICU/CCU admission with ECG monitoring until QTc normalizes (0.5 marks)
8. Repeat ECG - Monitor QTc every 6 hours to track improvement (0.5 marks)
9. Cardiology consult - To exclude congenital long QT syndrome and risk-stratify (0.5 marks)

Examiner Notes:

• Critical: Must include magnesium AND potassium correction (3 marks combined)
• Critical: Must stop culprit QT-prolonging drug (haloperidol) (0.5 marks)
• Accept: "Overdrive pacing" or "temporary pacing" for increasing heart rate
• Accept: "Electrical pacing" or "pharmacological pacing (isoprenaline)"
• Bonus (examiner discretion): If candidate mentions "Do NOT give amiodarone" → +0.5

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Australian Guidelines

ARC/ANZCOR

ANZCOR Guideline 11.8: Tachycardia

Key Recommendations (2021 update):

1. Broad-complex tachycardia should be assumed to be VT unless proven otherwise

   • Clinical features (haemodynamic stability, age) are unreliable for differentiation
   • If any doubt, manage as VT

2. Unstable patients (SBP below 90, altered mental status, chest pain, acute heart failure):

   • Immediate synchronized cardioversion: 120-200J biphasic
   • Sedation if time permits, but do NOT delay for sedation if patient is peri-arrest

3. Stable VT:

   • First-line: Amiodarone 300 mg IV over 20-60 minutes
   • Alternative: Procainamide 10-15 mg/kg IV over 30-60 minutes (max 17 mg/kg)
   • Avoid: Adenosine, verapamil, diltiazem (risk of cardiovascular collapse if VT)

4. Polymorphic VT (torsades de pointes):

   • Magnesium sulfate 2 g IV (first-line, even if Mg²⁺ normal)
   • Correct hypokalaemia (K⁺ greater than 4.5), hypomagnesaemia (Mg²⁺ greater than 1.0)
   • Increase heart rate if bradycardic (isoprenaline, pacing)
   • Do NOT use amiodarone (prolongs QT)

5. Pre-excited AF (WPW):

   • Avoid: Adenosine, verapamil, diltiazem, digoxin (precipitate VF)
   • Use: Amiodarone, procainamide, or electrical cardioversion

Key Differences from AHA/ERC

Australian-specific emphasis:

• Stronger recommendation to avoid adenosine in broad-complex tachycardia (ANZCOR: "assume VT, do not use AV nodal blockers")
• Higher initial amiodarone dose (300 mg vs AHA 150 mg)

Therapeutic Guidelines Australia

Cardiovascular Guidelines (2023):

1. Acute VT management:

   • Haemodynamically unstable: Cardioversion
   • Haemodynamically stable: Amiodarone 300 mg IV OR procainamide 10 mg/kg IV

2. Post-VT management:

   • Beta-blocker (if ischaemic VT): Metoprolol 25-50 mg PO q6-12h
   • Consider ICD if LVEF ≤35% or recurrent VT despite medical therapy

3. Drug interactions:

   • Amiodarone: Prolongs QT (avoid with other QT drugs), increases warfarin effect (reduce warfarin dose 30-50%)
   • Avoid combination of QT-prolonging drugs: Antipsychotics + macrolides + diuretics (hypokalaemia) = high torsades risk

State-Specific Protocols

NSW Ambulance Protocol

• Pre-hospital VT: If stable, transport without medication (defer to ED); if unstable, cardiovert (midazolam 0.05 mg/kg IV sedation)
• Pre-hospital adenosine: NOT indicated for broad-complex tachycardia

Victoria (Ambulance Victoria)

• Similar to NSW: Cardioversion for unstable BCT, withhold antiarrhythmics (defer to hospital)

Queensland

• Remote/rural protocols: If greater than 2 hours from PCI-capable centre, consider amiodarone during RFDS retrieval for stable VT

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Remote/Rural Considerations

Pre-Hospital

RFDS / Ambulance:

• ECG transmission: Use 12-lead ECG with telemetry to metro ED for interpretation (if local uncertainty about VT vs SVT)
• Medication availability: Amiodarone available in most RFDS aircraft and rural ambulances; procainamide less common
• Cardioversion: All RFDS aircraft and remote EDs have defibrillators; ensure staff training in synchronized mode

Challenges:

• Misdiagnosis of VT as SVT due to limited ECG interpretation experience → inappropriate adenosine use (reports of cardiovascular collapse)
• Delayed cardioversion due to lack of procedural sedation skills or equipment

Resource-Limited Setting

If procainamide, central line, or ICU unavailable:

1. Stable VT: Amiodarone 300 mg IV peripherally (use large vein, slow infusion to minimize phlebitis)
2. Unstable VT: Cardioversion (sedation with midazolam or ketamine if available; if not, cardiovert awake if life-threatening)
3. Electrolyte repletion: KCl 20 mmol peripherally over 1 hour (repeat as needed for K⁺ below 3.5); MgSO4 10 mmol IV over 30 min
4. Post-cardioversion: Continuous telemetry; if recurs and no antiarrhythmic drugs available, repeat cardioversion + urgent retrieval

Retrieval

Indications for retrieval to tertiary centre:

Retrieval preparation:

1. Stabilize: Cardiovert if unstable; amiodarone infusion if stable
2. Secure airway: If sedated for repeated cardioversions, consider intubation for transport
3. Documentation: 12-lead ECG (before and after cardioversion), rhythm strips, medication doses/times
4. Communication: Contact retrieval service (RFDS 1800 625 800; state-based) + receiving cardiology/EP team
5. Medications for transport: Amiodarone infusion (900 mg/24h), sedation (midazolam/propofol), resuscitation drugs (adrenaline, atropine)

RFDS capabilities:

• Cardioversion (defibrillator on all aircraft)
• Amiodarone infusion
• Temporary pacing (selected aircraft with critical care paramedics/doctors)
• Limitations: Limited blood products, no catheter lab access (need retrieval to metro)

Telemedicine

Applications:

1. ECG interpretation: Remote cardiologist/EP reviews 12-lead ECG via telehealth (apply Brugada criteria, confirm VT vs SVT)
2. Management advice: Drug choice, cardioversion timing, retrieval decision
3. Post-cardioversion monitoring: Daily ECG review via telemedicine until patient transferred or stable for discharge

Services available:

• NSW Telestroke (extends to cardiology consult in some LHDs)
• QLD Virtual ED (metro ED support for rural sites)
• NT TEHS Telehealth (Alice Springs/Darwin support for remote clinics)
• Private services: Telehealth companies provide on-demand cardiology reviews (fee-for-service)

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References

Guidelines

1. Australian Resuscitation Council. ANZCOR Guideline 11.8: Tachycardia. 2021. Available from: https://www.resus.org.au
2. Australian Resuscitation Council. ANZCOR Guideline 11.2: Protocols for Adult Advanced Life Support. 2021.
3. Therapeutic Guidelines. Cardiovascular. Version 7. Melbourne: Therapeutic Guidelines Limited; 2023.
4. National Heart Foundation of Australia. Guidelines for the diagnosis and management of acute coronary syndromes. 2016.

Key Evidence - Brugada Criteria & Differentiation

5. Brugada P, Brugada J, Mont L, et al. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation. 1991;83(5):1649-1659. PMID: 2022012
6. Vereckei A, Duray G, Szénási G, et al. Application of a new algorithm in the differential diagnosis of wide QRS complex tachycardia. Eur Heart J. 2007;28(5):589-600. PMID: 18084011
7. Pava LF, Perafán P, Badiel M, et al. R-wave peak time at DII: a new criterion for differentiating between wide complex QRS tachycardias. Heart Rhythm. 2010;7(7):922-926. PMID: 20643200
8. Jastrzebski M, Sasaki K, Kukla P, et al. The ventricular tachycardia score: a novel approach to electrocardiographic diagnosis of ventricular tachycardia. Europace. 2016;18(4):578-584. PMID: 22409943
9. Baxi RP, Hart KW, Vereckei A, et al. Verifying the principle of lead aVR in the differential diagnosis of wide QRS complex tachycardia. J Cardiovasc Electrophysiol. 2009;20(3):311-316. PMID: 19175849
10. Isenhour JL, Craig S, Gibbs M, et al. Wide-complex tachycardia: continued evaluation of diagnostic criteria. Acad Emerg Med. 2000;7(7):769-773. PMID: 10917325

Key Evidence - VT Epidemiology & Outcomes

11. Aliot EM, Stevenson WG, Almendral-Garrote JM, et al. EHRA/HRS Expert Consensus on Catheter Ablation of Ventricular Arrhythmias. Heart Rhythm. 2009;6(6):886-933. PMID: 19467519
12. Zipes DP, Camm AJ, Borggrefe M, et al. ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death. Circulation. 2006;114(10):e385-e484. PMID: 16935995
13. Akhtar M, Shenasa M, Jazayeri M, et al. Wide QRS complex tachycardia. Reappraisal of a common clinical problem. Ann Intern Med. 1988;109(11):905-912. PMID: 3056169
14. Buxton AE, Marchlinski FE, Doherty JU, et al. Hazards of intravenous verapamil for sustained ventricular tachycardia. Am J Cardiol. 1987;59(12):1107-1110. PMID: 3578050

Key Evidence - Pharmacotherapy (Amiodarone, Procainamide)

15. Tomlinson DR, Cherian P, Betts TR, et al. Intravenous amiodarone for the pharmacological termination of haemodynamically-tolerated sustained ventricular tachycardia: is bolus dose amiodarone an appropriate first-line treatment? Emerg Med J. 2008;25(1):15-18. PMID: 18156532
16. Marill KA, deSouza IS, Nishijima DK, et al. Amiodarone is poorly effective for the acute termination of ventricular tachycardia. Ann Emerg Med. 2006;47(3):217-224. PMID: 16492483
17. Gorgels AP, van den Dool A, Hofs A, et al. Comparison of procainamide and lidocaine in terminating sustained monomorphic ventricular tachycardia. Am J Cardiol. 1996;78(1):43-46. PMID: 8712116
18. Ortiz M, Martín A, Arribas F, et al. Randomized comparison of intravenous procainamide vs. intravenous amiodarone for the acute treatment of tolerated wide QRS tachycardia: the PROCAMIO study. Eur Heart J. 2017;38(17):1329-1335. PMID: 27354617

Key Evidence - Cardioversion

19. Botto GL, Politi A, Bonini W, et al. External cardioversion of atrial fibrillation: role of paddle position on technical efficacy and energy requirements. Heart. 1999;82(6):726-730. PMID: 10573502
20. Mittal S, Ayati S, Stein KM, et al. Transthoracic cardioversion of atrial fibrillation: comparison of rectilinear biphasic versus damped sine wave monophasic shocks. Circulation. 2000;101(11):1282-1287. PMID: 10725290

Key Evidence - Torsades de Pointes & Long QT

21. Roden DM. Drug-induced prolongation of the QT interval. N Engl J Med. 2004;350(10):1013-1022. PMID: 14999113
22. Tzivoni D, Banai S, Schuger C, et al. Treatment of torsade de pointes with magnesium sulfate. Circulation. 1988;77(2):392-397. PMID: 3338132
23. Khan IA. Long QT syndrome: diagnosis and management. Am Heart J. 2002;143(1):7-14. PMID: 11773903
24. Drew BJ, Ackerman MJ, Funk M, et al. Prevention of torsade de pointes in hospital settings: a scientific statement from the AHA and ACCF. Circulation. 2010;121(8):1047-1060. PMID: 20142454

Key Evidence - WPW & Pre-Excited AF

25. Gollob MH, Redpath CJ, Roberts JD. The short QT syndrome: proposed diagnostic criteria. J Am Coll Cardiol. 2011;57(7):802-812. PMID: 21310316
26. Blomström-Lundqvist C, Scheinman MM, Aliot EM, et al. ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias. Circulation. 2003;108(15):1871-1909. PMID: 14557344
27. Sellers TD Jr, Bashore TM, Gallagher JJ. Digitalis in the pre-excitation syndrome. Analysis during atrial fibrillation. Circulation. 1977;56(2):260-267. PMID: 872319

Key Evidence - ICD Therapy

28. Moss AJ, Zareba W, Hall WJ, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. N Engl J Med. 2002;346(12):877-883. PMID: 11907286
29. Bardy GH, Lee KL, Mark DB, et al. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. N Engl J Med. 2005;352(3):225-237. PMID: 15659722
30. Connolly SJ, Hallstrom AP, Cappato R, et al. Meta-analysis of the implantable cardioverter defibrillator secondary prevention trials. Eur Heart J. 2000;21(24):2071-2078. PMID: 11102258

Systematic Reviews & Meta-Analyses

31. Zipes DP, Wellens HJ. Sudden cardiac death. Circulation. 1998;98(21):2334-2351. PMID: 9826323
32. Katritsis DG, Boriani G, Cosio FG, et al. European Heart Rhythm Association (EHRA) consensus document on the management of supraventricular arrhythmias. Europace. 2017;19(3):465-511. PMID: 28175283
33. Neumar RW, Otto CW, Link MS, et al. Part 8: Adult Advanced Cardiovascular Life Support: 2010 AHA Guidelines for CPR and ECC. Circulation. 2010;122(18 Suppl 3):S729-S767. PMID: 20956224

Australian Context & Indigenous Health

34. Agostino JW, Wong D, Paige E, et al. Cardiovascular disease risk assessment for Aboriginal and Torres Strait Islander adults aged under 35 years: a cohort study. Aust N Z J Public Health. 2020;44(5):384-390. PMID: 32860284
35. Katzenellenbogen JM, Sanfilippo FM, Hobbs MS, et al. Incidence of and case fatality following acute myocardial infarction in Aboriginal and non-Aboriginal Western Australians (2000-2004). Heart. 2010;96(19):1548-1553. PMID: 20798059
36. Australian Institute of Health and Welfare. Cardiovascular disease in Aboriginal and Torres Strait Islander people. Cat. no. CVD 64. Canberra: AIHW; 2014.
37. Glover M, Kira A, Johnston V, et al. A systematic review of barriers and facilitators to participation in cardiac rehabilitation by Māori. J Prim Health Care. 2013;5(4):261-269. PMID: 24323067

Remote/Rural & Retrieval Medicine

38. Royal Flying Doctor Service. Annual Report 2021-22. Available from: https://www.flyingdoctor.org.au
39. Fatovich DM, Jacobs IG. The relationship between remoteness and trauma deaths in Western Australia. J Trauma. 2009;67(5):910-914. PMID: 19901648
40. Reeve C, Humphreys J, Wakerman J, et al. Strengthening primary health care: achieving health gains in a remote region of Australia. Med J Aust. 2015;202(9):483-488. PMID: 25971570

Additional Key Studies

41. Wellens HJ, Bär FW, Lie KI. The value of the electrocardiogram in the differential diagnosis of a tachycardia with a widened QRS complex. Am J Med. 1978;64(1):27-33. PMID: 623134
42. Stewart RB, Bardy GH, Greene HL. Wide complex tachycardia: misdiagnosis and outcome after emergent therapy. Ann Intern Med. 1986;104(6):766-771. PMID: 3706928