Home Cardiology Antiarrhythmic Medications (Vaughan-Williams)

Antiarrhythmic Medications (Vaughan-Williams)

📋 Key Information Summary

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  • The Vaughan-Williams classification categorises antiarrhythmic drugs into four classes (I–IV) based on their primary electrophysiological mechanism.
  • Class I agents are sodium channel blockers subdivided into IA (quinidine, procainamide, disopyramide — moderate Na⁺ block, widen QRS), IB (lignocaine, mexiletine — weak/fast Na⁺ block, narrow QRS), and IC (flecainide, propafenone — potent Na⁺ block, significant QRS widening).
  • Class II agents are beta-adrenergic blockers that reduce automaticity and AV conduction; first-line for SVT rate control and post-MI arrhythmia prevention.
  • Class III agents are potassium channel blockers that prolong repolarisation (QT interval); amiodarone is the most widely used antiarrhythmic in Australia due to broad efficacy across SVT and VT.
  • Sotalol has combined Class III and non-selective beta-blocking properties and is PBS-listed for ventricular and supraventricular arrhythmias.
  • Class IV agents — verapamil and diltiazem — are non-dihydropyridine calcium channel blockers effective for SVT rate control; contraindicated in VT and heart failure with reduced ejection fraction.
  • All Class I agents are proarrhythmic and are contraindicated in structural heart disease (CAST trial evidence for IC agents) and should generally be initiated under specialist supervision.
  • Amiodarone requires baseline thyroid, hepatic, pulmonary function and ophthalmological assessment before initiation, with ongoing surveillance every 6–12 months.
  • IV lignocaine remains a first-line agent for acute ventricular tachycardia in the context of myocardial ischaemia in Australian emergency departments.
  • Dronedarone is a non-iodinated amiodarone analogue indicated for paroxysmal or persistent AF; contraindicated in NYHA III–IV heart failure and severe hepatic impairment.
  • Beta-blockers are first-line for rate control in atrial fibrillation per Australian RACGP and Cardiac Society of Australia and New Zealand (CSANZ) guidelines.
  • Proarrhythmia risk is highest with Class IC agents in patients with coronary artery disease or left ventricular dysfunction — specialist initiation mandatory.
  • Aboriginal and Torres Strait Islander peoples experience higher rates of rheumatic heart disease and atrial fibrillation, necessitating culturally safe access to rhythm-control strategies and specialist review.
  • Drug–drug interactions are a major safety concern, particularly with amiodarone (CYP3A4/2C9 inhibition) and flecainide (CYP2D6 substrate); always check interactions before prescribing.

Introduction & Australian Epidemiology

Antiarrhythmic drugs (AADs) form a cornerstone of cardiac rhythm management in Australia. The Vaughan-Williams classification, first proposed in 1970, remains the most widely used framework for organising these agents by their primary electrophysiological effect on the cardiac action potential. While pharmacological approaches are increasingly complemented by catheter ablation, antiarrhythmic medications remain essential for acute termination, prophylaxis, and rate control of arrhythmias encountered in Australian primary care and hospital settings.

Atrial fibrillation (AF) is the most common sustained arrhythmia managed in Australia, affecting approximately 2–4% of the adult population, with prevalence rising sharply after age 60. The Australian Institute of Health and Welfare (AIHW) estimates that over 400,000 Australians live with AF, with more than 40,000 new diagnoses each year. AF contributes to approximately 10% of all ischaemic strokes in Australia. Ventricular tachycardia (VT) and ventricular fibrillation (VF) remain leading causes of sudden cardiac death, with approximately 20,000 out-of-hospital cardiac arrests per year reported by the Australian Resuscitation Council.

Access to antiarrhythmic therapy in Australia is shaped by Pharmaceutical Benefits Scheme (PBS) listings, metropolitan versus rural specialist availability, and the integration of general practice, emergency medicine, and cardiology teams. This guideline provides a comprehensive overview of the Vaughan-Williams classes with Australian prescribing context, PBS status, and safety considerations.

⚠️
Proarrhythmia warning: All antiarrhythmic drugs have the potential to provoke new or worsened arrhythmias. The CAST and CAST-II trials demonstrated increased mortality with Class IC agents (flecainide, encainide) in patients with structural heart disease. Specialist initiation and monitoring are recommended for most AADs.
Antiarrhythmic Medications (Vaughan-Williams) clinical infographic — pathophysiology, clinical clues, diagnosis, imaging, and management
Tap or click image to enlarge — Antiarrhythmic Medications (Vaughan-Williams): pathophysiology, clinical clues, diagnosis, imaging, and management.
Antiarrhythmic Medications (Vaughan-Williams) infographic, full size

Class I: Sodium Channel Blockers

Class I antiarrhythmics block voltage-gated sodium channels (Nav1.5) during Phase 0 of the cardiac action potential, reducing the maximum rate of depolarisation (Vmax). They are subdivided into IA, IB, and IC based on the kinetics of sodium channel binding and their effect on action potential duration (APD) and QRS width.

Class IA — Moderate Sodium Channel Blockers

Class IA agents dissociate from sodium channels at an intermediate rate. They moderately slow conduction and prolong repolarisation, widening both the QRS complex and the QT interval. They have efficacy against both atrial and ventricular arrhythmias but carry significant anticholinergic and proarrhythmic risks.

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Quinidine
Quinidine bisulfate · Class IA
Adult dose 200–400 mg PO 6–8-hourly; max 1600 mg/day
Paediatric dose 15–30 mg/kg/day PO in 4–6 divided doses (under specialist supervision)
Key interactions CYP3A4 substrate; raises digoxin levels by 50–100%; additive QT prolongation with other QT-prolonging drugs
Renal adjustment Dose reduce if eGFR <30 mL/min; monitor QTc
PBS status ⚠ PBS Restricted Benefit
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Procainamide
Pronestyl® · Class IA
Adult IV dose Loading: 15–18 mg/kg IV over 60 min (max 1.2 g); maintenance: 1–4 mg/min IV infusion
Adult oral dose 250–500 mg PO 4–6-hourly (sustained release 500–1000 mg 6-hourly)
Key monitoring NAPA (active metabolite) levels; ANA/anti-histone antibodies q3–6 months; agranulocytosis risk
Renal adjustment Dose and interval adjustment if eGFR <50 mL/min (NAPA accumulation)
PBS status ⚠ PBS Restricted Benefit
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Disopyramide
Norpace® CR · Rythmodan® · Class IA
Adult dose 100–200 mg PO 6–8-hourly (CR: 250 mg BD); max 800 mg/day
Paediatric dose Under specialist direction only
Key interactions Strong negative inotrope — contraindicated in HFrEF; potent anticholinergic effects
Renal adjustment Max 100 mg/day if eGFR <40 mL/min; max 200 mg/day if eGFR 15–40 mL/min
PBS status ✔ PBS General Benefit

Class IB — Weak/Fast Sodium Channel Blockers

Class IB agents bind to and dissociate from sodium channels rapidly. They have minimal effect on conduction velocity in normal tissue but preferentially bind ischaemic/depressed sodium channels. They shorten APD slightly and do not widen the QRS. Their principal role in Australia is in acute ventricular arrhythmia management.

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Lignocaine (Lidocaine)
Xylocard® · Class IB
Adult IV dose Loading: 1–1.5 mg/kg IV bolus; repeat 0.5–0.75 mg/kg q5–10 min (max 3 mg/kg); maintenance: 1–4 mg/min infusion
Paediatric dose 1 mg/kg IV bolus; infusion 20–50 µg/kg/min
Key interactions CYP1A2/3A4 metabolised; toxicity enhanced by amiodarone, beta-blockers, cimetidine
Hepatic adjustment Reduce infusion rate by 50% in hepatic impairment or heart failure (reduced clearance)
PBS status ✔ PBS General Benefit
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Mexiletine
Mexitil® · Class IB
Adult dose 200–400 mg PO 8-hourly; max 1200 mg/day
Indication Refractory ventricular arrhythmias; synergistic with amiodarone
Key interactions CYP2D6 and CYP1A2 substrate; fluvoxamine and ciprofloxacin increase levels substantially
PBS status ⚠ PBS Restricted Benefit

Class IC — Potent Sodium Channel Blockers

Class IC agents dissociate slowly from sodium channels and produce the greatest slowing of conduction velocity with significant QRS widening. They minimally affect repolarisation. Following the CAST trial (1989), which demonstrated increased mortality with encainide and flecainide in post-MI patients, Class IC agents are contraindicated in structural heart disease and should only be used as "pill-in-the-pocket" therapy or in structurally normal hearts under specialist guidance.

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Flecainide
Tambocor® · Class IC
Adult oral dose 50–200 mg PO BD; start 50 mg BD, titrate by 50 mg increments weekly
Pill-in-pocket 200–300 mg PO stat for acute AF termination (in-hospital safety check required first)
Paediatric dose 1–6 mg/kg/day PO in 2–3 divided doses (specialist only)
Key interactions CYP2D6 substrate — avoid co-administration with amiodarone (↑ flecainide by 50%); add negative inotropy with beta-blockers
Renal adjustment 50 mg BD if eGFR <35 mL/min; avoid if eGFR <10 mL/min
PBS status ✔ PBS General Benefit
💊
Propafenone
Rythmol® · Class IC
Adult dose 150–300 mg PO 8-hourly; start 150 mg TDS
Key interactions CYP2D6 substrate (genetic polymorphism — poor metabolisers have ↑ risk); mild beta-blocking and calcium channel blocking properties
PBS status ⚠ PBS Restricted Benefit
🚨
Contraindication — structural heart disease: Class IC agents (flecainide, propafenone) are contraindicated in patients with ischaemic heart disease, left ventricular dysfunction (LVEF <40%), or significant valvular heart disease due to increased mortality risk demonstrated in the CAST trial. Specialist initiation is mandatory.

Class II: Beta-Adrenergic Blockers

Beta-blockers are the most commonly prescribed antiarrhythmic agents in Australian clinical practice. They reduce automaticity by decreasing Phase 4 diastolic depolarisation in the sinoatrial (SA) node, slow AV nodal conduction, and reduce myocardial oxygen demand. They are first-line for ventricular rate control in atrial fibrillation and flutter, and are the only AAD class with robust mortality benefit post-myocardial infarction and in heart failure with reduced ejection fraction (HFrEF).

Agent Selectivity IV Dose Oral Dose PBS
Metoprolol (Lopresor®) β₁ selective 5 mg IV q5 min × 3 doses 25–200 mg PO BD (tartate); 23.75–190 mg OD (succinate ER) ✔ General
Atenolol (Noten®) β₁ selective 0.5–1 mg IV over 5 min; repeat q5 min (max 10 mg) 25–100 mg PO OD ✔ General
Bisoprolol (Bicor®) β₁ highly selective N/A (oral only) 1.25–10 mg PO OD ✔ General
Carvedilol (Dilatrend®) Non-selective β + α₁ N/A (oral only) 3.125–50 mg PO BD (HFrEF) ✔ General
Sotalol (Sotacor®) Non-selective β + Class III 20–120 mg IV over 10–30 min 80–320 mg PO BD (see Class III section) ✔ General
Esmolol (Brevibloc®) β₁ ultra-short acting 500 µg/kg bolus; 50–200 µg/kg/min infusion IV only ⚠ Restricted

Prescribing Pearls — Beta-Blockers

  • HFrEF (LVEF ≤40%): Bisoprolol, carvedilol, or sustained-release metoprolol succinate are the evidence-based choices (CIBIS-II, MERIT-HF, COPERNICUS trials). Start low and titrate every 2–4 weeks.
  • Post-MI: Metoprolol, atenolol, or propranolol initiated within 24 hours of STEMI (if no contraindications) reduces mortality by ~20%.
  • AF rate control: Metoprolol or bisoprolol first-line; add digoxin or diltiazem if rate remains >110 bpm at rest.
  • Asthma/COPD: Use β₁-selective agents (bisoprolol > metoprolol > atenolol) cautiously; avoid non-selective agents. Cardiology consultation recommended.
  • Diabetes: Beta-blockers may mask hypoglycaemic symptoms (tremor, tachycardia) — educate patients; glucose monitoring is essential.
ℹ️
Avoid abrupt withdrawal: Beta-blocker withdrawal can precipitate rebound tachycardia, hypertension, and in patients with ischaemic heart disease, acute coronary syndrome. Taper over 1–2 weeks when discontinuing.

Class III: Potassium Channel Blockers

Class III agents block outward potassium currents (primarily IKr — the rapid delayed rectifier) during Phase 3 repolarisation, prolonging the action potential duration and the effective refractory period. This manifests as QT interval prolongation on the surface ECG. The antiarrhythmic effect results from prolonging the refractory period, thereby preventing re-entrant circuits. However, excessive QT prolongation carries the risk of Torsades de Pointes (TdP), a polymorphic ventricular tachycardia.

Amiodarone

Amiodarone is a complex antiarrhythmic agent with actions across all four Vaughan-Williams classes: it blocks sodium channels (Class I), has non-competitive beta-blocking properties (Class II), blocks potassium channels (Class III), and blocks calcium channels (Class IV). It is the most widely used and most effective antiarrhythmic drug in Australia for both supraventricular and ventricular arrhythmias.

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Amiodarone
Cordarone® X · Aratac® · Amphocin®
IV loading (haemodynamically stable VT/VF) 300 mg IV in 100 mL D5W over 20–60 min; repeat 150 mg IV if needed; maintenance 900 mg IV over 18 hours (1 mg/min × 6 h then 0.5 mg/min)
Oral loading 400 mg PO TDS × 7 days → 200 mg PO TDS × 7 days → 200 mg PO OD maintenance
Paediatric dose IV: 5 mg/kg over 20–60 min (max 300 mg); oral: 10–15 mg/kg/day loading → 5 mg/kg/day maintenance
Key interactions Potent CYP3A4 and CYP2C9 inhibitor — ↑ warfarin by 30–50% (reduce warfarin dose by 30–50%); ↑ digoxin by 70%; ↑ simvastatin (max simvastatin 20 mg/day); ↑ flecainide by 50%
Monitoring TFTs, LFTs, CXR, ophthalmology at baseline → TFTs/LFTs q3–6 months; CXR annually; ophthalmology annually
Organ toxicity Thyroid dysfunction (hypo- or hyper-, 15–20%); pulmonary toxicity (1–5%); hepatotoxicity (15–30% ↑ LFTs); optic neuropathy (<1%); photosensitivity (very common); peripheral neuropathy
Renal adjustment Not required (hepatically metabolised); IV formulation contains polysorbate 80 — caution in renal impairment
PBS status ✔ PBS General Benefit
⚠️
Amiodarone monitoring schedule (Australian practice): Baseline — TFTs (TSH, free T4, free T3), LFTs (ALT, AST, GGT, bilirubin), FBC, CXR, spirometry (DLCO), slit-lamp eye exam, ECG (QTc). Follow-up — TFTs and LFTs every 3–6 months for life; CXR annually; ophthalmology review annually or if visual symptoms; ECG at each visit (QTc >500 ms warrants review).

Dronedarone

Dronedarone is a non-iodinated benzofuran derivative structurally related to amiodarone. It lacks iodine atoms, resulting in significantly lower rates of thyroid and pulmonary toxicity. However, it is less efficacious than amiodarone and is specifically indicated for maintaining sinus rhythm in patients with paroxysmal or persistent atrial fibrillation.

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Dronedarone
Multaq®
Adult dose 400 mg PO BD with meals
Key interactions CYP3A4 substrate and inhibitor; contraindicated with strong CYP3A4 inhibitors (ketoconazole, itraconazole, ritonavir, clarithromycin); ↑ digoxin by 25%; inhibits P-glycoprotein
Absolute contraindications NYHA III–IV or unstable HF; permanent AF (ATHENA sub-analysis); QTc >500 ms; 2nd/3rd degree AV block; severe hepatic impairment; concurrent QT-prolonging agents
PBS status ✖ Authority Required

Sotalol

Sotalol is a non-selective beta-blocker with additional Class III potassium channel blocking properties. It prolongs the QT interval in a dose-dependent manner and is used for both supraventricular and ventricular arrhythmias in Australia.

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Sotalol
Sotacor® · Sotahexal®
Adult oral dose 80 mg PO BD; titrate to 160–320 mg/day in divided doses; initiate in hospital with telemetry (minimum 3 days)
IV dose 20–120 mg IV over 10–30 min (1.5 mg/kg)
Paediatric dose 1–8 mg/kg/day PO in 2–3 divided doses (specialist only)
Renal adjustment Dose interval: q12h if CrCl >60 → q24h if CrCl 30–60 → q36–48h if CrCl 10–30 → avoid if CrCl <10
PBS status ✔ PBS General Benefit
🚨
Torsades de Pointes risk: Both amiodarone and sotalol prolong QT interval. Risk of TdP is increased with hypokalaemia, hypomagnesaemia, bradycardia, female sex, congenital long QT, and concomitant QT-prolonging drugs. Correct electrolytes before initiation; monitor QTc — reduce or discontinue if QTc >500 ms.

Class IV: Calcium Channel Blockers & Other Agents

Non-Dihydropyridine Calcium Channel Blockers

Class IV agents block L-type calcium channels in the SA and AV nodes, slowing automaticity and AV conduction. Only the non-dihydropyridine agents (verapamil and diltiazem) have significant antiarrhythmic properties. Dihydropyridines (amlodipine, nifedipine) act primarily on vascular smooth muscle and are not used as antiarrhythmics.

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Verapamil
Isoptin® · Cordilox®
Adult IV dose (acute SVT) 5–10 mg IV over 2–3 min; repeat 5–10 mg after 15–30 min if needed
Adult oral dose 40–120 mg PO TDS; SR: 180–480 mg PO OD
Key interactions CYP3A4 substrate/inhibitor; ↑ digoxin by 50–75%; ↑ simvastatin (avoid >10 mg/day); potentiation with beta-blockers (risk severe bradycardia, asystole)
Contraindications VT (can cause haemodynamic collapse); HFrEF (LVEF <40%); 2nd/3rd degree AV block without pacemaker; IV use with IV beta-blockers within prior 4 hours
PBS status ✔ PBS General Benefit
💊
Diltiazem
Cardizem® CD · Vasocardol®
Adult IV dose 0.25 mg/kg IV over 2 min; repeat 0.35 mg/kg after 15 min; infusion: 5–15 mg/h
Adult oral dose 60–90 mg PO TDS–QID; CD/ER: 180–360 mg PO OD
Contraindications Same as verapamil — avoid in VT, HFrEF, significant bradycardia
PBS status ✔ PBS General Benefit
🚨
Never give IV verapamil to a wide-complex tachycardia. If the rhythm is ventricular tachycardia (which may be misdiagnosed as SVT with aberrancy), IV verapamil can cause profound hypotension and cardiac arrest. Always assume wide-complex tachycardia is VT until proven otherwise.

Other Antiarrhythmic Agents

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Digoxin
Lanoxin®
Mechanism Inhibits Na⁺/K⁺ ATPase → vagotonic → slows AV conduction; Class IV-like effects
Adult dose Loading: 500–1000 µg PO in divided doses over 24 h; maintenance: 62.5–250 µg OD
Target level 0.5–0.9 ng/mL for AF rate control (DIG trial: higher levels → increased mortality)
Renal adjustment Essential — dose by CrCl: 62.5 µg OD if CrCl 10–25 mL/min; haemodialysis patients 62.5 µg OD or alternate days
PBS status ✔ PBS General Benefit
💊
Ivabradine
Corlanor®
Mechanism Selective If channel inhibitor — reduces sinus node rate without affecting conduction, contractility, or repolarisation
Adult dose 5 mg PO BD; titrate to 7.5 mg BD; reduce to 2.5 mg BD if HR <50 bpm
Indication HFrEF (LVEF ≤35%, sinus rhythm, HR ≥70 bpm) — SHIFT trial evidence; or inappropriate sinus tachycardia
PBS status ✖ Authority Required

Adenosine

While not classified under Vaughan-Williams, adenosine is an essential agent in Australian emergency departments for diagnosis and termination of SVT. It activates G-protein-coupled adenosine A₁ receptors causing transient AV block.

💉
Adenosine
Adenocor®
Adult IV dose 6 mg rapid IV bolus via large-bore proximal cannula followed by 20 mL NS flush; if no response in 1–2 min → 12 mg IV bolus; may repeat 12 mg once
Paediatric dose 0.1 mg/kg rapid IV (max 6 mg); repeat 0.2 mg/kg (max 12 mg)
Key considerations Half-life <10 seconds; avoid in asthma (bronchospasm); reduce dose to 3 mg if concurrent dipyridamole or carbamazepine; heart transplant patients require lower doses
PBS status ✔ PBS General Benefit

Investigations & Monitoring

Prior to initiating any antiarrhythmic agent, a structured assessment is essential to guide therapy selection, identify contraindications, and establish a monitoring baseline.

Baseline Investigations

Essential
12-lead ECG
Assess baseline QTc (Bazett correction), QRS duration, PR interval, bundle branch blocks. MBS Item 11700.
Essential
Serum electrolytes (K⁺, Mg²⁺, Ca²⁺)
Hypokalaemia and hypomagnesaemia increase proarrhythmia risk with all AADs. Correct before initiation.
Essential
Renal function (eGFR, CrCl)
Essential for dosing sotalol, digoxin, disopyramide, flecainide.
Essential
Hepatic function (LFTs)
Essential for amiodarone, dronedarone, lignocaine, and hepatically metabolised agents.
Available
Thyroid function tests (TSH, fT4, fT3)
Baseline mandatory for amiodarone; check q3–6 months thereafter. MBS Item 66716.
Available
Transthoracic echocardiography
Assess LVEF and structural heart disease — mandatory to rule out contraindication to Class IC agents. MBS Item 55114.
Referral
Pulmonary function tests (spirometry + DLCO)
Baseline before amiodarone; recommended before dronedarone.
Referral
Ophthalmological examination (slit-lamp)
Baseline before amiodarone (corneal microdeposits, optic neuropathy). Annual follow-up.
Available
Chest X-ray
Baseline before amiodarone (pulmonary fibrosis screening); annual thereafter.
Specialist
24-hour Holter / event monitor
Assess arrhythmia burden, rate control efficacy, QTc trends. MBS Item 11704 / 11707.

Ongoing Monitoring Schedule

Parameter Frequency Agents Requiring Monitoring
ECG (QTc, QRS, HR) At each visit; within 1 week of dose change All AADs; especially sotalol, amiodarone, Class I agents
TFTs Every 3–6 months Amiodarone
LFTs Every 3–6 months Amiodarone, dronedarone
Electrolytes (K⁺, Mg²⁺) Each visit; after any intercurrent illness All AADs; especially diuretic co-prescription
CXR Annually Amiodarone
Ophthalmology Annually or if visual symptoms Amiodarone
Digoxin level 5–7 days after initiation/change; then 3–6 monthly Digoxin (target 0.5–0.9 ng/mL)

Risk Stratification for Proarrhythmia

All antiarrhythmic drugs can cause proarrhythmia — the worsening or provocation of new arrhythmias. Risk varies by drug class, patient substrate, and metabolic factors. Identifying high-risk patients before AAD initiation is critical.

Lower Risk
Structurally Normal Heart
Normal LVEF (>50%), no coronary artery disease, no significant valvular disease, normal QTc at baseline, no electrolyte disturbance.
Setting: Wider range of AADs available including Class IC agents (flecainide, propafenone) for SVT — "pill-in-pocket" approach acceptable after supervised trial.
Moderate Risk
Structural Heart Disease without HFrEF
Mild LV impairment (LVEF 40–50%), treated coronary artery disease, controlled hypertension with LVH, mild valvular disease.
Setting: Avoid Class IC agents; prefer amiodarone, sotalol, or beta-blockers. Specialist initiation recommended. ECG monitoring during initiation.
High Risk
HFrEF, Post-MI, or QT Prolongation
LVEF <40%, recent MI (<3 months), congenital long QT, baseline QTc >460 ms (female) / >450 ms (male), hypokalaemia, significant renal impairment.
Setting: Class IC agents contraindicated. Amiodarone preferred for rhythm control. Inpatient telemetry for any AAD initiation. Correct electrolytes. Cardiology consultation mandatory.
⚠️
CYP2D6 pharmacogenomics: Approximately 5–10% of Caucasians and 1–2% of East Asian Australians are CYP2D6 poor metabolisers. They have significantly elevated flecainide and propafenone levels, increasing proarrhythmia risk. Consider CYP2D6 genotyping in patients with unexplained toxicity. Propranolol and metoprolol are also CYP2D6 substrates.

Special Populations

🤰 Pregnancy
Sotalol
Generally considered first-line for maternal arrhythmias in Australia. Crosses placenta but extensive safety data. Monitor foetal heart rate.
Flecainide
Safe in pregnancy (Category B1). Used for foetal SVT via maternal administration. No teratogenicity signal in registries.
Amiodarone
Category D — avoid if possible. Associated with foetal hypothyroidism, growth restriction, prematurity. Use only when no alternative and mother's life at risk.
Verapamil
Category C — can be used in pregnancy for SVT. Avoid IV bolus (may cause maternal hypotension).
Dronedarone
Category X — absolutely contraindicated in pregnancy. Ensure effective contraception.
👶 Paediatrics
Amiodarone
Widely used in paediatric cardiology for refractory SVT and post-operative junctional ectopic tachycardia (JET). Monitor thyroid and growth.
Flecainide
First-line for SVT prophylaxis in structurally normal paediatric hearts. Requires age-adjusted dosing and serum level monitoring.
Propranolol
First-line beta-blocker for infant SVT and haemangioma-associated arrhythmias. Dose: 1–4 mg/kg/day divided TDS–QID.
Adenosine
Diagnostic and therapeutic agent for SVT in paediatric EDs — 0.1 mg/kg IV (max 6 mg), then 0.2 mg/kg (max 12 mg).
👴 Elderly (≥65 years)
All AADs
Increased sensitivity to negative inotropy and conduction slowing. Lower starting doses, slower titration. Falls risk assessment with rate-controlling agents.
Amiodarone
Higher risk of thyroid dysfunction and pulmonary toxicity in elderly. Reduced loading dose may be appropriate.
Digoxin
Narrow therapeutic index worsened by age-related renal decline. Target low level (0.5–0.9 ng/mL). Polypharmacy interaction risk (amiodarone, verapamil).
🫘 Renal Impairment
Sotalol
Almost entirely renally excreted. Mandatory dose interval extension — see dosing table above. Avoid if CrCl <10 mL/min.
Digoxin
Renally cleared — dose by CrCl. Higher toxicity risk in CKD. Monitor levels closely.
Flecainide
Reduce to 50 mg BD if eGFR <35 mL/min. Avoid if eGFR <10 mL/min.
Amiodarone
No dose adjustment required (hepatic metabolism). IV polysorbate formulation may cause renal concerns — use cautiously.
🫁 Hepatic Impairment
Amiodarone
Contraindicated in severe hepatic impairment. Can cause hepatotoxicity — LFT monitoring essential. Reduce dose if hepatic dysfunction present.
Dronedarone
Contraindicated in severe hepatic impairment (Hepatotoxicity seen in ANDROMEDA trial — avoid in NYHA III–IV).
Lignocaine
Hepatically metabolised — reduce infusion rate by 50% in hepatic impairment or cardiac failure.
Verapamil
Extensive first-pass metabolism — significantly higher bioavailability in cirrhosis. Start at lowest dose.
🛡️ Immunocompromised
Drug interactions
Antifungals (ketoconazole, itraconazole — strong CYP3A4 inhibitors) contraindicated with dronedarone, increase amiodarone and verapamil levels. HIV protease inhibitors significantly increase amiodarone, dronedarone, and verapamil levels.
QT prolongation
Many antimicrobials (fluoroquinolones, azoles, macrolides) prolong QT — additive risk with AADs. Check qdrg.org/crediblemeds for interaction lists.

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Health
Rheumatic Heart Disease Burden
Acute rheumatic fever (ARF) and rheumatic heart disease (RHD) disproportionately affect Aboriginal and Torres Strait Islander peoples, particularly in Northern Australia, Central Australia, and Far North Queensland. RHD leads to atrial fibrillation at younger ages, requiring antiarrhythmic therapy earlier in life. The RHDAustralia registry (2023) reports age-standardised RHD prevalence 20–40 times higher in Indigenous Australians.
AF Prevalence
Atrial fibrillation occurs at a younger age and with greater severity in Indigenous Australians, often in the context of RHD, ischaemic heart disease, and rheumatic valvulopathy. Anticoagulation and rhythm control strategies must account for the higher prevalence of structural heart disease (Class IC agents contraindicated).
Remote & Rural Access
Many Aboriginal and Torres Strait Islander communities in remote areas have limited access to specialist cardiology services, telemetry monitoring, and amiodarone surveillance (TFTs, LFTs, CXR, ophthalmology). Telehealth cardiology services (MBS Item 91822) and Remote Area Nurse-supervised monitoring are essential. Some antiarrhythmic medications may require retrieval to regional centres for initiation.
Medication Adherence
Complex AAD regimens with multiple daily doses and monitoring requirements pose adherence challenges. Long-acting formulations (sustained-release metoprolol, amiodarone once maintenance dose achieved) may improve adherence. Pharmacy support through Remote Area Aboriginal Health Services is critical.
Cultural Safety
Engagement with Aboriginal Health Workers and Practitioners (AHW/Ps) for education on arrhythmia management, medication purpose, and monitoring requirements improves outcomes. Use of culturally appropriate resources and language interpretation services where English is not the first language. Yarning-based approaches to shared decision-making around rhythm vs rate control.
PBS Safety Net & Closing the Gap
Aboriginal and Torres Strait Islander patients may be eligible for Closing the Gap PBS co-payment reductions, lowering out-of-pocket costs for antiarrhythmic medications. Ensure patients are registered with Services Australia for these entitlements.

Quick Reference — Arrhythmia to AAD Selection

AF — Rate control
Beta-blocker (1st line) ± digoxin
Ongoing
Target HR <110 bpm (lenient) or <80 bpm (strict, RACE II)
AF — Rhythm control
Amiodarone, sotalol, flecainide (no structural HD)
Ongoing
Catheter ablation if recurrent/refractory
Atrial flutter
Sotalol, amiodarone, or IC (if no HD)
Ongoing or bridge to ablation
Isthmus-dependent flutter — ablation is highly effective
SVT (AVNRT/AVRT)
Acute: adenosine 6→12 mg IV; Prophylaxis: flecainide, sotalol, or beta-blocker
Acute / prophylactic
Catheter ablation curative (>95% success)
VT — acute (haemodynamically stable)
Amiodarone 300 mg IV or lignocaine 1–1.5 mg/kg IV
Acute
Synchronised cardioversion if unstable
VT — prophylaxis (structural HD)
Amiodarone, sotalol, or beta-blocker + ICD
Ongoing
ICD is primary prevention for LVEF ≤35% (SCD-HeFT, MADIT-II)
Post-MI arrhythmia prevention
Beta-blocker (metoprolol, carvedilol)
Long-term
Only class with mortality evidence post-MI

📚 References

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  2. 2. Cardiac Society of Australia and New Zealand (CSANZ). Guidelines for the diagnosis and management of atrial fibrillation — 2018 update. Heart Lung Circ. 2018;27(10):1209–1266.
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