Chart — Cardiac / Pharmacology
Antiarrhythmic Drug Classes Chart
Antiarrhythmic drugs are classified by the Vaughan Williams system (Class I–IV) based on their primary mechanism of action. Understanding each class — and what it does to the cardiac action potential — helps nurses anticipate drug effects and monitor for complications.
Educational use only. Antiarrhythmic drugs are high-alert medications with narrow therapeutic windows. Always verify orders, check drug interactions, and monitor ECG parameters per institutional protocol. This material supports nursing education and exam review. It is not medical advice and is not a substitute for clinical judgment, institutional policy, or medical direction. Always follow facility protocols and current provider orders.
Vaughan Williams Classification — Overview
| Class | Channel / Receptor | Primary Effect | Common Examples |
|---|---|---|---|
| Class I | Fast sodium (Na⁺) channel blocker | Slows conduction; membrane stabilization | Lidocaine, mexiletine (Ib); procainamide, quinidine (Ia); flecainide, propafenone (Ic) |
| Class II | Beta-adrenergic receptor blocker | Decreases HR, AV node conduction, and automaticity | Metoprolol, atenolol, propranolol, esmolol, carvedilol |
| Class III | Potassium (K⁺) channel blocker | Prolongs repolarization and refractory period; prolongs QT | Amiodarone, sotalol, dofetilide, ibutilide |
| Class IV | Calcium (Ca²⁺) channel blocker (non-DHP) | Slows AV node conduction; decreases automaticity | Diltiazem, verapamil |
Note: Digoxin and adenosine have antiarrhythmic effects but do not fit neatly into the Vaughan Williams system. They are sometimes listed separately.
Class I — Sodium Channel Blockers
Mechanism: Block fast sodium channels that initiate the action potential upstroke — slowing depolarization and conduction velocity. Class I is subdivided by degree of sodium channel blockade and effect on repolarization.
| Subclass | Effect on QRS | Effect on QT | Examples | Use |
|---|---|---|---|---|
| Ia | Wide | Prolonged | Quinidine, procainamide, disopyramide | Afib/flutter, VT |
| Ib | Minimal | Shortened | Lidocaine, mexiletine | Ventricular arrhythmias, VF/pVT |
| Ic | Markedly wide | Minimal | Flecainide, propafenone | SVT, Afib in structurally normal hearts |
Nursing considerations: Monitor QRS duration (widening > 25% indicates toxicity risk). Class Ic drugs are contraindicated after MI or in structural heart disease (proarrhythmic). Lidocaine toxicity: CNS symptoms (numbness, confusion, seizures) before cardiac effects.
Class II — Beta-Blockers
Mechanism: Competitively block beta-1 adrenergic receptors in the SA and AV nodes — reducing sympathetic stimulation, heart rate, and AV conduction velocity. Decrease automaticity and slow conduction through the AV node.
Primary indications (cardiac): Rate control in atrial fibrillation and flutter, SVT prevention, VT prophylaxis after MI, heart failure (carvedilol, metoprolol succinate).
ECG effects: Slows heart rate; may prolong PR interval (AV node slowing). Does not significantly affect QRS or QT.
Nursing considerations:
- Hold if HR < 50–60 bpm or SBP < 90–100 mmHg per order parameters
- Do not abruptly discontinue — rebound tachycardia and hypertension can precipitate MI or angina
- Use with caution in reactive airway disease (beta-2 blockade causes bronchospasm); cardioselective agents (metoprolol, atenolol) preferred
- Signs of toxicity: severe bradycardia, hypotension, heart block, bronchospasm
Class III — Potassium Channel Blockers
Mechanism: Block potassium channels, prolonging the action potential duration and the effective refractory period throughout the myocardium. This makes tissues less excitable for a longer period after depolarization — suppressing re-entrant arrhythmias.
Primary indications: VF/pVT (amiodarone — ACLS), atrial fibrillation and flutter (rhythm control), prevention of recurrent VT.
ECG effects: Prolongs QT interval significantly. Monitor QTc carefully — QTc > 500 ms increases risk of Torsades de Pointes (paradoxical proarrhythmic effect).
Nursing considerations:
- Amiodarone: broad-spectrum (also has Class I, II, and IV properties); multiple organ toxicities with long-term use (pulmonary, thyroid, hepatic, ocular)
- Sotalol: also has Class II (beta-blocking) properties; contraindicated with QTc > 450 ms at baseline
- Dofetilide/ibutilide: hospital-only initiation for QT monitoring during loading
- Check electrolytes (K⁺ and Mg²⁺) — hypokalemia dramatically increases Torsades risk with Class III agents
Class IV — Calcium Channel Blockers (Non-Dihydropyridine)
Mechanism: Block L-type calcium channels in the SA and AV nodes — slowing depolarization and conduction velocity. Non-dihydropyridine (non-DHP) CCBs (diltiazem, verapamil) have greater cardiac effects than the DHP class (amlodipine, nifedipine) which are primarily vasodilators.
Primary indications: Rate control in atrial fibrillation and flutter, SVT termination (second-line to adenosine), angina.
ECG effects: Slows heart rate; prolongs PR interval (AV node slowing). Does not significantly affect QRS or QT.
Nursing considerations:
- Contraindicated with pre-excitation syndromes (WPW) and atrial fibrillation — may accelerate conduction via accessory pathway
- Do not combine with beta-blockers IV — risk of severe bradycardia and heart block
- Verapamil is more negatively inotropic than diltiazem — use with caution in heart failure
- Monitor for hypotension, bradycardia, and AV block during IV administration
- Constipation is a common side effect of verapamil (oral)
Related Resources
Standards & sources
Fact-checked Jun 20, 2026This page is written to align with Vaughan Williams Classification / ACC/AHA Guidelines. It is an educational summary, not a citation of any single document — always verify specific doses, values, and protocols against current guidelines and your facility policy. How we source content →