- Pharmshala

Anti-Arrhythmic Drugs

The Vaughan Williams classification — how each class of anti-arrhythmic acts on a different phase of the cardiac action potential.

e.1

Why arrhythmias happen

An arrhythmia is any abnormal heart rhythm — too fast (tachycardia), too slow (bradycardia), or irregular. Mechanisms fall into two broad groups: abnormal impulse formation (a focus other than the SA node fires, or the SA node fires abnormally) and abnormal impulse conduction, classically re-entry, where an impulse re-circulates around a loop of tissue instead of dying out. Anti-arrhythmic drugs are classified by the Vaughan Williams system, based on which part of the cardiac action potential (see Unit I.A) each class acts on.

e.2

The Vaughan Williams classification

Class	Mechanism	Examples	Main use
I — Na⁺ channel blockers	Block the fast inward sodium current (phase 0), slowing conduction	see subtypes below	Various atrial and ventricular arrhythmias
Ia	Moderate Na⁺ block + prolongs repolarisation	Quinidine, procainamide, disopyramide	Broad-spectrum, now used less often
Ib	Weak Na⁺ block, shortens repolarisation; binds preferentially to ischaemic/fast-firing tissue	Lidocaine, mexiletine	Ventricular arrhythmias, especially post-MI
Ic	Strong Na⁺ block, little effect on repolarisation	Flecainide, propafenone	Supraventricular arrhythmias in patients with structurally normal hearts
II — Beta-blockers	Reduce sympathetic drive to the SA/AV node, slow conduction and automaticity	Propranolol, esmolol, metoprolol	Sinus and supraventricular tachycardias; reduce sudden cardiac death post-MI
III — K⁺ channel blockers	Block outward potassium current, prolonging repolarisation and the action potential (and the QT interval)	Amiodarone, sotalol, dofetilide	Broad-spectrum, including atrial fibrillation and ventricular arrhythmias; amiodarone is very widely used despite a long side-effect list (thyroid, lung, liver, skin)
IV — Non-dihydropyridine CCBs	Block the slow inward calcium current important at the SA/AV node	Verapamil, diltiazem	Supraventricular tachycardias, rate control in atrial fibrillation

Unclassified but important: adenosine and digoxin

Adenosine (IV) transiently blocks AV-node conduction via A₁ receptors (opening K⁺ channels, hyperpolarising the node) — the drug of choice to terminate acute supraventricular tachycardia, with a very short half-life (seconds). Digoxin slows AV conduction via vagal (parasympathetic) stimulation and is used for rate control in atrial fibrillation, especially when CHF coexists (see Unit I.B).

e.3

Key safety point: pro-arrhythmia

Anti-arrhythmics can cause arrhythmias

Every class above can, under some circumstances, provoke new arrhythmias (“pro-arrhythmic” effect) — most notably, Class Ia and Class III drugs can prolong the QT interval and precipitate torsades de pointes. This is why anti-arrhythmic therapy is usually started under ECG monitoring, and why non-drug options (catheter ablation of the re-entry circuit, implantable defibrillators/pacemakers) are preferred wherever appropriate.