Vaughan-Williams classification
| Class | Mechanism | Drugs |
| Ia | Sodium blockade – prolongs refractory period of cardiac muscle | Quinidine, Procainamide |
| Ib | Sodium blockade – shortens refractory period | Lidocaine, Phenytoin |
| Ic | Sodium blockade – no effect of refractory period | Flecainide |
| II | Beta blockade – prolongs phase 4 | Propranolol, Atenolol |
| III | Potassium channel blockade – slows rate of repolarisation and prolongs action potential | Amiodarone, Sotalol |
| IV | Calcium channel blockade (L-type) – prevents maintenance of action potential | Verapamil, Dilatiazem |
Class I
Sodium blockade, therefore membrane stabilisers.
Class II
Block the effect of catecholamines at the Beta-1 adrenergic receptor, decreasing sympathetic activity on the heart. Decrease conduction through the AV node.
Class III
Potassium channel blockers, therefore prolong repolarisation and action potential duration
Class IV
Decrease conduction through the AV node
Shorten phase II (plateau phase)
Reduce contractility
Adrenergic control of heart rate maintained
An alternative classification
Digoxin, adenosine and magnesium do not fit into the Vaughan-Williams classification.
| Drugs that work on | |
| Supraventricular tachycardias | Class Ic – Flecainide |
| Class II – Beta blockers | |
| Class IV – Ca channel blockers | |
| Digoxin | |
| Adenosine | |
| Ventricular tachycardias | Class Ia – Procainamide |
| Class Ib – Lidocaine and Phenytoin | |
| Both | Class III – Amiodarone |
Review: Myocyte action potential, Pacemaker action potential.
critnotes 