Medication                                                                                              

Drugs with anti arrhythmic effects are classified according to their principle site of action. This may be on various phases of the action potential or the autonomic nervous system. Many of their actions overlap and in the clinical situation, where are understanding of the molecular biology of the arrhythmia substrate is imperfect, in any group of patient with the same clinical arrhythmia some may be efficacious whilst others are not.

Class 1 Agents

These are sodium channel blocking agents that reduce the ability of the cell to depolarize and hence they primarily slow conduction. They are subcategorized according to their effect on the refractory period. 1A agents eg. disopyramide prolong the refractory period, 1B agents eg. lignocaine shorten the refractory period whilst 1C agents eg. flecainide have little effect on refractory period.

Class 2 Agents

These are the β blockers and hence their action is mediated by the autonomic nervous system. They are also subcategorized into IIA agents that are cardioselective eg atenolol, IIB agents those with partial agonist activity, IIC agents with membrane stabilizing activity eg. propranolol, IID agents lipid solubility.

Class 3 Agents

These agents block the rapid potassium influx and hence predominantly prolong refractoriness eg amioderone and sotalol.

Class 4 Agents

This is the group of calcium channel blockers eg verapamil which reduce automaticity of the SA and AV node and also prolong the action potential.

Class 5 Agents

These are the cardiac glycosides eg digoxin. Its predominant effect is via the vagus

Class 6 Agents

Purinergic agonists eg adenosine act directly on the SA and AV node. Adenosine is extremely rapidly metabolized by the erythrocytes and has a half life measured in seconds. It is able to provide rapid and complete blockade of the nodes and prevent atrio-ventricular conduction. It is therefore useful as a diagnostic test differentiating atrial from ventricular arrhythmias and atrial reentrant from automatic mechanisms. In those arrhythmias requiring AV conduction as part of the reentrant mechanism it may terminate the arrhythmia although as its effects are transitory recurrence is common.

This page was last edited 14/2/2004