Cardiac arrhythmias arise from disturbances in the functioning of the specific ion channels that normally control excitation or from the functional expression of previously latent channels. Antiarrhythmic agents act by blocking the membrane sodium, potassium, and calcium channels, but no agent has exclusive action on a given type of channel. Arrhythmias resulting from reentry form the largest group of clinically significant arrhythmias. Most arrhythmias result from depressed sodium channel function. The local anesthetic class of sodium channel blockers (class I agents) acts by slowing conduction and converting regions of unidirectional block to bidirectional block. Class III agents act by prolonging the action potential duration. Because potassium currents are normally responsible for repolarization of the cardiac action potentials, these agents are generally assumed to be potassium channel blockers. Class IV antiarrhythmics--calcium channel blockers--are used when a group of reentrant arrhythmias arises in regions in which conduction is primarily sustained by increases in permeability to calcium ions. The mechanisms of action of antiarrhythmic agents are discussed with respect to the basic cellular mechanisms of cardiac arrhythmias.