Flecainide acetate depresses both the upstroke of the intracellular action potential and the rate of diastolic depolarisation in isolated tissue preparations of atrial myocardium. It produces no consistent effect on action potential duration. Predictably, in the human heart, studied by clinical cardiac electrophysiological techniques, conduction velocity through atrial myocardium, the atrioventricular (AV) node and anomalous tissue is depressed following flecainide administration. Refractoriness of normal atrial or AV nodal myocardium is not prolonged but the recovery time of anomalous or abnormal tissue is lengthened by the drug. In response to the intravenous injection of flecainide, atrial fibrillation (90%), atrial tachycardia (100%), intra-AV nodal tachycardia (89%) and atrioventricular re-entrant tachycardia (80%) are generally terminated, and although atrial flutter is slowed, only a small proportion (20%) is terminated. There is little experience of the long term treatment of supraventricular tachycardia with oral flecainide. However, preliminary results suggest that flecainide is equally effective in the treatment of both supraventricular and ventricular arrhythmias. Thus, flecainide acetate is a 'broad spectrum' antiarrhythmic agent.