Encainide is an antiarrhythmic drug, developed by Bristol Myers Co supplied 25 and 35 mg capsules for oral administration. Encainide is no longer used because of its frequent proarrhythmic side effects. The mechanisms of the antiarrhythmic effects of Enkaid are unknown but probably are the result of its ability to slow conduction, reduce membrane responsiveness, inhibit automaticity, and increase the ratio of the effective refractory period to action potential duration. Enkaid produces a differentially greater effect on the ischemic zone as compared with normal cells in the myocardium. This could result in the elimination of the disparity in the electrophysiologic properties between these two zones and eliminate pathways of abnormal impulse conduction, development of boundary currents and/or sites of abnormal impulse generation. The absorption of Enkaid after oral administration is nearly complete with peak plasma levels present 30 to 90 minutes after dosing. There are two major genetically determined patterns of encainide metabolism. In over 90% of patients, the drug is rapidly and extensively metabolized with an elimination half-life of 1 to 2 hours. These patients convert encainide to two active metabolites, O-demethylencainide (ODE) and 3-methoxy-O-demethylencainide (MODE), that are more active (on a per mg basis) than encainide itself. In less than 10% of patients, metabolism of encainide is slower and the estimated encainide elimination half-life is 6 to 11 hours. Slow metabolism of encainide is associated with a diminished ability to metabolize debrisoquin. Enkaid should be administered only after appropriate clinical assessment and the dosage of Enkaid must be individualized for each patient on the basis of therapeutic response and tolerance. The recommended initial dosing schedule for adults is one 25 mg Enkaid capsule t.i.d. at approximately 8-hour intervals.