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The electrophysiological effects of flecainide on the action potential were examined in guinea pig ventricular muscles using microelectrode recording methods. Under the control conditions, flecainide (0.5-1 microgram/ml) did not alter the resting potential, action potential duration (APD) or effective refractory period (ERP). The major effect of flecainide was on maximum upstroke velocity (Vmax), which was depressed in a dose-dependent manner. In high [K+] medium (potassium concentration = 10 mM), Vmax was depressed by 16.8% at a concentration of 1.0 microgram/ml (8.8% in normal [K+]o). In metabolic acidosis (pH = 6.89), it was depressed by 15.7% at the same concentration of the drug (8.3% in normal condition). The changes in ERP and ERP/APD90% in high [K+]o and metabolic acidosis were not significantly different from the normal condition. After hypoxic perfusion for 15 min, Vmax depression by flecainide was 16.3% (7.4% in control medium). The increase of ERP/APD90% was also greater in hypoxia. These data indicate that the most prominent effect of flecainide is Vmax depression which is enhanced under the high K+, acidic and hypoxic conditions. Therefore, it is suggested that flecainide may be most effective for ventricular arrhythmias occurring in myocardial ischemia.

Electrophysiological effects of flecainide on guinea pig ventricular muscle in high (K+)o, acidosis and hypoxia.