The goal of this study was to examine the effect of AC currents on a cardiac fiber. The study is the second in a series of two articles devoted to the subject. The initial study demonstrated that low-strength sinusoidal currents can cause hemodynamic collapse without inducing ventricular fibrillation. The present modeling study examines possible electrophysiologic mechanisms leading to such hemodynamic collapse. A strand of cardiac myocytes was subjected to an extracellular sinusoidal current stimulus. The stimulus was located 100 microm over one end. Membrane dynamics were described by the Luo-Rudy dynamic model. Examination of the interspike intervals (ISI) revealed that they were dependent on the phase of the stimulus and, as a result, tended to take on discrete values. The frequency dependency of the current threshold to induce an action potential in the cable had a minimum, as has been found experimentally. When a sinus beat was added to the cable, the sinus beat dominated at low-stimulus currents, whereas at high currents the time between action potentials corresponded to the rate observed in a cable without the sinus beat. In between there was a transition region with a wide dispersion of ISIs. The following phenomena observed in the initial study were reproduced and explained by the present simulation study: insignificant effect of temporal summation of subthreshold stimuli, frequency dependency of the extrasystole threshold, discrete nature of the ISI, and increase in regularity of the ISI with increasing stimulus strength.