Strength-interval curves in canine myocardium at very short cycle lengths.

While ventricular electrophysiological properties have been intensively studied at normal heart rates, little is known about these properties at the very short cycle lengths (approximately 100 msec), which are present in ventricular fibrillation. We examined refractoriness in the right ventricles of six dogs at stimulation intervals of 80 to 300 msec. Starting at 300 msec, the basic (S1) cycle length was decremented by 10 msec each beat to 200, 150, or 125 msec. A 1-msec premature (S2) stimulus of 1, 5, 10, or 20 mA was then introduced. The S1-S2 interval was decremented until capture was lost. The refractory period was considered to be the shortest interval that captured the heart for each S2 strength. Only pacing episodes that did not induce fibrillation were included. Strength-interval curves maintained the same hyperbolic shape but shifted to very short refractory periods as the S1-S1 interval was decreased. At the shortest S1-S1 intervals, premature stimuli were capable of capturing the heart without inducing ventricular fibrillation for S1-S2 intervals as short as 83 +/- 3 msec. Thus, decremental rapid pacing can produce refractory periods shorter than the cycle length during ventricular fibrillation. This finding suggests that there is no need to postulate a discontinuous jump to new electrophysiological properties or relationships at the onset of fibrillation, but that the capability for fibrillation is an integral part of normal electrophysiological parameters when they are pushed to values that do not occur normally. The results of this study should be useful in the further development of active membrane models and cellular automata models of cellular electrical behavior.