While ventricular electrophysiological properties have been intensivel
y studied at normal heart rates, little is known about these propertie
s 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 ms
ec. Starting at 300 msec, the basic (S-1) cycle length was decremented
by 10 msec each beat to 200, 150, or 125 msec. A 1-msec premature (S-
2) stimulus of 1, 5, 10, or to mA was then introduced. The S-1-S-2 int
erval was decremented until capture was lost. The refractory period wa
s considered to be the shortest interval that captured the heart for e
ach S-2 strength. Only pacing episodes that did not induce fibrillatio
n were included. Strength-interval curves maintained the same hyperbol
ic shape but shifted to very short refractory periods as the S-1-S-1 i
nterval was decreased. At the shortest S-1-S-1 intervals, premature st
imuli were capable of capturing the heart without inducing ventricular
fibrillation for S-1-S-2 intervals as short as 83 +/- 3 msec. Thus, d
ecremental rapid pacing can produce refractory periods shorter than th
e cycle length during ventricular fibrillation. This finding suggests
that there is no need to postulate a discontinuous jump to new electro
physiological properties or relationships at the onset of fibrillation
, but that the capability for fibrillation is an integral part of norm
al 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 automat
a models of cellular electrical behavior.