Refractory period extension (RPE) has been proposed as a basic mechani
sm for defibrillation but it remains unclear if RPE exists at the fast
rates associated with ventricular fibrillation. In 7 pentobarbital an
esthetized dogs, we measured refractory periods with and without 8 ms
rectangular transcardiac shocks at left ventricular pacing rates of 20
0-600 beats/min. To achieve these high rates, an incremental rate paci
ng method was used to produce pacing train timing sequences requiring
4.5-27 seconds, A variably timed premature stimulus followed the last
stimulus in each pacing train. To determine refractoriness, a 128 elec
trode array(4 x 4 cm) was used to detect the presence, or absence of a
n activation sequence sweeping away from the pacing site. At each rate
, a control refractory period (RPc) was measured and refractory period
s were also measured for 8 and 12 V/cm shocks with coupling intervals
of 60% to 90% of RPc. RPc decreased as the rare increased with a minim
um RPc of 94 ms at a rate of 600 beats/min (100 ms cycle length). RPE/
RPc versus shock coupling interval was similar at all pacing rates. RP
E/RPc increased with increased coupling interval or higher shock inten
sity. We conclude that during ventricular pacing at fibrillatory rates
tissue is nearly always in a refractory state; that RPE exists at fib
rillatory activation rates; and that RPE/RPc versus shock coupling int
erval does not vary strongly with pacing rate. These findings support
the hypothesis that RPE contributes to defibrillation.