Alferness C, Bayly P V, Krassowska W, Daubert J P, Smith W M, Ideker R E
Department of Medicine, Duke University, Durham, North Carolina.
Pacing Clin Electrophysiol. 1994 May;17(5 Pt 1):876-81. doi: 10.1111/j.1540-8159.1994.tb01428.x.
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.
虽然在正常心率下对心室电生理特性进行了深入研究，但对于心室颤动时出现的极短周期长度（约100毫秒）下的这些特性却知之甚少。我们在6只犬的右心室中，以80至300毫秒的刺激间隔检查了不应期。从300毫秒开始，基础（S1）周期长度每搏减少10毫秒，直至200、150或125毫秒。然后引入强度为1、5、10或20毫安的1毫秒期前（S2）刺激。S1 - S2间隔逐渐减小，直至失去夺获。不应期被认为是每种S2强度下使心脏夺获的最短间隔。仅纳入未诱发颤动的起搏发作。强度 - 间隔曲线保持相同的双曲线形状，但随着S1 - S1间隔缩短，移向极短的不应期。在最短的S1 - S1间隔时，对于短至83±3毫秒的S1 - S2间隔，期前刺激能够使心脏夺获而不诱发心室颤动。因此，递减快速起搏可产生比心室颤动时周期长度更短的不应期。这一发现表明，在颤动开始时无需假定向新的电生理特性或关系的不连续跳跃，而是当正常电生理参数被推至正常情况下不会出现的值时，颤动能力是其正常电生理参数的一个组成部分。本研究结果应有助于有源膜模型和细胞电行为的细胞自动机模型的进一步发展。
