Leja F, Scanlon P J, Euler D E
Am Heart J. 1987 Feb;113(2 Pt 1):296-301. doi: 10.1016/0002-8703(87)90268-7.
To determine the mechanism for postcountershock ventricular ectopy, internal and external shocks were delivered to 20 anesthetized dogs. Shock energies of 25 and 50 joules were employed internally while 100 and 200 joules were delivered externally. Experiments were performed in both the presence and absence of a nearly toxic dose of ouabain. All shocks resulted in the occurrence of nonsustained (less than 15 seconds) ventricular tachycardia. When bursts of rapid ventricular pacing were synchronized with a shock, the pacing stimuli invariably captured the ventricles and overdrove the shock-induced ventricular tachycardia. However, the burst pacing never appeared to break a tachycardia, since the termination of pacing was followed immediately by the resumption of the shock-induced ventricular tachycardia. The presence of ouabain did not alter the response of the ventricles to postshock burst pacing. Administration of verapamil (0.5 mg/kg) had no effect on the duration of shock-induced ventricular arrhythmia. Elevation of the serum potassium level to 8.5 +/- 0.6 mEq/L drastically reduced the duration of postshock ventricular tachycardia in both the presence and absence of ouabain. The results suggest that postshock ventricular ectopy results from an abnormality of impulse initiation rather than reentry.
为确定电击后室性异位心律的机制，对20只麻醉犬进行了体内和体外电击。体内电击能量采用25焦耳和50焦耳，而体外电击能量为100焦耳和200焦耳。实验在给予近中毒剂量哇巴因和未给予哇巴因的情况下均进行。所有电击均导致非持续性（少于15秒）室性心动过速的发生。当快速心室起搏脉冲与电击同步时，起搏刺激总是能夺获心室并超速驱动电击诱发的室性心动过速。然而，起搏脉冲似乎从未终止过速，因为起搏终止后紧接着电击诱发的室性心动过速就会恢复。哇巴因的存在并未改变心室对电击后起搏脉冲的反应。静脉注射维拉帕米（0.5毫克/千克）对电击诱发的室性心律失常持续时间无影响。血清钾水平升高至8.5±0.6毫当量/升时，无论有无哇巴因，均显著缩短电击后室性心动过速的持续时间。结果提示，电击后室性异位心律是由冲动起始异常而非折返所致。
