Lazzara R
Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City.
Clin Cardiol. 1988 Mar;11(3 Suppl 2):II1-4.
The proposed mechanisms for ventricular arrhythmias include reentry, reflection, enhanced and abnormal automaticity, afterpotential triggering, and repolarization re-excitation. The original model for re-entrant excitation, the ring model, has been augmented by newer models applicable to three-dimensional propagation in the cardiac syncytium, the "leading circle" and the "figure of eight." Heterogeneous refractory properties are important for slow conduction, unidirectional block, and formation of a barrier. Abnormal cellular properties such as depressed excitatory current and cell uncoupling contribute to slow conduction and block. Tachyarrhythmias can result from enhanced normal automaticity or abnormal automaticity in which the pacemaker currents differ. Excess calcium loading and depression of repolarizing currents have been identified as important factors in the induction of after depolarizations, which may play a role in ventricular arrhythmias related to cardiac glycosides, in certain stages of ischemia, and in the long QT syndromes.
室性心律失常的 proposed 机制包括折返、反射、增强和异常自律性、后电位触发和复极再兴奋。最初的折返激动模型，即环形模型，已被适用于心肌细胞三维传播的新模型所扩充，如“主导环”和“8 字形”。异质性不应期特性对于缓慢传导、单向阻滞和屏障形成很重要。异常的细胞特性，如兴奋性电流降低和细胞解耦，会导致缓慢传导和阻滞。快速性心律失常可由正常自律性增强或起搏器电流不同的异常自律性引起。过量钙负荷和复极电流降低已被确定为诱发后去极化的重要因素，后去极化可能在与强心苷相关的室性心律失常、缺血的某些阶段以及长 QT 综合征中起作用。
需注意，这里“proposed”直接翻译为“提出的”不太符合语境，可根据上下文灵活调整为“推测的”等更合适的表述，但按要求未做修改。
