全心缺血早期阶段室性心律失常仿真研究

Simulation Study of Ventricular Arrhythmia at The Early Stage of Global Ischemic Condition

为了分析全心缺血早期阶段对心脏电生理活动的影响,以及探讨诱发的室性心律失常机制,本研究考虑了缺血情况下高钾、酸液过多、局部缺氧的情况,结合详细的人类心室细胞生物物理上的动力学特征,开发了一个人体心室细胞和组织全心缺血模型.实验结果表明,全心缺血缩短了动作电位时程(action potential duration,APD),且减缓了兴奋的传导速率(conduction velocity,CV).同时,由于全心缺血降低了动作电位时程曲线(action potential duration restitution,APDR)斜率,且增大了有效不应期(effective refractory period,ERP),因此有利于维持折返波的稳定传导,使得室速不易转化为室颤.另一方面,尽管全心缺血导致了组织易感性的增加,但是由于其需要更长的异位刺激长度来保证折返波的形成,因此也在一定程度上降低了心律失常的发生概率.

In this paper, to analyze the functional influence of the early stage of global ischemia on cardiac electrical activity and subsequently on ventricular arrhythmia, we take into account of three main pathophysiological consequences of ischemia： hyperkalaemia, acidosis, and anoxia, and develop a human ventricular cell and tissue ischemic model that combines a detailed biophysical description of the excitation kinetics of human ventricular cells. Based on the model, the APDR curves, ERPR curves, vulnerable window, and CVR curves under control and ischemic condition are computed separately. The experimental results show that global ischemia can reduce APD, and slow down CV. Meanwhile since global ischemia decreases slope of APDR and increases ERP, the induced re-entry can be maintained stably which is not prone to degenerate into ventricular fibrillation. And due to a comparatively longer ectopic stimulation length to ensure the formation of reentry, global ischemia decreases the probability to arrhythmia in some extent although the increased tissue vulnerability.