心肌缺血下人体心室电生理建模和心电图仿真

Modeling of Electrophysiology and Simulation of ECG under Ischemic Condition in Human Ventricular Tissue

为了分析心肌缺血下心肌细胞电生理变化以及对心室传导波的影响,本文考虑了缺血情况下高钾、酸液过多、局部缺氧的实际情况,开发了一个人体心室缺血模型。基于该模型,文中模拟了不同缺血程度下心内膜细胞、M细胞和心外膜细胞的动作电位(AP),并探讨了心肌缺血的三个单一因素分别对细胞AP的影响,最后定量分析了二维人体左心室组织心肌缺血下心电图(ECG)的改变情况。实验结果表明,在缺血情况下,心肌细胞动作电位时程(APD)均有不同程度的缩短。大多数情况下,缺血区域越大,或者缺血情况越严重,ECG的ST-T波变化幅度也越大。在上述三个心肌缺血因素中,高钾对ST-T波变化起到关键的作用,这与之前在动物模型上得到的实验结论保持一致。

In this paper, to analyze the functional influence of ischemia on cardiac cell electrical activity and subsequently on ventricular electrical wave conduction, a human ventricular ischemic model was developed, which took into account three major pathophysiological components of ischemia, hyperkalaemia, acidosis, and anoxia. This model simulated the action potential （AP） propagations of endocardial, midmycardial and epicardial cells with different levels of isehemia, and the influence of each factor on cell AP was analyzed. Finally the ECG waveform under ischemia was quantified by using a 2D model of human left ventricular tissue based on the anatomical structure of human heart. The experimental results showed that under ischemia action potential durations （APD） were reduced. In most cases, the larger the size of ischemie region or the more severe the ischemic level, the more dramatic the changes in the amplitude of ST-T wave were observed. For the three components of ischemia, hyperkalaemia was the dominant contributor to ST-T wave changes, which was in agreement with the results obtained on animal models.