Electric defibrillation is a life-saving therapy for clinically dangerous ventricular arrhythmias. Unfortunately, direct-current (DC) shock treatment often induces or worsens other tachyarrhythmias. The adverse effects of electric shock delivered to human ventricular cardiomyocytes are not fully understood. This study thus uses computer simulation to investigate the pathogenesis of the electrophoresis in epicardial and endocardial human tissue. The O’Hara-Rudy dynamic human ventricular cell model incorporated with Ohuchi’s mathematical DC shock model is used. The effect of electroporation is described as a transmembrane pore, mimicking the reversible breakdown of the cell membrane. The aftershock effects on epiardial and endocardial ventricular cardiomyocytes are evaluated. The effects of delivering shock from the endocardium and epicardium using a multicellular one-dimensional strand model are also investigated. Ventricular tachycardia can be terminated by a low-strength shock to endocardial cardiomyocytes. However, an excessively strong shock to epicardial cardiomyocytes induces early afterdepolarization and is arrhythmogenic. The aftershock effect of the electroporation is serious for epicardial ventricular myocytes. The optimization of defibrillation energy delivery to the maximum membrane potential and the pathogenesis of the aftershock effect during ventricular tachycardia are also investigated. The aftershock effect of electroporation is more serious in epicardial cells than it is in endocardial cells. It is suggested that the DC shock be delivered to endocardium cells before the maximum membrane potential of the epicardial cell in a multicellular one-dimensional strand model is reached, which is before the electrocardiogram R wave spike.