Effects of Strong Electrical Shock on Cardiac Muscle Tissue a

Electrical shock is deliberately applied to the heart in the clinical setting for pacemaking, cardioversion, defibrillation, and ablation.' The strength of the applied shock varies with the intended application, from low values used for pacemaking, to higher levels used first for cardioversion and then for defibrillation, and ultimately to destructive levels utilized for electrical ablation. The region of tissue targeted by the current may in some cases be highly localized (e.g., with pacemaking or electrical ablation) or in other cases global in extent (e.g., with defibrillation). In the case of automatic implantable cardioverter-defibrillators (AICDs), the shock is commonly delivered through two flexible patch electrodes situated on the epicardial surface of the ventricles.2 This configuration deserves special consideration with respect to unintentional injury to the heart. It is believed that successful defibrillation is achieved when the bulk of the heart is subjected to a minimum level of potential gradient. On the other hand, the potential gradient is unavoidably nonuniform, with the highest level in the region adjacent to the shock electrodes. With high shock levels, animal experiments have clearly shown that tissue in this region can undergo depression in cardiac function. Although the extent of myocardial damage is less clear in h ~ r n a n s , ~ mild electrocardiographic changes can be observed even following the lower intensity shock used for cardioversion.3 Effects observed in animal studies include altered electrophysiology, arrhythmia, coronary artery dilatation, impaired contractility, ultrastructural changes, hemorrhage, depletion of essential enzymes, and ultimately tissue n e c r o s i ~ . ~ , ~ One of the most immediate indices of myocardial injury in the heart is electrophysiological, in the form of rhythm abnormalities (cardiac arrest, bradycardia, tachycardia, altered conduction), morphological changes in the ECG (QRS complex, ST segment, T wave), or decreases in cellular resting potential. There is substantial experimental and theoretical evidence suggesting that the electropathological effects of high-intensity electrical shock on cardiac muscle originate from electroporation of the cell membrane.6 The pathways by which applied electrical shock is coupled to the cardiac cetl membrane are shown in FIGURE 1.Ohm's law modified for volume conductors states that the potential gradient (i.e., voltage per unit length, or electric field) for a resistive medium is proportional to the current density (current per unit cross-