Internal cardiac defibrillation threshold: effects of acute ischemia.

The influence of myocardial ischemia on defibrillation success was studied using two different lead orientations in halothane-anesthetized pigs. Ischemia was induced by ligating the left anterior descending artery in its distal third. Controls had loosely tied ligatures placed around the artery at the same site. Ventricular fibrillation was induced by electrical stimulation 30 minutes after coronary artery ligation. Defibrillation used a single truncated pulse of approximately 6 ms duration passed to either: a transvenous electrode catheter (Medtronic, 6880) with the cathode in the apex of the right ventricle and the anode in the superior vena cava-atrial junction region, or the cathode in the apex of the right ventricle and a mesh plaque on the epicardium of the basal lateral left ventricle as anode. Ten seconds after the onset of ventricular fibrillation, defibrillation was attempted with increasing incremental energies until defibrillation was achieved. Fibrillation episodes were repeated at 15-minute intervals until the minimum first shock was successful in defibrillating the animal (i.e., defibrillation threshold). The number of animals successfully defibrillated with a minimum energy above or below 30 J was not different between normal and ischemic animals for either electrode configuration (i.e., 3 out of 20 vs 1 out of 13 for the catheter and 5 out of 6 vs 6 out of 7 for the epicardial plaque, respectively). Also, the cumulative percent success as a function of defibrillation energy was similar in both the normal and ischemic groups. There was a significant reduction in the minimum energy necessary for defibrillation when passing current between the right ventricular apex and the left ventricular epicardial plaque. The present results indicate that, despite differences in lead orientations, acute ischemia in the anesthetized pig does not appear to influence defibrillation success.