The Mechanisms of Defibrillation During Acute Myocardial Ischemia

The overall objective of this research is to increase our understanding of the mechanisms for ventricular defibrillation and the conditions of ischemic cardiac disease.  Specifically, we focus on unraveling the cause-and-effect relationship between electrophysiological changes during acute myocardial ischemia and defibrillation shock efficacy.  Our specific aim is to, using a realistic model of the rabbit ventricles, analyze the relationship between defibrillation threshold and cellular-level manifestations of acute ischemia, such as elevated extracellular potassium, acidosis, and anoxia.  Our hypothesis is the defibrillation threshold increases under the conditions of elevated extracellular potassium, acidosis, and anoxia due to:  1) elevated threshold for the generation of post-shock break excitations, 2) decrease in the conduction velocity of the break excitations, and 3) decrease in the shock-induced extension of action potential duration.