Use of calcium blockers in electromechanical dissociation

Calcium antagonists have been shown to protect the myocardium against the deleterious effects of ischemia and reperfusion in both focal and global models. The mechanism of this protection is probably related to their ability to decrease the rapid and massive cytosolic and mitochondrial calcium overloading that occurs with reperfusion of severely ischemic myocardium. This calcium overloading uncouples oxidative phosphorylation, preventing repletion of ischemia-depleted ATP stores. The mode of action of calcium antagonists in protecting heart muscle is complex, and may ultimately depend on their ability to preserve sufficient energy to maintain intracellular ionic homeostasis. The cellular events that occur with prolonged cardiac ischemia have been well documented in animal studies, and are reflected in the clinical picture of electromechanical dissociation (EMD). ATP production is decreased during ischemia and quickly results in depleted energy stores. The electrical and mechanical activities of the heart are energy-consuming processes that gradually come to a halt in the presence of prolonged ischemia. In excised totally ischemic hearts, electrical activity persists for a time after contractions have ceased, resulting in the clinical picture of EMD. Eventually electrical activity stops as well, causing asystole. Calcium antagonists administered during resuscitation from EMD, as well as other terminal arrhythmias, may protect the myocardium from reperfusion injury and preserve the ATP stores necessary for normal cardiac function.