Myocardial ischemia. Nature of ischemic electrocardiographic patterns in the mammalian ventricles as determined by intracellular electrographic and metabolic changes.

Abstract Severe ischemia results in serious damage to myocardial cells and their membranes. As a consequence, K+ is lost from these cells and intracellular Na+ concentration probably rises. These changes produce a decrease in the transmembrane ionic gradient for these substances and probably hypopolarization of the cell membranes. This is manifested in the intracellular electrogram by a decrease in negativity of the membrane resting potential of the individual subepicardial ischemic cells. In direct electrograms from the epicardium over these cells the T-Q segment becomes depressed. This T-Q depression is indicated in the clinical electrocardiogram as S-T elevation. Perfusion of nonischemic myocardium with solutions of high K+ or low Na+ concentration produces intracellular and surface electrographic changes similar to those of severe ischemia. This supports the theory that metabolic changes such as those just described are at least part of the fundamental cause of the electrocardiographic changes of severe ischemia. In all probability, other chemical and metabolic factors also play a role in their production. Mild ischemia produces an increased uptake of K+ and probably glucose by the myocardial cells. As a result, the transmembrane ionic gradient for K+ increases and a state of hyperpolarization may occur. This causes an increase in membrane resting potential of the individual cells, manifested in the overlying surface electrogram by elevation of the T-Q segment. In the clinical electrocardiogram this appears as S-T depression. Perfusion of nonischemic myocardium with solutions of low K+ or high Na+ ion concentration produces intracellular and surface electrocardiographic changes similar to those of mild ischemia. This again provides support for the belief that such metabolic changes may be in part responsible for the electrocardiographic phenomena of mild ischemia. The increase in amplitude of the R wave often observed early in severe ischemia appears to be the result of delayed conduction in the ischemic muscle. The tall R wave is also widened because of this delay. The S wave is buried in the wide R wave and thus becomes smaller or entirely invisible. The increase in intracellular K+ and glucose in mild ischemia may represent a homeostatic mechanism by which the cells prepare themselves for injury by severe ischemia. The fact that the electrographic and electrocardiographic phenomena of the two kinds of ischemia are almost opposite in nature then becomes understandable as a manifestation of such a mechanism.