Electrophysiologic effects of acute myocardial ischemia. A mechanistic investigation of action potential conduction and conduction failure

Circulation Research
R M Shaw, Y Rudy

Abstract

A multicellular ventricular fiber model was used to determine mechanisms of slowed conduction and conduction failure during acute ischemia. We simulated the three major pathophysiological component conditions of acute ischemia: elevated [K+]o, acidosis, and anoxia. Elevated [K+]o was the major determinant of conduction, causing supernormal conduction, depressed conduction, and conduction block as [K+]o was gradually increased from 4.5 to 14.4 mmol/L. Only elevated [K+]o caused conduction failure when varied within the range reported for acute ischemia. Before block, depressed upstrokes consisted of two distinct components: the first to the fast Na+ current (INa) and the second to the L-type Ca2+ current (ICa(L)). Even in highly depressed conduction, excitability was maintained by INa, with conduction block occurring at 95% INa inactivation. However, because ICa(L) supported the later phase of the depressed upstroke, ICa(L) enhanced conduction and delayed block by increasing the electrotonic source current. At [K+]o = 18 mmol/L, slow action potentials generated by ICa(L) were obtained with 10% ICa(L) augmentation. However, in the presence of acidosis and anoxia, significantly larger (120%) ICa(L) augmentation was required. The d...Continue Reading

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