Alterations in the electrophysiology of cardiac tissue produced by myocardial ischemia may result in potentially lethal arrhythmias. The purpose of this manuscript is to review the alterations documented to occur in vivo and in vitro. Peripheral Purkinje fibers, after a transient period during which they demonstrate depressed electrophysiologic characteristics, survive myocardial ischemia and infarction, whereas ventricular muscular fibers do not. Ischemic ventricular fibers exhibit a decrease in the resting potential and in the upstroke velocity of action potentials, as well as loss of cellular excitability. These changes appear responsible for slow and inhomogeneous conduction which, in turn, is manifest by delayed onset and fractionation of bipolar electrograms recorded from ischemic myocardium. The electrophysiologic alterations observed during ischemia can be considered to result from the effects of multiple factors, among which are hypoxia, intracellular and extracellular acidosis and accumulation in the extracellular space of K+, lactate, and many other metabolic byproducts. The changes in ventricular fibrillation threshold (VFT), when measured from the ischemic zone, are characterized by a rapid decrease within the first 2 min after one-stage coronary artery occlusion, followed by a return to, and above control values. Changes in inhomogeneity of recovery of excitability and in the level of the diastolic threshold of excitability influence the time course of the VFT. The relevance of these observations to the genesis of cardiac arrhythmias are discussed.
|Original language||English (US)|
|Number of pages||17|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|State||Published - Jan 1 1977|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)