What are the electrophysiological changes and mechanisms leading to ventricular fibrillation during repetitive myocardial ischemia in dogs?
Experimental coronary occlusion in dogs causes rapid shortening of action potential duration and prolonged conduction time, strongly supporting re-entry as the mechanism for early ventricular fibrillation.
Electrophysiological changes occurring soon after experimental coronary occlusion have been examined in 13 dogs by combined recording of epicardial action potential, endocardial-epicardial con- duction time, and epicardial ST segment elevation during successive 5-minute occlusions of the left anterior descending coronary artery. Mter initial coronary occlusion, action potential duration shortened from 182 9 ms to 113 9 ms at 2 minutes and conduction time was prolonged from 24 i 1 ms to 71 17 ms associated with progressive ST segment elevation. These changes were followed by the appearance of potentials of 'slow response' type morphology, alternans of action potential duration and amplitude, alternans of epicardial and endocardial ST segment elevation, and intermittent conduction block. Ventricular fibrillation was preceded by action potential alternans in 95 per cent and by conduction block in 65 per cent of instances and occurred at a time of maximum conduction delay. These data strongly support the concept of re-entry in the pathogenesis of early ventricular fibrillation.
Russell et al. (1979) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: