Electric Instability of the Heart

Abstract

Normally oxygenated dog hearts and hearts rendered uniformly anoxic exhibit electric stability: there is no difference in resting electric potentials, and spontaneous ventricular fibrillation does not occur. When an area of myocardium is rendered ischemic, the resulting "trigger" may destroy the coordinated mechanism of the heart. A current of oxygen differential is produced across the zone of contact between red and blue myocardium resulting in "electric instability." In the electrically stable, uniformly anoxic heart, perfusion of an area with red blood produces a "reverse trigger" and electric instability. Application of these concepts and therapeutic implications to human coronary disease appears justified.