Ventricular fibrillation. Its effect on myocardial flow, distribution, and performance

Abstract

Subendocardial ischemia develops in hearts that are fibrillated during cardiopulmonary bypass when: (1) the normal ventricle is fibrillated with a sustained electrical stimulus, (2) the hypertrophied ventricle is allowed to fibrillate spontaneously, (3) the fibrillating heart becomes distended, or (4) the perfusion pressure is reduced to approximately 50 mm Hg. Myocardial hypothermia reduces cardiac oxygen requirements during fibrillation but does not prevent ischemia when perfusion pressure falls to levels frequently attained during clinical open-heart operations. The ischemia occurs because flow cannot rise sufficiently to meet the metabolic demands of ventricular fibrillation. The forces interacting to impede adequate flow to the subendocardium during ventricular fibrillation are: (1) the compressive forces exerted on subendocardial muscle by the strength of fibrillation, (2) the compressive forces resulting from raised intracavitary pressure due to occlusion or malfunction of the ventricular vent, and (3) the evolution of myocardial edema as ischemia is prolonged. We have abandoned the use of ventricular fibrillation in clinical open-heart operations and now allow the heart to beat continually with adequate perfusion pressure. We have not needed to use inotropic drugs postoperatively after aortic or mitral valve replacement since adopting this technique.