Studies of the effects of ventricular fibrillation on the adequacy of regional myocardial flow

This report analyzes the mechanisms of subendocardial ischemia during ventricular fibrillation in normal and hypertrophied hearts and focuses primarily upon (1) the role of the fibrillating stimulus, (2) how ventricular distention impedes flow, and (3) why coronary vascular resistance progressively rises as the duration of fibrillation is prolonged. The forces interacting to impede the adequacy of 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 the ischemia is prolonged. These compressive forces may become exaggerated in hypertrophied hearts where increased wall thickness may add to the distortion of subendocardial vessels.