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Ventricular fibrillation. Its effect on myocardial flow, distribution, and performance
1Division of Thoracic Surgery, UCLA School of Medicine 90024.
Insights
Ventricular fibrillation during cardiopulmonary bypass can cause subendocardial ischemia due to inadequate blood flow. Avoiding fibrillation and maintaining adequate perfusion pressure prevents this ischemia and reduces the need for postoperative inotropic drugs.
Area of Science:
- Cardiology
- Cardiac Surgery
- Physiology
Background:
- Subendocardial ischemia is a risk during cardiopulmonary bypass when the heart is in ventricular fibrillation.
- Conditions promoting ischemia include sustained electrical stimulus, spontaneous fibrillation in hypertrophied ventricles, cardiac distension, and reduced perfusion pressure.
Purpose of the Study:
- To identify the conditions under which subendocardial ischemia develops during ventricular fibrillation in hearts undergoing cardiopulmonary bypass.
- To explain the mechanisms impeding adequate myocardial blood flow during fibrillation.
- To present an alternative surgical technique to mitigate ischemic complications.
Main Methods:
- The study analyzes factors contributing to subendocardial ischemia during ventricular fibrillation in the context of cardiopulmonary bypass.
- It examines the interplay of fibrillation forces, intracavitary pressure, and myocardial edema in reducing subendocardial flow.
- The research contrasts the outcomes of ventricular fibrillation with a technique of allowing continuous cardiac beating with adequate perfusion pressure.
Main Results:
- Subendocardial ischemia occurs during ventricular fibrillation due to insufficient blood flow to meet metabolic demands.
- Key impeding forces include fibrillation strength, elevated intracavitary pressure, and myocardial edema.
- Myocardial hypothermia offers limited protection against ischemia when perfusion pressure drops significantly.
Conclusions:
- Ventricular fibrillation during cardiopulmonary bypass leads to subendocardial ischemia.
- Abandoning ventricular fibrillation in favor of continuous cardiac beating with adequate perfusion pressure has eliminated the need for postoperative inotropic drugs in aortic or mitral valve replacement surgeries.
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.