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Irvin B. Krukenkamp
Sidney Levitsky
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Ann Thorac Surg 1991;52:949-954
© 1991 The Society of Thoracic Surgeons

Articles

Myocardial oxygen consumption after fibrillation in the nonhypertrophied porcine ventricle

Irvin B. Krukenkamp, MD, Sidney Levitsky, MD*

Division of Cardiothoracic Surgery, Department of Surgery, Harvard Medical School, New England Deaconess Hospital, Boston, Massachusetts USA

* Address reprint requests to Dr Levitsky, Division of Cardiothoracic Surgery, New England Deaconess Hospital, 110 Francis St, Suite 2C, Boston, MA 02215.

Prior studies of nonischemic ventricular fibrillation have identified variable bioenergetic defects that depend on the prevailing frequency of electrical activation, coronary perfusion pressure, and left ventricular wall tension. In hearts in the adequately perfused, vented, and nondistended state the myocardial oxygen consumption of ventricular fibrillation may not be significantly different than that of the empty, beating heart. Thus, the present study investigated both global normothermic ischemic and nonischemic prolonged ventricular fibrillation effects on cardiac energetics when quantitated in the same heart under constant and defined nonworking conditions. At constant heart rate and perfusion pressure, preload recruitable stroke work was preserved in the nonischemic group but depressed to 41% of control postischemically (p = 0.018). Under control conditions, no significant differences in myocardial oxygen consumption between the various nonworking cardiac states were detected. However, postischemic empty, beating hearts and empty, fibrillating hearts both extracted (31%) and consumed (26%) less oxygen (p < 0.03 each) without concomitant coronary hyperemia. Prolonged nonischemic ventricular fibrillation increased coronary blood flow 158% (p < 0.03) without augmenting myocardial oxygen consumption. These data contrast with the previously reported increased oxygen demand of ventricular fibrillation and suggest that postischemic fibrillation is not bioenergetically deleterious in the nonhypertrophied heart under controlled working conditions.






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Copyright © 1991 by The Society of Thoracic Surgeons.