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Ann Thorac Surg 1996;61:87
© 1996 The Society of Thoracic Surgeons
Division of Cardiothoracic Surgery, New England Deaconess Hospital, 110 Francis St, Suite 2C, Boston, MA 02215
There is perhaps no other subject that elicits such a strong and visceral (and always biased) response from the cardiac surgeon than ventricular fibrillation. The spectrum ranges from those (few) who routinely use intermittent aortic cross-clamping and fibrillation as an intraoperative myocardial management strategy to those who ``never'' allow the heart to fibrillate during cardioplegia, and rapidly defibrillate if needed early in reperfusion to prevent myocellular damage. Who is right? The simple answer to the question is probably both. Why? The metrics used to assess any fibrillation effects often confound determinant variables such as the duration and method of fibrillation induction, internal and external cardiac workload, endocardial wall tension, coronary perfusion pressure and flow, oxygen extraction, left ventricular hypertrophy, and the heart rate in the beating comparison group. It is no surprise that electrically induced and sustained ventricular fibrillation in a hypertrophied, distended ventricle is bioenergetically and mechanically deleterious compared with the electrically quiescent, nondistended heart. Is there a significant difference, however, between the spontaneously fibrillating, empty, nondistended, nonhypertrophied, well-perfused (high coronary perfusion pressure and flow) heart and one that is in a similar state, but beating?
Most well conducted and controlled experimental studies, as well as clinical series, would suggest not. This is not a surprise if one considers that the oxygen cost of electrical activation alone without the resultant mechanical activity has been previously reported at less than 1% of the total working myocardial oxygen consumption per beat [1]. As indicated by this excellent study by Jessen and associates, for the neonatal myocardium, the oxygen utilization cost of ventricular fibrillation versus the empty beating, vented state is small, about 15%. If the heart were cooled to a myocardial temperature of 15°C, the absolute difference would be predictably less, because the greatest reduction in myocardial oxygen consumption is realized (at least 90%) attendant to empty, nonworking, vented hypothermia whether induced by cold perfusion or cardioplegia. This was the observation of the present study. The central question, however, is what is the postischemic, postfibrillation or reperfusion residual functional capacity, as all of us desire a rapid and successful wean from bypass at the end of the operation. Perhaps differences between cold perfusion alone, cold plus fibrillation, or cold plus cardioplegia would be better assessed by preintervention and postintervention mechanical indices, where the relative impact of each intervention on depleting adenosine triphosphate stores, altering calcium homeostasis and buffering capacity, and exacerbating transmural flow maldistribution and edema formation are immediately evident. Such data were not reported by Jessen and colleagues for the neonatal heart, but serve as fertile soil for future investigation.
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