Myocardial Preservation during Hypothermic Cardiopulmonary Bypass: A Team Endeavor

____________ _ Myocardial failure is the primary cause of death following operation using hypothermic cardiopulmonary bypass. The mean mortality rate for coronary bypass in Medicare patients in the United States for 1984 was 5.5%.1njury to the heart is caused by aortic cross-clamping or total circulatory arrest. The lesion of hypoxia is characterized by progressive acidosis. The severity of acidosis correlates with the degree of post-operative myocardial dysfunction. In decision making concerning the management of perfusion or of operative technique, prevention and/ or treatment of myocardial acidosis takes precedence over other considerations. Recent advances in understanding the effect of temperature on acidbase equilibria, and the recent introduction of online blood gas monitoring devices have given the perfusionist the necessary means to achieve perfusion which keeps the patient on the alkaline side of biological neutrality. Similarly, the surgeon should utilize the protective value of frequent coronary infusions with a cold, oxygenated, alkaline, buffered, anti-oxidant blood cardiopreservation solution. Figures and tables are presented which enable the perfusionist to understand hypothermic acidbase management, and to use appropriately hyperventilation and high flow perfusion, avoiding any use of C02 gas, while monitoring the patient's course using venous blood samples which are uncorrected for temperature. With this team approach, improvement in operative mortality can be expected. Presented at The Mechanisms of Perfusion III Meeting in Tampa, Florida, April9, 1988. *Research institute for Biological Sciences Lakewood, Colorado 80227 124 The Journal of Extra-Corporeal Technology Heart surgery is major surgery and causes a significant mortality rate. In the only large scale national study available, the Department of Health and Human Resources released late in 1985 an analysis of the death rate in all 57,804 patients whose coronary bypass procedures in 1984 were paid for by Medicare. The analysis was by hospital in every state of the country. The average death rate following surgery in these patients was 5.5%. This paper explores in depth the major component of that risk and discusses the means available to diminish it. What are the operative sequellae which are the cause of mortality and morbidity? In the opinion of every cardiac surgeon with whom I have discussed this problem, myocardial failure is No. I. Difficulty in weaning the patient from the pump and the necessity for post-operative circulatory support is a dreaded scenario for all. Slow and progressive myocardial insufficiency may also prove eventually to be terminal. True, other sequellae also occur. Technical failure is the one to which the surgeon is most sensitive, and strives to perfect his skills and judgment so these will not occur. Embolic episodes, clotting disturbances, pulmonary or renal complications are important too, but myocardial failure apparently is a more frequent cause of death than all these put together. To lower the risk of heart surgery, attention should be concentrated on protection and preservation of the myocardium, which must not be allowed to develop acidosis. The myocardium was adequately supporting the life of the patient when he or she was on the way to the operating room in all but a very few instances. If it fails to achieve this capability after surgery, one must face up to the fact that injury inflicted during the operation is the chief cause of its failure. Procedures in the interior of the heart involving valve excision and replacement, insertion of baffles, suture closure of defects, or myomectomy inflict significant myocardial surgical trauma. Mechanical muscular injury is intrinsic to these procedures and cannot be avoided, only minimized. In today's cardiac surgery scenario, Volume 20, Number 4, Winter 1988 however, the great majority of operations are performed with the intact heart immobilized and cold. Bypass procedures do not require cardiac incision beyond cannulation; they only require aortic cross clamping. The damage is inflicted by circulatory abuse. Ischemic myocardial acidosis can and is being surgically inflicted in large and potentially lethal doses throughout the world. However, with careful management this type of myocardial impairment can and should be largely prevented and successfully treated. It has been known for years that acidosis reduces myocardial contractility (1). If the acidosis becomes severe enough, it will lead to structural damage and eventual cell necrosis. At some point in this progression, the damage is irreversible, and the heart is doomed. At normothermia, this occurs between 15 and 30 minutes of ischemia. And even deep hypothermia will not prevent these changes but will only delay them for about two hours. The degree of post operative myocardial disability correlates exactly with the level of maximum depression in myocardial pH irrespective of myocardial temperature or duration of ischemia. In a careful study by Takash et al. (2) using micro-myocardial pH and temperature probes in ischemic left ventricles in sheep, any terminal intramyocardial pH less than 7.0 resulted in marked decrease in left ventricular function whether that pH level was reached rapidly during normothermic ischemic or more slowly during hypothermic (25°C) ischemia. In both instances, a pH of 6.8 resulted in only about 50% return ofleft ventricular function, and of6.6 in about 30% return of function at one hour. Below 6.5 no animal could be weaned from the pump without circulatory assist. It is clear that intramyocardial acidosis is damaging to the functional integrity of the heart. Before irreversibility sets in, the myocardium will still look essentially normal under the microscope; but if reperfusion with an oxygenated acidotic fluid is instituted there is an explosive change in the micropathologic characteristics. Hypoxically distorted enzyme systems fail to supress the violent formation of oxygen free radicals. Superoxides and hydrogen peroxides flood the cell structures causing damage everywhere. Edema forms in the matrix; calcium floods the mitochondria and precipitates as phosphate conglomerates. This is the cataclysm of the so-called' 'reperfusion injury.'' But it can be successfully prevented by the avoidance of hypoxic acidosis and it can be essentially ablated by reperfusion which is strongly