Hypothermia and anoxic arrest

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Myocardial hypothermia, induced by topical cooling, selective cooling by perfusion of the coronary arteries, or by a combination of these methods, has proved to be an effective method for protection of the myocardium during cardiac surgical procedures which require interruption of normal coronary perfusion. For patients undergoing coronary bypass grafting procedures, selective myocardial hypothermia (15 to 18 C) resulting in cardiac arrest over a period of several minutes has been shown to be superior to ventricular fibrillation and moderate hypothermia (30 to 35 C) as assessed by rate of physiologic recovery of ventricular function, myocardial creatine phosphokinase (MB CK) isoenzyme release, and by study of myocardial ultrastructure.1 Hypothermic cardioplegia, produced by a cold, potassium-containing solution, has also been shown to be an effective method of myocardial protection. The latter technique produces almost immediate and complete cessation of electromechanical activity, thereby further reducing metabolic demands during the period of aortic clamping. Potassium-induced cardioplegia has been shown experimentally to result in less depletion and more rapid restoration of myocardial energy stores than anoxic arrest at similar temperatures.2 Despite the theoretical advantages of hypothermic cardioplegia, few clinical studies, particularly in patients undergoing coronary artery grafting procedures, are available to document the beneficial effects noted in the experimental studies.

To evaluate these two methods of myocardial protection (hypothermic anoxic arrest, hypothermic cardioplegia), 50 consecutive patients undergoing multiple coronary bypass grafting procedures on one surgical service during a 4-month period were evaluated using serial MB CK determinations and electrocardiographic changes as indices of myocardial injury.



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