Despite advances in anesthetic and surgical management, a substantial number of patients still sustain some degree of myocardial damage during cardiac operations designed to repair their hearts. Although myocardial necrosis can occur at any time during the perioperative period, damage most often results from inadequate myocardial preservation during cardiopulmonary bypass.1 The purpose of this publication is to discuss first, some of the mechanisms and manifestations of myocardial damage during cardiopulmonary bypass; and second, some interventions that can be made during the bypass interval to protect jeopardized myocardium.
Although the precise mechanism of cell death remains controversial, the process is probably initiated by a period of ischemia. If the ischemia is prolonged, depletion of cellular glycogen, high energy phosphate and other metabolites occurs followed by cell swelling and membrane disruption.2 Structural damage may be detected at autopsy or clinically by electrocardiography, and enzyme and radionuclide imaging techniques. Structural damage predisposes to functional impairment manifest clinically as low cardiac output with the need for inotropic or mechanical support. Persistent ventricular arrhythmias may be a subtle manifestation of myocardial damage. A not so subtle but fortunately uncommon sign of damage is ischemic contracture (“stone heart”).
It is not clear whether impaired cardiac function always indicates that structural damage has occurred. It may be possible for ischemia to induce temporary reversible dysfunction of the sub-cellular mechanisms of energy production or excitation contraction coupling or both without permanent structural damage. Further investigation in this area is needed. Data presently available suggest that persistently low cardiac . . .