Abstract

Changes in oxyhemoglobin dissociation compensate partially for decreased O2 transport caused by high altitude, anemia, and cardiac disease. This investigation determined whether similar changes occurred in patients undergoing myocardial revascularization and the possible significance of such changes. In 15 patients scheduled for coronary vein bypass surgery the following were inserted: a #7 French catheter into the coronary sinus or great cardiac vein, a pulmonary arterial catheter (Swan-Ganz), and a radial arterial catheter. Patients were anesthetized with either halothane-N2O 50% or morphine (2 mg/kg IV) with N2O 50%. Hemodynamic status was measured and blood samples were taken from the catheters in the preoperative period and after endotracheal intubation, sternotomy, bypass, and chest closure. Blood samples were analyzed for pH, blood gas tensions, and O2 saturation. Values for P50 for mixed venous and coronary sinus blood were calculated from O2 tension and saturation. Patients were divided into two groups on the basis of peroperative mixed venous P50 values: group I had normal P50 levels of 26.1 +/- 2.0 torr (mean +/- SD); group II had elevated values for mixed venous blood P50 of 32.5 +/- 1.6 (mean +/- SD). Unlike group I, group II had depressed ventricular function and higher P50 values for coronary sinus blood than for mixed venous blood. Induction of anesthesia increased P50 values in group I but not in group II and removed the significant differences between group I and group II mixed venous P50 values. In group II patients, cardiopulmonary bypass lowered the elevated P50 of coronary sinus blood so that it equaled P50 for mixed venous blood. It is concluded that induction of anesthesia may elevate P50 in patients who have normal preoperative P50 values. The already elevated P50 values of patients with ventricular dysfunction did not change. Cardiopulmonary bypass decreased coronary sinus P50 in group II patients, and this change might be deleterious if the original elevation represents a compensatory response to a reduction in O2 transport.

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