Temporary Incomplete Ischemia of the Legs Induced by Aortic Clamping in Man Metabolic and Hemodynamic Effects of Temporary Extracorporeal By-pass

The effects on central hemodynamics and skeletal muscle metabolism during surgery for abdominal aortic aneurysm were compared in 6 patients given a preoperative adrenergic block (group B) and in 6 patients who additionally had a temporary brachio-femoro-femoral by-pass during the aortic clamping (group B+S). The cardiac output, heart rate, arterial and pulmonary artery pressures and the cardiac filling pressure were studied. Biopsy specimens from the lateral vastus muscle and blood samples from the radial artery and the iliac vein were taken before aortic clamping and also before and 30 minutes, 4 and 16 hours after the aortic declamping. Intramuscular temperature and pH were measured. The glycogen, glucose, lactate, pyruvate, ATP, ADP, AMP, phosphocrea-tine (PCr) and creatine (Cr) contents of the muscle and the lactate and pyruvate concentration in iliac venous and radial arterial blood were determined, using enzymatic fluorometric techniques. In group B, aortic clamping induced severe temporary incomplete ischemia with a 300 % increase in lactate/pyruvate (L/P) ratio and a fall in intramuscular pH (pHm). The adenylate energy charge (EC) decreased, but the creatine (PCr + CR) and the adenylate (ATP + ADP + AMP) pool remained unchanged. After aortic declamping, the L/P ratio, EC and pHm regained their preclamping values, but the pools of energy phosphate compounds were reduced, indicating dysfunction or damage of the muscle cells. In group B+S there were no major muscle metabolic changes during clamping or after declamping of the aorta. In group B the systemic vascular resistance (SVR), mean arterial blood pressure (MAP) and left ventricular stroke work (LVSW) increased during the occlusion. On release of the clamp, cardiac output rose, possibly due to the sudden reduction of SVR. A temporary marked fall of MAP occurred. In group B+S, no increase of SVR, MAP or LVSW was observed during aortic clamping. After the declamping, only a minor MAP drop was observed. In both groups, a brief rise in pulmonary vascular resistance after the aortic declamping suggested transient pulmonary microembolism. If a high-risk patient is to undergo reconstructive surgery of the abdominal aorta and/or technical difficulties can be expected to necessitate prolonged cross-clamping during the operation, a temporary extracorporeal by-pass may be a favorable adjuvant, improving cardiac performance and preventing derangement of muscle metabolism.