Clowes GH; Del Guercio LR;
Circulatory response to trauma of surgical operations. Metabolism. 1960;9:67-81. (NOTE THE DATE)
To determine the nature of the normal cardiovascular response of man to surgical operations, thirteen patients making uncomplicated recoveries after thoracotomy for pulmonary surgery were studied by measuring cardiac output and arterial and venous pressure before, during and for one week after surgery. Arterial pH, blood gas and electrolytes were analyzed simultaneously. Through out the observations, arterial blood pressure was more or less constantly maintained; but during the operation cardiac output fell an average of 33 per cent with a decrease of stroke volume, and the calculated peripheral arterial resistance rose. Venous pressure was elevated in all patients during the induction of anesthesia and remained so to the end of the operation. Upon awakening and during extubation, the situation was promptly reversed. Cardiac output rose to 130 per cent of the resting value; peripheral resistance fell below normal; and venous pressure returned to levels below 10 cm. of H20 . These changes persisted to the end of the first post operative week. Three patients, who recovered satisfactorily after cardiac operations, followed a similar pattern of circulatory response. Arterial pH and pCO2 were maintained within normal limits in all patients who recovered; however, all showed some degree of arterial oxygen desaturation postoperatively. Metabolic acidosis, as indicated by an elevation of lactic acid, took place during and after the operation but returned to pre-operative values within three days. Sodium fell, on the average, to 129 mEq./L. on the second postoperative day. Ionized calcium fell to 4.1 mg. per cent on the first day. Potassium remained unchanged. Three patients who recovered from open heart operations responded in the same fashion with a postoperative in crease in cardiac output.
Two patients died postoperatively. Both failed to show the normal post operative elevation of cardiac output; metabolic acidosis increased until respiratory compensation failed, and arterial pH fell below 7.3.