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.