Electrocardiographic studies during operation for coarctation of the aorta.

Considerable attention has recently been focussed upon the disturbance of cardiac rhythm that may occur during intrathoracic surgery (Meek et al., 1937, and Burstein, 1946). These arrhythmias may vary from the relatively innocuous nodal rhythm and shifting pacemaker to cardiac standstill and ventricular fibrillation. Several initiating factors have been described, among which are cyclopropane anesthesia, endotracheal intubation, cutting and spreading of ribs, hilar stimulation, opening of the pericardium, and dislocation of the heart (Burstein, 1947). The mechanisms by which such abnormal cardiac action has been brought into play have not always been clearly defined. In certain cases increased vagal tone or direct vagal stimulation has appeared to be the most probable cause. The work of Sloan (1949) showing the increase in vagal sensitivity with anoxia has shed considerable light on this. It seems clear then that hypoxia and hypercapncea play a very important role in precipitating these abnormalities, whether mediated through a vagal mechanism or not. Surgery for coarctation of the aorta has been complicated by the occurrence of several serious disturbances of cardiac function during or shortly after operation (Shapiro, 1949, and Clagett, 1949). In 100 operations reported recently by Gross (1950), there appeared to be three phases of the operation during which cardiac irregularities are especially apt to occur. The first is during the period of hypertension following the clamping of the aorta. This has proved even more hazardous if the subclavian artery also has been occluded. One patient died three days after operation and necropsy showed cerebral hemorrhage; both aorta and subclavian artery had been clamped off during aortic anastomosis, and it is believed that the resultant excessive hypertension caused the cerebral hlmorrhage. Another patient had severe convulsions during this phase. The second danger point proved to be immediately after the release of the aortic clamps. One patient died suddenly at this juncture, and temporary cardiac arrest occurred in three, and shock in several more. Other surgeons are known to have encountered difficulties of similar nature at this point. The end of the operation marks the third phase that has been associated with a number of cardiac disturbances. Two patients developed severe shock at the end of operation and subsequently died. Only one patient, who developed marked pulmonary cedema and died shortly after the opening of the chest, showed a severe disturbance of cardiac function at an interval unrelated to the three just mentioned. Many of these accidents were quite unrelated to vagal reflexes. Shock and death on release of the aortic clamps were probably due to rapid change in hemodynamics effected by sudden removal of peripheral resistance added to previous blood loss. Shock following cyclopropane