Etiology and prevention of topical cardiac hypothermia-induced phrenic nerve injury and left lower lobe atelectasis during cardiac surgery.

Left hemidiaphragm elevation is frequently noted following cardiac surgery employing topical hypothermia. We speculate that contact of the left phrenic nerve with ice causes nerve injury, resulting in left hemidiaphragm paresis or paralysis and left lower lobe atelectasis. Left diaphragm elevation was noted on postoperative chest x-ray examination of 36 of 60 (60 percent) consecutive patients in whom topical cooling of the heart with a cold slush solution was administered prior to use of a cardiac insulation pad (CIP, Shiley Laboratories, Irvine, California). Following the use of the CIP in a similar group of 60 consecutive patients, only five (8 percent) showed evidence of diaphragmatic elevation. The difference in the incidence of diaphragmatic elevation between these two groups is statistically significant (p less than 0.001). A comparison of postoperative left lower lobe atelectasis prior to the use of the CIP was also statistically significant (p less than 0.001). There was no significant difference in the aortic cross-clamp time or the volume of intraaortic cardioplegia used in these two groups. The use of topical cardiac hypothermia has been shown to protect the myocardium. Phrenic nerve injury secondary to the use of ice in this method has been documented. The use of a cold solution without ice chips or slush, or the insertion of a CIP prior to the use of topical cardiac hypothermia (when ice chips or slush are used) decreases the exposure of the phrenic nerve to cold injury and decreases the incidence of paresis of the left diaphragm and resultant atelectasis.

Ischemic contracture of the left ventricle. Production and prevention.

Ischemic contracture of the left ventricle ("stone heart") is a recognized complication of prolonged periods of interruption of the coronary circulation during open-heart surgery. We have examined the effects of moderate hypothermia (28 degrees C.) and preoperative beta-adrenergic blockade (propranolol, 0.5 mg. per kilogram; 1.0 mg. per kilogram) on contracture development during ischemic arrest of the heart. Four groups of 8 dogs each were placed on total cardiopulmonary bypass, and ischemic arrest of the heart was produced by cross-clamping the ascending aorta and venting the left ventricle. Intramyocardial carbon dioxide tension was continuously monitored by mass spectrometry. When anaerobic energy production ceased, as indicated by a final plateau in the intramyocardial carbon dioxide accumulation curve, the ischemic arrest was terminated and the contractile state of the heart observed. These results are given in the text. We conclude that beta-adrenergic blockade delays, but does not prevent, the onset of ischemic contracture of the left ventricle under normothermic conditions. Moderate hypothermia appears to prevent this complication completely.

Comparison of effects of prostaglandin E1 and nitroprusside on pulmonary vascular resistance in children after open-heart surgery.

Prostaglandin E1 (PGE1) is a vasodilator. Because the drug is metabolized by lung, we postulated a selective effect on pulmonary vasculature. Twenty-six patients aged 3 months to 16 year (mean, 6.5 years) were studied after repair of atrial septal defect (5), ventricular septal defect (10), tetralogy of Fallot (3), and other lesions (8). Fourteen patients also received nitroprusside. PGE1 (0.1 to 1.0 micrograms/kg/min) or nitroprusside (0.59 to 8.7 micrograms/kg/min) was infused through a central venous catheter until mean pulmonary or mean systemic arteria pressure decreases at least 10%. Prostaglandin E1 and nitroprusside both decreased mean systemic arterial pressure and systemic vascular resistance (P less than 0.05). Although both drugs caused an average decrease in pulmonary arterial pressure and resistance, nitroprusside produced a more consistent response. Side-effects limited the use of PGE1 in 5 patients. PGE1 is an effective vasodilator and has advantages for some patients, but it does not produce selective vasodilation of pulmonary vessels.

Effects of nitroprusside and dopamine on pulmonary arterial vasculature in children after cardiac surgery.

The hemodynamic effects of nitroprusside and dopamine were studied in 28 children early after intracardiac repair. Children were placed in six groups, five according to their anatomic lesion and one made up of those who had postoperative pulmonary artery hypertension, to evaluate the possible differences in response of the pulmonary arterial vasculature to the drugs. Seven children had repair of an atrial septal defect; six, repair of tetralogy of Fallot; four, repair of ventricular septal defect; five, surgery for pulmonary stenosis; one, closure of a left ventricular to right atrial tunnel; and five, postoperative pulmonary artery hypertension. Dopamine was infused at 8 microgram/kg/min, and nitroprusside at 3 microgram/kg/min. With dopamine, the heart rate increased an average of 10% and the cardiac index 11%; both increases were statistically significant. Changes in systemic and pulmonary vascular resistance, however, were not. With nitroprusside, the heart rate increased an average of 9% and the cardiac index 5%, while there was a significant decrease in both systemic (-20%) and pulmonary (-27%) vascular resistance. With the combination of dopamine and nitroprusside, both the cardiac index (+13%) and heart rate (+20%) increased significantly while systemic vascular resistance fell an average of 23% from control, and the pulmonary vascular resistance decreased 21%. Drug response among all five anatomic subgroups tended to be similar. We conclude that an afterload-reducing agent, such as nitroprusside and an inotropic drug such as dopamine, may have potential clinical advantages when used together in children providing heart rate does not become excessive.