Risk of spinal cord dysfunction in patients undergoing thoracoabdominal aortic replacement.

The records of 150 consecutive patients undergoing thoracoabdominal aortic replacement from 1980 to 1991 were retrospectively reviewed. There were 89 men and 61 women; mean age was 67.8 years (range: 33 to 88 years). Since June 1989, a multimodality prospective perioperative protocol was used to reduce the risk of spinal cord dysfunction. Ischemia is minimized by complete intercostal reimplantation whenever possible, cerebrospinal fluid drainage, and maintenance of proximal hypertension during cross-clamping. Spinal cord metabolism is reduced by moderate hypothermia, high-dose barbiturates, and avoidance of hyperglycemia. Reperfusion injury is minimized by the use of mannitol, steroids, and calcium channel blockers. Ninety-seven percent of patients survived long enough for evaluation of their neurologic function. Spinal cord dysfunction was reduced from 6 of 108 (6%) in the preprotocol group to 0 of 42 in the protocol group (0%) (p less than 0.01). The overall 30-day operative mortality was not significantly different between the groups (9% versus 12%, p = NS). A multimodality protocol appears to be effective in reducing the risk of spinal cord injury during thoracoabdominal aortic replacement.

The Blalock-Taussig shunt: an analysis of trends and techniques in the fourth decade.

The original description of the Blalock-Taussig shunt was published in 1945 and represented the first direct surgical procedure for the treatment of cyanotic congenital heart disease. The present study analyzes the results of Blalock-Taussig shunts performed at Duke University Medical Center during the fourth decade since the original description of the procedure. From 1975 to 1984, 53 classic and 24 modified Blalock-Taussig shunts were performed with a hospital mortality of 8%. These deaths occurred in critically ill patients with either pulmonary atresia or complex congenital cardiac lesions. The results of the early group (1975-1979) were compared to the late group (1980-1984) of patients. There was a greater proportion of infants less than 1 week of age in the late group, and the actuarial event-free shunt survival following operation was significantly better in the late group. This improvement in the late group was apparent both in patients receiving classic and modified Blalock-Taussig shunts and probably represents the effects of advances in microsurgical technique as well as improvement in the support of critically ill infants at the time of surgery by pediatric anesthesiologists and neonatologists. The data in the present study indicate that the mortality associated with Blalock-Taussig shunting is related to the condition of the patient at the time of surgery and the underlying cardiac pathology rather than the age of the patient at the time of shunting. The efforts to further reduce morbidity and mortality associated with Blalock-Taussig shunting should therefore be directed primarily to the support of infants during the preoperative and intraoperative phases of care.

The electrophysiological effects of calcium channel blockade during standard hyperkalemic hypothermic cardioplegic arrest.

The addition of calcium channel-blocking agents to a standard hyperkalemic hypothermic cardioplegic solution has been examined both experimentally and clinically. None of these studies, however, have investigated the effect of calcium blockade during cardioplegic arrest on the specialized cardiac conduction tissues and on the subsequent development of arrhythmias after arrest. The present study examined the effect of adding nifedipine to standard cardioplegic solution administered in a canine experimental preparation modeled on routine clinical techniques. The time to and duration of electrical arrest following the administration of cardioplegia and the functional electrophysiological variables before and after arrest were measured using a 32-channel data acquisition system. The addition of nifedipine shortened the time to electrical arrest and prolonged the duration of arrest compared with standard potassium cardioplegic solution alone, without a deleterious effect on conduction function immediately after arrest. The occurrence of low-amplitude electrical activity (LEA) in both atria and ventricles during arrest was significantly reduced by the addition of nifedipine, thereby suggesting a possible correlation between LEA and calcium-mediated conduction occurring under conditions of standard cardioplegic arrest.

Monitoring of the electrical status of the ventricle during cardioplegic arrest.

Present methods used to assess the status of myocardial preservation during cardioplegic arrest include monitoring the peripheral electrocardiogram (ECG) and ventricular myocardial temperature, and visual inspection of the heart to verify complete mechanical arrest. This study was designed to determine if these parameters are adequate to ensure complete electromechanical arrest after the application of standard cardioplegic techniques. The electrical status of the ventricle in adult mongrel dogs was monitored continuously during elective hyperkalemic hypothermic arrest for the presence of electrical activity in either the atrium or ventricle with 25 intramural electrodes, three epicardial reference electrodes, a His bundle catheter, and three peripheral ECGs. Occurrence of ventricular electrical activity was documented in the arrested heart (determined visually) when the peripheral ECG was quiescent; the activity persisted for a significant period of time before electromechanical activity could be detected by standard monitoring techniques. This electrical activity is believed to originate in the lower atrial septum and to conduct through the AV node to the ventricles at myocardial temperatures previously thought to be safe. Thus, continuous monitoring of intramural electrical activity would appear to be a more reliable technique than those currently used to determine the adequacy of myocardial preservation during elective cardioplegic arrest.

Conduction block after cardioplegic arrest: prevention by augmented atrial hypothermia.

Atrioventricular conduction abnormalities have become more frequent since the reintroduction of cardioplegic techniques for myocardial preservation during cardiac surgery. An animal model was developed to clarify the role of atrial septal hypothermia in the preservation of the primary site of postoperative conduction delay, the AV node. In our study, 10 animals served as the control group. They were subjected to 40 min of cardioplegic arrest during which the heart was protected with multidose cold potassium cardioplegia. Atrial septal temperatures averaged 27.4 degrees +/- 1.2 degrees C during cardioplegic arrest. We treated 10 additional animals (study group) similarly, except that atrial hypothermia was augmented by intracavitary or specialized topical techniques, which resulted in an average atrial septal temperature of 20.8 degrees +/- 3.3 degrees C (p less than .05). Detailed electrophysiologic studies of both groups were performed at 37 degrees C before and after cardioplegic arrest. Significant prolongation of AV nodal, and to a lesser extent His-Purkinje, conduction times was noted in the control group, but no conduction abnormalities occurred in the study group receiving augmented atrial hypothermia. Thus, conduction block in the specialized conduction system after cardioplegic arrest appears to be related to the adequacy of hypothermic preservation of the atrial septum and can be prevented by augmented atrial hypothermia.