Faculty Bibliography

Patients with cystic fibrosis who have end-stage respiratory failure and associated liver cirrhosis have been considered poor candidates for lung transplantation because of high morbidity and mortality resulting from hepatic insufficiency after the operation. Since April 1989, our policy has been to combine heart-lung or lung and liver transplantation in this group of patients. Between June 1990 and March 1995, among 25 patients accepted in the program for combined transplantation, nine died awaiting transplantation and 10 underwent one of the following procedures: heart-lung-liver transplantation (n = 5), en bloc double lung-liver transplantation (n = 1), sequential double lung-liver transplantation (n = 3), and bilateral lobar lung transplantation from a split left lung and reduced liver transplantation (n = 1). There were 5 male and 5 female patients. The ages of the recipients ranged from 10 to 24 years. Mean forced expiratory volume in 1 second was 29% and mean forced vital capacity was 35% of predicted values. All patients were infected with resistant Pseudomonas, three with Pseudomonas cepaceia, and two patients had Aspergillus species in addition. All patients had severe cirrhosis with portal hypertension. Four patients had a history of esophageal variceal bleeding and two had had previous portosystemic shunts. The operation was performed as a two-stage procedure, the intrathoracic operation being completed before the abdominal stage was begun. Cardiopulmonary bypass was used in all patients because of poor clinical condition. Immunosuppression consisted of azathioprine, cyclosporine, and prednisone, as for isolated lung transplantation. There were two perioperative deaths, one caused by primary liver failure and the second by early lung dysfunction. For the first 3 months after transplantation pulmonary infection was the most common cause of morbidity. Other complications included tracheal stenosis (n = 1), bronchial stenosis (n = 1), biliary stricture (n = 2), and severe ascites (n = 3). All were successfully treated. Obliterative bronchiolitis developed in three patients. This was stabilized with FK 506 in two patients; the other patient underwent retransplantation at 38 months but eventually died of bleeding. Actuarial survival was 70% at 1 year and remained unchanged at 3 years. Significant functional improvement was observed in all survivors. For patients who have chronic respiratory failure with advanced cirrhosis, lung transplantation combined with liver transplantation can be performed with a satisfactory outcome

The purpose of this study was to test the hypothesis that isoproterenol could reverse bupivacaine toxicity. In eight isolated rabbit hearts an electrophysiologic evaluation was performed then repeated during infusion of bupivacaine (1 microgram/mL) alone and bupivacaine plus isoproterenol (1-2 micrograms/mL). Bupivacaine alone increased electrocardiographic intervals (P wave, QRS complex, PR, AV, and QTc interval) and refractory periods of the myocardium and atrioventricular junction as well as the Wenckebach cycle and pacing thresholds. The addition of isoproterenol corrected partially or completely all bupivacaine-induced abnormalities, and decreased sinus cycle length, suggesting a potential therapeutic value in the treatment of bupivacaine intoxication

To assess the direct electrophysiologic effects of bupivacaine, we examined the spontaneous sinus rhythm and induced rapid and premature atrial and ventricular pacing in 11 isolated rabbit hearts perfused in the Langendorff apparatus with varying concentrations (designated by []) of bupivacaine (control, n = 2; 0.3 microgram/mL, n = 3; 1.5 micrograms/mL, n = 3; 3.0 micrograms/mL, n = 3). There was no change in sinus node automaticity or sinus node recovery time at any concentration and no evidence of abnormal automaticity. Depression of conduction was reflected by prolongation of the PR interval at the following concentrations: 1.5 micrograms/mL (65.0 ms before, 96.6 ms after) and 3.0 micrograms/mL (61.6 ms before, 103.3 ms after) and increase in atrial and ventricular pacing thresholds at 3.0 micrograms/mL (atrial: 0.86-8.6 mA, ventricular: 2.0-10.0 mA). No spontaneous tachyarrhythmias occurred; 2:1 spontaneous atrioventricular block (n = 1) and a decrease in maximal paced rate with 1:1 anterograde or retrograde atrioventricular conduction were noted at all concentrations of bupivacaine. Thus bupivacaine did not change automaticity but had a depressant effect on conduction at the atrial, ventricular, and atrioventricular levels, providing a basis for clinically occurring atrioventricular block and reentrant arrhythmias