The Journal of thoracic and cardiovascular surgery
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J. Thorac. Cardiovasc. Surg. · Jun 1987
Comparative StudyContinuous epidural infusion of morphine for pain relief after cardiac operations.
Postoperative pain relief and stress hormones were examined during the use of continuous epidural infusion of morphine at a rate of 0.1 mg/hr in 30 patients (Group B) after coronary artery bypass grafting. This was compared to our routine method of postoperative analgesia of intravenous morphine 2 mg/2 hr and as needed in another 30 patients (Group A). Continuous epidural morphine infusion required occasional supplementation with intravenous morphine and achieved effective analgesia in 80% of the patients. ⋯ Levels of postoperative stress, serum cortisol, and beta-endorphin were significantly lower in Group B than in Group A. This study shows that continuous epidural infusion of morphine at a rate of 0.1 mg/hr provides selective and effective pain relief and reduces postoperative stress after cardiac operations. This method of analgesia was also associated with minimal side effects and provides an alternate approach for treatment of pain after cardiac operations.
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J. Thorac. Cardiovasc. Surg. · Jun 1987
Case ReportsLife-threatening postoperative pulmonary complications in patients with previous amiodarone pulmonary toxicity undergoing cardiothoracic operations.
Amiodarone therapy for cardiac arrhythmias is increasingly being recognized to be associated with pulmonary toxicity. In this report, we describe the case histories of four patients with previously diagnosed amiodarone pulmonary toxicity in whom the adult respiratory distress syndrome developed after cardiothoracic operations for malignant ventricular arrhythmias. Three patients underwent endocardial resection (two died), and a fourth patient had implantation of an automatic defibrillator unit. ⋯ In the two patients who died, desethylamiodarone levels were 510 and 4,400 micrograms/gm in pulmonary tissue. Histologic examination showed "honeycomb" appearance of the lung with prominent septae, alveolar foamy macrophages, and hyperplasia of alveolar lining cells, consistent with amiodarone pulmonary toxicity. Causes including pump-oxygenator time, oxygen toxicity, anesthetic agents, congestive heart failure, and pulmonary infection superimposed on amiodarone pulmonary toxicity are discussed with a review of the literature.