Understanding cardiovascular drug interactions.
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Biomedical subjects
Publications and source records attributed to J G Porterfield.
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The new anti-arrhythmic agent, amiodarone, is increasingly recognized as a cause of pulmonary toxicity (APT). In the present series, 11 of 171 patients (6.4%) receiving the drug had APT develop. Clinical symptoms varied from mild cough and dyspnea to acute respiratory failure. Chest x-rays demonstrated alveolar and/or interstitial opacities in all 11 patients. The microscopic appearance of APT resembled that seen in lung injury from other drugs. The features were those of diffuse alveolar damage, ranging from the early acute to the organizing phase. Mural and intraalveolar foam cells were a prominent component. The epithelial origin of these cells was confirmed by positive immunoperoxidase staining for carcinoembryonic antigen. They were further identified as type II pneumocytes by electron microscopic examination. These findings support the concept that amiodarone is responsible for a drug-induced phospholipidosis. APT was clinically reversible in all patients; however, five patients (45%) died of arrhythmia shortly after discontinuation of amiodarone.
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BACKGROUND AND OBJECTIVE: The ability of a shock to defibrillate the heart depends on its waveform and energy. Past studies of biphasic truncated exponential (BTE) shocks for external defibrillation focused on low energy levels. This prospective, randomized, double-blind clinical trial compared the first-shock efficacies of 200-joule (J) BTE, 130-J BTE, and 200-J monophasic damped sine wave shocks. METHODS: Ventricular fibrillation (VF) was induced in 115 patients during evaluation of implantable cardioverter-defibrillator function and 39 patients during electrophysiologic evaluation of ventricular arrhythmias. After 19 +/- 10 seconds of VF, a randomized transthoracic shock was administered. Mean first-shock success rates of the three groups were compared using a "Tukey-like" statistical test, adjusting for multiple comparisons. Blood pressures and arterial oxygen saturations were measured before VF induction and 30, 90, and 150 seconds after successful defibrillation. RESULTS: First-shock success rates were 61/68 (90%) for 200-J monophasic, 39/39 (100%) for 200-J biphasic, and 39/47 (83%) for 130-J biphasic shocks. The 200-J biphasic shocks were simultaneously superior in first-shock efficacy to both 200-J monophasic and 130-J biphasic shocks (experimentwise error rate, alpha < 0.01). There was no significant difference between the efficacies of 200-J monophasic and 130-J biphasic shocks, nor was there any significant difference between the three groups in hemodynamic parameters after successful shocks. CONCLUSIONS: Biphasic shocks of 200 J provide better first-shock defibrillation efficacy for short-duration VF than 200-J monophasic and 130-J biphasic shocks and thus may allow earlier termination of VF in cardiac arrest patients.
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