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Ann Thorac Surg 1996;61:1118-1123
© 1996 The Society of Thoracic Surgeons
Department of Surgery, University of Colorado Health Sciences Center and the Department of Veterans Affairs Medical Center, Denver, Colorado
Background. Pulmonary hypertension secondary to increased pulmonary vascular resistance may greatly complicate the perioperative management of patients having cardiac operations. Adenosine may have a therapeutic role as a selective pulmonary vasodilator. The purpose of this study was to examine the pulmonary hemodynamic effects of a central venous infusion of adenosine in cardiac operative patients with pulmonary hypertension.
Methods. Ten cardiac patients with pulmonary hypertension (age, 62 ± 6 years) were studied in the operating room under general anesthesia after weaning from cardiopulmonary bypass. Cardiac output, pulmonary vascular resistance, systemic vascular resistance, mean pulmonary arterial pressure, and mean systemic arterial pressure were determined before, during, and after central venous infusion of adenosine (50 µg kg-1 min-1) for 15 minutes. Statistical analysis was by analysis of variance, and significance was accepted at p < 0.05.
Results. Adenosine produced significant pulmonary vasodilation. Mean pulmonary arterial pressure was lowered from 36 ± 1 to 28 ± 2 mm Hg (p < 0.05), and pulmonary vascular resistance was lowered from 560 ± 30 to 260 ± 30 dynes s cm-5 (p < 0.05) during adenosine administration. At the same time, cardiac output rose from 4.0 ± 0.6 to 6.2 L/min (p < 0.05). Pulmonary vascular resistance, mean pulmonary arterial pressure, and cardiac output returned to baseline after the adenosine infusion was stopped. There was no change in systemic mean arterial pressure during adenosine infusion.
Conclusions. Adenosine may be used clinically as a selective pulmonary vasodilating agent to optimize pulmonary hemodynamic indices without adverse systemic hemodynamic effects in patients with pulmonary hypertension having cardiac operations. It may be particularly valuable in patients with right heart dysfunction by selectively lowering right ventricular afterload.
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