Esmolol for Potentiation of Nitroprusside-Induced Hypotension: Impact on the Cardiovascular, Adrenergic, and Renin-Angiotensin Systems in Man

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Esmolol infusion at rates of 200, 300, and 400 μg·kg−1·mm−1 was used to potentiate hypotension (mean arterial pressure = 60 mm Hg) induced with sodium nitroprusside (SNP) in 10 male patients undergoing radical cancer surgery during nitrous oxide-oxygen and fentanyl anesthesia. Heart rate (HR), blood pressure (radial arterial catheter), and plasma levels of renin activity (PRA), norepmephrine (N), epinephrine (E), and dopamine (D) were measured: 1) while patients were awake; 2) after induction of anesthesia (nitrous oxide, 60% in oxygen, fentanyl = 5 μg/kg followed by an infusion at 10 μg·kg−1 ·hr−1); 3) after surgery had begun: 4) after 20 minutes of SNP-induced hypotension; 5) after 20 minutes of esmolol at each of the above infusion rates; and 6) after the completion of surgery. Compared to awake values, SNP-induced hypotension (mean infusion rate = 3.1 μg·kg−1·min−1 ± 0.6 SE] during surgery resulted in significant (P < 0.05) increases in heart rate, PRA, N, and D. Infusion of esmolol resulted in significant (P < 0.05) dose-dependent reductions in SNP requirement to maintain MAP = 60 mm Hg. At 200 μg·kg−1·min−1, SNP requirement was 2.1 μg·kg−1·min−1 ±0.4, at 300 μg·kg−1·min−2, it was 1.0 μg·kg−1·min−1 ±0.2, and at 400 μg·kg−1·min−1, was 0.5 μg·kg−1·min−1 ±0.3. Concomitant with the decrease in SNP requirement, there were significant reductions in HR and PRA at all infusion rates of esmolol. At 300 μg·kg−1·min−1, there was a significant (P < 0.05) increase in PaO2 (141 mm Hg ± 18 to 162 mm Hg ± 16, and decrease in N (615 pg/ml ± 105 to 356 pg/ml ± 56) and E (74 pg/ml ± 20 to 57 ± 10). No rebound hypertension was observed at the end of SNP-esmolol infusion, and HR, BP, PaO2, PRA, N, and D levels were not different from awake values. Only E levels were elevated postoperatively (460 pg/ ml ± 98 vs 63 pg/ml ± 8 preoperatively, P < 0.05). The authors conclude that esmolol infusion is a safe and effective pharmacologic means of potentiating SNP-induced hypotension during fentanyl-N2O-O2 anesthesia. Esmolol acts by counteracting many of the adverse endocrine and baroreceptor-mediated effects of SNP, and the short half-lives of esmolol and SNP permit contemporaneous termination of action when they are simultaneously discontinued.

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