HYPOTENSIVE ANESTHESIA WITH ISOFLURANE IN RADICAL MASTECTOMY

Abstract

We performed isoflurane-induced hypotensive anesthesia for 8 patients, and isoflurane-induced normotensive anesthesia for 8 patients undergoing radical mastectomy. We measured the hemodynamic parameters : systolic arterial pressure, diastolic arterial pressure, and heart rate, plasma catecholamine concentration (epinephrine, norepinephrine), plasma renin-activity, and plasma-aldosterone concentration in each group. All patients were premedicated with 0.5 mg atropine sulfate, and 50 mg hydroxyzine. Anesthesia was induced with thiamylal and the trachea was intubated after vecronium or succinylcholine. Isoflurane was administered until systolic blood pressure decreased to 80-90 mmHg in the hypotensive group. In the normotensive group (control group), a concentration of 1-2 % isoflurane was administered. Hemodynamic data (blood pressure, heart rate) and blood samples for measurement of plasma epinephrine (EP), norepinephrine (NEP), plasma renin activity (PRA) and plasma aldosterone (PA) were collected : 1) before induction (S₁), 2) 30 min after starting to operate (S2), 3) 60 min after starting to operate (S₃), and 4) 90 min after starting to operate (S₄) . Decreases in mean blood pressure below baseline were significantly greater in the hypotensive group than in the control group. Heart rate did not change in the control group, but in the hypotensive group it increased significantly. NEP concentration did not change in the control group but increased significantly above the baseline (S₁) in the hypotensive group. NEP concentration (S₂·S₃) was significantly greater in the hypotensive group than in the control group. AD was significantly above the baseline (S₁) in the control group, but did not change in the hypotensive group. PA increased significantly in both groups, and PA (S₃) increased significantly more in the hypotensive group than in the control group. The results suggest that isoflurane-induced hypotension preserves the effect of homeostatic response, and this increases stress hormones. The cardiac depressing effect of isoflurane was believed to be less than those of halothane or enflurane, and at higher concentration the direct vasodilation effect of isoflurane predominated. We conclude that isoflurane can be employed safely and effectively as a hypotensive agent.