Moderate hypothermia depresses arterial baroreflex control of heart rate during, and delays its recovery after, general anesthesia in humans.

BACKGROUND Effects of hypothermia on arterial baroreflex function during, and on its recovery after, general anesthesia were examined in humans. METHODS Twenty healthy volunteers were randomly assigned to a normothermic group (n = 10 each, active forced-air warming) or to a hypothermic group (no active warming) during anesthesia. Measurements of R-R intervals and systolic blood pressure were made at conscious baseline and at 20, 60, and 120 min after the induction and 20, 60, 120, and 180 min after emergence from general anesthesia with sevoflurane for 2 h. Ventilation was mechanically controlled, and end-tidal sevoflurane concentration was maintained at 2% during anesthesia. Baroreflex responses were triggered by bolus intravenous injections of phenylephrine and nitroprusside. The linear portions of the baroreflex curves relating R-R intervals and systolic blood pressure were determined to obtain baroslopes. RESULTS During anesthesia, the mean lowest tympanic temperature of the hypothermia group (33.9+/-0.5 degrees C [mean +/- SD]) was significantly lower than that of the normothermia group (36.1+/-0.7 degrees C, P < 0.001). The baroslopes of the pressor and depressor tests were decreased by 19-39% during and by 27-53% after general anesthesia in the hypothermia group, compared with the normothermia group (P < 0.05). The baroslopes of the normothermia group returned to the baseline values at 60 min after anesthesia, whereas the pressor test sensitivity of the hypothermia group was significantly less than that of the normothermia group for the entire course of recovery. CONCLUSIONS The results indicate that moderate hypothermia enhances anesthesia-induced depression of baroreflex function in anesthetized humans and delays its recovery after general anesthesia.