PHYSIOLOGICAL-RESPONSES TO HYPERTHERMIA DURING EPIDURAL-ANESTHESIA AND COMBINED EPIDURAL ENFLURANE ANESTHESIA IN WOMEN

Background. During combined epidural/isoflurane anesthesia, the core temperature triggering finger-tip vasoconstriction is almost-equal-to 1-degrees C less than that triggering redilation. This hysteresis suggests that thermoregulatory responses are not dependent entirely on current thermal status (state-dependence), but may be influenced also by the system's recent thermal history (direction-dependence). Once triggered, the gain and maximum response intensity of many thermoregulatory responses is nearly normal during isoflurane anesthesia. However, it remains unknown whether preserved gain and maximum response intensities are a characteristic paradigm describing thermoregulatory responses to general anesthetics. Also unknown is whether the sweating and pre-capillary vasodilation thresholds are comparably impaired by different volatile anesthetics. Accordingly, the authors tested the hypotheses that, during one minimum alveolar concentration of enflurane anesthesia: (1) there is a direction-dependent hysteresis for sweating; (2) the sweating and active vasodilation thresholds increase almost-equal-to 1.2-degrees-C, as they do during one minimum alveolar concentration of isoflurane; and (3) the gain and maximum intensity of sweating are well preserved. Methods: Six female volunteers each were studied on 2 days, once during epidural anesthesia alone and once with combined enflurane (1.7%)/epidural anesthesia. On each study day, core hyperthermia was induced by cutaneous warming restricted to the legs. Warming continued until chest sweating reached maximal values; the volunteers then were cooled gradually until sweating stopped. The core temperature at which the sweating rate departed from baseline values was considered the activation threshold. Gain was expressed as the slope of the sweating rate versus core temperature curve within the range 25-75% of the maximum sweating rate. Hysteresis was evaluated by subtracting the tympanic membrane temperature at which the sweating rate suddenly increased during warming (approximately 25% above baseline values) from that at which sweating precipitously decreased during cooling (approximately 75% of maximum values). Results. The sweating threshold was 1.4 +/- 0.7-degrees-C higher during combined enflurane/epidural anesthesia than during epidural anesthesia alone. Maximum intensity was almost-equal-to 700 g.m-2-h-1, and the gain almost-equal-to 1,300 g.m-2.h-1.-degrees-C-1 during each treatment. No hysteresis was detected on either study day. Conclusions. One minimum alveolar concentration of enflurane increased the sweating threshold only slightly more than previously reported for isoflurane. As in previous studies of sweating and vasoconstriction during isoflurane anesthesia, gain and maximum response intensity were well preserved during enflurane anesthesia. An increase in the interthreshold range (temperatures not triggering thermoregulatory responses), with little change in gain and maximum response intensities, appears to be the typical effect of volatile anesthetics. Sweating during enflurane anesthesia appears to be state-dependent and little influenced by the direction of core temperature perturbations.