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BACKGROUND Sufficient hypothermia during anesthesia provokes thermoregulatory responses, but the clinical significance of these responses remains unknown. Nonshivering thermogenesis does not increase metabolic heat production in anesthetized adults. Vasoconstriction reduces cutaneous heat loss, but the initial decrease appears insufficient to cause a thermal steady state (heat production equaling heat loss). Accordingly, the authors tested the hypotheses that: 1) thermoregulatory vasoconstriction prevents further core hypothermia; and 2) the resulting stable core temperature is not a thermal steady state, but, instead, is accompanied for several hours by a continued reduction in body heat content. METHODS Six healthy volunteers were anesthetized with isoflurane (0.8%) and paralyzed with vecuronium. Core hypothermia was induced by fan cooling, and continued for 3 h after vasoconstriction in the legs was detected. Leg heat content was calculated from six needle thermocouples and skin temperature, by integrating the resulting parabolic regression over volume. RESULTS Core temperature decreased 1.0 +/- 0.2 degrees C in the 1 h before vasoconstriction, but only 0.4 +/- 0.3 degrees C in the subsequent 3 h. This temperature decrease, evenly distributed throughout the body, would reduce leg heat content 10 kcal. However, measured leg heat content decreased 49 +/- 18 kcal in the 3 h after vasoconstriction. CONCLUSIONS These data thus indicate that thermoregulatory vasoconstriction produces a clinically important reduction in the rate of core cooling. This core temperature plateau resulted, at least in part, from sequestration of metabolic heat to the core which allowed core temperature to remain nearly constant, despite a continually decreasing body heat content.

Generalized autonomic stimulation enhances hemodynamic responses and may, in a similar fashion, facilitate thermoregulatory responses. We thus tested the hypothesis that painful stimulation increases the central temperature threshold for vasoconstriction during general anesthesia. Healthy volunteers were anesthetized with 1.3% end-tidal enflurane on 2 separate days. On 1 day (randomly assigned), painful stimulation was produced by tetanic electrical stimulation. On the other day, electrical stimulation was not given. Significant thermoregulatory vasoconstriction was defined as a forearm-fingertip skin-surface temperature gradient exceeding 4 degrees C. The distal esophageal temperature triggering significant vasoconstriction was considered the thermoregulatory threshold. The threshold was 35.5 +/- 0.8 degrees C during electrical stimulation and 35.1 +/- 0.6 degrees C without stimulation (P = 0.050, 95% confidence interval for the difference = 0-0.7 degree C). These data suggest that thresholds determined in nonsurgical volunteers will be slightly (but not clinically significantly) less than those in operative patients. Similarly, intraoperative vasoconstriction thresholds likely will be slightly less when surgical pain is prevented by simultaneous regional or local analgesia.

Background The pupillary light reflex often is evaluated in the perianesthetic period to assess drug effects and brainstem function. Mild hypothermia alone or combined with isoflurane does not impair pupillary responses. Although perioperative hyperthermia is less common than hypothermia, abnormal increases in core temperature remain an important thermal disturbance. Accordingly, the pupillary effects of hyperthermia alone and hyperthermia combined with isoflurane and enflurane were evaluated. Additionally, the effects of nitrous oxide on pupillary responses were determined. Methods The pupillary light reflex was evaluated in 31 non-surgical volunteers participating in concurrent thermoregulatory studies. Pupillary reflexes were quantified using a portable infrared pupillometer during (1) hyperthermia alone (n = 9), (2) hyperthermia with 0.8% and 1.2% end-tidal isoflurane (n = 8), (3) hyperthermia with 1.7% end-tidal enflurane (n = 5), and (4) inhalation of 60% N2O (n = 9). Results Mild hyperthermia alone (core temperature 38.5 +/- 0.3 degrees C) produced no clinically significant change in the pupillary light reflex. Pupillary responses were decreased markedly with 0.8% isoflurane, 1.2% isoflurane, and 1.7% enflurane when the volunteers were normothermic. Mild hyperthermia combined with isoflurane or enflurane dilated the pupil and increased the amplitude of the light reflex. Sixty-percent nitrous oxide decreased the pupillary reflex only 26 +/- 4%. Conclusions Anesthetic-induced inhibition of the pupillary response to light is reversed partially by core hyperthermia. In contrast to enflurane and isoflurane, 60% N2O has little effect on the pupil.