Fructose administration increases intraoperative core temperature by augmenting both metabolic rate and the vasoconstriction threshold

BACKGROUND: The authors tested the hypothesis that intravenous fructose ameliorates intraoperative hypothermia both by increasing metabolic rate and the vasoconstriction threshold (triggering core temperature). METHODS: Forty patients scheduled to undergo open abdominal surgery were divided into two equal groups and randomly assigned to intravenous fructose infusion (0.5 g . kg(-1) . h(-1) for 4 h, starting 3 h before induction of anesthesia and continuing for 4 h) or an equal volume of saline. Each treatment group was subdivided: Esophageal core temperature, thermoregulatory vasoconstriction, and plasma concentrations were determined in half, and oxygen consumption was determined in the remainder. Patients were monitored for 3 h after induction of anesthesia. RESULTS: Patient characteristics, anesthetic management, and circulatory data were similar in the four groups. Mean final core temperature (3 h after induction of anesthesia) was 35.7 degrees +/- 0.4 degrees C (mean +/- SD) in the fructose group and 35.1 degrees +/- 0.4 degrees C in the saline group (P = 0.001). The vasoconstriction threshold was greater in the fructose group (36.2 degrees +/- 0.3 degrees C) than in the saline group (35.6 degrees +/- 0.3 degrees C; P < 0.001). Oxygen consumption immediately before anesthesia induction in the fructose group (214 +/- 18 ml/min) was significantly greater than in the saline group (181 +/- 8 ml/min; P < 0.001). Oxygen consumption was 4.0 l greater in the fructose patients during 3 h of anesthesia; the predicted difference in mean body temperature based only on the difference in metabolic rates was thus only 0.4 degrees C. Epinephrine, norepinephrine, and angiotensin II concentrations and plasma renin activity were similar in each treatment group. CONCLUSIONS: Preoperative fructose infusion helped to maintain normothermia by augmenting both metabolic heat production and increasing the vasoconstriction threshold.     

Effect of Amino Acid Infusion on Central Thermoregulatory Control in Humans

Background: Administration of protein or amino acids enhances thermogenesis, presumably by stimulating oxidative metabolism. However, hyperthermia results even when thermoregulatory responses are intact, suggesting that amino acids also alter central thermoregulatory control. Therefore, the authors tested the hypothesis that amino acid infusion increases the thermoregulatory set point.

Methods: Nine male volunteers each participated on 4 study days in randomized order: (1) intravenous amino acids infused at 4 kJ [middle dot] kg-1 [middle dot] h-1 for 2.5 h combined with skin-surface warming, (2) amino acid infusion combined with cutaneous cooling, (3) saline infusion combined with skin-surface warming, and (4) saline infusion combined with cutaneous cooling.

Results: Amino acid infusion increased resting core temperature by 0.3 +/- 0.1[degrees]C (mean +/- SD) and oxygen consumption by 18 +/- 12%. Furthermore, amino acid infusion increased the calculated core temperature threshold (triggering core temperature at a designated mean skin temperature of 34[degrees]C) for active cutaneous vasodilation by 0.3 +/- 0.3[degrees]C, for sweating by 0.2 +/- 0.2[degrees]C, for thermoregulatory vasoconstriction by 0.3 +/- 0.3[degrees]C, and for thermogenesis by 0.4 +/- 0.5[degrees]C. Amino acid infusion did not alter the incremental response intensity (i.e., gain) of thermoregulatory defenses.     

Nefopam, a Nonsedative Benzoxazocine Analgesic, Selectively Reduces the Shivering Threshold in Unanesthetized Subjects

Background: The analgesic nefopam does not compromise ventilation, is minimally sedating, and is effective as a treatment for postoperative shivering. The authors evaluated the effects of nefopam on the major thermoregulatory responses in humans: sweating, vasoconstriction, and shivering.

Methods: Nine volunteers were studied on three randomly assigned days: (1) control (saline), (2) nefopam at a target plasma concentration of 35 ng/ml (low dose), and (3) nefopam at a target concentration of 70 ng/ml (high dose, approximately 20 mg total). Each day, skin and core temperatures were increased to provoke sweating and then reduced to elicit peripheral vasoconstriction and shivering. The authors determined the thresholds (triggering core temperature at a designated skin temperature of 34[degrees]C) by mathematically compensating for changes in skin temperature using the established linear cutaneous contributions to control of each response.

Results: Nefopam did not significantly modify the slopes for sweating (0.0 +/- 4.9[degrees]C [middle dot] [mu]g-1 [middle dot] ml; r2 = 0.73 +/- 0.32) or vasoconstriction (-3.6 +/- 5.0[degrees]C [middle dot] [mu]g-1 [middle dot] ml; r2 = -0.47 +/- 0.41). In contrast, nefopam significantly reduced the slope of shivering (-16.8 +/- 9.3[degrees]C [middle dot] [mu]g-1 [middle dot] ml; r2 = 0.92 +/- 0.06). Therefore, high-dose nefopam reduced the shivering threshold by 0.9 +/- 0.4[degrees]C (P < 0.001) without any discernible effect on the sweating or vasoconstriction thresholds.     

Amino acid infusion induces thermogenesis and reduces blood loss during hip arthroplasty under spinal anesthesia

The thermic effect of amino acids is augmented under general anesthesia and counteracts hypothermia. Mild hypothermia may increase surgical bleeding. We studied whether amino acids also induce thermogenesis under spinal anesthesia and whether this endogenous heat production reduces bleeding during hip arthroplasty. Rectal temperature, oxygen uptake, and perioperative bleeding were measured in 22 patients receiving an IV amino acid mixture (Vamin 18), 240 kJ/h) for 1 h before and then during spinal anesthesia and in 24 control patients receiving acetated Ringer's solution. Blood loss was calculated after surgery by weighing the swabs and the content of the suction tubes after subtraction of the saline used. After surgery, the closed drains were weighed after 24 h. In the amino acid group, the preanesthesia temperature increased by 0.4 degrees C +/- 0.2 degrees C (P < 0.01) and was unchanged in controls. At end of surgery, core temperature had decreased by 0.9 degrees C +/- 0.4 degrees C in controls and by 0.4 degrees C +/- 0.3 degrees C in the amino acid patients (P < 0.01). Oxygen uptake increased by 26 +/- 7 mL/min, or 16% +/- 5% (P < 0.05), from baseline in the amino acid patients, whereas it was unchanged in the controls. Blood loss during surgery was significantly larger in the control patients (702 +/- 344 mL) than in the amino acid patients (516 +/- 272 mL) (P < 0.05). After surgery, there were no significant differences in shed blood volume. In conclusion, amino acid infusion also induced a thermogenic response under spinal anesthesia. In addition, the prevention of temperature decrease during spinal anesthesia seemed to have a positive effect on intraoperative blood loss. IMPLICATIONS: Infusion of a balanced mixture of amino acids during spinal anesthesia prevented core body temperature decrease. Bleeding was also less pronounced.     

Thermoregulatory Thresholds for Vasoconstriction in Patients Anesthetized with Various 1-Minimum Alveolar Concentration Combinations of Xenon, Nitrous Oxide, and Isoflurane

Background: Nitrous oxide limits intraoperative hypothermia because the vasoconstriction threshold with nitrous oxide is higher than with equi-minimum alveolar concentrations of sevoflurane or isoflurane, presumably because of its stimulating actions on the sympathetic nervous system. Xenon, in contrast, does not cause sympathetic activation. Therefore, the authors tested the hypothesis that the vasoconstriction threshold during xenon-isoflurane anesthesia is less than during nitrous oxide-isoflurane anesthesia or isoflurane alone.

Methods: Fifteen patients each were randomly assigned to one of three 1-minimum alveolar concentration anesthetic regimens: (1) xenon, 43% (0.6 minimum alveolar concentration) and isoflurane, 0.5% (0.4 minimum alveolar concentration); (2) nitrous oxide, 63% (0.6 minimum alveolar concentration) and isoflurane 0.5%; or (3) isoflurane, 1.2%. Ambient temperature was maintained near 23[degrees]C and the patients were not actively warmed. Thermoregulatory vasoconstriction was evaluated using forearm-minus-fingertip skin temperature gradients. A gradient exceeding 0[degrees]C indicated significant vasoconstriction. The core-temperature threshold that would have been observed if skin had been maintained at 33[degrees]C was calculated from mean skin and distal esophageal temperatures at the time of vasoconstriction.

Results: The patients' demographic variables, preinduction core temperatures, ambient operating room temperatures, and fluid balance were comparable among the three groups. Heart rates were significantly less during xenon anesthesia than with nitrous oxide. The calculated vasoconstriction threshold was lowest with xenon (34.6 +/- 0.8[degrees]C, mean +/- SD), intermediate with isoflurane alone (35.1 +/- 0.6[degrees]C), and highest with nitrous oxide (35.7 +/- 0.6[degrees]C). Each of the thresholds differed significantly.     

Core Cooling by Central Venous Infusion of Ice-cold (4°C and 20°C) Fluid: Isolation of Core and Peripheral Thermal Compartments

Background: Central venous infusion of cold fluid may be a useful method of inducing therapeutic hypothermia. The aim of this study was to quantify systemic heat balance and regional distribution of body heat during and after central infusion of cold fluid.

Methods: The authors studied nine volunteers, each on two separate days. Anesthesia was maintained with use of isoflurane, and on each day 40 ml/kg saline was infused centrally over 30 min. On one day, the fluid was 20[degrees]C and on the other it was 4[degrees]C. By use of a tympanic membrane probe core (trunk and head) temperature and heat content were evaluated. Peripheral compartment (arm and leg) temperature and heat content were estimated with use of fourth-order regressions and integration over volume from 18 intramuscular thermocouples, nine skin temperatures, and "deep" hand and foot temperature. Oxygen consumption and cutaneous heat flux estimated systemic heat balance.

Results: After 30-min infusion of 4[degrees]C or 20[degrees]C fluid, core temperature decreased 2.5 +/- 0.4[degrees]C and 1.4 +/- 0.2[degrees]C, respectively. This reduction in core temperature was 0.8[degrees]C and 0.4[degrees]C more than would be expected if the change in body heat content were distributed in proportion to body mass. Reduced core temperature resulted from three factors: (1) 10-20% because cutaneous heat loss exceeded metabolic heat production; (2) 50-55% from the systemic effects of the cold fluid per se; and (3) approximately 30% because the reduction in core heat content remained partially constrained to core tissues. The postinfusion period was associated with a rapid and spontaneous recovery of core temperature. This increase in core temperature was not associated with a peripheral-to-core redistribution of body heat because core temperature remained warmer than peripheral tissues even at the end of the infusion. Instead, it resulted from constraint of metabolic heat to the core thermal compartment.     

The Effects of Hydration on Core Temperature in Pediatric Surgical Patients

Background: Reduced vascular volume might influence body temperature by diverting heat flow from peripheral tissues to the central organs. We therefore tested the hypothesis that mild hypovolemia helps to prevent intraoperative hypothermia in pediatric patients.

Methods: Twenty-two pediatric patients (aged 1-3 yr) undergoing prolonged minor surgery were randomly assigned to conservative (n = 12) or aggressive (n = 10) perioperative fluid management. The conservative group fasted 8 h before surgery and received a crystalloid at 1 ml [middle dot] kg-1 [middle dot] h-1 during surgery. The aggressive group was allowed to drink liquids until 3 h before surgery and was given a maintenance crystalloid at 8 ml [middle dot] kg-1 [middle dot] h-1. Anesthesia was induced and maintained with halothane in nitrous oxide. Ambient temperature was kept near 25[degrees]C, but the patients were not actively warmed. During recovery from anesthesia, additional fluid was given to the conservative group so that perioperative fluid totaled 9.5 ml [middle dot] kg-1 [middle dot] h-1 in both groups.

Results: Intraoperative body weight remained unchanged in the aggressive group and decreased only 1% in patients managed conservatively. Heart rate was slightly greater in the conservative group (107 +/- 9 vs. 95 +/- 4 beats/min, P = 0.002), but blood pressure was similar. Esophageal temperature in patients whose fluid was managed conservatively increased significantly, by 0.4 +/- 0.3[degrees]C, to 37.1[degrees]C; in contrast, temperature in the aggressive group decreased significantly, by 0.4 +/- 0.2[degrees]C, to 36.4[degrees]C (P < 0.001 between groups). Temperatures remained significantly different 1 h after surgery.     

Desflurane Reduces the Febrile Response to Administration of Interleukin-2

Background: Intraoperative fever is relatively rare considering how often pyrogenic causes are likely to be present and how common fever is postoperatively. This low incidence suggests that general anesthesia per se inhibits the normal response to pyrogenic stimulation. The authors therefore tested the hypothesis that desflurane-induced anesthesia produces a dose-dependent inhibition of the febrile response.

Methods: Eight volunteers were studied, each on 3 study days. Each was given an intravenous injection of 50,000 IU/kg of interleukin-2 (elapsed time, 0 h), followed 2 h later by 100,000 IU/kg. One hour after the second dose, the volunteers were assigned randomly to three doses of desflurane to induce anesthesia: (1) 0.0 minimum alveolar concentration (MAC; control), (2) 0.6 MAC, and (3) 1.0 MAC. Anesthesia continued for 5 h. Core temperatures were recorded from the tympanic membrane. Thermoregulatory vasoconstriction was evaluated using forearm-minus-fingertip skin temperature gradients; shivering was evaluated with electromyography. Integrated and peak temperatures during anesthesia were compared with repeated-measures analysis of variance and Scheffe's F tests.

Results: Values are presented as mean +/- SD. Desflurane reduced the integrated (area under the curve) febrile response to pyrogen, from 7.7 +/- 2.0 [degree sign]C [center dot] h on the control day to 2.1 +/- 2.3 [degree sign]C [center dot] h during 0.6 MAC and to -1.4 +/- 3.1 [degree sign]C [center dot] h during 1.0 MAC desflurane-induced anesthesia. Peak core temperature (elapsed time, 5-8 h) decreased in a dose-dependent fashion: 38.6 +/- 0.5 [degree sign]C on the control day, 37.7 +/- 0.7 [degree sign]C during 0.6 MAC and 37.2 +/- 1.0 [degree sign]C during 1.0 MAC desflurane anesthesia. Rising core temperature was always associated with fingertip vasoconstriction and often with shivering.     

Intraoperative phenylephrine infusion decreases the magnitude of redistribution hypothermia.

Core hypothermia during the first hour after induction of general anesthesia results largely from an internal core-to-peripheral redistribution of body heat. This redistribution results from both central inhibition of tonic thermoregulatory vasoconstriction in the arteriovenous shunt and anesthetic-induced vasodilation. We therefore tested the hypothesis that acute administration of phenylephrine, a pure alpha-adrenergic agonist, reduces the magnitude of anesthetic-induced core-to-peripheral redistribution of body heat. Patients undergoing minor oral surgery were randomly assigned to an infusion of 0.5 microgram.kg-1.min-1 phenylephrine i.v. or no treatment (control). The phenylephrine infusion was started immediately before anesthesia was induced with 2.5 mg/kg propofol i.v. Subsequently, anesthesia was maintained with sevoflurane and 60% nitrous oxide in oxygen. Calf minus toe, skin-temperature gradients < 0 degree C were considered indicative of significant arteriovenous shunt vasodilation. Ambient temperature and end-tidal concentrations of maintenance sevoflurane were comparable in each group. Although there were no significant differences in skin-temperature gradients, core temperatures in the untreated patients decreased significantly more (1.2 +/- 0.4 degrees C) than in those given phenylephrine (0.5 +/- 0.2 degree C, P < 0.001). These data suggest that maintaining precapillary vasoconstriction of blood vessels, not in the arteriovenous shunt reduces the magnitude of redistribution hypothermia. Implications: Core hypothermia immediately after induction of general anesthesia results largely from core-to-peripheral redistribution of body heat. Core temperature reduction during the first hour of anesthesia decreased less in patients given phenylephrine than in untreated controls. These data suggest that maintaining precapillary vasoconstriction possibly reduces the magnitude of redistribution hypothermia.     

Covering the head and face maintains intraoperative core temperature

PURPOSE: To determine the effect of covering the patient's head and face on the prevention of intraoperative hypothermia (<35.5 degrees C). METHODS: This randomized, prospective trial included 44 adults undergoing elective abdominal surgery. After the induction of anesthesia with thiopental, in 44 patients their extremities and trunk were covered with towels and sheets. In addition, 22 patients (covered group) had their face and head fully covered. Anesthesia was maintained with N2O 50-66% (2-3 L x min(-1)) and isoflurane (相似文献   

Effect of amino acid infusion on central thermoregulatory control in humans

BACKGROUND: Administration of protein or amino acids enhances thermogenesis, presumably by stimulating oxidative metabolism. However, hyperthermia results even when thermoregulatory responses are intact, suggesting that amino acids also alter central thermoregulatory control. Therefore, the authors tested the hypothesis that amino acid infusion increases the thermoregulatory set point. METHODS: Nine male volunteers each participated on 4 study days in randomized order: (1) intravenous amino acids infused at 4 kJ x kg(-1) x h(-1) for 2.5 h combined with skin-surface warming, (2) amino acid infusion combined with cutaneous cooling, (3) saline infusion combined with skin-surface warming, and (4) saline infusion combined with cutaneous cooling. RESULTS: Amino acid infusion increased resting core temperature by 0.3 +/- 0.1 degrees C (mean +/- SD) and oxygen consumption by 18 +/- 12%. Furthermore, amino acid infusion increased the calculated core temperature threshold (triggering core temperature at a designated mean skin temperature of 34 degrees C) for active cutaneous vasodilation by 0.3 +/- 0.3 degrees C, for sweating by 0.2 +/- 0.2 degrees C, for thermoregulatory vasoconstriction by 0.3 +/- 0.3 degrees C, and for thermogenesis by 0.4 +/- 0.5 degrees C. Amino acid infusion did not alter the incremental response intensity (i.e., gain) of thermoregulatory defenses. CONCLUSIONS: Amino acid infusion increased the metabolic rate and the resting core temperature. However, amino acids also produced a synchronous increase in all major autonomic thermoregulatory defense thresholds; the increase in core temperature was identical to the set point increase, even in a cold environment with amble potential to dissipate heat. In subjects with intact thermoregulatory defenses, amino acid-induced hyperthermia seems to result from an increased set point rather than increased metabolic rate per se.     

Relative Contribution of Skin and Core Temperatures to Vasoconstriction and Shivering Thresholds during Isoflurane Anesthesia

Background: Thermoregulatory control is based on both skin and core temperatures. Skin temperature contributes [approximate] 20% to control of vasoconstriction and shivering in unanesthetized humans. However, this value has been used to arithmetically compensate for the cutaneous contribution to thermoregulatory control during anesthesia-although there was little basis for assuming that the relation was unchanged by anesthesia. It even remains unknown whether the relation between skin and core temperatures remains linear during anesthesia. We therefore tested the hypothesis that mean skin temperature contributes [approximate] 20% to control of vasoconstriction and shivering, and that the contribution is linear during general anesthesia.

Methods: Eight healthy male volunteers each participated on 3 separate days. On each day, they were anesthetized with 0.6 minimum alveolar concentrations of isoflurane. They then were assigned in random order to a mean skin temperature of 29, 31.5, or 34 [degree sign]C. Their cores were subsequently cooled by central-venous administration of fluid at [almost equal to] 3 [degree sign]C until vasoconstriction and shivering were detected. The relation between skin and core temperatures at the threshold for each response in each volunteer was determined by linear regression. The proportionality constant was then determined from the slope of this regression. These values were compared with those reported previously in similar but unanesthetized subjects.

Results: There was a linear relation between mean skin and core temperatures at the vasoconstriction and shivering thresholds in each volunteer: r2 = 0.98 +/- 0.02 for vasoconstriction, and 0.96 +/- 0.04 for shivering. The cutaneous contribution to thermoregulatory control, however, differed among the volunteers and was not necessarily the same for vasoconstriction and shivering in individual subjects. Overall, skin temperature contributed 21 +/- 8% to vasoconstriction, and 18 +/- 10% to shivering. These values did not differ significantly from those identified previously in unanesthetized volunteers: 20 +/- 6% and 19 +/- 8%, respectively.     

Lack of Nonshivering Thermogenesis in Infants Anesthetized with Fentanyl and Propofol

Background: Sweating, vasoconstriction, and shivering have been observed during general anesthesia. Among these, vasoconstriction is especially important because-once triggered-it minimizes further hypothermia. Surprisingly, the core-temperature plateau associated with vasoconstriction appears to preserve core temperature better in infants and children than adults. This observation suggests that vasoconstriction in anesthetized infants may be accompanied by hypermetabolism. Consistent with this theory, unanesthetized infants rely on nonshivering thermogenesis to double heat production when vasoconstriction alone is insufficient. Accordingly, the authors tested the hypothesis that intraoperative core hypothermia triggers nonshivering thermogenesis in infants.

Methods: With Ethics Committee approval and written parental consent, the authors studied six infants undergoing abdominal surgery. All were aged 1 day to 9 months and weighed 2.4-9 kg. Anesthesia was maintained with propofol and fentanyl. The infants were mechanically ventilated and allowed to cool passively until core (distal esophageal) temperatures reached 34-34.5 degrees Celsius. Oxygen consumption-the authors' index of metabolic rate- was recorded throughout cooling. Because nonshivering thermogenesis triples circulating norepinephrine concentrations, arterial blood was analyzed for plasma catecholamines at [nearly equal] 0.5 degrees Celsius intervals. Thermoregulatory vasoconstriction was evaluated using forearm - fingertip, skin-surface gradients, with gradients exceeding 4 degrees Celsius, indicating intense vasoconstriction. The patients were subsequently rapidly rewarmed to 37 degrees Celsius. Regression analysis was used to correlate changes in oxygen consumption and plasma catecholamine concentrations with core temperature.

Results: All patients were vasoconstricted by the time core temperature reached 36 degrees Celsius. Further reduction in core temperature to 34-34.5 degrees Celsius did not increase oxygen consumption. Instead, oxygen consumption decreased linearly. Hypothermia also failed to increase plasma catecholamine concentrations.     

The effects of urapidil on thermoregulatory thresholds in volunteers

In a previous study we have shown that the antihypertensive drug, urapidil, stops postanesthetic shivering. One possible mechanism in the inhibition of postanesthetic shivering by urapidil may be alterations in thermoregulatory thresholds. We therefore studied the effects of urapidil on vasoconstriction and shivering thresholds during cold-induced shivering in volunteers. Seven healthy male volunteers were cooled by an infusion of saline at 4 degrees C on two study days separated by 48 h. Thermoregulatory vasoconstriction was estimated using forearm minus fingertip skin-temperature gradients, and values exceeding 0 degrees C were considered to represent significant vasoconstriction. The rectal core temperatures at the beginning of shivering and at vasoconstriction were considered the thermoregulatory thresholds. Before cooling, either 25 mg of urapidil or placebo was administered randomly and blindly to each volunteer. When shivering occurred continuously for 10 min, another 25 mg of urapidil was administered IV to completely stop shivering. Urapidil led to a decrease in core temperature at vasoconstriction and shivering threshold by 0.4 degrees C plus/minus 0.2 degrees C (P < 0.001) and 0.5 degrees C plus/minus 0.3 degrees C (P < 0.01), respectively. Oxygen consumption increased during shivering by 70% plus/minus 30% (P < 0.01) in comparison with baseline and decreased levels after shivering stopped, despite the continued low core temperature. Our investigation shows that urapidil stops postanesthetic shivering by decreasing important thermoregulatory thresholds. This means that shivering, not hypothermia, is treated, and hypothermia will need more attention in the postanesthesia care unit. IMPLICATIONS: In this study we show that the antihypertensive drug urapidil stops cold-induced shivering and decreases normal thermoregulatory responses, i.e., the thresholds for vasoconstriction and shivering, in awake volunteers.     

Chronic treatment with antipsychotics enhances intraoperative core hypothermia

Antipsychotics can induce hypothermia, but intraoperative temperature regulation in schizophrenic patients taking antipsychotics remains unclear. We investigated intraoperative temperature regulation and postoperative shivering in chronic schizophrenic patients receiving antipsychotics. We studied 30 schizophrenic patients and 30 control patients who underwent orthopedic surgery. Tympanic membrane temperatures (35.7 degrees C +/- 0.5 degrees C, 35.6 degrees C +/- 0.5 degrees C, 35.6 degrees C +/- 0.4 degrees C, 35.5 degrees C +/- 0.4 degrees C, 35.4 degrees C +/- 0.5 degrees C, and 35.4 degrees C +/- 0.3 degrees C) 15, 30, 45, 60, 75, and 90 min, respectively, after induction in schizophrenic patients were significantly (P < 0.001) lower than those (36.5 degrees C +/- 0.5 degrees C, 36.4 degrees C +/- 0.5 degrees C, 36.3 degrees C +/- 0.4 degrees C, 36.2 degrees C +/- 0.5 degrees C, 36.2 degrees C +/- 0.4 degrees C, and 36.1 degrees C +/- 0.4 degrees C) in control patients. Mean skin temperatures (31.1 degrees C +/- 0.4 degrees C [P = 0.008], 31.1 degrees C +/- 0.3 degrees C [P = 0.007], and 31.1 degrees C +/- 0.2 degrees C [P = 0.006]) 60, 75, and 90 min, respectively, after induction in schizophrenic patients were significantly lower than those (31.5 degrees C +/- 0.3 degrees C, 31.5 degrees C +/- 0.3 degrees C, and 31.5 degrees C +/- 0.3 degrees C) in control patients. Four of 30 schizophrenic patients and 7 of 30 control patients developed postanesthesia shivering. There were no significant differences within 1 h after tracheal extubation in tympanic membrane temperatures between patients who shivered and those who did not shiver. In conclusion, chronic schizophrenic patients were more hypothermic during anesthesia. The incidence of postanesthesia shivering was not significantly increased. IMPLICATIONS: Antipsychotics inhibit autonomic thermoregulation. This is caused by decreased heat production, increased heat loss, and impaired central action at the hypothalamus. Thus, schizophrenic patients receiving antipsychotics may have impaired intraoperative temperature regulation.     

The thermoregulatory threshold in humans during nitrous oxide-fentanyl anesthesia

Narcotics and nitrous oxide (N2O) inhibit thermoregulatory responses in animals. The extent to which N2O/fentanyl anesthesia lowers the thermoregulatory threshold in humans was tested by measuring peripheral cutaneous vasoconstriction using skin-surface temperature gradients (forearm temperature-fingertip temperature) and the laser Doppler perfusion index. Fifteen unpremedicated patients were anesthetized with N2O (70%) and fentanyl (10 micrograms/kg iv bolus followed by 4 micrograms.kg-1.h-1 infusion) during elective, donor nephrectomy. Patients were randomly assigned to undergo additional warming (humidified respiratory gases, warmed intravenous fluids, and a heating blanket over the legs; n = 5) or standard temperature management (no special warming measures; n = 10). Significant vasoconstriction was prospectively defined as a skin-surface temperature gradient between forearm surface and finger-tip surface greater than or equal to 4 degrees C, and the thermoregulatory threshold was defined as the esophageal temperature at which such vasoconstriction occurred. Vasoconstriction did not occur in the patients who received additional warming and thus remained nearly normothermic [average minimum esophageal temperature = 35.8 +/- 0.4 degrees C (SD)] but did in six hypothermic patients at a mean esophageal temperature of 34.2 +/- 0.5 degrees C. Four hypothermic patients developed a passive thermal steady state without becoming sufficiently cold to trigger vasoconstriction. Thus, active thermoregulation occurs during N2O/fentanyl anesthesia but does not occur until core temperatures are approximately 2.5 degrees C lower than normal. The thermoregulatory threshold during N2O/fentanyl anesthesia is similar to that previously determined during halothane (34.4 +/- 0.2 degrees C).(ABSTRACT TRUNCATED AT 250 WORDS)     

Upright posture reduces thermogenesis and augments core hypothermia

We recently reported that baroreceptor-mediated reflexes modulate thermoregulatory vasoconstriction during lower abdominal surgery. Accordingly, we examined the hypothesis that postural differences and the related alterations in baroreceptor loading similarly modulate the thermogenic (i.e., shivering) response to hypothermia in humans. In healthy humans (n = 7), cold saline was infused IV (30 mL/kg at 4 degrees C) for 30 min to decrease core temperature. Each participant was studied on 2 separate days, once lying supine and once sitting upright. Tympanic membrane temperature and oxygen consumption were monitored for 40 min after each saline infusion. The decrease in core temperature upon completion of the infusion in the upright posture position was 1.24 degrees C +/- 0.07 degrees C, which was significantly greater than the 1.02 degrees C +/- 0.06 degrees C seen in the supine position. The core temperature was reduced by 0.59 degrees C +/- 0.07 degrees C in the upright position but only by 0.37 degrees C +/- 0.05 degrees C in the supine position when the increase in oxygen consumption signaling thermogenic shivering occurred. Thus, the threshold temperature for thermogenesis was significantly less in the upright than the supine position. The gain of the thermogenic response did not differ significantly between the positions (363 +/- 69 mL. min(-1). degrees C(-1) for upright and 480 +/- 80 mL. min(-1). degrees C(-1) for supine). The skin temperature gradient was significantly larger in the upright than in the supine posture, suggesting that the peripheral vasoconstriction was augmented by upright posture. Plasma norepinephrine concentrations increased in response to cold saline infusion under both conditions, but the increase was significantly larger in the upright than in the supine posture. Baroreceptor unloading thus augments the peripheral vasoconstrictor and catecholamine response to core hypothermia but simultaneously reduces thermogenesis, which consequently aggravated the core temperature decrease in the upright posture. IMPLICATIONS: Upright posture attenuates the thermogenic response to core hypothermia but augments peripheral vasoconstriction. This divergent result suggests that input from the baroreceptor modifies the individual thermoregulatory efferent pathway at a site distal to the common thermoregulatory center or neural pathway.     

The threshold and gain of thermoregulatory vasoconstriction differs during anesthesia in the dependent and upper arms in the lateral position

Increased intraluminal pressure may help maintain vasodilation in a dependent arm even after hypothermia triggers centrally mediated thermoregulatory vasoconstriction. We therefore tested the hypotheses that the threshold (triggering core temperature) and gain (increase in vasoconstriction per degree centigrade) of cold-induced vasoconstriction is reduced in the dependent arm during anesthesia. Anesthesia was maintained with 0.4 minimum alveolar anesthetic concentration of desflurane in 10 volunteers in the left-lateral position. Mean skin temperature was reduced to 31 degrees C to decrease core body temperature. Fingertip blood flow in both arms was measured, as was core body temperature.The vasoconstriction threshold was slightly, but significantly, less in the dependent arm (36.2 degrees C +/- 0.3 degrees C, mean +/- SD) than in the upper arm (36.5 degrees C +/- 0.3 degrees C). However, the gain of vasoconstriction in the dependent arm was 2.3-fold greater than in the upper arm. Consequently, intense vasoconstriction (i.e., a fingertip blood flow of 0.15 mL/min) occurred at similar core temperatures. In the lateral position, the vasoconstriction threshold was reduced in the dependent arm; however, gain was also increased in the dependent arm. The thermoregulatory system may thus recognize that hydrostatic forces reduce the vasoconstriction threshold and may compensate by sufficiently augmenting gain. IMPLICATIONS: The threshold for cold-induced vasoconstriction is reduced in the dependent arm, but the gain of vasoconstriction is increased. Consequently, the core temperature triggering intense vasoconstriction was similar in each arm, suggesting that the thermoregulatory system compensates for the hydrostatic effects of the lateral position.     

Thermal balance and tremor patterns during epidural anesthesia

Five healthy, nonpregnant volunteers were studied before and after induction of lumbar epidural anesthesia to determine the cause of central hypothermia during epidural anesthesia. Cutaneous heat loss was measured from 10 area-weighted sites using thermal flux transducers. Oxygen consumption was measured and converted to heat production in watts (W). After a 2-h control period at approximately 20 degrees C, epidural anesthesia was induced by injection of 30-50 ml 3% chloroprocaine. Additional boluses were given to extend the sensory blockade to at least the T5 dermatome. Tremor during epidural anesthesia was compared with normal shivering induced by rapid central venous infusion of approximately 4 l iced saline in six unanesthetized volunteers. Average skin temperature and cutaneous heat loss decreased during the control period, while tympanic membrane temperature remained stable. During the 1st h of epidural blockade, tympanic membrane temperature decreased 1.1 +/- 0.3 degrees C, and average skin temperature increased 0.9 +/- 0.5 degrees C. Cutaneous heat loss increased 16 +/- 6% (15 +/- 5 W), but metabolic heat production increased even more (and was associated with a shivering-like tremor). Tremor during epidural anesthesia and shivering induced by iced saline infusion had similar synchronous waxing-and-waning patterns. No abnormal EMG patterns were detected during epidural anesthesia. We conclude that central hypothermia during the 1st h of epidural anesthesia does not result from heat loss to the environment in excess of metabolic heat production, but results primarily from redistribution of body heat from central to peripheral tissues. Analysis of the tremor patterns suggests that oscillations recorded during epidural anesthesia in nonpregnant individuals is normal thermoregulatory shivering. Shivering occurred sooner and was more intense during iced saline infusion than during epidural anesthesia, despite comparable central hypothermia. The low intensity of shivering during epidural anesthesia, and in some individuals the delay in onset, may result from blockade of afferent cutaneous cold signals.     

The vasoconstriction threshold is increased in obese patients during general anaesthesia

BACKGROUND: In anaesthetized patients, body temperature decreases often, but overweight patients become less hypothermic. Obesity in itself protects body heat, and thermoregulatory reflexes may maintain normothermia in obese patients. We tested the hypothesis that even slight obesity increases the vasoconstriction threshold. METHODS: Twenty male patients aged 30-65 years scheduled for open abdominal surgery were allocated to two groups: body fat >/=25% (obese group, n = 10), or <25% (normal weight group, n = 10). Anaesthesia was maintained with 0.4% isoflurane and opioid. The thermoregulatory vasoconstriction threshold was defined by the tympanic membrane temperature at which the skin temperature gradient equalled 0 degrees C. Plasma adrenaline, noradrenaline and leptin were measured. RESULTS: Age, height, heart rate and blood pressure did not differ between the two groups of patients. In the obese group the vasoconstriction threshold was higher than that in the normal weight group: 36.0 +/- 0.1 vs. 35.5 +/- 0.2 degrees C. Consequently, after 4 h of anaesthesia, the core temperature was highest in the obese patients: 36.4 +/- 0.1 vs. 35.5 +/- 0.2 degrees C. CONCLUSIONS: These results suggest that core temperature is maintained in obese patients because their vasoconstriction threshold to a low environmental temperature is high.