Blood pressure response to thermoregulatory vasoconstriction during isoflurane and desflurane anesthesia.

BACKGROUND: Mild perioperative hypothermia produces morbid cardiac outcomes that may result from sympathetically induced hypertension. However, volatile anesthetics produce vasodilatation that may reduce the hemodynamic response to hypothermia. We tested the hypothesis that the volatile anesthetics isoflurane and desflurane blunt the normal cold-induced hypertensive response. METHODS: We analyzed prospective data from three analogous studies: 1) 10 volunteers given desflurane (2.6 volume percentage) maintained in left-lateral position; 2) nine volunteers without anesthesia or anesthetized with various doses of desflurane; and 3) eight volunteers given various concentrations of isoflurane. Mean skin temperature was reduced to 31 C, which decreased core body temperature and triggered thermoregulatory vasoconstriction. Mean arterial pressures were determined before and after hypothermia provoked intense thermoregulatory vasoconstriction. RESULTS: The hemodynamic responses to thermoregulatory vasoconstriction were similar without anesthesia and at all concentrations of desflurane and isoflurane. On average, mean arterial pressure increased 14 (SD = 5) mmHg with and without anesthesia. CONCLUSION: We conclude that thermoregulatory vasoconstriction significantly increases arterial pressure with or without isoflurane or desflurane anesthesia.

Neither nalbuphine nor atropine possess special antishivering activity.

The special antishivering action of meperidine may be mediated by its kappa or anticholinergic actions. We therefore tested the hypotheses that nalbuphine or atropine decreases the shivering threshold more than the vasoconstriction threshold. Eight volunteers were each evaluated on four separate study days: 1) control (no drug), 2) small-dose nalbuphine (0.2 microg/mL), 3) large-dose nalbuphine (0.4 microg/mL), and 4) atropine (1-mg bolus and 0.5 mg/h). Body temperature was increased until the patient sweated and then decreased until the patient shivered. Nalbuphine produced concentration-dependent decreases (mean +/- SD) in the sweating (-2.5 +/- 1.7 degrees C. microg(-1). mL; r(2) = 0.75 +/- 0.25), vasoconstriction (-2.6 +/- 1.7 degrees C. microg(-1). mL; r(2) = 0.75 +/- 0.25), and shivering (-2.8 +/- 1.7 degrees C. microg(-1). mL; r(2) = 0.79 +/- 0.23) thresholds. Atropine significantly increased the thresholds for sweating (1.0 degrees C +/- 0.4 degrees C), vasoconstriction (0.9 degrees C +/- 0.3 degrees C), and shivering (0.7 degrees C +/- 0.3 degrees C). Nalbuphine reduced the vasoconstriction and shivering thresholds comparably. This differs markedly from meperidine, which impairs shivering twice as much as vasoconstriction. Atropine increased all thresholds and would thus be expected to facilitate shivering. Our results thus fail to support the theory that activation of kappa-opioid or central anticholinergic receptors contribute to meperidine's special antishivering action.

Core cooling by central venous infusion of ice-cold (4 degrees C and 20 degrees 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. CONCLUSIONS: Central venous infusion of cold fluid decreases core temperature more than would be expected were the reduction in body heat content proportionately distributed. It thus appears to be an effective method of rapidly inducing therapeutic hypothermia. When the infusion is complete, there is a spontaneous partial recovery in core temperature that facilitates rewarming to normothermia.

Resistive heating is more effective than metallic-foil insulation in an experimental model of accidental hypothermia: A randomized controlled trial.

STUDY OBJECTIVE: We study a resistive-heating blanket in a volunteer model of severe accidental hypothermia to evaluate differences in rates of rewarming, core temperature afterdrop, and body heat content and distribution during active and passive rewarming. METHODS: Eight volunteers participated in a crossover design on 2 days. The volunteers were anesthetized and cooled to 33 degrees C (91.4 degrees F); anesthesia was subsequently discontinued, and shivering was prevented with meperidine. On one randomly assigned day, the volunteers were rewarmed passively with reflective foil (passive insulation), whereas on the other they were covered with a carbon fiber-resistive heating blanket set to 42 degrees C (107.6 degrees F; active rewarming). Trunk and head temperature and heat content were calculated from core (tympanic membrane) temperature. Peripheral (arm and leg) tissue temperature and heat content were estimated by using fourth-order regressions and integration over volume from 30 tissue and skin temperatures. RESULTS: Core heat content increased 73+/-14 kcal (mean+/-SD) during 3 hours of active warming, but only 31+/-24 kcal with passive insulation, a difference of 41+/-20 kcal (95% confidence interval [CI] 27 to 55 kcal; P <. 001). Peripheral tissue heat content increased linearly by 111+/-16 kcal during active warming but only by 38+/-31 kcal during passive warming, a difference of 74+/-34 kcal (95% CI 50 to 97; P <.001). Consequently, total body heat increased 183+/-22 kcal during active warming but only 68+/-54 kcal with passive insulation, a difference of 115+/-42 kcal (95% CI 86 to 144 kcal; P <.001). Core temperature increased from 32.9 degrees C+/-0.2 degrees C to 35.2 degrees C+/-0. 4 degrees C during 3 hours of active warming, a difference of 2.3 degrees C+/-0.4 degrees C. In contrast, core temperature with foil insulation only increased from 32.9 degrees C+/-0.2 degrees C to 33. 8 degrees C+/-0.5 degrees C, a difference of only 0.8 degrees C+/-0. 4 degrees C. The difference in the core temperature increase between the two treatments was thus 1.5 degrees C+/-0.4 degrees C (95% CI 1. 2 degrees C to 1.7 degrees C; P <.001 between treatments). Active warming was not associated with an afterdrop, whereas the afterdrop was 0.2 degrees C+/-0.2 degrees C and lasted a median of 45 minutes (interquartile range, 41 to 64 minutes) with passive insulation. CONCLUSION: Resistive heating more than doubles the rewarming rate compared with that produced by reflective metal foil and does so without producing an afterdrop. It is therefore likely to be useful in the prehospital setting.

Supplemental oxygen reduces the incidence of postoperative nausea and vomiting.

BACKGROUND: Despite new anesthetic drugs and antiemetics, particularly 5-hydroxytryptamines, the incidence of postoperative nausea or vomiting remains between 20% and 70%. The authors tested the hypothesis that supplemental perioperative oxygen administration reduces the incidence of postoperative nausea or vomiting. METHODS: Patients undergoing colon resection were anesthetized with fentanyl and isoflurane. During and for 2 h after surgery they were randomly assigned to (1) 30% oxygen, balance nitrogen (n = 119); or (2) 80% oxygen, balance nitrogen (n = 112). The incidence of nausea or vomiting during the first 24 postoperative hours was evaluated by nurses blinded to group assignment and oxygen concentration. Data were analyzed with unpaired t or Mann-Whitney U tests. Results are presented as means +/- SD; P < 0.05 was considered significant. RESULTS: Factors known to influence nausea and vomiting were comparable in the two groups. Perioperative oxygen saturation was well within normal limits in each treatment group; saturations the first postoperative morning were comparable in each group. Supplemental oxygen reduced the incidence of postoperative nausea or vomiting from 30% in the patients given 30% oxygen to 17% in those given 80% oxygen (P = 0.027). CONCLUSIONS: Supplemental oxygen reduced the incidence of postoperative nausea or vomiting nearly twofold after colorectal surgery. The mechanism by which oxygen administration reduces the incidence of these postoperative sequelae remains unknown but may be related to subtle intestinal ischemia. Because oxygen is inexpensive and essentially risk-free, supplemental oxygen appears to be an effective method of reducing postoperative nausea and vomiting.

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 approximately 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 approximately 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 degrees C. Their cores were subsequently cooled by central-venous administration of fluid at approximately 3 degrees 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. CONCLUSIONS: The results in anesthetized volunteers were virtually identical to those reported previously in unanesthetized subjects. In both cases, the cutaneous contribution to control of vasoconstriction and shivering was linear and near 20%. These data indicate that a proportionality constant of approximately 20% can be used to compensate for experimentally induced skin-temperature manipulations in anesthetized as well as unanesthetized subjects.