Biomedical subjects

D I Sessler

Publications and source records attributed to D I Sessler.

At least 181 records · Page 10Linked to original sources

PubMed1995

Mild hypothermia alters propofol pharmacokinetics and increases the duration of action of atracurium.

Mild intraoperative hypothermia is common. We therefore studied the effects of mild hypothermia on propofol pharmacokinetics, hepatic blood flow, and atracurium duration of action in healthy volunteers. Six young volunteers were studied on two randomly assigned days, at either 34 degrees C or 37 degrees C. Anesthesia was induced with thiopental, 3 mg/kg, and maintained with 70% N2O and 0.6% isoflurane. Core hypothermia was induced by conductive and convective cooling. On the other study day, normothermia was maintained by a Bair Hugger (Augustine Medical, Inc., Eden Prairie, MN) forced-air warmer. Propofol, 1 mg/kg lean body mass (LBM), then was given, followed by a 4-h infusion at 5 mg.kg-1.h-1. After 2 h, atracurium 0.5 mg/kg was administered as an intravenous bolus. Indocyanine green was administered for estimation of hepatic blood flow. Arterial blood was assayed for propofol and indocyanine green concentration. Pharmacokinetic analysis was performed using NONMEM. Results are reported as means +/- SEM. Propofol blood concentrations averaged approximately 28% more at 34 degrees C than at 37 degrees C (P < 0.05). Hepatic blood flow decreased 23% +/- 11% in normothermic volunteers during the propofol infusion, and 33% +/- 11% in hypothermic volunteers (P = not significant). A three-compartment mamillary model fitted the data best. Inclusion of hepatic blood flow change from the prepropofol baseline as a covariate for total body clearance significantly improved the fit. The intercompartmental clearances were decreased in the presence of hypothermia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1995

Nitrous oxide decreases the threshold for vasoconstriction less than sevoflurane or isoflurane.

The core temperature triggering thermoregulatory arteriovenous shunt constriction is designated the threshold for vasoconstriction. High thresholds are generally desirable because vasoconstriction helps prevent further core hypothermia by decreasing cutaneous heat loss and constraining metabolic heat to the core thermal compartment. Previous studies suggest that nitrous oxide (N2O) may inhibit thermoregulatory vasoconstriction less than comparable doses of volatile anesthetics. To confirm this impression, we tested the hypothesis that 0.5 minimum alveolar anesthetic concentration (MAC) N2O combined with 0.5 MAC sevoflurane or isoflurane would reduce the vasoconstriction threshold less than 1.0 MAC sevoflurane or isoflurane. With institutional review board approval, we studied 40 patients, aged 20-60 yr, undergoing open abdominal surgery. No premedication was given. Ten patients each were anesthetized with: 1) N2O (50%) and 0.5 MAC sevoflurane (1%); 2) sevoflurane alone (2%); 3) N2O (60%) and 0.5 MAC isoflurane (0.6%); and, 4) isoflurane alone (1.2%). A forearm minus fingertip, skin temperature gradient > or = 0 degree C was considered significant vasoconstriction; the esophageal temperature triggering vasoconstriction identified the threshold. Morphometric characteristics were comparable in each group. The threshold for vasoconstriction was 35.8 +/- 0.3 degrees C in the patients given 50% N2O combined with 0.5 MAC sevoflurane, which was significantly greater than that in those given 1.0 MAC sevoflurane: 35.1 +/- 0.4 degrees C. Similarly, the threshold for vasoconstriction was 35.9 +/- 0.3 degrees C in the patients given 60% N2O combined with 0.5 MAC isoflurane, which was significantly greater than that in those given 1.0 MAC isoflurane: 35.0 +/- 0.5 degrees C. We thus conclude that N2O impairs thermoregulation less than sevoflurane or isoflurane.

Adult↗

PubMed1995

Midazolam minimally impairs thermoregulatory control.

Perioperative hypothermia usually results largely from pharmacologic inhibition of normal thermoregulatory control. Midazolam is a commonly used sedative and anesthetic adjuvant whose thermoregulatory effects are unknown. We therefore tested the hypothesis that midazolam administration impairs thermoregulatory control. Eight volunteers were studied on 2 days each, once without drug and once at a target total plasma midazolam concentration of 0.3 micrograms/mL (corresponding to administration of approximately 40 mg over approximately 4 h). Each day, skin and core temperatures were increased sufficiently to provoke sweating, and then reduced to elicit peripheral vasoconstriction and shivering. We mathematically compensated for changes in skin temperature using the established linear cutaneous contributions to control of each response. From these calculated thresholds (core temperatures triggering responses at a designated skin temperature of 34 degrees C), we determined the thermoregulatory effects of midazolam. The sweating threshold was decreased approximately 0.3 degrees C by midazolam administration: 37.3 +/- 0.2 degrees C vs 37.0 +/- 0.3 degrees C (P = 0.0004, paired t-test). Midazolam decreased the core temperature that triggered vasoconstriction somewhat more: 37.1 +/- 0.2 degrees C vs 36.3 +/- 0.5 degrees C (P = 0.0002). Similarly, midazolam decreased the shivering threshold: 35.9 +/- 0.3 degrees C vs 35.3 +/- 0.6 degrees C (P = 0.03). The sweating-to-vasoconstriction (interthreshold) range, therefore, increased from 0.2 +/- 0.1 degrees C to 0.7 +/- 0.3 degrees C (P = 0.002). Although statistically significant, this relatively small increase contrasts markedly with the 3-5 degrees C interthreshold ranges produced by clinical doses of volatile anesthetics, propofol, and opioids.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1995

Pancuronium does not decrease oxygen consumption during hypothermic or normothermic cardiopulmonary bypass.

Muscle relaxation reportedly reduces systemic oxygen consumption 30% during hypothermic cardiopulmonary bypass. A potential mechanism is inhibition of hypothermia-induced subclinical muscle tone ("microshivering"). Accordingly, we tested the hypothesis that pancuronium administration would decrease systemic oxygen consumption during hypothermic cardiopulmonary bypass, but not during normothermic bypass. We studied 20 patients undergoing normothermic cardiopulmonary bypass at a nasopharyngeal temperature of 37.6 +/- 0.8 degrees C (mean +/- SD) and 15 patients undergoing hypothermic bypass at a nasopharyngeal temperature of 28.2 +/- 1.2 degrees C. Oxygen consumption during bypass was determined, using the Fick principle, before and after administration of pancuronium 0.15 mg/kg. Morphometric characteristics and anesthetic management were similar in the two groups. Oxygen consumption averaged 93 +/- 28 mL.min-1.m-2 in the normothermic patients and 43 +/- 10 mL.min-1.m-2 in the hypothermic group. Administration of pancuronium decreased oxygen consumption only 2% in the normothermic patients. However, muscle relaxation also decreased oxygen consumption only 2% in the hypothermic patients. We were thus unable to confirm our hypothesis because muscle relaxation induced by administration of pancuronium did not significantly reduce oxygen consumption in either group.

Aged↗

PubMed1995

Isoflurane and sevoflurane produce a dose-dependent reduction in the shivering threshold in rabbits.

All general anesthetics markedly impair thermoregulatory responses; nonetheless, sufficient hyperthermia or hypothermia will trigger most protective reflexes. Shivering, however, remains an exception among thermo-regulatory responses: it is common during postanesthetic recovery, but is rare at typical anesthetic concentrations. This observation suggests that general anesthesia impairs shivering far more than other thermoregulatory defenses. Accordingly, we tested the hypothesis that low concentrations of isoflurane and sevoflurane would virtually obliterate shivering. Japanese white rabbits were anesthetized with isoflurane or sevoflurane at end-tidal concentrations of 0.2, 0.3, and 0.4 minimum alveolar anesthetic concentration (MAC) (n = 6 in each group); the normal core temperature for these rabbits is approximately 39 degrees C. Core temperatures were subsequently reduced by a water-perfused thermode positioned in the colon. The core temperature triggering shivering identified the threshold for this response. Five of the six rabbits given 0.2 MAC isoflurane shivered at a mean core temperature of 36.3 +/- 0.3 degrees C (mean +/- SD), and one rabbit failed to shiver at a minimum core temperature of 35.0 degrees C. Four of the six rabbits given 0.3 MAC isoflurane shivered at a mean core temperature of 36.2 +/- 0.6 degrees C, and two of these rabbits failed to shiver at a minimum core temperature of 35.0 degrees C. However, no rabbit given 0.4 MAC isoflurane shivered, even at minimum core temperatures of 35.0 degrees C. All of the rabbits given 0.2 MAC sevoflurane shivered at a mean core temperature of 36.6 +/- 0.7 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetics↗

PubMed1995

Propofol blood concentration and the Bispectral Index predict suppression of learning during propofol/epidural anesthesia in volunteers.

Propofol is often used for sedation during regional anesthesia. We tested the hypothesis that propofol blood concentration, the Bispectral Index and the 95% spectral edge frequency predict suppression of learning during propofol/epidural anesthesia in volunteers. In addition, we tested the hypothesis that the Bispectral Index is linearly related to propofol blood concentration. Fourteen healthy, male volunteers were studied on three randomly ordered days: no propofol, target propofol blood concentration 1 microgram/mL, and target propofol blood concentration 2 micrograms/mL. Each day, epidural anesthesia (approximately T11 level) was induced using 2% 2-chloroprocaine. Propofol was infused by a computer-controlled pump, and propofol concentration measured in central venous blood. We administered a Trivial Pursuit-type question task on all 3 days. The electroencephalogram was monitored continuously (Fp1, Fp2; reference, Cz; ground, mastoid). Propofol caused concentration-related impairment of learning. The propofol blood concentration suppressing learning by 50% was 0.66 +/- 0.1 microgram/mL. The Bispectral Index value when learning was suppressed by 50% was 91 +/- 1. In contrast, the 95% spectral edge frequency did not correlate well with learning. The Bispectral Index decreased linearly as propofol blood concentration increased (Bispectral Index = -7.4.[propofol] + 90; r2 = 0.47, n = 278). There was no significant correlation between the 95% spectral edge frequency and propofol concentration. In order to suppress learning, propofol blood concentrations reported to produce amnesia may be targeted. Alternatively, the Bispectral Index may be used to predict anesthetic effect during propofol sedation.

Adult↗

PubMed1995

Heat flow and distribution during induction of general anesthesia.

BACKGROUND: Core hypothermia after induction of general anesthesia results from an internal core-to-peripheral redistribution of body heat and a net loss of heat to the environment. However, the relative contributions of each mechanism remain unknown. The authors evaluated regional body heat content and the extent to which core hypothermia after induction of anesthesia resulted from altered heat balance and internal heat redistribution. METHODS: Six minimally clothed male volunteers in an approximately 22 degrees C environment were evaluated for 2.5 control hours before induction of general anesthesia and for 3 subsequent hours. Overall heat balance was determined from the difference between cutaneous heat loss (thermal flux transducers) and metabolic heat production (oxygen consumption). Arm and leg tissue heat contents were determined from 19 intramuscular needle thermocouples, 10 skin temperatures, and "deep" foot temperature. To separate the effects of redistribution and net heat loss, we multiplied the change in overall heat balance by body weight and the specific heat of humans. The resulting change in mean body temperature was subtracted from the change in distal esophageal (core) temperature, leaving the core hypothermia specifically resulting from redistribution. RESULTS: Core temperature was nearly constant during the control period but decreased 1.6 +/- 0.3 degree C in the first hour of anesthesia. Redistribution contributed 81% to this initial decrease and required transfer of 46 kcal from the trunk to the extremities. During the subsequent 2 h of anesthesia, core temperature decreased an additional 1.1 +/- 0.3 degree C, with redistribution contributing only 43%. Thus, only 17 kcal was redistributed during the second and third hours of anesthesia. Redistribution therefore contributed 65% to the entire 2.8 +/- 0.5 degree C decrease in core temperature during the 3 h of anesthesia. Proximal extremity heat content decreased slightly after induction of anesthesia, but distal heat content increased markedly. The distal extremities thus contributed most to core cooling. Although the arms constituted only a fifth of extremity mass, redistribution increased arm heat content nearly as much as leg heat content. Distal extremity heat content increased approximately 40 kcal during the first hour of anesthesia and remained elevated for the duration of the study. CONCLUSIONS: The arms and legs are both important components of the peripheral thermal compartment, but distal segments contribute most. Core hypothermia during the first hour after induction resulted largely from redistribution of body heat, and redistribution remained the major cause even after 3 h of anesthesia.

Adult↗

PubMed1995

Optimal duration and temperature of prewarming.

BACKGROUND: Core hypothermia developing immediately after induction of anesthesia results largely from an internal core-to-peripheral redistribution of body heat. Although difficult to treat, redistribution can be prevented by prewarming. The benefits of prewarming may be limited by sweating, thermal discomfort, and efficacy of the warming device. Accordingly, the optimal heater temperature and minimum warming duration likely to substantially reduce redistribution hypothermia were evaluated. METHODS: Sweating, thermal comfort, and extremity heat content were evaluated in seven volunteers. They participated on two study days, each consisting of a 2-h control period followed by 2 h of forced-air warming with the heater set on "medium" (approximately 40 degrees C) or "high" (approximately 43 degrees C). Arm and leg tissue heat contents were determined from 19 intramuscular needle thermocouples, ten skin temperatures, and "deep" foot temperature. RESULTS: Half the volunteers started sweating during the second hour of warming. None of the volunteers felt uncomfortably warm during the first hour of heating, but many subsequently did. With the heater set on "high," arm and leg heat content increased 69 kcal during the first 30 min of warming and 136 kcal during the first hour of warming, representing 38% and 75%, respectively, of the values observed after 2 h of warming. The increase was only slightly less when the heater was set to "medium." CONCLUSIONS: Neither sweating nor thermal discomfort limited heat transfer during the first hour of warming. Thirty minutes of forced-air warming increased peripheral tissue heat content by more than the amount normally redistributed during the first hour of anesthesia. The large increase in arm and leg heat content during prewarming thus explains the observed efficacy of prewarming.

Arm↗

PubMed1995

Thermoregulatory vasoconstriction impairs active core cooling.

BACKGROUND: Many clinicians now consider hypothermia indicated during neurosurgery. Active cooling often will be required to reach target temperatures < 34 degrees C sufficiently rapidly and nearly always will be required if the target temperature is 32 degrees C. However, the efficacy even of active cooling might be impaired by thermoregulatory vasoconstriction, which reduces cutaneous heat loss and constrains metabolic heat to the core thermal compartment. The authors therefore tested the hypothesis that the efficacy of active cooling is reduced by thermoregulatory vasoconstriction. METHODS: Patients undergoing neurosurgical procedures with hypothermia were anesthetized with either isoflurane/nitrous oxide (n = 13) or propofol/fentanyl (n = 13) anesthesia. All were cooled using a prototype forced-air cooling device until core temperature reached 32 degrees C. Core temperature was measured in the distal esophagus. Vasoconstriction was evaluated using forearm minus fingertip skin-temperature gradients. The core temperature triggering a gradient of 0 degree C identified the vasoconstriction threshold. RESULTS: In 6 of the 13 patients given isoflurane, vasoconstriction (skin-temperature gradient = 0 degrees C) occurred at a core temperature of 34.4 +/- 0.9 degree C, 1.7 +/- 0.58 h after induction of anesthesia. Similarly, in 7 of the 13 patients given propofol, vasoconstriction occurred at a core temperature of 34.5 +/- 0.9 degree C, 1.6 +/- 0.6 h after induction of anesthesia. In the remaining patients, vasodilation continued even at core temperatures of 32 degrees C. Core cooling rates were comparable in each anesthetic group. However, patients in whom vasodilation was maintained cooled fastest. Patients in whom vasoconstriction occurred required nearly an hour longer to reach core temperatures of 33 degrees C and 32 degrees C than did those in whom vasodilation was maintained (P < 0.01). CONCLUSIONS: Vasoconstriction did not produce a full core temperature "plateau," because of the extreme microenvironment provided by forced-air cooling. However, it markedly decreased the rate at which hypothermia developed. The approximately 1-h delay in reaching core temperatures of 33 degrees C and 32 degrees C could be clinically important, depending on the target temperature and the time required to reach critical portions of the operation.

Adult↗

PubMed1995

Increasing mean skin temperature linearly reduces the core-temperature thresholds for vasoconstriction and shivering in humans.

BACKGROUND: The contribution of mean skin temperature to the thresholds for sweating and active precapillary vasodilation has been evaluated in numerous human studies. In contrast, the contribution of skin temperature to the control of cold responses such as arteriovenous shunt vasoconstriction and shivering is less well established. Accordingly, the authors tested the hypothesis that mean skin and core temperatures are linearly related at the vasoconstriction and shivering thresholds in men. Because the relation between skin and core temperatures might vary by gender, the cutaneous contribution to thermoregulatory control also was determined in women. METHODS: In the first portion of the study, six men participated on 5 randomly ordered days, during which mean skin temperatures were maintained near 31, 34, 35, 36, and 37 degrees C. Core hypothermia was induced by central venous infusion of cold lactated Ringer's solution sufficient to induce peripheral vasoconstriction and shivering. The core-temperature thresholds were then plotted against skin temperature and a linear regression fit to the values. The relative skin and core contributions to the control of each response were calculated from the slopes of the regression equations. In the second portion of the study, six women participated on three randomly ordered days, during which mean skin temperatures were maintained near 31, 35, and 37 degrees C. At each designated skin temperature, core hypothermia sufficient to induce peripheral vasoconstriction and/or shivering was again induced by central venous infusion of cold lactated Ringer's solution. The cutaneous contributions to control of each response were then calculated from the skin- and core-temperature pairs at the vasoconstriction and shivering thresholds. RESULTS: There was a linear relation between mean skin and core temperatures at the response thresholds in the men: r = 0.90 +/- 0.06 for vasoconstriction and r = 0.94 +/- 0.07 for shivering. Skin temperature contributed 20 +/- 6% to vasoconstriction and 19 +/- 8% to shivering. Skin temperature in the women contributed to 18 +/- 4% to vasoconstriction and 18 +/- 7% to shivering, values not differing significantly from those in men. There was no apparent correlation between the cutaneous contributions to vasoconstriction and shivering in individual volunteers. CONCLUSIONS: These data indicate that skin and core temperatures contribute linearly to the control of vasoconstriction and shivering in men and that the cutaneous contributions average approximately 20% in both men and women. The same coefficients thus can be used to compensate for experimental skin temperature manipulations in men and women. However, the cutaneous contributions to each response vary among volunteers; furthermore, the contributions to the two responses vary within volunteers.

Adult↗

PubMed1995

Propofol linearly reduces the vasoconstriction and shivering thresholds.

BACKGROUND: Skin temperature is best kept constant when determining response thresholds because both skin and core temperatures contribute to thermoregulatory control. In practice, however, it is difficult to evaluate both warm and cold thresholds while maintaining constant cutaneous temperature. A recent study shows that vasoconstriction and shivering thresholds are a linear function of skin and core temperatures, with skin contributing 20 +/- 6% and 19 +/- 8%, respectively. (Skin temperature has long been known to contribute approximately 10% to the control of sweating). Using these relations, we were able to experimentally manipulate both skin and core temperatures, subsequently compensate for the changes in skin temperature, and finally report the results in terms of calculated core-temperature thresholds at a single-designated skin temperature. METHODS: Five volunteers were each studied on 4 days: (1) control; (2) a target blood propofol concentration of 2 micrograms/ml; (3) a target concentration of 4 micrograms/ml; and (4) a target concentration of 8 micrograms/ml. On each day, we increased skin and core temperatures sufficiently to provoke sweating. Skin and core temperatures were subsequently reduced to elicit peripheral vasoconstriction and shivering. We mathematically compensated for changes in skin temperature by using the established linear cutaneous contributions to the control of sweating (10%) and to vasoconstriction and shivering (20%). From these calculated core-temperature thresholds (at a designated skin temperature of 35.7 degrees C), the propofol concentration-response curves for the sweating, vasoconstriction, and shivering thresholds were analyzed using linear regression. We validated this new method by comparing the concentration-dependent effects of propofol with those obtained previously with an established model. RESULTS: The concentration-response slopes for sweating and vasoconstriction were virtually identical to those reported previously. Propofol significantly decreased the core temperature triggering vasoconstriction (slope = -0.6 +/- 0.1 degrees C.micrograms-1.ml-1; r2 = 0.98 +/- 0.02) and shivering (slope = -0.7 +/- 0.1 degrees C.micrograms -1.ml-1; r2 = 0.95 +/- 0.05). In contrast, increasing the blood propofol concentration increased the sweating threshold only slightly (slope = 0.1 +/- 0.1 degrees C.micrograms -1.ml-1; r2 = 0.46 +/- 0.39). CONCLUSIONS: Advantages of this new model include its being nearly noninvasive and requiring relatively little core-temperature manipulation. Propofol only slightly alters the sweating threshold, but markedly reduces the vasoconstriction and shivering thresholds. Reductions in the shivering and vasoconstriction thresholds are similar; that is, the vasoconstriction-to-shivering range increases only slightly during anesthesia.

Adult↗

PubMed1995

Alfentanil slightly increases the sweating threshold and markedly reduces the vasoconstriction and shivering thresholds.

BACKGROUND: Hypothermia is common in surgical patients and victims of major trauma; it also results from environmental exposure and drug abuse. In most cases, hypothermia results largely from drug-induced inhibition of normal thermoregulatory control. Although opioids are given to a variety of patients, the thermoregulatory effects of opioids in humans remain unknown. Accordingly, the hypothesis that opioid administration impairs thermoregulatory control was tested. METHODS: Eight volunteers were studied, each on 3 days: (1) a target total plasma alfentanil concentration of 100 ng/ml, (2) control (no drug), and (3) a target alfentanil concentration of 300 ng/ml. Each day, skin and core temperatures were increased sufficiently to provoke sweating. Temperatures subsequently were reduced to elicit peripheral vasoconstriction and shivering. Mathematical compensations were made for changes in skin temperature using the established linear cutaneous contributions to control of sweating (10%) and to vasoconstriction and shivering (20%). From the calculated thresholds (core temperatures triggering responses at a designated skin temperature of 34 degrees C) and unbound plasma alfentanil concentrations, the individual concentration-response relationship was determined. The concentration-response relationship for all the volunteers was determined similarly using total alfentanil concentrations. RESULTS: In terms of unbound concentration, alfentanil increased the sweating threshold (slope = 0.021 +/- 0.016 degrees C.ng-1.ml; r2 = 0.92 +/- 0.06). Alfentanil also significantly decreased the vasoconstriction (slope = -0.075 +/- 0.067 degrees C.ng-1.ml; r2 = 0.92 +/- 0.07) and shivering thresholds (slope = -0.063 +/- -0.037 degrees C.ng-1.ml; r2 = 0.98 +/- 0.04). In terms of total alfentanil concentration (degrees C.ng-1.ml), the sweating threshold increased according to the equation: threshold (degrees C) = 0.0014[alfentanil] + 37.2 (r2 = 0.33). In contrast, alfentanil produced a linear decrease in the core temperature, triggering vasoconstriction: threshold (degrees C) = -0.0049[alfentanil] + 36.7 (r2 = 0.64). Similarly, alfentanil linearly decreased the shivering threshold: threshold (degrees C) = -0.0057[alfentanil] + 35.9 (r2 = 0.70). CONCLUSIONS: The observed pattern of thermoregulatory impairment is similar to that produced by most general anesthetics: a slight increase in the sweating threshold and a substantial, linear decrease in the vasoconstriction and shivering thresholds.

Adult↗

PubMed1995

Heat balance and distribution during the core-temperature plateau in anesthetized humans.

BACKGROUND: Once triggered, intraoperative thermoregulatory vasoconstriction is remarkably effective in preventing further hypothermia. Protection results from both vasoconstriction-induced decrease in cutaneous heat loss and altered distribution of body heat. However, the independent contributions of each mechanism have not been quantified. Accordingly, we evaluated overall heat balance and distribution of heat within the body during the core-temperature plateau. METHODS: Nine minimally clothed male volunteers were anesthetized with propofol and isoflurane and maintained in an approximately 22 degrees C environment. They were monitored for approximately 2 h before vasoconstriction and for 3 h subsequently. Overall heat balance was determined from the difference between cutaneous heat loss (thermal flux transducers) and metabolic heat production (oxygen consumption). Arm and leg tissue heat contents were determined from 19 intramuscular temperatures, ten skin temperatures, and "deep" foot temperature. Heat constrained by vasoconstriction to the trunk and head was calculated by subtracting the expected change in that region (overall heat balance multiplied by the fractional weight of the trunk and head) from the actual change (change in distal esophageal temperature multiplied by the specific heat of human tissue and the weight of the trunk and head); the result represents the amount by which core heat exceeded that which would be expected based on overall heat balance, assuming that the change was evenly distributed throughout the body. RESULTS: Vasoconstriction and passive tissue cooling decreased heat loss but not to the level of heat production. Consequently, heat loss exceeded metabolic heat production throughout the study. Core temperature decreased approximately 1.3 C during the 2-h prevasoconstriction period; however, core temperature remained virtually constant during the subsequent 3 h. In the 3 h after vasoconstriction, arm and leg heat content decreased 57 +/- 9 kcal, and vasoconstriction constrained 22 +/- 8 kcal to the trunk and head. CONCLUSIONS: These results confirm the efficacy of thermo-regulatory vasoconstriction in preventing additional core hypothermia. Decreased cutaneous heat loss and constraint of metabolic heat to the core thermal compartment contributed to the plateau.

Adult↗

PubMed1995

Heat flow and distribution during epidural anesthesia.

BACKGROUND: Core hypothermia after induction of epidural anesthesia results from both an internal core-to-peripheral redistribution of body heat and a net loss of heat to the environment. However, the relative contributions of each mechanism remain unknown. The authors thus evaluated regional body heat content and the extent to which core hypothermia after induction of anesthesia resulted from altered heat balance and internal heat redistribution. METHODS: Twelve minimally clothed male volunteers were evaluated in a approximately 22 degrees C environment for 2.5 control hours before induction of epidural anesthesia and for 3 subsequent hours. Epidural anesthesia produced a bilateral sympathetic block in only six volunteers, and only their results are reported. Shivering, when observed, was treated with intravenous meperidine. Overall heat balance was determined from the difference between cutaneous heat loss (thermal flux transducers) and metabolic heat production (oxygen consumption). Arm and leg tissue heat contents were determined from 19 intramuscular needle thermocouples, 10 skin temperatures, and "deep" foot temperature. To separate the effects of redistribution and net heat loss, we multiplied the change in overall heat balance by body weight and the specific heat of humans. The resulting change in mean body temperature was subtracted from the change in esophageal or tympanic membrane (core) temperatures, leaving the core hypothermia specifically resulting from redistribution. RESULTS: Arm heat content decreased approximately 5 kcal/h after induction of anesthesia, but leg heat content increased markedly. Most of the increase in leg heat content was in the lower legs and feet. Core temperature increased slightly during the control period but decreased 0.8 +/- 0.3 degrees C in the 1st hour of anesthesia. Redistribution, contributing 89% to this initial decrease, required a net transfer of 20 kcal from the trunk to the extremities. During the subsequent 2 h of anesthesia, core temperature decreased an additional 0.4 +/- 0.3 degrees C, with redistribution contributing 62%. Thus, only 7 kcal were redistributed during the 2nd and 3rd hours of anesthesia. Redistribution therefore contributed 80% to the entire 1.2 +/- 0.3 degrees C decrease in core temperature during the 3 h of anesthesia. CONCLUSIONS: Core hypothermia during the 1st hour after induction of epidural anesthesia resulted largely from redistribution of body heat from the core thermal compartment to the distal legs. Even after 3 h of anesthesia, redistribution remained the major cause of core hypothermia. Despite the greater fractional contribution of redistribution during epidural anesthesia, core temperature decreased only half as much as during general anesthesia because metabolic rate was maintained and the arms remained vasoconstricted.

Adjuvants, Anesthesia↗

PubMed1995

Shivering threshold during spinal anesthesia is reduced in elderly patients.

BACKGROUND: Both accidental and perioperative hypothermia are common in the elderly. The elderly are at risk because their responses to hypothermia may be delayed or less efficient than in those of younger subjects. For example, the vasoconstriction threshold during isoflurane anesthesia is approximately 1 degree C less in elderly than younger patients. However, the extent to which other cold defenses are impaired in the elderly remains unclear, especially in those older than 80 yr. Operations suitable for spinal anesthesia provided an opportunity to quantify shivering thresholds in patients of varying ages. Accordingly, the hypothesis that the shivering threshold is reduced as a function of age during spinal anesthesia was tested. METHODS: Twenty-eight ASA Physical Status 1-3 patients undergoing lower extremity orthopedic procedures were studied. Spinal anesthesia was induced without preanesthetic medication, using bupivacaine sufficient to produce a dermatomal level near T9. Electrocardiogram signals were recorded at 10-min intervals. Subsequently, an observer masked to patient age and core temperature identified the onset of sustained electromyographic artifact consistent with shivering. The tympanic membrane temperature triggering shivering identified the threshold. RESULTS: Three patients did not shiver at minimum core temperatures exceeding 36.2 degrees C. Fifteen patients aged < 80 yr (58 +/- 10 yr) shivered at 36.1 +/- 0.6 degrees C; in contrast, ten patients aged > or = 80 yr (89 +/- 7 yr) shivered at a significantly lower mean temperature, 35.2 +/- 0.7 degrees C (P = 0.002). The shivering thresholds in seven of the ten patients older than 80 yr was less than 35.5 degrees C, whereas the threshold equaled or exceeded this value in all younger patients (P = 0.0002). CONCLUSIONS: Age-dependent inhibition of autonomic thermoregulatory control in the elderly might be expected to result in hypothermia. That it usually does not suggests that behavioral regulation (e.g., increasing ambient temperature, dressing warmly) compensates for impaired autonomic control. Elderly patients undergoing spinal anesthesia, however, may be especially at risk of hypothermia because low core temperatures may not trigger protective autonomic responses. Furthermore, hypothermia in the elderly given regional anesthesia may not be perceived by the patient (who typically feels less cold after induction of the block), or by the anesthesiologist (who does not observe shivering). Consequently, temperature monitoring and management usually is indicated in these patients.

Adult↗

PubMed1995

Desflurane slightly increases the sweating threshold but produces marked, nonlinear decreases in the vasoconstriction and shivering thresholds.

BACKGROUND: Shivering is rare during general anesthesia. This observation suggests that anesthetics profoundly impair shivering. However, the effects of surgical doses of volatile anesthetics on control of shivering have yet to be evaluated. Furthermore, the effects of desflurane on sweating and thermoregulatory vasoconstriction remain unknown. Accordingly, the authors determined the concentration-dependent effects of desflurane on sweating, vasoconstriction, and shivering. METHODS: Nine volunteers each were studied on three randomly ordered days: (1) control (no anesthesia); (2) a target end-tidal desflurane concentration of 0.5 minimum alveolar concentration (MAC; 3.5%); and (3) a target concentration of 0.8 MAC (5.6%). Each day, volunteers were warmed until sweating was induced and subsequently cooled until peripheral vasoconstriction and shivering was observed. Changes in skin temperature were arithmetically compensated using the established linear cutaneous contributions to control of each response. From the calculated thresholds (core temperatures triggering responses at a designated skin temperature of 34 degrees C), the concentration-response relationship was determined. RESULTS: Desflurane significantly and linearly increased the sweating threshold from 37.1 +/- 0.3 degrees C on the control day (mean +/- SD), to 37.6 +/- 0.4 degrees C at 0.5 MAC, and to 38.1 +/- 0.3 degrees C at 0.8 MAC. Desflurane significantly, but nonlinearly, reduced the vasoconstriction and shivering thresholds. The sweating-to-vasoconstriction (interthreshold) range thus increased from 0.5 +/- 0.3 degrees C to 2.3 +/- 0.7 degrees C at 0.5 MAC and further to 4.6 +/- 2.0 degrees C at 0.8 MAC. The vasoconstriction-to-shivering range (difference between the respective thresholds) remained between 1.1 and 1.5 degrees C on the three study days. CONCLUSIONS: The observed linear increase in the sweating threshold was similar in pattern and magnitude to that produced by most general anesthetics. The approximately 3 degrees C reduction in the vasoconstriction threshold by 0.8 MAC desflurane was similar to that observed previously during isoflurane and propofol anesthesia. However, the threshold was reduced less than expected at 0.5 MAC, suggesting that the dose-response relationship for vasoconstriction is nonlinear. Shivering was induced without difficulty in this study although the response is rare in surgical patients. It is likely that shivering during general anesthesia is rare because thermoregulatory vasoconstriction usually prevents body temperature from decreasing the required additional 1-1.5 degrees C.

Adult↗

PubMed1995

Desflurane reduces the gain of thermoregulatory arteriovenous shunt vasoconstriction in humans.

BACKGROUND: Thermoregulatory responses, such as arteriovenous shunt vasoconstriction, provide substantial protection against core hypothermia. A response can be characterized by its threshold (core temperature triggering response), gain (rate at which response intensity increases, once triggered), and maximum response intensity. Reduced gain decreases the efficacy of a thermoregulatory response at a given threshold because response intensity will increase more slowly than usual. The effects of general anesthesia on the gain of arteriovenous shunt vasoconstriction have not been reported. Accordingly, we tested the hypothesis that desflurane decreases the gain of centrally mediated vasoconstriction. METHODS: We studied seven healthy male volunteers. Each was studied twice: (1) desflurane (end-tidal concentration 0.4 minimum alveolar concentration); and (2) control (no anesthesia). Mean skin and fingertip temperatures were controlled at 35.5 degrees C throughout the study. Core temperature was reduced at a rate of 1.5 degrees C/h by central venous infusion of cold fluid. Fingertip arteriovenous shunt flow was measured using venous occlusion volume plethysmography at 1-min intervals. Flow was also evaluated using the perfusion index and laser Doppler flowmetry. Vasoconstriction thresholds were calculated as the core temperatures triggering fingertip flows of 1.0 ml/min (beginning of vasoconstriction) and 0.25 ml/min (intense vasoconstriction). The gain of vasoconstriction was considered to be the slope of the fingertip flow versus core temperature regression within the linear range from 1.0 ml/min to 0.15 ml/min. The minimum observed flow was considered maximum vasoconstriction intensity. Data are presented as means +/- SD; P < 0.01 was considered statistically significant. RESULTS: The vasoconstriction threshold (when defined using a flow of 1.0 ml/min) was reduced from 36.8 +/- 0.3 degrees C to 35.6 +/- 0.3 degrees C by desflurane anesthesia (P < 0.01). Desflurane reduced the gain of vasoconstriction by a factor of three, from 2.4 to 0.8 ml.min-1.degrees C-1 (P < 0.01). Gains, as determined by the perfusion index and laser Doppler flowmetry, were likewise reduced (P < 0.01). The threshold on the control day was only 0.2 +/- 0.1 degrees C less when significant vasoconstriction was defined as a flow of 0.25 ml/min rather than 1.0 ml/min. Because gain was reduced, however, the threshold during desflurane administration was 0.8 +/- 0.2 degrees C less when significant vasoconstriction was defined by a flow of 0.25 ml/min. Minimum flows were comparable and near zero with and without anesthesia. CONCLUSIONS: The threshold reduction (1.2 degrees C/0.4 minimum alveolar concentration) was similar to that observed previously during isoflurane anesthesia. Similarly, it is established already that maximum vasoconstriction intensity is comparable with and without isoflurane anesthesia. However, the data also indicate that even relatively low desflurane concentrations markedly reduce the gain of vasoconstriction. It is likely that reduced gain (i.e., slow onset of vasoconstriction) contributes to core hypothermia in some surgical patients.

Adult↗

PubMed1995

Deliberate mild hypothermia.

Core body temperature is normally rigidly regulated by effective thermoregulatory responses that are triggered by small deviations in core and skin temperature. All general anesthetics so far tested markedly impair thermoregulatory control, increasing the range of temperatures not triggering protective responses by approximately 20-fold. Inhibition of thermoregulatory control--and reemergence of protective responses--are major factors influencing intraoperative temperature. Mild hypothermia provides dramatic protection against cerebral ischemia and therefore is frequently indicated during neurosurgery. Hypothermia to core temperatures near 34 degrees C can usually be instituted passively so long as thermoregulatory vasoconstriction is inhibited by sufficient anesthesia or neurosurgery per se. When core temperature must be rapidly reduced, or reduced to values approaching 32 degrees C, active cooling will usually be needed. Forced air appears to be the most effective clinically practical cooling method. Mild hypothermia is also associated with serious complications including myocardial ischemia, impaired resistance to surgical wound infections, coagulopathies, and postoperative shivering. Consequently, patients deliberately made hypothermic during neurosurgery should subsequently be actively rewarmed.

Anesthesia, General↗