Redistribution Of Body Heat Research Articles

Tissue Heat Content and Distribution During and After Cardiopulmonary Bypass at 17[degree sign

We measured afterdrop and peripheral tissue temperature distribution in eight patients cooled to approximately 17 degrees C during cardiopulmonary bypass and subsequently rewarmed to 36.5 degrees C. A nasopharyngeal probe evaluated trunk and head temperature and heat content. Peripheral tissue temperature (arm and leg temperature) and heat content were estimated using fourth-order regressions and integration over volume from 30 tissue and skin temperatures. Peripheral tissue temperature decreased to 19.7+/-0.9 degrees C during bypass and subsequently increased to 34.3+/-0.7 degrees C during 104+/-18 min of rewarming. The core-to-peripheral tissue temperature gradient was -5.9+/-0.9 degrees C at the end of cooling and 4.7+/-1.5 degrees C at the end of rewarming. The core-temperature afterdrop was 2.2+/-0.4 degrees C and lasted 89+/-15 min. It was associated with 1.1+/-0.7 degrees C peripheral warming. At the end of cooling, temperatures at the center of the upper and lower thigh were (respectively) 8.0+/-5.2 degrees C and 7.3+/-4.2 degrees C cooler than skin temperature. On completion of rewarming, tissue at the center of the upper and lower thigh were (respectively) 7.0+/-2.2 degrees C and 6.4+/-2.3 degrees C warmer than the skin. When estimated systemic heat loss was included in the calculation, redistribution accounted for 73% of the afterdrop, which is similar to the contribution observed previously in nonsurgical volunteers. Temperature afterdrop after bypass at 17 degrees C was 2.2+/-0.4 degrees C, with approximately 73% of the decrease in core temperature resulting from core-to-peripheral redistribution of body heat. Cooling and rewarming were associated with large radial tissue temperature gradients in the thigh.

Less Core Hypothermia when Anesthesia Is Induced with Inhaled Sevoflurane Than with Intravenous Propofol

Hypothermia after the induction of anesthesia results initially from core-to-peripheral redistribution of body heat. Sevoflurane and propofol both inhibit central thermoregulatory control, thus causing vasodilation. Propofol differs from sevoflurane in producing substantial peripheral vasodilation. This vasodilation is likely to facilitate core-to-peripheral redistribution of heat. Once heat is dissipated from the core, it cannot be recovered. We therefore tested the hypothesis that the induction of anesthesia with IV propofol causes more core hypothermia than induction with inhaled sevoflurane. We studied patients undergoing minor oral surgery randomly assigned to anesthetic induction with either 2.5 mg/kg propofol (n = 10) or inhalation of 5% sevoflurane (n = 10). Anesthesia in both groups was subsequently maintained with sevoflurane and 60% nitrous oxide in oxygen. Calf minus toe skin temperature gradients <0[degree sign]C were considered indicative of significant vasodilation. Ambient temperature and end-tidal concentrations of maintenance sevoflurane were comparable in each group. Patients in both groups were vasodilated throughout most of the surgery. Nonetheless, core temperatures in patients who received propofol were significantly lower than those in patients who received inhaled sevoflurane. These data support our hypothesis that even a brief period of vasodilation causes substantial redistribution hypothermia that persists throughout surgery. Implications: Core temperatures in patients who received IV propofol were consistently lower than those in patients who received inhaled sevoflurane, although anesthesia was subsequently maintained with sevoflurane in nitrous oxide in both groups. This suggests that even a brief period of propofol-induced vasodilation during anesthetic induction causes substantial redistribution hypothermia that persists throughout surgery. (Anesth Analg 1999;88:921-4)

Changes in body temperature following deflation of limb pneumatic tourniquet

Study Objectives: To investigate changes in both core and peripheral skin-surface temperatures during and after application of a unilateral leg pneumatic tourniquet in adult patients. Design: Prospective, observational clinical study. Setting: University hospital. Patients: 21 ASA physical status I and II adult patients scheduled for elective leg orthopedic surgery with lumbar epidural anesthesia. Interventions: Rectal and fingertip skin-surface temperatures were recorded every minute after steady-state lumbar epidural anesthesia was established. Measurements and Main Results: Significant ( p < 0.05) increases in both rectal and fingertip temperatures were observed during tourniquet application for 91 ± 6 minutes from 36.5 ± 0.14 °C to 37.0 ± 0.17 °C and from 32.6 ± 0.79 °C to 35.5 ± 0.44 °C, respectively. In contrast, both rectal and fingertip temperatures progressively decreased following tourniquet release; significant ( p < 0.05) decreases in the rectal and fingertip temperatures were observed 6 and 5 minutes after tourniquet release, respectively. Decreases (≈maximum) in the rectal and fingertip temperatures 15 minutes after tourniquet release were 0.25 ± 0.05 °C and 1.26 ± 0.26 °C, respectively. In each case, changes in fingertip temperature were approximately six times greater than those in the rectal temperature. Conclusions: Limb tourniquets appear to cause thermal perturbations during epidural anesthesia. The progressive increases in core temperature during tourniquet application presumably resulted from constraint of metabolic heat to the core thermal compartment, and the greater increases in the skin-surface temperature during tourniquet application appear to represent vasodilation in response to the core hyperthermia. On the other hand, redistribution of body heat and the efflux of hypothermic venous blood from the tourniqueted area into systemic circulation following tourniquet deflation probably decreased the core temperature, which might switch off the thermoregulatory vasodilation, leading to the decreases in skin-surface temperature. Recognition of these thermal perturbations are useful in diagnosing intraoperative thermal perturbations.

A Study in the Comparison of Body Temperature Change between General Anesthesia and Epidural Anesthesia

Background : Core hypothermia after induction of anesthesia results from an core-to-peripheral redistribution of body heat and a loss of body heat to environment. The purpose of this study is finding body temperatures during operation by either general of epidural anesthesia and evaluates content of total body heat. Methods : We measured tympanic membrane temperature, 4 point skin temperature (mid calf, mid thigh, upper extremity, nipple). And we calculate mean skin temperature, mean body temperature, total body heat content changes based on tympanic membrane temperature and 4 point skin temperature. Results : Tympanic membrane temperature of the first group decreased significantly after 10 minutes of induction(P＜0.005), the second group decreased after 45 minutes of induction. Although upper extremity temperature has continuously increased as time passed, there was no significant difference in both group. Lower extremity temperature has significantly increased after 30 minutes of induction in the first group, and the second group has significantly increased after 10 minutes of induction(P＜0.05). Mean skin temperature hasdecreasd temperaturily in both group after 10 minutes of induction and increased as time passed. Mean body temperature of the first group has significantly decreased after 10 minutes of induction(P＜0.05) and second group has no significant changes. Total body heat content has continuously decreased after induction with no significance. Conclusions : General anesthesia reveals more significant decrease than epidural anesthesia. Both groups show significant decrease of body temperature after induction. We think that we need to close attention to temperature changes after induction for preventing possible side effects due to core hypothermia. (Korean J Anesthesiol 1997; 33: 477∼484)

Skeletal Muscle Is Responsible for Heat Production in Porcine Malignant Hyperthermia

In Response: It is well established that the primary defect associated with porcine malignant hyperthermia resides within skeletal muscle. It is further established that, during fulminant episodes of malignant hyperthermia, skeletal muscle is the primary source of heat production [1]. Our data and Discussion do not dispute this notion. Our text stated that "the increase in core temperature associated with the malignant hyperthermia episodes in these animals resulted from: 1) increased organ metabolism; 2) muscle contractures; and 3) decreased ability to dissipate heat via peripheral tissues" [2]. It was novel to find that "during the initial stages of an acute episode of malignant hyperthermia, compared to pulmonary artery temperature, temperatures within the liver and kidney were significantly greater" than "those in several different skeletal muscles." During the initial period after halothane administration, temperatures within the very proximal longissimus dorsi muscle and those within other muscles considered to be important for developing limb rigidity had surprisingly lower interior temperatures than those of the investigated internal organs. The Second Law of Thermodynamics thus specifies that, as blood leaves the heart and flows into these skeletal muscles, heat will be transferred from the blood to the muscles. Interestingly, central organ temperature increased even before any clinical signs of malignant hyperthermia could be detected. This suggests that these organs responded to systemic needs by increasing metabolic rate. This can be explained either by these organs responding to a subclinical change in skeletal muscle metabolism or by an abnormal response to anesthetic administration per se. The latter possibility is supported by evidence that Ca2+ regulation in nonmuscle cells including hepatocytes may be abnormally altered by triggering anesthetics [3,4]. Induction of general anesthesia causes a core-to-peripheral redistribution of body heat, which increases muscle temperature [5]. The fact that core temperature increased faster than muscle temperatures is thus especially impressive. The ability of halothane to trigger muscle contractures is temperature dependent such that even a slight reduction to 35 degrees C significantly decreases responsiveness [6,7]. Increases in metabolic rate and heat production within nonmuscle tissues during a malignant hyperthermia crisis may thus indirectly potentiate the dysregulation of Ca2+ within skeletal muscle by increasing overall body temperature. The aim of our report was to explore the integrative physiology of acute malignant hyperthermia in susceptible swine. We hope that our data encourage clinicians to consider not just treating the primary defect in such an episode, but consider the role of other organ systems in such an event. Paul A. Iaizzo, PhD Departments of Anesthesiology and Physiology University of Minnesota Minneapolis, MN 55455 Daniel I. Sessler, MD Department of Anesthesia University of California, San Francisco San Francisco, CA 94143-0648 and Department of Anesthesia and Intensive Care University of Vienna Vienna, Austria

Heat Flow and Distribution during Induction of General Anesthesia

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. 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. 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. 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.

Optimal Duration and Temperature of Prewarming

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. 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. 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." 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.

Morphometric influences on intraoperative core temperature changes.

Intraoperative core hypothermia develops in three characteristic phases: 1) core-to-peripheral redistribution of body heat that is most prominent during the first hour after induction of anesthesia; 2) subsequent slow linear decrease in core temperature resulting largely from heat loss exceeding metabolic heat production; and 3) core temperature plateau resulting when thermoregulatory vasoconstriction decreases cutaneous heat loss and constrains metabolic heat to the core thermal compartment. Accordingly, we tested the hypotheses that: 1) core cooling does not depend on body fat (BF) or the ratio of weight-to-surface area (Wt/SA) during the initial redistribution phase; 2) the core cooling phase; 2) the core cooling rate is a function of the Wt/SA ratio during the second phase; and 3) the rate of core cooling during the plateau phase (after vasoconstriction) will be determined by the percentage of BF. In 40 patients undergoing elective colon surgery, the amount of redistribution hypothermia was inversely proportional to the percentage of BF (delta TC = 0.034.BF-2.2, r2 = 0.63) and the Wt/SA ratio (delta TC = 0.052.Wt/SA-3.35, r2 = 0.66). The core cooled linearly during the second phase, and the cooling rate was inversely proportional to the Wt/SA ratio (rate = 0.035.(Wt/SA)-2.2, r2 = 0.29). Thermoregulatory vasoconstriction was effective in virtually all patients independent of their morphology, and produced a four-fold reduction in the core cooling rate. These results indicate that patient morphometric characteristics substantially influence intraoperative core temperature changes, and that the effect depends on the hypothermia phase.

Perianesthetic thermoregulation and heat balance in humans.

General anesthesia markedly impairs normal control of body temperature, reducing the threshold (triggering core temperature) for thermoregulatory vasoconstriction from approximately 37 to approximately 34.5 degrees C. Sweating and active vasodilation thresholds similarly are increased, widening the range of temperatures not triggering regulatory compensations from approximately 0.2 to approximately 4 degrees C. However, once initiated, the gains (slopes of response intensity vs. core temperature curves) and maximum intensities of thermoregulatory responses are nearly normal. Intraoperative core temperature initially decreases rapidly because anesthetic-induced inhibition of tonic thermoregulatory vasoconstriction causes a core-to-peripheral redistribution of body heat. The subsequent slower, linear decrease in body temperature results from heat loss exceeding metabolic heat production. And finally, after 3-4 h of anesthesia, core temperature stabilizes at an abnormally low value. In patients experiencing minimal heat loss, and therefore not becoming sufficiently hypothermic to trigger vasoconstriction, this plateau can be passive steady state in which heat loss equals production. Conversely, patients becoming sufficiently hypothermic will trigger thermoregulatory vasoconstriction that both decreases cutaneous heat loss and sequesters some metabolic heat in the core. Epidural and spinal anesthesia also cause core hypothermia by inhibiting tonic thermoregulatory vasoconstriction, producing an internal redistribution of heat from the warm core to cooler peripheral tissues. Core hypothermia provokes thermoregulatory responses including vasoconstriction (above the block level) and shivering. Nonetheless, many patients feel warmer after induction of regional anesthesia, apparently because perceived skin temperature is elevated. The following review will focus on anesthetic-induced impairment of normal thermoregulatory control and the resulting alterations in heat balance.

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.

Redistribution of Body Heat during Anaesthesia

Epidural anaesthesia and high dose fentanyl (50 micrograms/kg) when used to supplement nitrous oxide and oxygen anaesthesia for a standard lower abdominal operation were associated with a mean fall in deep body temperature, as measured in the external auditory meatus, of 0.46 degrees C and 0.6 degrees C/hr respectively. This is significantly different from the mean values of 0.14 degrees C and 0.2 degrees C/hr which were recorded when moderate dose fentanyl (10 micrograms/kg) or 0.5% halothane were used to supplement anaesthesia. When mean skin temperature is combined with the core temperature to provide an estimate for total body heat, there is no difference between the groups. Redistribution of body heat occurs and this may be related to reduced adrenergic stimulation and altered regional blood flow. Where the facilities and environments are inadequate for the maintenance of normothermia, care should be taken in the choice of anaesthetic technique. In the recovery period mean body heat gain showed a wide scatter of results but those patients receiving epidural anaesthesia were slow to rewarm despite a high incidence of shivering in this group. The implications of this are discussed.

Mechanisms of cold acclimatization in the cat.

Thermoregulatory control in cats living at 25 C was compared to the regulation of body temperature in the same species after continuous whole-body cold exposure to an ambient temperature of 5 C for periods exceeding 2 months. Rectal and extremity temperatures and metabolic rates for the two groups were examined during acute (2-hr) air exposures to 23, 10, and 0 C. Cold acclimatizing mechanisms in the cat involve a redistribution of body heat at 23 C, obligating increased heat flux at the expense of elevated metabolism, an improved peripheral vascular defense (increase functional tissue insulation) during moderate cold exposure (10 C), and a greater ability to increase heat production accompanied by more labile peripheral vasomotion, during more severe cold air exposure (0 C). Although resting at 23 C, cold-acclimatized cats had lower rectal temperatures and were able to maintain higher internal body temperatures during both levels of cold stress compared to noncold-acclimatized animals. Submitted on November 1, 1962