Richard Christensen

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.

Meperidine decreases the shivering threshold twice as much as the vasoconstriction threshold

Background: Meperidine administration is a more effective treatment for shivering than equianalgesic doses of other opioids. However, it remains unknown whether meperidine also profoundly impairs other thermoregulatory responses, such as sweating or vasoconstriction. Proportional inhibition of vasoconstriction and shivering suggests that the drug acts much like alfentanil and anesthetics but possesses greater thermoregulatory than analgesic potency. In contrast, disproportionate inhibition would imply a special antishivering mechanism. Accordingly, the authors tested the hypothesis that meperidine administration produces a far greater concentration‐dependent reduction in the shivering than vasoconstriction threshold. Methods: Nine volunteers were each studied on three days: 1) control (no opioid); 2) a target total plasma meperidine concentration of 0.6 micro gram/ml (40 mg/h); and 3) a target concentration of 1.8 micro gram/ml (120 mg/h). Each day, skin and core temperatures were increased to provoke sweating and then subsequently reduced to elicit vasoconstriction and shivering. Core‐temperature thresholds (at a designated skin temperature of 34 degrees Celsius) were computed using established linear cutaneous contributions to control sweating (10%) and vasoconstriction and shivering (20%). The dose‐dependent effects of unbound meperidine on thermoregulatory response thresholds was then determined using linear regression. Results are presented as means +/‐ SDs. Results: The unbound meperidine fraction was [nearly equal] 35%. Meperidine administration slightly increased the sweating threshold (0.5 +/‐ 0.8 degrees Celsius [center dot] micro gram sup ‐1 [center dot] ml; r2 = 0.51 +/‐ 0.37) and markedly decreased the vasoconstriction threshold (‐3.3 +/‐ 1.5 degrees Celsius [center dot] micro gram sup ‐1 [center dot] ml; r sup 2 = 0.92 +/‐ 0.08). However, meperidine reduced the shivering threshold nearly twice as much as the vasoconstriction threshold (‐6.1 +/‐ 3.0 degrees Celsius [center dot] micro gram sup ‐1 [center dot] ml; r2 = 0.97 +/‐ 0.05; P = 0.001). Conclusions: The special antishivering efficacy of meperidine results at least in part from an uncharacteristically large reduction in the shivering threshold rather than from exaggerated generalized thermoregulatory inhibition. This pattern of thermoregulatory impairment differs from that produced by alfentanil, clonidine, propofol, and the volatile anesthetics, all which reduce the vasoconstriction and shivering thresholds comparably.

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.

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 micro gram/mL (corresponding to administration of approximate equals 40 mg over approximate equals 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 approximate equals 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. Thus, plasma concentrations of midazolam far exceeding those used routinely produce relatively little impairment of thermoregulatory control. (Anesth Analg 1995;81:393-8)

Tissue Heat Content and Distribution during and after Cardiopulmonary Bypass at 31 [degree sign]C and 27 [degree sign]C

Background Afterdrop following cardiopulmonary bypass results from redistribution of body heat to inadequately warmed peripheral tissues. However, the distribution of heat between the thermal compartments and the extent to which core‐to‐peripheral redistribution contributes to post‐bypass hypothermia remains unknown. Methods Patients were cooled during cardiopulmonary bypass to nasopharyngeal temperatures near 31 [degree sign]C (n = 8) or 27 [degree sign]C (n = 8) and subsequently rewarmed by the bypass heat exchanger to [almost equal to] 37.5 [degree sign]C. A nasopharyngeal probe evaluated core (trunk and head) temperature and heat content. Peripheral compartment (arm and leg) temperature and heat content were estimated using fourth‐order regressions and integration over volume from 19 intramuscular needle thermocouples, 10 skin temperatures, and “deep” foot temperature. Results In the 31 [degree sign]C group, the average peripheral tissue temperature decreased to 31.9 +/‐ 1.4 [degree sign]C (means +/‐ SD) and subsequently increased to 34 +/‐ 1.4 [degree sign]C at the end of bypass. The core‐to‐peripheral tissue temperature gradient was 3.5 +/‐ 1.8 [degree sign]C at the end of rewarming, and the afterdrop was 1.5 +/‐ 0.4 [degree sign]C. Total body heat content decreased 231 +/‐ 93 kcal. During pump rewarming, the peripheral heat content increased to 7 +/‐ 27 kcal below precooling values, whereas the core heat content increased to 94 +/‐ 33 kcal above precooling values. Body heat content at the end of rewarming was thus 87 +/‐ 42 kcal more than at the onset of cooling. In the 27 [degree sign]C group, the average peripheral tissue temperature decreased to a minimum of 29.8 +/‐ 1.7 [degree sign]C and subsequently increased to 32.8 +/‐ 2.1 [degree sign]C at the end of bypass. The core‐to‐peripheral tissue temperature gradient was 4.6 +/‐ 1.9 [degree sign]C at the end of rewarming, and the afterdrop was 2.3 +/‐ 0.9 [degree sign]C. Total body heat content decreased 419 +/‐ 49 kcal. During pump rewarming, core heat content increased to 66 +/‐ 23 kcal above precooling values, whereas peripheral heat content remained 70 +/‐ 42 kcal below precooling values. Body heat content at the end of rewarming was thus 4 +/‐ 52 kcal less than at the onset of cooling. Conclusions Peripheral tissues failed to fully rewarm by the end of bypass in the patients in the 27 [degree sign]C group, and the afterdrop was 2.3 +/‐ 0.9 [degree sign]C. Peripheral tissues rewarmed better in the patients in the 31 [degree sign]C group, and the afterdrop was only 1.5 +/‐ 0.4 [degree sign]C.

Postanesthetic vasoconstriction slows peripheral-to-core transfer of cutaneous heat, thereby isolating the core thermal compartment

Forced-air warming during anesthesia increases core temperature comparably with and without thermoregulatory vasoconstriction. In contrast, postoperative forced-air warming may be no more effective than passive insulation. Nonthermoregulatory anesthesia-induced vasodilation may thus influence heat transfer. We compared postanesthetic core rewarming rates in volunteers given cotton blankets or forced air. Additionally, we compared increases in peripheral and core heat contents in the postanesthetic period with data previously acquired during anesthesia to determine how much vasomotion alters intercompartmental heat transfer. Six men were anesthetized and cooled passively until their core temperatures reached 34 [degree sign] C. Anesthesia was then discontinued, and shivering was prevented by giving meperidine. On one day, the volunteers were covered with warmed blankets for 2 h; on the other, volunteers were warmed with forced air. Peripheral tissue heat contents were determined from intramuscular and skin thermocouples. Predicted changes in core temperature were calculated assuming that increases in body heat content were evenly distributed. Predicted changes were thus those that would be expected if vasomotor activity did not impair peripheral-to-core transfer of applied heat. These results were compared with those obtained previously in a similar study of anesthetized volunteers. Body heat content increased 159 +/- 35 kcal (mean +/- SD) more during forced-air than during blanket warming (P < 0.001). Both peripheral and core temperatures increased significantly faster during active warming: 3.3 +/- 0.7[degree sign]C and 1.1 +/- 0.4[degree sign]C, respectively. Nonetheless, predicted core temperature increase during forced-air warming exceeded the actual temperature increase by 0.8 +/- 0.3[degree sign]C (P < 0.001). Vasoconstriction thus isolated core tissues from heat applied to the periphery, with the result that core heat content increased 32 +/- 12 kcal less than expected after 2 h of forced-air warming (P < 0.001). In contrast, predicted and actual core temperatures differed only slightly in the anesthetized volunteers previously studied. In contrast to four previous studies, our results indicate that forced-air warming increases core temperature faster than warm blankets. Postanesthetic vasoconstriction nonetheless impeded peripheral-to-core heat transfer, with the result that core temperatures in the two groups differed less than might be expected based on systemic heat balance estimates. Implications: Comparing intercompartmental heat flow in our previous and current studies suggests that anesthetic-induced vasodilation influences intercompartmental heat transfer and distribution of body heat more than thermoregulatory shunt vasomotion. (Anesth Analg 1997;85:899-906)

Thermoregulatory vasoconstriction does not impede core warming during cutaneous heating

Background Although forced‐air warming rapidly increases intraoperative core temperatures, it is reportedly ineffective postoperatively. A major difference between these two periods is that arteriovenous shunts are usually dilated during surgery, whereas vasoconstriction is uniform in hypothermic postoperative patients. Vasoconstriction may decrease efficacy of warming because its major physiologic purposes are to reduce cutaneous heat transfer and restrict heat transfer between the two thermal compartments. Accordingly, we tested the hypothesis that thermoregulatory vasoconstriction decreases cutaneous transfer of applied heat and restricts peripheral‐to‐core flow of heat, thereby delaying and reducing the increase in core temperature. Methods Eight healthy male volunteers anesthetized with propofol and isoflurane were studied. Volunteers were allowed to cool passively until core temperature reached 33 degrees C. On one randomly assigned day, the isoflurane concentration was reduced, to provoke thermoregulatory arteriovenous shunt vasoconstriction; on the other study day, a sufficient amount of isoflurane was administered to prevent vasoconstriction. On each day, forced‐air warming was then applied for 2 h. Peripheral (arm and leg) tissue heat contents were determined from 19 intramuscular needle thermocouples, 10 skin temperatures, and “deep” foot temperature. Core (trunk and head) heat content was determined from core temperature, assuming a uniform compartmental distribution. Time‐dependent changes in peripheral and core tissue heat contents were evaluated using linear regression. Differences between the vasoconstriction and vasodilation study days, and between the peripheral and core compartments, were evaluated using two‐tailed, paired t tests. Data are presented as means +/‐SD; P < 0.01 was considered statistically significant. Results Cutaneous heat transfer was similar during vasoconstriction and vasodilation. Forced‐air warming increased peripheral tissue heat content comparably when the volunteers were vasodilated and vasoconstricted: 48+/‐7 versus 53+/‐10 kcal/h. Core compartment tissue heat content increased similarly when the volunteers were vasodilated and vasoconstricted: 51+/‐8 versus 44+/‐ 11 kcal/h. Combining the two study days, the increase in peripheral and core heat contents did not differ significantly: 51+/‐8 versus 48 +/‐10 kcal/h, respectively. Core temperature increased at essentially the same rate when the volunteers remained vasodilated (1.3 degrees C/h) as when they were vasoconstricted (1.2 degrees Celsius/h). Conclusions The authors failed to confirm their hypothesis that thermoregulatory vasoconstriction decreases cutaneous transfer of applied heat and restricts peripheral‐to‐core flow of heat in anesthetized subjects. The reported difference between intraoperative and postoperative rewarming efficacy may result from nonthermoregulatory anesthetic‐induced vasodilation.

The effect of opioids on thermoregulatory responses in humans and the special antishivering action of meperidine.

In summary, both mu-receptor and combined mu/kappa-receptor opioids impair thermoregulatory control. Alfentanil, a pure mu-receptor agonist slightly increased the thresholds for sweating and markedly decreased the thresholds for vasoconstriction and shivering. However, the vasoconstriction-to-shivering range remained normal during alfentanil administration as it does during general anesthesia. Meperidine, a combined mu- and kappa-receptor agonist, also slightly increased the threshold for sweating and reduced the thresholds for vasoconstriction. However, meperidine reduced the shivering threshold twice as much as the vasoconstriction threshold, thus significantly increasing the vasoconstriction-to-shivering range. Furthermore, shivering during meperidine administration, once triggered, was of low intensity suggesting that the drug also decreased the gain of shivering. The special antishivering action of meperidine appears to result, at least in part, from its kappa-receptor activity.

Thermoregulatory vasoconstriction does not impede core warming during cutaneous heating.

Recent studies evaluating perioperative cutaneous-to-core heat transfer indicate that: Thermoregulatory vasoconstriction prevents further core cooling in anesthetized subjects during mild cooling. Thermoregulatory vasoconstriction only slightly decreases core cooling rates in anesthetized subjects during vigorous cooling. Thermoregulatory vasoconstriction does not impair vigorous core rewarming during anesthesia. Vigorous postanesthetic cutaneous warming increases core temperature much faster than passive insulation. Under conditions of mild thermal stress, thermoregulatory vasoconstriction is thus able to protect core temperature by reducing cutaneous heat transfer and functionally isolating the peripheral and core thermal compartment. Consequently, anesthetic-induced alterations in vasomotor tone is one of the major factors influencing core temperature in patients who are not actively cooled or warmed. In contrast, thermoregulatory tone is insufficient to prevent core temperature perturbations in patients undergoing vigorous cutaneous cooling or warming.