Induction of anesthesia with ketamine reduces the magnitude of redistribution hypothermia

Hypothermia after induction of general anesthesia results largely from core-to-peripheral redistribution of body heat. Both central inhibition of tonic thermoregulatory vasoconstriction in arteriovenous shunts and anesthetic-induced arteriolar and venous dilation contribute to this redistribution. Ketamine, unique among anesthetics, increases peripheral arteriolar resistance; in contrast, propofol causes profound venodilation that other anesthetics do not. We therefore tested the hypothesis that induction of anesthesia with ketamine causes less core hypothermia than induction with propofol. Twenty patients undergoing elective surgery were randomly assigned to anesthetic induction with either 1.5 mg/kg ketamine (n = 10) or 2.5 mg/kg propofol (n = 10). Anesthesia in both groups was subsequently maintained with sevoflurane and 60% nitrous oxide in oxygen. Forearm minus finger, skin-temperature gradients <0 degrees C were considered indicative of significant arteriovenous shunt vasodilation. Ketamine did not cause vasodilation just after induction, whereas propofol rapidly induced vasodilation. Core temperatures in the patients given ketamine remained significantly greater than those in the patients induced with propofol. These data suggest that maintaining vasoconstriction during induction of anesthesia reduces the magnitude of redistribution hypothermia. IMPLICATIONS: Core hypothermia during the first hour of anesthesia was less after induction of anesthesia with ketamine than propofol. Maintaining arteriovenous shunt vasoconstriction during induction of anesthesia reduces the magnitude of redistribution hypothermia.     

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 i.v. 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 degrees 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 i.v. 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.     

Perioperative heat balance

Hypothermia during general anesthesia develops with a characteristic three-phase pattern. The initial rapid reduction in core temperature after induction of anesthesia results from an internal redistribution of body heat. Redistribution results because anesthetics inhibit the tonic vasoconstriction that normally maintains a large core-to-peripheral temperature gradient. Core temperature then decreases linearly at a rate determined by the difference between heat loss and production. However, when surgical patients become sufficiently hypothermic, they again trigger thermoregulatory vasoconstriction, which restricts core-to-peripheral flow of heat. Constraint of metabolic heat, in turn, maintains a core temperature plateau (despite continued systemic heat loss) and eventually reestablishes the normal core-to-peripheral temperature gradient. Together, these mechanisms indicate that alterations in the distribution of body heat contribute more to changes in core temperature than to systemic heat imbalance in most patients. Just as with general anesthesia, redistribution of body heat is the major initial cause of hypothermia in patients administered spinal or epidural anesthesia. However, redistribution during neuraxial anesthesia is typically restricted to the legs. Consequently, redistribution decreases core temperature about half as much during major conduction anesthesia. As during general anesthesia, core temperature subsequently decreases linearly at a rate determined by the inequality between heat loss and production. The major difference, however, is that the linear hypothermia phase is not discontinued by reemergence of thermoregulatory vasoconstriction because constriction in the legs is blocked peripherally. As a result, in patients undergoing large operations with neuraxial anesthesia, there is the potential of development of serious hypothermia. Hypothermic cardiopulmonary bypass is associated with enormous changes in body heat content. Furthermore, rapid cooling and rewarming produces large core-to-peripheral, longitudinal, and radial tissue temperature gradients. Inadequate rewarming of peripheral tissues typically produces a considerable core-to-peripheral gradient at the end of bypass. Subsequently, redistribution of heat from the core to the cooler arms and legs produces an afterdrop. Afterdrop magnitude can be reduced by prolonging rewarming, pharmacologic vasodilation, or peripheral warming. Postoperative return to normothermia occurs when brain anesthetic concentration decreases sufficiently to again trigger normal thermoregulatory defenses. However, residual anesthesia and opioids given for treatment of postoperative pain decreases the effectiveness of these responses. Consequently, return to normothermia often needs 2-5 h, depending on the degree of hypothermia and the age of the patient.     

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 Celsius sufficiently rapidly and nearly always will be required if the target temperature is 32 degrees Celsius. 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 Celsius. 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 Celsius identified the vasoconstriction threshold.

Results: In 6 of the 13 patients given isoflurane, vasoconstriction (skin-temperature gradient = 0 degree Celsius) occurred at a core temperature of 34.4 plus/minus 0.9 degree Celsius, 1.7 plus/minus 0.5 h after induction of anesthesia. Similarly, in 7 of the 13 patients given propofol, vasoconstriction occurred at a core temperature of 34.5 plus/minus 0.9 degree Celsius, 1.6 plus/minus 0.6 h after induction of anesthesia. In the remaining patients, vasodilation continued even at core temperatures of 32 degrees Celsius. 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 Celsius and 32 degrees Celsius than did those in whom vasodilation was maintained (P < 0.01).     

Thermal care in the perioperative period

Perioperative hypothermia is, even today, 15 years after the development of active warming devices, a common complication of anesthesia and surgery.The combination of anesthetic-induced thermoregulatory impairment and exposure to cold operating room environments makes most surgical patients hypothermic. Hypothermia results initially from a core-to-peripheral redistribution of body heat, and subsequently from heat loss exceeding heat production. Patients becoming sufficiently hypothermic during general anesthesia develop a core-temperature plateau when arterio-venous shunt tone is re-established.General anesthesia produces marked and dose-dependent inhibition of thermoregulatory control, typically increasing the sweating and vasodilation thresholds by approximately 1 °C and reducing the vasoconstriction and shivering thresholds by approximately 3 °C. As a result, the inter-threshold range increases roughly 20-fold, leaving patients poikilothermic over an approximately 4 °C range of core temperatures. Regional anesthesia also impairs thermoregulatory control, producing both peripheral and central inhibition.Even mild perioperative hypothermia, which can easily be prevented, is associated with adverse outcomes including morbid cardiac events, coagulopathy, surgical wound infections, and prolonged hospitalization. Consequently, body temperature should be measured in most surgical patients. Unless hypothermia is specifically indicated (e.g. for protection against ischemia), intraoperative core temperature should be maintained above 36 °C.     

The effect of sedation with propofol and fentanyl during epidural catheter insertion on intraoperative temperatures

General anesthesia inhibits thermoregulation by suppressing tonic vasoconstriction and facilitates a core-to-peripheral redistribution of body heat, which is the major cause of core hypothermia during the first hour of anesthesia. We randomly assigned 16 patients to two groups; 1) patients who received fentanyl (1 microgram.kg-1, i.v.) and propofol (1.5 mg.kg-1.h-1) during insertion of epidural catheters (P group), and 2) no drug (control) group (C group). We measured tympanic (Ttym) and skin temperatures at the time of admission to operating rooms, after dural catheter insertion, before induction of anesthesia, just after induction of anesthesia, and one hour after induction. After dural catheter insertion, forearm-finger tip skin temperature gradient of P group was significantly smaller than C group. One hour after induction of anesthesia, Ttym of P group was significantly higher than C group. We can conclude that a sedative dose of propofol and fentanyl before induction of general anesthesia inhibits redistribution hypothermia during general anesthesia.     

IM droperidol as premedication attenuates intraoperative hypothermia

PURPOSE: Perioperative hypothermia results largely from core-to-peripheral heat redistribution. Droperidol, which is often used for premedication, promotes vasodilation, and thus may affect redistribution of heat. Accordingly, we tested the hypothesis that preanesthetic droperidol would affect perioperative hypothermia. METHODS: Twenty-three ASA physical status I patients scheduled for arthroscopic ligament reconstruction were randomly assigned to two groups to receive no premedication or im droperidol 0.1 mg x kg(-1) 30 min before anesthesia. Anesthesia was induced and maintained with propofol and fentanyl. We monitored core (tympanic) and peripheral (palm) temperatures, and skin (fingertip) blood flow for two hours after the induction of anesthesia during surgery. RESULTS: Before the induction of anesthesia, patients given droperidol were more deeply sedated than those given no premedication. Core temperature, which was similar in both groups before induction, decreased significantly more in the control than in the droperidol patients (0.75 +/- 0.34 degrees C and 0.37 +/- 0.20 degrees C, respectively, at 75 min after induction; P <0.01). Preinduction peripheral temperature and skin blood flow were lower in the control group than in the droperidol group, but the two variables became similar in both groups after induction. CONCLUSION: The results of the present study confirm our hypothesis that premedication with droperidol affects perioperative hypothermia. Droperidol may prevent core-to-peripheral heat redistribution after the induction of anesthesia.     

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 [nearly equal] 22 degrees Celsius 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 plus/minus 0.3 degrees Celsius 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 plus/minus 0.3 degrees Celsius, 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 plus/minus 0.5 degrees Celsius 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 [nearly equal] 40 kcal during the first hour of anesthesia and remained elevated for the duration of the study.     

Thermoregulatory vasoconstriction during isoflurane anesthesia minimally decreases cutaneous heat loss.

The authors tested the extent to which thermoregulatory vasoconstriction decreases cutaneous heat loss during isoflurane anesthesia. Thermoregulatory vasoconstriction was provoked by central hypothermia in five nonsurgical volunteers given isoflurane anesthesia. Peripheral arteriovenous shunt flow was quantified using forearm-fingertip skin-surface temperature gradients and volume plethysmography. Capillary blood flow on the chest was evaluated using laser Doppler flowmetry. The central temperature triggering peripheral vasoconstriction (the thermoregulatory threshold) was 34.6 +/- 0.4 degrees C. Central body temperature decreased less than or equal to 0.2 degrees C in the period from 1 h preceding onset of significant vasoconstriction until 1.5 h afterward. Chest skin-surface blood flow decreased 21% during the period from 2 h before to 1 h after significant fingertip vasoconstriction. In contrast, fingertip blood flow decreased approximately 50-fold in the same period. The correlation between fingertip blood flow and skin-temperature gradient was excellent. Total heat loss decreased approximately 26% (25.3 +/- 3.9 W) in the period from 2 h before significant peripheral vasoconstriction to 1 h afterward. Loss from the arms and legs (upper arm, lower arm, thigh, and calf) decreased approximately 24% in the same period. Heat loss from the trunk and head decreased only 14%; in contrast, loss from the hands and feet decreased approximately 57%. There were no clinically important changes in blood pressure or heart rate during vasoconstriction, but oxyhemoglobin saturation (measured by pulse oximetry) increased slightly. These data suggest that thermoregulatory vasoconstriction only minimally decreases cutaneous heat loss.     

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" ([nearly equal] 40 degrees Celsius) or "high" ([nearly equal] 43 degrees Celsius). 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."     

Isoflurane-induced vasodilation minimally increases cutaneous heat loss

Central body temperature, which usually is well controlled, typically decreases more than 1 degree C during the 1st h of general anesthesia. This hypothermia has been attributed partially to an anesthetic-induced peripheral vasodilation, which increases cutaneous heat loss to the environment. Based on the specific heat of humans, heat loss would have to increase more than 70 W for 1 h (in a 70-kg person) to explain hypothermia after induction of general anesthesia. However, during epidural anesthesia, sympathetic blockade increases heat loss only slightly. Furthermore, thermoregulatory vasoconstriction in unanesthetized humans decreases heat loss to the environment only 15 W. Therefore, we tested the hypothesis that the hypothermia that follows induction of general anesthesia does not result from increased cutaneous heat loss. Heat loss and skin-surface and tympanic membrane temperatures, before and after induction of isoflurane anesthesia, were measured in five minimally clothed volunteers. Peripheral skin blood flow was evaluated with venous-occlusion volume plethysmography and skin-surface temperature gradients. Cutaneous heat losses in watts were summed from ten area-weighted thermal flux transducers. Tympanic membrane temperature, which was stable during the 30-min control period preceding induction, decreased 1.2 +/- 0.2 degrees C in the 50 min after induction. Isoflurane anesthesia decreased mean arterial blood pressure approximately 20%. Average skin-surface temperature increased over 15 min to 0.5 degree C above control. Heat loss from the trunk, head, arms, and legs decreased slightly, whereas loss from the hands and feet (10.5% of the body surface area) doubled (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of anaesthesia on thermoregulation

Hypothermia is a common and serious complication during anaesthesia and surgery. It mainly results from anaesthetic-induced inhibition of thermoregulatory control and exposure to cold operating room environment. Perioperative hypothermia develops in three distinct phases: (1) anaesthetic-induced vasodilation during induction of anaesthesia results in core-to-peripheral redistribution of body heat and decreases core temperature 1–1.5°C during the first hour of general anaesthesia; (2) subsequently core temperature decreases linearly as heat loss to the environment exceeds metabolic heat production; (3) after 3–5 h of anaesthesia, core temperature often stops decreasing. This core temperature plateau results from reactivation of thermoregulatory vasoconstriction which decreases cutaneous heat loss and constrains metabolic heat to the core thermal compartment. Perioperative hypothermia is associated with numerous complications such as myocardial ischaemia, increased risk of wound infection and coagulopathy. On the other hand temperatures only 1–3°C below normal provide substantial protection against cerebral ischaemia and hypoxaemia in numerous animal species. Consequently, most anaesthesiologists believe mild hypothermia is indicated during operations likely to cause cerebral ischaemia such as carotid endarterectomy and neurosurgery or cardiac procedures. Thermal perturbations, therefore, deserve the same risk/benefit analysis as other medical interventions. Fortunately, effective methods of cooling and warming surgical patients are now available.     

Influence of Thermoregulatory Vasomotion and Ambient Temperature Variation on the Accuracy of Core-temperature Estimates by Cutaneous Liquid-crystal Thermometers

Background: Recently, liquid crystal skin-surface thermometers have become popular for intraoperative temperature monitoring. Three situations during which cutaneous liquid-crystal thermometry may poorly estimate core temperature were monitored: (1) anesthetic induction with consequent core-to-peripheral redistribution of body heat, (2) thermoregulatory vasomotion associated with sweating (precapillary dilation) and shivering (minimal capillary flow), and (3) ambient temperature variation over the clinical range from 18-26 degrees Celsius.

Methods: The core-to-forehead and core-to-neck temperature difference was measured using liquid-crystal thermometers having an [nearly equal] 2 degrees Celsius offset. Differences exceeding 0.5 degrees Celsius (a 1 degree Celsius temperature range) were a priori deemed potentially clinically important. Seven volunteers participated in each protocol. First, core-to-peripheral redistribution of body heat was produced by inducing propofol/desflurane anesthesia; anesthesia was then maintained for 1 h with desflurane. Second, vasodilation was produced by warming unanesthetized volunteers sufficiently to produce sweating; intense vasoconstriction was similarly produced by cooling the volunteers sufficiently to produce shivering. Third, a canopy was positioned to enclose the head, neck, and upper chest of unanesthetized volunteers. Air within the canopy was randomly set to 18, 20, 22, 24, and 26 degrees Celsius.

Results: Redistribution of body heat accompanying induction of anesthesia had little effect on the core-to-forehead skin temperature difference. However, the core-to-neck skin temperature gradient decreased [nearly equal] 0.6 degrees Celsius in the hour after induction of anesthesia. Vasomotion associated with shivering and mild sweating altered the core-to-skin temperature difference only a few tenths of a degree centigrade. The absolute value of the core-to-forehead temperature difference exceeded 0.5 degrees Celsius during [nearly equal] 35% of the measurements, but the difference rarely exceeded 1 degree Celsius. The core-to-neck temperature difference typically exceeded 0.5 degrees Celsius and frequently exceeded 1 degree Celsius. Each 1 degree Celsius increase in ambient temperature decreased the core-to-forehead and core-to-neck skin temperature differences by less than 0.2 degree Celsius.     

The etiology and management of inadvertent perioperative hypothermia

Mild perioperative hypothermia is a frequent complication of anesthesia and surgery. Core temperature should be monitored during general anesthesia and during regional anesthesia for large operations. Reliable sites of core temperature monitoring include the tympanic membrane, nasopharynx, esophagus, bladder, rectum, and pulmonary artery. The skin surface is not an acceptable site for monitoring core temperature. Anesthetic-induced vasodilation initially rapidly decreases core temperature secondary to an internal redistribution of heat rather than an increased heat loss to the environment. Both general and regional anesthetics impair thermoregulation, increasing the interthreshold range; that is, the range of core temperatures over which no autonomic respose to cold or warmth occurs. Preinduction skin surface warming is the only means to prevent this initial redistribution hypothermia. Forced-air warming is the most effective method of rewarming hypothermic patients intraoperatively.     

Intraoperative Wärmekonservierung Viel Lärm um heiße Luft?

Thermoregulation and its impairment by anaesthesia and surgery has recently been brought back into focus by researchers and clinicians. All volatile and IV anaesthetics, opioids, as well as spinal and epidural anaesthesia increase the inter-threshold range of thermoregulation from 0.2°?C to 4°?C between vasodilation and vasoconstriction. Thermoregulatory vasoconstriction and shivering occurs in anaesthetized patients at lower core temperatures than in awake subjects. Following induction of general or spinal/epidural anaesthesia, core temperature decreases significantly due to internal redistribution of body heat from the core thermal compartment to peripheral tissues. About 1?h after induction of general anaesthesia and initial redistribution hypothermia, a real reduction in body heat occurs as heat loss exceeds metabolic heat production. Heat loss is further increased due to low operating room temperatures, evaporation from open body cavities, and cold IV fluids. Peripheral thermoregulatory vasoconstriction is triggered by core temperatures between 33°?C and 35°?C, and is able to slow heat loss. However, body heat content continues to decrease even though core temperatures remain nearly constant. During spinal or epidural anaesthesia thermoregulation remains intact in the unblocked body segments, leading to reduced real heat loss when compared to general anaesthesia. Inadvertent hypothermia markedly decreases drug metabolism. Coagulation is impaired by cold-induced defects of platelet function. Hypothermia reduces neutrophil phagocytosis and oxidative killing capacity, causing wound infections. Postoperative hypothermia represents an unnecessary stress for the circulatory system, elevating plasma catecholamines and leading to myocardial ischaemia and arrhythmias. These hypothermia-related morbidities therefore have consequences reaching fare into the postoperative period. Prevention of inadvertent hypothermia is always indicated. Forced-air warming is the most effective and safest method to prevent perioperative hypothermia.     

Effects of isoflurane and sevoflurane anesthesia on arteriovenous shunt flow in the lower limb of diabetic patients without autonomic neuropathy

BACKGROUND: Failure of sympathetic nerve control caused by diabetic neuropathy results in vasodilation of arteriovenous shunts. The aim of this study was to test the hypothesis that the function of arteriovenous anastomoses was disordered in mild diabetic patients without apparent neuropathy, and that volatile anesthetics opened arteriovenous shunts more greatly in nondiabetic patients than diabetic patients. METHODS: Autonomic system function was assessed by cardiovascular reflex tests. Arterial-venous oxygen content difference (A-VDeltaO2) and partial oxygen pressure index (Pvo2/Pao2, the ratio of oxygen tension in femoral vein blood to that in femoral artery blood) were measured before and during isoflurane or sevoflurane anesthesia in 16 diabetic and 22 nondiabetic patients. Skin temperatures of the foot and leg were measured in 14 diabetic and 15 nondiabetic patients using thermography before and during anesthesia. RESULTS: Pvo2/Pao2 before anesthesia was significantly higher in diabetic patients. In nondiabetics, venous oxygen content significantly increased and A-VDeltaO2 markedly decreased during anesthesia, but these parameters were unchanged in diabetics. Foot temperatures were higher in diabetics before anesthesia, and increased gradually and significantly in both groups during anesthesia, but with a greater increase in nondiabetic patients. Induction of anesthesia caused a larger decrease in leg temperature in diabetics than in nondiabetics. CONCLUSIONS: Diabetic patients have a higher Pvo2/Pao2 and a small core-to-peripheral temperature gradient before anesthesia, suggesting latent dysfunction of the autonomic nerve system, even in the absence of autonomic neuropathy. Volatile anesthesia opens the arteriovenous shunt in nondiabetics to a greater extent than in diabetic patients.     

Thermoregulatory response to intraoperative head-down tilt.

Thermoregulation interacts with cardiovascular regulation within the central nervous system. We therefore evaluated the effects of head-down tilt on intraoperative thermal and cardiovascular regulation. Thirty-two patients undergoing lower-abdominal surgery were randomly assigned to the 1) supine, 2) 15 degrees -20 degrees head-down tilt, 3) leg-up, or 4) combination of leg-up and head-down tilt position. Core temperature and forearm minus fingertip skin-temperature gradients (an index of peripheral vasoconstriction) were monitored for 3 h after the induction of combined general and lumbar epidural anesthesia. We also determined cardiac output and central-venous and esophageal pressures. Neither right atrial transmural pressure nor cardiac index was altered in the Head-Down Tilt group, but both increased significantly in the Leg-Up groups. The vasoconstriction threshold was reduced in both leg-up positions but was not significantly decreased by head-down tilt. Final core temperatures were 35.2 degrees C +/- 0.2 degrees C (mean +/- SEM) in the Supine group, 35.0 degrees C +/- 0.2 degrees C in the Head-Down Tilt group, 34.2 degrees C +/- 0.2 degrees C in the Leg-Up group (P < 0.05 compared with supine), and 34.3 degrees C +/- 0.2 degrees C when leg-up and head-down tilt were combined (P < 0.05 compared with supine). These results confirm that elevating the legs increases right atrial transmural pressure, reduces the vasoconstriction threshold, and aggravates intraoperative hypothermia. Surprisingly, maintaining a head-down tilt did not increase right atrial pressure. IMPLICATIONS: Intraoperative hypothermia is exaggerated when patients are maintained in the leg-up position because the vasoconstriction threshold is reduced. However, head-down tilt (Trendelenburg position) does not reduce the vasoconstriction threshold or aggravate hypothermia. The head-down tilt position thus does not require special perioperative thermal precautions or management unless the leg-up position is used simultaneously.     

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).     

Postoperative Pain Facilitates Nonthermoregulatory Tremor

Background: Spontaneous tremor is relatively common in normothermic patients after operation and has been attributed to many causes. The hypothesis that nonthermoregulatory shivering-like tremor is facilitated by postoperative pain was tested. In addition, the effects of intravenous lidocaine on nonthermoregulatory tremor were evaluated.

Methods: Patients undergoing knee surgery were anesthetized with 2 [mu]g/kg intravenous fentanyl and 0.2 mg/kg etomidate. Anesthesia was maintained with 1.7 +/- 0.8% (mean +/- SD) isoflurane. Intraoperative forced-air heating maintained normothermia. The initial 44 patients were randomly allocated to receive an intra-articular injection of 20 ml saline (n = 23) or lidocaine, 1.5% (n = 21). The subsequent 30 patients were randomly allocated to receive an intravenous bolus of 250 [mu]g/kg lidocaine followed by an infusion of 13 [mu]g [middle dot] kg-1 [middle dot] h-1 lidocaine or an equivalent volume of saline when shivering was observed. Patient-controlled analgesia was provided for all patients: 3.5 mg piritramide, with a lockout interval of 5 min, for an unlimited total dose. Shivering was graded by a blinded investigator using a four-point scale. Pain was assessed by a 100-mm visual analog scale (0 = no pain and 100 = worst pain). The arteriovenous shunt status was evaluated with forearm-minus-fingertip skin-temperature gradients.

Results: Morphometric characteristics and hemodynamic responses were similar in the four groups. Core and mean skin temperature remained constant or increased slightly compared with preoperative values, and postoperative skin-temperature gradients were negative (indicating vasodilation) in nearly all patients. After intra-articular injection of saline, pain scores for the first postoperative hour averaged 46 +/- 32 mm (mean +/- SD), and 10 of the 23 (43%) patients shivered. In contrast, the pain scores of patients who received intra-articular lidocaine were significantly reduced to 5 +/- 9 mm and shivering was absent in this group (P < 0.05). In the second portion of the study, neither intravenous lidocaine nor saline reduced the magnitude or duration of nonthermoregulatory tremor or the patients' pain scores.     

Prevention of hypothermia in children under combined epidural and general anesthesia: a comparison between upper- and lower-body warming

BACKGROUND: Children receiving combined epidural and general anesthesia may be at greater risk of hypothermia. Active warming should be undertaken to combat heat loss. With combined epidural and general anesthesia heat loss from the lower body may be greater than from the upper body because of shift of blood towards the vasodilated lower body. We assumed that application of the warming blanket to the lower body might provide better protection against hypothermia. To test this hypothesis, lower-body warming (LBW) was compared with upper-body warming (UBW) in a randomized comparative study. METHODS: Children subjected to open urologic surgery under combined epidural and general anesthesia were randomly allocated to either UBW n = 38 or LBW n = 35 using a forced-air warming blanket. Core and peripheral skin temperatures were monitored. Temperature gradients between forearm and fingertip during LBW and between leg and toe during UBW were calculated. The warmer was set at 32 degrees C, room temperature was around 22 degrees C and fluids were infused at ambient room temperature. RESULTS: The changes in core temperature were comparable and parallel in both groups. Core temperature decreased significantly in each group at 1 h after induction compared with basal values. Temperature gradients at forearm-fingertip and at leg-toe were also comparable in both groups. Recovery was uneventful and no patient shivered in the recovery room. CONCLUSIONS: Lower body warming is as effective as UBW in prevention of hypothermia in children subjected to combined epidural and general anesthesia.