Biomedical subjects
D I Sessler
Publications and source records attributed to D I Sessler.
Thermoregulatory vasoconstriction increases the difference between femoral and radial arterial pressures.
OBJECTIVE: Thermoregulatory vasoconstriction locally increases arterial wall tension and arteriolar resistance, thereby altering physical properties of the arteries. The arterial pressure waveform is an oscillatory phenomenon related to those physical characteristics; accordingly, we studied the effects of thermoregulatory vasomotion on central and distal arterial pressures, using three hydraulic coupling systems having different dynamic responses. METHODS: We studied 7 healthy volunteers. Central arterial pressure was measured from the femoral artery and distal pressure was measured from the radial artery, using 10.8-cm long, 20-gauge catheters. Three hydraulic coupling systems were used: (1) a 10-cm-long, 2-mm internal diameter connector; (2) a 150-cm-long, 1-mm internal diameter connector (Combidyn 520-5689, B. Braun, Melsungen, Germany); (3) a 180-cm long, 2-mm internal diameter connector (Medex MX564 and MX562, Medex Inc., Hillard, OH). Brachial artery pressure was measured oscillometrically. Core temperature was measured at the tympanic membrane. The vasomotor index, defined as finger temperature minus room temperature, divided by core temperature minus room temperature, was used to estimate the degree of vasoconstriction. Constriction was considered near maximal when the index was less than 0.1, and minimal when it exceeded 0.75. Measurements were taken every 3 min. Baseline readings were obtained when subjects were warm. They then were cooled by exposure to 20 degrees C to 22 degrees C room air and a circulating-water mattress set at 4 degrees C until index was less than 0.1. They then were rewarmed by increasing water temperature to 42 degrees C and adding a forced-air warmer until the vasomotor index exceeded 0.75. Data were analyzed by ANOVA and linear regression. RESULTS: Thermoregulatory vasoconstriction was associated with marked arterial pressure waveform changes. Radial pressure showed, in lieu of a dicrotic notch, large oscillations of decreasing amplitude. Femoral pressure showed a single diastolic oscillation of smaller amplitude. The waveforms appeared different, depending on the hydraulic coupling system used, artifact being more marked with the longer connectors. On the average, radial systolic pressure exceeded femoral systolic pressure during vasoconstriction; however, during vasodilatation, femoral systolic pressure exceeded radial systolic pressure (p < 0.05). Oscillometric measurements underestimated systolic pressure, and did so more markedly during vasoconstriction. There were no differences in the values of mean and diastolic pressures. CONCLUSION: Thermoregulatory vasoconstriction alters radial arterial pressure waveform, artifactually increasing its peak systolic pressure compared with the femoral artery. Poor dynamic responses of recording systems further distort the waveforms. Consequently, radial artery pressure may be misleading in vasoconstricted patients.
Rewarming and sweating during cardiopulmonary bypass.
The hypothesis was tested that facial sweating at the end of cardiopulmonary bypass (CPB) is a thermoregulatory phenomenon. Twenty-two patients undergoing cardiac surgery with fentanyl anesthesia were studied. Nasopharyngeal temperature, nasal skin temperature, rectal temperature, and mean skin temperature were monitored for 90 minutes after the start of rewarming on CPB. Calf-toe and forehead-nose skin temperature gradients were followed as a measure of peripheral and facial thermoregulatory vasoactive responses. Facial sweating was defined as grade 1 (noticeable) or grade 2 (obvious droplets). Fourteen patients (64%) sweated during rewarming at the end of CPB. In 11 cases the onset of sweating was preceded by a dramatic increase in nasal skin temperature (mean +/- SEM, 4.6 +/- 0.3 degrees C in 5 min), suggesting facial vasodilation. The maximum rate of increase (degree C/5 min) in nasal skin temperature was significantly greater in patients who sweated than in those who did not, 4.1 +/- 0.4 degrees C versus 2.6 +/- 0.3 degrees C (P < 0.015). There was no difference in the age, weight, or BSA between patients who sweated during CPB and those who did not. The nasopharyngeal temperature threshold for the onset of sweating was not elevated (grade 1, 36.4 +/- 0.5 degrees C; grade 2, 37.6 +/- 0.4 degrees C), but there was a 5 to 6 degrees C interpatient variation. It was concluded that facial sweating during rewarming on CPB is typical of a thermoregulatory response. Absence of sweating in one third of patients may be due to pharmacokinetic or pharmacodynamic differences in the response to anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)
Mild hypothermia during halothane-induced anesthesia decreases resistance to Staphylococcus aureus dermal infection in guinea pigs.
Because various immune functions are impaired at temperatures only 1 degrees to 3 degrees C less than normal, we tested the hypothesis that mild hypothermia during anesthesia impairs resistance to dermal infections. Guinea pigs were anesthetized for 6 hours with 1% inspired halothane. Their core temperatures were maintained at either 39 degrees C (normal for guinea pigs, n = 12) or 36 degrees C (n = 12). Two hours after induction of anesthesia, three doses each of Staphylococcus aureus (10(8), 10(7), and 10(6) organisms) were injected intradermally at nine sites on each animal's back. Core temperatures were not controlled after recovery from the anesthetic, and animals in each group were maintained in the same environment. Four days after anesthesia, each injection site was excised to obtain a count of viable bacteria. Subcutaneous oxygen partial pressure values, averaged over time, were 53 +/- 3 mm Hg (mean +/- SEM) in the hypothermic group and 62 +/- 4 mm Hg in the normothermic group (p = 0.06). Capillary perfusion, as assessed by laser Doppler flowmetry, was comparable in the two groups. One day after injection of 10(8) bacteria, the area of induration was 89 +/- 11 mm(2) in the hypothermic group but only 61 +/- 6 mm(2) in the normothermic group (p < 0.05). On postanesthetic day 4, the area of induration was 72 +/- 6 and 59 +/- 6 mm(2) in the hypothermic and normothermic groups, respectively (p > 0.05). After inoculation with 10(8) bacteria, the fraction recovered was 1.0 +/- 0.2 in the hypothermic groups and 0.6 +/- 0.2 in the normothermic group (p < 0.05). After inoculation with 10(7) and 10(6) bacteria, the fraction recovered was less than 0.2, and no difference was found between the hypothermic and normothermic animals. Thus mild hypothermia during halothane-induced anesthesia slightly impairs resistance to dermal infection.
Nifedipine and intraoperative core body temperature in humans.
BACKGROUND: Initial anesthetic-induced hypothermia results largely from core-to-peripheral redistribution of heat. Nifedipine administration may minimize hypothermia by inducing vasodilation well before induction of anesthesia. Although vasodilation would redistribute heat to peripheral tissues, thermoregulatory responses would maintain core temperature. After equilibration, the patient would be left vasodilated, with a small core-to-peripheral temperature gradient. Minimal redistribution hypothermia may accompany subsequent induction of anesthesia, because heat flow requires a temperature gradient. In contrast, similar vasodilation concurrent with anesthetic-induced vasodilation may augment redistribution hypothermia. Accordingly, the authors tested the hypothesis that nifedipine treatment for 12 h before surgery would minimize intraoperative redistribution hypothermia, whereas nifedipine treatment immediately before induction of anesthesia would aggravate hypothermia. METHODS: Patients undergoing hip arthroplasty were randomly assigned to: (1) 20 mg long-acting nifedipine orally 12 h before surgery, and 10 mg sublingually 1.5 h before surgery (n = 10); (2) nifedipine 10 mg sublingually just before induction of anesthesia (n = 10); and (3) no nifedipine (control, n = 10). Anesthesia was maintained with isoflurane and 60% nitrous oxide. Administered intravenous fluids were heated, but the patients were not otherwise actively warmed. RESULTS: Core temperature decreased 0.8 degree C in the first hour of surgery in the patients given nifedipine the night before and the morning of surgery, which was significantly less than in the control group (1.7 degree C in the first hour). In contrast, core temperature decreased 2.0 degrees C in the first hour of surgery in the patients given nifedipine immediately before induction of anesthesia. During the subsequent 70-130 min of anesthesia, core temperature decreased at roughly comparable rates in each group. After 130 min of anesthesia, core temperature in the two nifedipine-treated groups differed by 1.6 degrees C, and the temperatures in all three groups differed significantly. CONCLUSIONS: Vasodilation induced by nifedipine well before induction of anesthesia minimized redistribution hypothermia, presumably by decreasing the core-to-peripheral tissue temperature gradient. In contrast, redistribution hypothermia was aggravated by administration of the same drug immediately before induction of anesthesia. Drug-induced modulation of vascular tone thus produces clinically important alterations in intraoperative core temperature.
Epidural anesthesia impairs both central and peripheral thermoregulatory control during general anesthesia.
BACKGROUND: The authors tested the hypotheses that: (1) the vasoconstriction threshold during combined epidural/general anesthesia is less than that during general anesthesia alone; and (2) after vasoconstriction, core cooling rates during combined epidural/general anesthesia are greater than those during general anesthesia alone. Vasoconstriction thresholds and heat balance were evaluated under controlled circumstances in volunteers, whereas the clinical importance of intraoperative thermoregulatory vasoconstriction was evaluated in patients. METHODS: Five volunteers were each evaluated twice. On one of the randomly ordered days, epidural anesthesia (approximately T9 dermatomal level) was induced and maintained with 2-chloroprocaine. On both study days, general anesthesia was induced and maintained with isoflurane (0.7% end-tidal concentration), and core hypothermia was induced by surface cooling and continued for at least 1 h after fingertip vasoconstriction was observed. Patients undergoing colorectal surgery were randomly assigned to combined epidural/enflurane anesthesia (n = 13) or enflurane alone (n = 13). In appropriate patients, epidural anesthesia was maintained by an infusion of bupivacaine. The core temperature that triggered fingertip vasoconstriction identified the threshold. RESULTS: In the volunteers, the vasoconstriction threshold was 36.0 +/- 0.2 degrees C during isoflurane anesthesia alone, but significantly less, 35.1 +/- 0.7 degrees C, during combined epidural/isoflurane anesthesia. Cutaneous heat loss and the rates of core cooling were similar 30 min before vasoconstriction with and without epidural anesthesia. In the 30 min after vasoconstriction, heat loss decreased 33 +/- 13 W when the volunteers were given isoflurane alone, but only 8 +/- 16 W during combined epidural/isoflurane anesthesia. Similarly, the core cooling rates in the 30 min after vasoconstriction were significantly greater during combined epidural/isoflurane anesthesia (0.8 +/- 0.2 degrees C/h) than during isoflurane alone (0.2 +/- 0.1 degrees C/h). In the patients, end-tidal enflurane concentrations were slightly, but significantly, less in the patients given combined epidural/enflurane anesthesia (0.6 +/- 0.2% vs. 0.8 +/- 0.2%). Nonetheless, the vasoconstriction threshold was 34.5 +/- 0.6 degrees C in the epidural/enflurane group, which was significantly less than that in the other patients, 35.6 +/- 0.8 degrees C. When the study ended after 3 h of anesthesia, patients given combined epidural/enflurane anesthesia were 1.2 degrees C more hypothermic than those given general anesthesia alone. The rate of core cooling during the last hour of the study was 0.4 +/- 0.2 degrees C/h during combined epidural/enflurane anesthesia, but only 0.1 +/- 0.3 degrees C/h during enflurane alone. CONCLUSIONS: These data indicate that epidural anesthesia reduces the vasoconstriction threshold during general anesthesia. Furthermore, the markedly reduced rate of core cooling during general anesthesia alone illustrates the importance of leg vasoconstriction in maintaining core temperature.
Rate and gender dependence of the sweating, vasoconstriction, and shivering thresholds in humans.
BACKGROUND: The range of core temperatures not triggering thermoregulatory responses ("interthreshold range") remains to be determined in humans. Although the rates at which perioperative core temperatures vary typically range from 0.5 to 2 degrees C/h, the thermoregulatory contribution of different core cooling rates also remains unknown. In addition, sweating in women is triggered at a slightly greater core temperature than in men. However, it is unknown whether the vasoconstriction and shivering thresholds are comparably greater in women, or if women tolerate a larger range of core temperatures without triggering thermoregulatory responses. Accordingly, the authors sought to (1) define the interthreshold range; (2) test the hypothesis that, at a constant skin temperature, the vasoconstriction and shivering thresholds are greater during rapid core cooling than during slowly induced hypothermia; and (3) compare the sweating, vasoconstriction, and shivering thresholds in men and women. METHODS: Eight men and eight women participated. The men participated on 2 separate days; no anesthesia or sedatives were administered. On each day, they were cutaneously warmed until sweating was induced and then were cooled by a central venous infusion of cold fluid. The cooling rates were 0.7 +/- 0.1 degrees C/h on 1 day and 1.7 +/- 0.4 degrees C/h on the other, randomly ordered. Skin temperature was maintained near 36.7 degrees C throughout each trial. The women were studied only once, in the follicular phase of their menstrual cycles, at the greater cooling rate. RESULTS: The interthreshold range was approximately 0.2 degrees C in both men and women, but all thermoregulatory response thresholds were approximately 0.3 degrees C higher in women. All thresholds were virtually identical during slow and fast core cooling. CONCLUSIONS: Our findings confirm the existence of an interthreshold range and document that its magnitude is small. They also demonstrate that the interthreshold range does not differ in men and women, but that women thermoregulate at a significantly higher temperature than do men. Typical clinical rates of core cooling do not alter thermoregulatory responses.
Thermoregulatory thresholds during epidural and spinal anesthesia.
BACKGROUND: There are significant physiologic differences between spinal and epidural anesthesia. Consequently, these two types of regional anesthesia may influence thermoregulatory processing differently. Accordingly, in volunteers and in patients, we tested the null hypothesis that the core-temperature thresholds triggering thermoregulatory sweating, vasoconstriction, and shivering are similar during epidural and spinal anesthesia. METHODS: Six male volunteers participated on three consecutive study days: epidural or spinal anesthesia were randomly assigned on the 1st and 3rd days (approximately T10 level); no anesthesia was given on the 2nd day. On each day, the volunteers were initially warmed until they started to sweat, and subsequently cooled by central venous infusion of cold fluid until they shivered. Mean skin temperature was kept constant near 36 degrees C throughout each study. The tympanic membrane temperatures triggering a sweating rate of 40 g.m-2.h-1, a finger flow less than 0.1 ml/min, and a marked and sustained increase in oxygen consumption (approximately 30%) were considered the thermoregulatory thresholds for sweating, vasoconstriction, and shivering, respectively. Twenty-one patients were randomly assigned to receive epidural (n = 10) or spinal (n = 11) anesthesia for knee and calf surgery (approximately T10 level). As in the volunteers, the shivering threshold was defined as the tympanic membrane temperature triggering a sustained increase in oxygen consumption. RESULTS: The thresholds and ranges were similar during epidural and spinal anesthesia in the volunteers. However, the sweating-to-vasoconstriction (inter-threshold) range, the vasoconstriction-to-shivering range, and the sweating-to-shivering range all were significantly increased by regional anesthesia. The shivering thresholds in patients assigned to epidural and spinal anesthesia were virtually identical. CONCLUSIONS: Comparable sweating, vasoconstriction, and shivering thresholds during epidural and spinal anesthesia suggest that thermoregulatory processing is similar during each type of regional anesthesia. However, thermoregulatory control was impaired during regional anesthesia, as indicated by the significantly enlarged inter-threshold and sweating-to-shivering ranges.
Epidural anesthesia increases apparent leg temperature and decreases the shivering threshold.
BACKGROUND: Lower core temperatures than usual are required to trigger shivering during epidural and spinal anesthesia, but the etiology of this impairment remains unknown. In this investigation, we propose and test a specific mechanism by which a peripheral action of regional anesthesia might alter centrally mediated thermoregulatory responses. Conduction anesthesia blocks all thermal sensations; however, cold signals are disproportionately affected because at typical leg temperatures mostly cold receptors fire tonically. It thus seems likely that epidural and spinal anesthesia increase the leg temperature perceived by the thermoregulatory system. Because skin temperature reportedly contributes 5-20% to thermoregulatory control, increased apparent (as distinguished from actual) leg temperature would produce a complimentary decrease in the core temperature triggering thermoregulatory shivering. Accordingly, we tested the hypothesis that abnormal tolerance for hypothermia during epidural anesthesia coincides with an increase in apparent leg temperature. We defined apparent temperature as the leg-skin temperature required to induce a reduction in the shivering threshold comparable to that produced by epidural anesthesia. METHODS: Six women were studied on 4 randomly ordered days: (1) leg-skin temperature near 32 degrees C; (2) leg-skin temperature near 36 degrees C; (3) leg-skin temperature near 38 degrees C; and (4) epidural anesthesia without leg-warming (leg-skin temperature approximately 34 degrees C). At each designated leg temperature, core hypothermia sufficient to evoke shivering was induced by central venous infusion of cold fluid. Upper-body skin temperature was kept constant throughout. In each volunteer, linear regression was used to calculate the correlation between the shivering thresholds on the 3 non-epidural days and concurrent leg temperatures. The slope of these regression equations thus indicated the extent to which leg-warming increased thermoregulatory tolerance for core hypothermia, and was expressed as a percentage leg-skin and leg-tissue contribution to total thermal afferent input. The skin and tissue temperatures that would have been required to produce the observed shivering threshold during epidural anesthesia, the apparent temperatures, were then interpolated from the regression. RESULTS: There was a good linear relation between the shivering threshold and leg-skin temperature (r2 = 0.94 +/- 0.06). The contribution of leg-skin temperature to the shivering threshold was 11 +/- 3% of the total thermal input. Apparent leg-skin temperature during epidural anesthesia was 37.8 +/- 0.5 degrees C, which exceeded actual leg-skin temperature by approximately 4 degrees C. The contribution of leg-tissue temperature to the shivering threshold was 19 +/- 7% of the total. Apparent leg-tissue temperature during epidural anesthesia was 37.1 +/- 0.4 degrees C, which exceeded actual leg-skin temperature by approximately 2 degrees C. CONCLUSIONS: Because leg-skin contributed approximately 11% to the shivering threshold, it is unlikely that the entire skin surface contributes at much less than 20%. These data suggest that the shivering threshold during epidural anesthesia is reduced by a specific mechanism, namely that conduction block significantly increases apparent (as distinguished from actual) leg temperature.
Propofol causes a dose-dependent decrease in the thermoregulatory threshold for vasoconstriction but has little effect on sweating.
BACKGROUND: Volatile anesthetics increase the core temperature required to trigger sweating and decrease the core temperature required to trigger vasoconstriction. However, little is known about the effects of intravenous anesthetics on thermoregulation. We therefore tested the hypothesis that propofol increases the sweating threshold and decreases the vasoconstriction threshold, thereby increasing the inter-threshold range (core temperatures not triggering autonomic thermoregulatory responses). The study was conducted using a new model in which thermal manipulations were restricted to insensate skin, and sensate skin temperature was controlled. METHODS: Six healthy, male volunteers were studied on 3 randomly ordered days: no propofol, target propofol blood concentration 2 micrograms/ml, and target blood propofol concentration 4 micrograms/ml. Each day, epidural anesthesia (approximately T11 level) was induced, using 2% 2-chloroprocaine (one volunteer received bupivacaine). Thermal manipulations were confined to the legs, and we attempted to maintain upper-body (sensate) skin temperature constant. Propofol was infused by a computer-controlled infusion pump. Volunteers were heated until sweating was observed, then cooled until fingertip vasoconstriction was observed. The sweating threshold was defined as the tympanic membrane temperature triggering sustained evaporative heat loss > 40 g.m-2.h-1. Similarly, the vasoconstriction threshold was defined as the tympanic membrane temperature triggering a sustained reduction in fingertip blood flow to < 0.25 ml/min. Central venous blood was assayed for propofol blood concentration. RESULTS: Increasing propofol concentration produced a linear decrease the vasoconstriction threshold (slope = -0.53 +/- 0.34 degrees C.microgram-1.ml-1; R2 = 0.98 +/- 0.04 [mean +/- SD]), but had little effect on the sweating threshold. The inter-threshold range was 0.51 +/- 0.46 degrees C during epidural anesthesia alone, and increased significantly, by 0.49 +/- 0.31 degrees C.microgram-1.ml-1 during propofol administration. CONCLUSIONS: Like volatile anesthetics, propofol reduces the vasoconstriction threshold and increases the inter-threshold range. However, propofol differs in leaving the sweating threshold unchanged.
Thermoregulatory and anesthetic-induced alterations in the differences among femoral, radial, and oscillometric blood pressures.
BACKGROUND: A decrease in radial artery blood pressure relative to central arterial blood pressure is commonly associated with the rewarming phase of cardiopulmonary bypass. Decreased hand vascular resistance has been suggested as a possible mechanism. Although decreased blood viscosity due to hemodilution may contribute to decreased hand vascular resistance, thermoregulatory vascular responses to core hyperthermia also may be important. METHODS: Seven healthy volunteers were studied. Volunteers first were cooled until thermoregulatory vasoconstriction was evident. Next, each was warmed until intense sweating developed. After a cool-down period, general anesthesia was induced with propofol and N2O. Femoral artery pressure (a surrogate for central arterial pressure) and radial artery and oscillometric (brachial artery) pressures were compared during each of six defined thermoregulatory and anesthetic study conditions. To determine the effect of hand vascular resistance on blood pressure differences, measurements were compared before and after occlusion of hand blood flow. Upper-extremity blood flow was evaluated by forearm and fingertip plethysmography and laser Doppler flowmetry. RESULTS: Forearm, fingertip, and cutaneous blood flow increased significantly during warming and were maximal during intense sweating. During thermoregulatory vasoconstriction, femoral, radial, and oscillometric mean blood pressures were similar. In contrast, radial artery mean pressure was 5 +/- 1 mmHg less than femoral artery mean pressure and 12 +/- 8 mmHg less than oscillometric mean pressure during intense sweating. Hand compression reduced these differences. The contour of the radial artery pressure waveform was dramatically altered by thermoregulatory and anesthetic conditions. Radial artery systolic pressure exceeded both femoral artery and oscillometric systolic pressures during vasoconstriction but was less than these during intense sweating. Hand compression reestablished the exaggerated radial artery systolic pressure during all study conditions. CONCLUSIONS: Thermoregulatory and anesthetic-induced alterations in upper-extremity blood flow substantially influence the relations among femoral artery, radial artery, and oscillometric blood pressure measurements.
Mild hypothermia during isoflurane anesthesia decreases resistance to E. coli dermal infection in guinea pigs.
Small changes in core temperature profoundly alter cutaneous blood flow, a major factor influencing resistance to wound infection. Furthermore, when measured in vitro, various immune functions are temperature dependent in the physiological range. Accordingly, we tested the hypothesis that mild hypothermia impairs and mild hyperthermia improves resistance to dermal infections. Thirty-two guinea pigs were anesthetized for 6 h using 1.5% (1.25 MAC) inspired isoflurane. Their core temperatures were maintained at either 39 degrees C (normal for guinea pigs, n = 11), 36 degrees C (n = 12), or 41 degrees C (n = 9). One h after induction of anesthesia, 2 x 10(8) E. coli were injected intradermally with a 26-g needle at eight sites on each animal's back. Core temperatures were not controlled after recovery from anesthesia, and animals in each group were maintained in the same environment. Twenty-four h after injection, the area of induration surrounding each injection site was measured. This is a standard test of resistance to wound infection. Values were compared using one-way ANOVA and Scheffé's S tests. Results are presented as means +/- standard deviations; differences were considered significant when P < 0.05. Areas of inflammation on the hypothermic animals were significantly larger (48 +/- 10 mm2) than those on normothermic (36 +/- 10 mm2) or hyperthermic (37 +/- 6 mm2) animals. These data suggest that mild hypothermia during anesthesia significantly impairs resistance to dermal infection. In contrast, mild hyperthermia does not appear to be protective.
Treatment of mild immersion hypothermia by direct body-to-body contact.
Body-to-body contact is often recommended for rewarming mildly hypothermic victims in the field. This procedure involves a euthermic individual donating heat to the recipient by direct contact in an insulated bag. However, this technique has not been critically evaluated and may not be beneficial because there is limited direct contact between recipient and donor, peripheral vasoconstriction may impair heat transfer to the core, skin warming may blunt the recipient's shivering response, and cold stress to the donor may be excessive. The present study was designed to evaluate whether donation of heat by a donor would be sufficient to enhance rewarming of a hypothermic subject (recipient). Six pairs of recipients (5 men, 1 woman) and donors (2 men, 4 women) participated in the study. Esophageal and skin temperatures, cutaneous heat flux, and oxygen consumption were measured. Recipients were immersed in 8 degrees C water until esophageal temperature decreased to a mean of 34.6 +/- 0.7 degrees C (SD). They then were rewarmed by one of three methods: rewarming by the endogenous heat generated by shivering only (SH), body-to-body rewarming (BB), or rewarming with a constant-heat source manikin (MAN). Mean afterdrop for the three conditions was 0.54 +/- 0.2, 0.54 +/- 0.2, and 0.57 +/- 0.2 degrees C for SH, BB, and MAN, respectively (NS), and the rate of rewarming was 2.40 +/- 0.8, 2.46 +/- 1.1 and 2.55 +/- 0.9 degrees C/h for SH, BB, and MAN, respectively (NS).(ABSTRACT TRUNCATED AT 250 WORDS)
The effect of hypothermia on adductor pollicis twitch tension during continuous infusion of vecuronium in isoflurane-anesthetized humans.
The effect of total body cooling on force of contraction of the adductor pollicis was determined during a constant rate infusion of vecuronium. Anesthesia was induced with thiopental and maintained with isoflurane/nitrous oxide in eight volunteers (study group) and seven surgical patients (control group). After train-of-four (TOF) stimulation of the ulnar nerve, we measured the amplitude of the first response (T1) in the train and the ratio of the fourth-to-first response (TOF ratio). Vecuronium was then administered as an intravenous (i.v.) bolus, 25 micrograms/kg, followed by continuous i.v. infusion, 25 micrograms.kg-1 x h-1; central body (core) temperature was maintained stable for 60 min, at the end of which T1 and TOF responses were constant. In the study group, core temperature was then reduced (using circulating-water blankets) by a mean of 2.6 degrees C, decreasing the T1 and TOF ratio, respectively, by 19% and 18% per degrees C reduction in adductor pollicis temperature. Normothermia was maintained in the control group for a mean of 111 min, with no significant change in T1 and TOF responses. We conclude that, during a constant-rate infusion of vecuronium, the magnitude of neuromuscular block increases significantly when adductor pollicis temperature decreases secondary to core cooling.
Routine postoperative oxygen supplementation.
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Leg temperature and heat content in humans during immersion hypothermia and rewarming.
Core temperature afterdrop following cold water immersion has previously been shown to be greater during treadmill exercise than shivering (J. Appl. Physiol. 1987; 63:2375-9). To test the hypothesis that this results from increased transfer of heat from the core to exercising muscles, we quantified the changes in leg temperature and heat content during cooling and exercise/shivering protocols. Upper and lower leg muscle temperatures were measured at multiple depths in five thin healthy male subjects immersed in 8 degrees C water until core temperatures reached 32.8-34.9 degrees C. In these thin subjects there was a significant but small difference between exercise and shivering afterdrop (approximately 0.2 degrees C), and total leg heat content was unchanged during this period with both protocols. Subsequent heat gain was similar in both treatments but, in the lower leg, was greater during exercise than shivering, suggesting that shivering is less effective than exercise in increasing lower leg heat content.
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.