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D I Sessler

Publications and source records attributed to D I Sessler.

At least 217 records · Page 12Linked to original sources

Leg heat content continues to decrease during the core temperature plateau in humans anesthetized with isoflurane.

BACKGROUND: Sufficient hypothermia during anesthesia provokes thermoregulatory responses, but the clinical significance of these responses remains unknown. Nonshivering thermogenesis does not increase metabolic heat production in anesthetized adults. Vasoconstriction reduces cutaneous heat loss, but the initial decrease appears insufficient to cause a thermal steady state (heat production equaling heat loss). Accordingly, the authors tested the hypotheses that: 1) thermoregulatory vasoconstriction prevents further core hypothermia; and 2) the resulting stable core temperature is not a thermal steady state, but, instead, is accompanied for several hours by a continued reduction in body heat content. METHODS: Six healthy volunteers were anesthetized with isoflurane (0.8%) and paralyzed with vecuronium. Core hypothermia was induced by fan cooling, and continued for 3 h after vasoconstriction in the legs was detected. Leg heat content was calculated from six needle thermocouples and skin temperature, by integrating the resulting parabolic regression over volume. RESULTS: Core temperature decreased 1.0 +/- 0.2 degrees C in the 1 h before vasoconstriction, but only 0.4 +/- 0.3 degrees C in the subsequent 3 h. This temperature decrease, evenly distributed throughout the body, would reduce leg heat content 10 kcal. However, measured leg heat content decreased 49 +/- 18 kcal in the 3 h after vasoconstriction. CONCLUSIONS: These data thus indicate that thermoregulatory vasoconstriction produces a clinically important reduction in the rate of core cooling. This core temperature plateau resulted, at least in part, from sequestration of metabolic heat to the core which allowed core temperature to remain nearly constant, despite a continually decreasing body heat content.

Anesthesia, Inhalation↗

Physiologic responses to hyperthermia during epidural anesthesia and combined epidural/enflurane anesthesia in women.

BACKGROUND: During combined epidural/isoflurane anesthesia, the core temperature triggering finger-tip vasoconstriction is approximately 1 degree C less than that triggering redilation. This hysteresis suggests that thermoregulatory responses are not dependent entirely on current thermal status (state-dependence), but may be influenced also by the system's recent thermal history (direction-dependence). Once triggered, the gain and maximum response intensity of many thermoregulatory responses is nearly normal during isoflurane anesthesia. However, it remains unknown whether preserved gain and maximum response intensities are a characteristic paradigm describing thermoregulatory responses to general anesthetics. Also unknown is whether the sweating and pre-capillary vasodilation thresholds are comparably impaired by different volatile anesthetics. Accordingly, the authors tested the hypotheses that, during one minimum alveolar concentration of enflurane anesthesia: (1) there is a direction-dependent hysteresis for sweating; (2) the sweating and active vasodilation thresholds increase approximately 1.2 degrees C, as they do during one minimum alveolar concentration of isoflurane; and (3) the gain and maximum intensity of sweating are well preserved. METHODS: Six female volunteers each were studied on 2 days, once during epidural anesthesia alone and once with combined enflurane (1.7%)/epidural anesthesia. On each study day, core hyperthermia was induced by cutaneous warming restricted to the legs. Warming continued until chest sweating reached maximal values; the volunteers then were cooled gradually until sweating stopped. The core temperature at which the sweating rate departed from baseline values was considered the activation threshold. Gain was expressed as the slope of the sweating rate versus core temperature curve within the range 25-75% of the maximum sweating rate. Hysteresis was evaluated by subtracting the tympanic membrane temperature at which the sweating rate suddenly increased during warming (approximately 25% above baseline values) from that at which sweating precipitously decreased during cooling (approximately 75% of maximum values). RESULTS: The sweating threshold was 1.4 +/- 0.7 degrees C higher during combined enflurane/epidural anesthesia than during epidural anesthesia alone. Maximum intensity was approximately 700 g.m-2.h-1, and the gain approximately 1,300 g.m-2.h-1.degrees C-1 during each treatment. No hysteresis was detected on either study day. CONCLUSIONS: One minimum alveolar concentration of enflurane increased the sweating threshold only slightly more than previously reported for isoflurane. As in previous studies of sweating and vasoconstriction during isoflurane anesthesia, gain and maximum response intensity were well preserved during enflurane anesthesia. An increase in the interthreshold range (temperatures not triggering thermoregulatory responses), with little change in gain and maximum response intensities, appears to be the typical effect of volatile anesthetics. Sweating during enflurane anesthesia appears to be state-dependent and little influenced by the direction of core temperature perturbations.

Adult↗

Heat loss during surgical skin preparation.

BACKGROUND: Hypothermia develops rapidly during the 1st h of anesthesia and results in part from evaporative heat loss during surgical skin preparation. The authors tested the hypothesis that evaporation of skin preparation solution contributes significantly to hypothermia. METHODS: Five healthy, unanesthetized volunteers were studied in a 22 +/- 0.4 degrees C environment. One thigh of each volunteer was washed for 10 min, using each of the following representative solutions: (1) water; (2) 50% ethanol in water (EtOH/H2O; similar to tincture of iodine); and (3) povidone-iodine gel. Water and EtOH/H2O each were tested at ambient temperature (cold), warmed to 40 degrees C before application (warm), and with radiant heating of the skin, and gel only at ambient temperatures, resulting in seven study states. Heat loss and skin temperatures on the washed thighs were measured using thermal flux transducers, and values compared with the data obtained from the contralateral unwashed thighs. Change in mean body temperature (per 70 kg) due to washing was calculated by integrating measured heat loss over time and multiplying by the specific heat of human tissue. A mathematical model was developed to predict cutaneous heat loss using only skin temperature, independent of the type and temperature of skin-preparation solution or the use of radiant heating during preparation. RESULTS: Heat loss from the unwashed thigh was approximately 14 kcal/m2 during radiant warming and approximately 39 kcal/m2 without warming. Net heat loss (increment produced by washing) was approximately 30 kcal/m2 with water and gel without radiant warming, but loss was larger with EtOH/H2O than with water under all study conditions. Radiant warming reduced total heat loss (increment produced by washing and environment) during both the EtOH/H2O and water trials, compared with warm or cold EtOH/H2O and water alone. The calculated decreases in mean body temperature per 70 kg ranged from -0.2 to -0.7 degree C/m2. The smallest decrease occurred during radiant warming and washing with water, and the largest decreases during warm or cold EtOH/H2O. CONCLUSIONS: Heat loss was significantly less with water-based than with alcohol-based solutions. Though heating the solutions and radiant warming decreased heat loss, such loss under each tested condition, even per square meter of washed surface, was small compared to other causes of perioperative hypothermia. Consequently, the authors recommend that efforts to maintain intraoperative normothermia be directed elsewhere.

Adult↗

The pupillary light reflex. Effects of anesthetics and hyperthermia.

BACKGROUND: The pupillary light reflex often is evaluated in the perianesthetic period to assess drug effects and brainstem function. Mild hypothermia alone or combined with isoflurane does not impair pupillary responses. Although perioperative hyperthermia is less common than hypothermia, abnormal increases in core temperature remain an important thermal disturbance. Accordingly, the pupillary effects of hyperthermia alone and hyperthermia combined with isoflurane and enflurane were evaluated. Additionally, the effects of nitrous oxide on pupillary responses were determined. METHODS: The pupillary light reflex was evaluated in 31 non-surgical volunteers participating in concurrent thermoregulatory studies. Pupillary reflexes were quantified using a portable infrared pupillometer during (1) hyperthermia alone (n = 9), (2) hyperthermia with 0.8% and 1.2% end-tidal isoflurane (n = 8), (3) hyperthermia with 1.7% end-tidal enflurane (n = 5), and (4) inhalation of 60% N2O (n = 9). RESULTS: Mild hyperthermia alone (core temperature 38.5 +/- 0.3 degrees C) produced no clinically significant change in the pupillary light reflex. Pupillary responses were decreased markedly with 0.8% isoflurane, 1.2% isoflurane, and 1.7% enflurane when the volunteers were normothermic. Mild hyperthermia combined with isoflurane or enflurane dilated the pupil and increased the amplitude of the light reflex. Sixty-percent nitrous oxide decreased the pupillary reflex only 26 +/- 4%. CONCLUSIONS: Anesthetic-induced inhibition of the pupillary response to light is reversed partially by core hyperthermia. In contrast to enflurane and isoflurane, 60% N2O has little effect on the pupil.

Adult↗

Pupillary assessment of sensory block level during combined epidural/general anesthesia.

BACKGROUND: Currently, no reliable method exists to determine the level of sensory block during combined epidural/general anesthesia. However, the pupil dilates markedly in response to noxious electrical stimulation during general anesthesia. Presumably, sensory block produced by epidural anesthesia decreases or obliterates this autonomic response. Accordingly, we tested the hypothesis that pupillary dilation in response to noxious stimulation would predict the level of sensory block achieved during combined epidural/general anesthesia. METHODS: We studied eight volunteers and ten patients during combined epidural/general anesthesia. The volunteers were given an epidural infusion of 2% 2-chloroprocaine while general anesthesia was maintained with 0.8% isoflurane and 60% N2O. In the patients, an epidural infusion of 0.25% bupivacaine was combined with isoflurane and vecuronium. Noxious electrical stimulation was administered to dermatomal segments in a caudal-to-rostral progression. A twofold increase in pupil size following electrical stimulation was considered the predicted block level in volunteers. In patients, an increase in pupil size exceeding 50% was considered the predicted level. After general anesthesia was discontinued, observers blinded to the pupillary measurements independently determined the actual epidural block level using pain in response to a pinprick as the criterion. RESULTS: The level predicted by pupillary responses was within two dermatomal segments of the actual level in all the volunteers. The predicted and actual block levels were within two segments in eight of the ten patients and never differed by more than four dermatomes. CONCLUSIONS: We conclude that dilation of the pupil in response to electrical stimulation is an accurate test of the sensory block level during combined epidural/general anesthesia.

Adult↗

The effects of preinduction warming on temperature and blood pressure during propofol/nitrous oxide anesthesia.

BACKGROUND: Core temperature decreases rapidly after induction of anesthesia, largely because heat is redistributed to peripheral tissues. The hypothesis that warming peripheral tissues before induction of general anesthesia (prewarming) minimizes hypothermia was tested. Because circulating blood volume may be greater during exposure to heat compared to cold, the hypothesis that prewarming decreases the amount of hypotension associated with induction of anesthesia was tested also. Finally, the hypothesis that the difference between direct radial arterial blood pressure and blood pressure measured oscillometrically at the brachial artery depends on thermoregulatory and anesthetic conditions was tested. METHODS: Each of six volunteers underwent general anesthesia (propofol and nitrous oxide) twice on the same day. Each anesthetic lasted 1 h and was preceded by either 2 h of active warming with forced air or 2 h of passive cooling by exposure to a typical operating room environment. After induction of each anesthetic, volunteers were fully exposed to the ambient environment. Volunteers recovered for 2 h before starting the second preinduction treatment. RESULTS: Initial tympanic membrane temperatures were similar before each preinduction treatment: 36.7 +/- 0.4 degrees C when volunteers were not warmed and 36.7 +/- 0.6 degrees C when volunteers were warmed. Tympanic membrane temperature did not change during the preinduction period without warming but increased slightly (delta T = 0.4 +/- 0.2 degree C) during warming. After induction of anesthesia, core temperatures decreased to 36.1 +/- 0.4 degree C over 1 h when volunteers were prewarmed but decreased to 34.9 +/- 0.4 degrees C when they were not. Radial arterial systolic, diastolic, and mean blood pressures were lower before induction of anesthesia when volunteers were warmed compared to when no warming was given. Oscillometric diastolic and mean pressures also were lower during prewarming; however, oscillometric systolic pressure did not differ significantly. Prewarming did not result in less hypotension after induction. Without warming, the difference (radial arterial minus oscillometric) in systolic blood pressure measurements was approximately 17 mmHg. Warming was associated with a reversal of the systolic pressure difference to approximately -6 mmHg. After induction of anesthesia, the differences in systolic and mean pressure measurements became more negative with respect to the preinduction values regardless of preinduction warming treatment. CONCLUSIONS: These data confirm our hypothesis that redistribution hypothermia can be minimized by preinduction warming of peripheral tissues. Prewarming decreases blood pressure but does not prevent subsequent hypotension after induction. The difference between radical arterial blood pressure and oscillometric blood pressure depends on thermoregulatory vasomotor changes but also may be influenced by vasodilation associated with administration of propofol and nitrous oxide.

Adult↗

The threshold for thermoregulatory vasoconstriction during nitrous oxide/isoflurane anesthesia is lower in elderly than in young patients.

BACKGROUND: Thermoregulatory vasoconstriction minimizes further core hypothermia during anesthesia. Elderly patients become more hypothermic during surgery than do younger patients, and take longer to rewarm postoperatively. These data indicate that perianesthetic thermoregulatory responses may be especially impaired in the elderly. Accordingly, the authors tested the hypothesis that the thermoregulatory threshold for vasoconstriction during nitrous oxide/isoflurane anesthesia is reduced more in elderly than in young patients. METHODS: The authors studied 12 young patients aged 30-50 yr and 12 elderly patients aged 60-80 yr. All were undergoing major orthopedic or open abdominal surgery. Anesthesia was induced with thiopental and fentanyl, and maintained only with nitrous oxide (70%) and isoflurane (0.6-0.8%). Core temperature was measured in the distal esophagus. Fingertip vasoconstriction was evaluated using forearm minus fingertip, skin-temperature gradients. A gradient of 4 degrees C identified significant vasoconstriction, and the core temperature triggering vasoconstriction identified the thermoregulatory threshold. RESULTS: The vasoconstriction threshold was significantly less in the elderly patients (33.9 +/- 0.6 degree C) than in the younger ones (35.1 +/- 0.3 degrees C) (P < 0.01). The gender distribution, weight, and height of the elderly and young patients did not differ significantly. The end-tidal isoflurane concentration at the time of vasoconstriction did not differ significantly in the two groups. CONCLUSIONS: These data indicate that thermoregulatory responses in the elderly are initiated at temperatures approximately 1.2 degrees C less than that in younger patients. Thus, it is likely that elderly surgical patients become more hypothermic than do younger patients, at least in part, because they fail to trigger protective thermoregulatory responses.

Adult↗

Clonidine comparably decreases the thermoregulatory thresholds for vasoconstriction and shivering in humans.

BACKGROUND: Clonidine stops postoperative shivering, but its underlying mechanism of action is unknown. Clonidine may impair central control of thermoregulation or act on peripheral receptors. Accordingly, the authors tested the hypothesis that clonidine reduces both the vasoconstriction and shivering thresholds, a pattern consistent with central thermoregulatory impairment. METHODS: Seven healthy volunteers participated in the study. Thermoregulatory vasoconstriction was evaluated using forearm minus fingertip, skin-temperature gradients; values exceeding 4 degrees C were considered to be significant vasoconstriction. Systemic oxygen consumption (VO2) was measured with a canopy system. In addition, shivering was qualitatively evaluated using a simple scale, graduated from 0 (no shivering) to 2 (intense shivering). The tympanic membrane temperatures triggering significant vasoconstriction and grade 1 shivering were considered to be the thresholds for the two thermoregulatory responses. Measurements were performed after a 10-min steady state period and during cooling by central venous infusion of Ringer's lactate solution at 4 degrees C. Each subject was evaluated at two sessions, separated by at least 48 h. They were randomly and blindly assigned to received either an intravenous bolus of 75 micrograms clonidine or a placebo before cooling. When the shivering score equaled 2, 75 micrograms clonidine was injected intravenously, and repeated if necessary, to completely stop shivering.

Adult↗

Clonidine and ketanserin both are effective treatment for postanesthetic shivering.

BACKGROUND: Although meperidine is an effective treatment of postanesthetic shivering, its mechanism of action remains unknown. Investigation of other drugs might help clarify the mechanisms by which shivering can be controlled. Accordingly, we investigated the efficacy of clonidine, an alpha 2-adrenergic agonist, and ketanserin, a 5-hydroxytryptamine antagonist, in treating postanesthetic shivering. METHODS: First, 54 patients shivering after general anesthesia were allocated randomly to receive an intravenous bolus of saline, 150 micrograms clonidine, or 10 mg ketanserin. A second study explored the dose-dependence of clonidine. Forty shivering patients were given saline or clonidine, 37.5, 75, or 150 micrograms. RESULTS: The duration of shivering was significantly shorter in those given clonidine (2.1 +/- 0.9 min) than in the other two groups and shorter in the ketanserin group (4.3 +/- 0.9 min) than in the saline group (12.0 +/- 1.6 min). Clonidine and ketanserin significantly decreased systolic arterial blood pressure when compared to saline. Core rewarming was significantly slower in the clonidine group. In the second study, 37.5 micrograms clonidine was no more effective than saline. Two minutes after treatment, 150 micrograms obliterated shivering in all patients. Five minutes after treatment, all patients given 75 micrograms had stopped shivering. Systolic arterial pressure and heart rate decreased significantly in patients given 75 and 150 micrograms clonidine. CONCLUSIONS: Clonidine (150 micrograms) and ketanserin (10 mg) both are effective treatment for postanesthetic shivering. The effect of clonidine on shivering is dose-dependent: whereas 37.5 micrograms had no effect, 75 micrograms clonidine stopped shivering within 5 min.

Adult↗

Absence of nonshivering thermogenesis in anesthetized adult humans.

BACKGROUND: Typically, core temperature rapidly decreases after induction of anesthesia, but reaches a stable plateau after several hours. This plateau typically occurs in conjunction with the onset of thermoregulatory vasoconstriction. Decreased heat loss, caused by vasoconstriction, may not be sufficient to establish thermal steady state without a concomitant increase in heat production. Accordingly, the authors tested the hypothesis that nonshivering thermogenesis contributes to thermal steady state during anesthesia. Rewarming from hypothermia is often associated with an afterdrop (a further reduction in core temperature, despite cutaneous warming). Because total body heat content increases during cutaneous warming, heat storage during afterdrop must reflect increased temperature and heat content of the peripheral tissue mass. Thermal balance was measured during rewarming to estimate the thermal capacity of the peripheral tissues. METHODS: Five volunteers were anesthetized with isoflurane and paralyzed with vecuronium. Oxygen consumption was measured during cooling to a core temperature at least 1 degree C less than that which triggered vasoconstriction. Volunteers were subsequently rewarmed using a circulating-water blanket and forced-air warmer. Oxygen consumption and cutaneous heat flux were measured to assess thermal balance and peripheral tissue heat storage during rewarming. RESULTS: The core temperature threshold for vasoconstriction was 35.2 +/- 0.8 degrees C. Oxygen consumption decreased 9 +/- 5%/degrees C during active cooling before vasoconstriction and 9 +/- 3%/degrees C after vasoconstriction. After the start of rewarming, core temperature continued to decrease for an additional 32 +/- 8 min. The magnitude of this afterdrop was 0.6 +/- 0.1 degree C. Peripheral tissue heat storage measured from the start of rewarming until the first net increase in core temperature was 144 +/- 60 kcal, which approximately equals 2 h of resting metabolic heat production. CONCLUSIONS: The authors concluded that nonshivering thermogenesis is not an important thermoregulatory response in adults anesthetized with isoflurane. Afterdrop and delayed core temperature recovery during rewarming reflect the large heat storage capacity of peripheral tissues.

Adult↗

Naloxone, meperidine, and shivering.

BACKGROUND: Meperidine, which binds both mu and kappa opioid receptors, is reportedly more effective in treating shivering than are equianalgesic doses of morphine (a nearly pure mu-receptor agonist). Furthermore, butorphanol, a kappa-receptor agonist/antagonist, treats shivering better than does fentanyl, which mostly binds mu receptors. These data indicate that much of meperidine's special antishivering activity may be mediated by its kappa activity. Accordingly, the authors tested the hypothesis that the antishivering activity of meperidine will be minimally impaired by low-dose naloxone (blocking most mu-receptors), but largely prevented by high-dose naloxone (blocking all mu and most kappa receptors). METHODS: Twelve volunteers each participated on 2 days. On both days, shivering was induced by central venous infusion of cold fluid. Twenty minutes later, six volunteers were given a placebo infusion of saline on one day, or an infusion of 0.5 microgram.kg-1.min-1 naloxone hydrochloride ("low-dose," designed to block mu receptors) on the other. The second group of six volunteers was given a saline bolus and infusion on one day, or a bolus of 11.5 micrograms/kg naloxone hydrochloride followed by an infusion of naloxone at 5 micrograms.kg-1.min-1 ("high-dose," designed to block both mu and kappa receptors) on the other day. The infusions were continued for the duration of the study. The order of the treatment days (saline vs. naloxone) was randomly assigned, and the study was double blinded. Fifteen minutes after the test infusion was started, all 12 volunteers were given an intravenous bolus of 1 mg/kg meperidine hydrochloride. Pupillary diameter and light reflex amplitude were used to quantify opioid-receptor agonist activity; shivering intensity was evaluated using oxygen consumption. RESULTS: Administration of naloxone alone did not alter oxygen consumption, pupil size, or the pupillary light reflex. No pupillary constriction was detected in either group when naloxone and meperidine were combined; in contrast, meperidine alone decreased pupil size and amplitude of the light reflex 30%. The meperidine bolus decreased oxygen consumption nearly to control values when the volunteers were given saline placebo. Combined administration of meperidine and low-dose naloxone also significantly reduced oxygen consumption, but the reduction and the duration of the reduction was less than during saline. When the volunteers were given high-dose naloxone, meperidine only slightly reduced oxygen consumption, and the values rapidly returned to premeperidine levels. CONCLUSIONS: These data indicate that the antishivering property of meperidine is not fully mediated by mu-receptors. Although meperidine has well-known nonopioid actions, stimulation of kappa receptors seems a likely alternative explanation for much of the drug's antishivering action.

Adult↗

Thermoregulatory responses to hyperthermia during isoflurane anesthesia in humans.

The authors tested the hypotheses that isoflurane anesthesia increases the threshold for sweating but minimally decreases the gain (sensitivity) or maximum intensity of this response and that thermoregulatory responses to hyperthermia are similar in anesthetized men and women. Sweating in response to core hyperthermia was studied in five men and five women during 0, 0.8, and 1.2% end-tidal isoflurane anesthesia. Thigh sweating was quantified by measuring gas flow, relative humidity, and temperature passing over a known surface area. The distal esophageal temperature triggering sweating was considered the sweating threshold, and gain was defined as the core temperature increment required to increase sweating rate from 25 to 75% of maximum observed intensity. The sweating threshold increased linearly with isoflurane concentration from 36.6 +/- 0.1 to 38.1 +/- 0.1 degrees C in the men and from 37.1 +/- 0.3 to 38.3 +/- 0.2 degrees C in the women. The thresholds were significantly higher in women than in men. Gain and maximum sweating intensities were similar at each anesthetic concentration and in men and women. These data indicate that isoflurane anesthesia significantly increases the threshold triggering thermoregulatory sweating but that gain and maximum sweating rate are relatively well preserved.

Anesthesia↗

Mild hypothermia does not impair postanesthetic recovery in infants and children.

We tested the hypothesis that mild perioperative hypothermia (e.g., central temperature 34-36 degrees C) does not impair postanesthetic recovery in infants and children. The postoperative course was evaluated in 84 ASA Physical Status 1 or 2 patients, weighing 5-50 kg, who were recovering from peripheral surgery lasting less than 3 h. Postoperative monitoring initiated in the Post Anesthesia Care Unit (PACU) included: 1) rectal (central) temperature; 2) oxyhemoglobin saturation (Spo2) while breathing 21% oxygen; 3) apnea (using impedance pneumography); and 4) duration of recovery determined by an anesthesiologist not involved with the study and unaware of the patients' central temperatures. Data were stratified according to patients' weights and central temperatures on admission to PACU. Recovery was rapid in all patients, with no statistically significant differences in duration of recovery among the groups. Only three patients had Spo2 values less than 90%, and in each case desaturation was observed during only one 15-min epoch and resolved without specific treatment. The lowest observed Spo2 was 82%. These three patients weighed between 10 and 20 kg and had initial temperatures exceeding 36 degrees C. No patient had an apneic episode exceeding 15 s. We conclude that mild hypothermia per se neither impairs respiratory function, nor prolongs postanesthetic recovery in generally infants and children undergoing peripheral surgery.

Anesthesia Recovery Period↗

Pupillary response to noxious stimulation during isoflurane and propofol anesthesia.

We studied the effects of noxious stimuli on arterial blood pressure, heart rate, pupil size, and the pupillary light reflex in 13 volunteers anesthetized with either isoflurane or propofol. Those given isoflurane (n = 8) were anesthetized twice, in a randomly selected order, once at an end-tidal concentration of 0.8% and once at 1.2%. An intense noxious stimulus was provided by electrical stimulation applied to skin of the abdominal wall (65-70 mA, 100 Hz). Hemodynamic values and pupillary responses were recorded immediately before stimulation and at 15-60-s intervals during 8 subsequent min. In the volunteers given isoflurane (both concentrations), stimulation significantly increased pupil size (265 +/- 44%) and the amplitude of the light reflex (233 +/- 23%). In contrast, mean heart rate and systolic blood pressure increased only 19 +/- 7% and 13 +/- 7% after stimulation. Five additional volunteers were anesthetized twice with propofol (approximately 3 micrograms/mL plasma concentration) and 60% nitrous oxide. The same electrical stimulus was applied, and hemodynamic and pupillary measurements were obtained. During one propofol anesthetic, an esmolol infusion (100 micrograms.kg-1 x min-1) was started 10 min before stimulation to determine whether this agent would blunt the pupillary response. The pupillary light reflex increased more than 200% during both propofol anesthetics with or without esmolol; once again, heart rate and blood pressure changed little. We conclude that with these experimental conditions, the pupil is a more sensitive measure of noxious stimulation than the commonly used variables of arterial blood pressure and heart rate.

Adult↗

Heat loss in humans covered with cotton hospital blankets.

We evaluated mean skin temperature, cutaneous heat loss, and perceived warmth in six volunteers covered with one or three cotton hospital blankets, warmed or unwarmed. Mean skin temperatures were significantly higher during each treatment than during the control periods preceding each blanket application. Total cutaneous heat loss during the control period was 81 +/- 11 watts. Covering the volunteers with a single warmed or unwarmed blanket for 60 min reduced heat loss 33% +/- 5%; when they were covered with three warmed or unwarmed blankets, heat loss was reduced an additional 18% +/- 6%. Warmed blankets reduced heat loss 9-16 watts more than unwarmed ones, but the benefit dissipated in approximately 10 min. The volunteers' perception of warmth was similar when they were covered with three warmed or unwarmed blankets; it also was similar when they were covered with a single warmed or unwarmed blanket. These data indicate that increasing the number of covering blankets from one to three decreases heat loss only slightly. Similarly, warming the blankets is relatively ineffective and the benefit short-lived. The reduction in heat loss, even by three warmed blankets replaced at 10-min intervals, was small compared to that provided by available active warming systems.

Adult↗

Preanesthetic skin-surface warming reduces redistribution hypothermia caused by epidural block.

Redistribution of heat from the core to the cool peripheral compartments of the body causes hypothermia during epidural anesthesia. Diminishing the temperature gradient between the core and peripheral tissues by warming the body via the skin before anesthesia should prevent this hypothermia. We measured core temperature, skin temperatures, and cutaneous heat loss in seven volunteers who received two lidocaine epidural injections during a single study day. One epidural injection was given after the volunteer had rested in a cool room (approximately 22 degrees C) ("no prewarming") for 2 h, and one injection was given after the volunteer had been covered with a forced air warming mattress (approximately 38 degrees C) ("prewarming") for 2 h. Skin temperatures were higher after prewarming. The decrease in core temperature during epidural anesthesia was smaller after prewarming [mean within patient difference (prewarming-no prewarming): 0.41; P = 0.003]. However, heat loss was greater after prewarming (mean within patient difference: 26.4; P = 0.02). Shivering was less after prewarming. We conclude that prewarming decreases redistribution hypothermia caused by epidural block. These results support the hypothesis that redistribution of heat within the body, not heat loss, is the most important etiology of hypothermia from epidural anesthesia.

Adult↗

Thermoregulatory response thresholds during spinal anesthesia.

Reportedly, during spinal anesthesia, the shivering threshold is reduced approximately 1 degree C but the vasoconstriction threshold remains normal. Such divergence between the shivering and vasoconstriction thresholds is an unusual pattern of thermoregulatory impairment and suggests that the mechanisms of impairment during regional anesthesia may be especially complex. Accordingly, we sought to define the pattern of thermoregulatory impairment during spinal anesthesia by measuring response thresholds. Seven healthy women volunteered to participate on two study days. On one day, we evaluated thermoregulatory responses to hypothermia and hyperthermia during spinal anesthesia; on the other day, responses were evaluated without anesthesia. Upper body skin temperature was kept constant throughout the study. The volunteers were warmed via the lower body and cooled by central venous infusion of cold fluid. The core temperatures triggering a sweating rate of 40 g.m-2 x h-1, a finger flow of 0.1 mL/min, and a marked and sustained increase in oxygen consumption were considered the thermoregulatory thresholds for sweating, vasoconstriction, and shivering, respectively. Spinal anesthesia significantly decreased the thresholds for vasoconstriction and shivering, and the decrease in each was approximately 0.5 degree C. The range of temperatures not triggering thermoregulatory responses (those between sweating and vasoconstriction) was 0.9 +/- 0.6 degree C during spinal anesthesia. The synchronous decrease in the shivering and vasoconstriction thresholds during spinal anesthesia is consistent with thermoregulatory impairment resulting from altered afferent thermal input.

Adult↗

The direction dependence of thermoregulatory vasoconstriction during isoflurane/epidural anesthesia in humans.

We tested the hypothesis that once thermoregulatory vasoconstriction is triggered at a given core temperature during isoflurane anesthesia, redilation starts at a substantially higher core temperature. To avoid direct perception of cutaneous cooling and warming, we used epidural anesthesia and limited our thermal manipulations to the blocked area. Seven volunteers were anesthetized with isoflurane/epidural anesthesia (approximately T9 dermatomal level). Core hypothermia was induced by surface cooling restricted to the legs. Cooling was continued until fingertip blood flow suddenly decreased (vasoconstriction threshold). The core was then rewarmed by heating the legs until fingertip flow suddenly increased toward initial values (redilation threshold). The difference between the two thresholds defined the direction-dependent hysteresis. Vasoconstriction occurred at 35.2 +/- 0.6 degrees C and vasodilation at 36.2 +/- 0.5 degrees C (P < 0.01, paired t-test); consequently, the hysteresis was 1.0 +/- 0.6 degrees C. The observed hysteresis suggests that thermoregulatory responses during combined isoflurane/epidural anesthesia are not determined simply by instantaneous thermal input to central controllers, but may also depend on the direction of core temperature change.

Adult↗