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Biomedical subjects

D I Sessler

Publications and source records attributed to D I Sessler.

At least 163 records · Page 9Linked to original sources
PubMed1996

Rapid core-to-peripheral tissue heat transfer during cutaneous cooling.

Perioperative thermal manipulations are usually directed at the skin surface because methods of directly warming the core are invasive or ineffective. However, inadequate heat flow between peripheral and core compartments will decrease the rate at which core temperature changes. We therefore determined whether core hypothermia is delayed after initiation of surface cooling. Six volunteers were anesthetized with propofol and midazolam, and maintained under three layers of passive insulation for 2.5-4 h. Subsequently, the skin surface was cooled using forced air, 1000 L/min, at 10 degrees C. Isoflurane was added as necessary to maintain arteriovenous shunt vasodilation. Overall heat balance was determined from the difference between cutaneous heat loss (thermal flux transducers) and metabolic heat production (oxygen consumption). Average arm and leg (peripheral) tissue temperatures were determined from 19 intramuscular needle thermocouples, 10 skin temperatures, and "deep" foot temperature. Overall body heat content decreased approximately 234 kcal during 2.5 h of active cooling. Core temperature, which was nearly constant before active cooling, decreased approximately 1.3 degrees C/h. There was no delay between initiation of active cooling and the decrease in core temperature. Furthermore, peripheral (arm and leg) and core (trunk and head) tissue heat contents decreased at virtually the same rates: approximately 50 kcal/h and approximately 47 kcal/h, respectively. These data indicate that there is little restriction of heat flow between peripheral and core tissues in vasodilated, anesthetized subjects.

Adult↗
PubMed1996

Enflurane decreases the threshold for vasoconstriction more than isoflurane or halothane.

Intraoperative hypothermia results largely from anesthetic-induced inhibition of tonic thermoregulatory vasoconstriction. Sufficient hypothermia, however, triggers peripheral vasoconstriction, which usually prevents further decrease in core temperature. The thermoregulatory effects of all volatile anesthetics have been tested in adults and/or children, but different anesthetics have not been directly compared. We therefore evaluated thermoregulatory responses during enflurane, isoflurane, and halothane administration. Anesthesia was maintained with 1 minimum alveolar anesthetic concentration (MAC) of halothane, isoflurane, or enflurane in 27 patients undergoing intraabdominal surgery. Patients were maintained normovolemic and normocapnic but were allowed to cool passively. A forearm minus fingertip, skin-temperature gradient of 4 degrees C identified significant vasoconstriction; the core temperature triggering vasoconstriction identified the threshold. Morphometric characteristics, initial core temperatures, ambient operating room temperatures, blood pressures, and anesthetic potencies were similar in each group. All eight patients given halothane vasoconstricted at a core temperature of 35.5 +/- 0.6 degrees C. Eight of the patients given isoflurane vasoconstricted at a core temperature of 35.2 +/- 0.5 degrees C. However, two others did not at minimum core temperatures of 34.0 and 33.8 degrees C. Only one patient given enflurane vasoconstricted at a core temperature of 34.6 degrees C. The other six patients never vasoconstricted, at minimum core temperatures of 33.6 +/- 0.4 degrees C. Our data indicate that enflurane profoundly inhibits thermoregulatory responses in children. The mechanism for this extraordinary inhibition remains unknown but does not result from any obvious anesthetic pharmacology or thermoregulatory physiology. We conclude that unwarmed pediatric patients will become colder when anesthetized with enflurane than with halothane or isoflurane.

Anesthetics, Inhalation↗
PubMed1996

Clonidine increases the sweating threshold, but does not reduce the gain of sweating.

We tested the hypothesis that clonidine produces a dose-dependent increase in the sweating threshold but does not reduce the gain of sweating. Six healthy male volunteers were evaluated, each on three separate days in random order. In one, saline was administered; in another, a 2-micrograms/kg bolus of clonidine was followed by an infusion at 2 micrograms.kg-1.h-1, and on a third day, a 4-micrograms/kg bolus was followed by an infusion at 4 micrograms.kg-1.h-1. Core temperature was measured at the tympanic membrane and mean skin temperature was determined from four sites. A chest sweating rate of 40 g.m-2.h-1 was considered significant. The core temperature triggering sweating, adjusted to a designated mean skin temperature of 34 degrees C, identified the threshold for this response. Gain was defined by the adjusted core temperature increase required to augment sweating from 100 to 300 g.m-2.h-1. degree C-1. Plasma clonidine concentrations were 0.8 +/- 0.1 and 1.6 +/- 0.2 ng/mL on the small- and large-dose days, respectively. Clonidine administration increased the sweating threshold approximately 0.4 degree C (P < 0.05), but the increase was comparable at each dose. The gain of sweating was approximately 0.2 degree C and was not influenced by clonidine administration. The thermoregulatory effects of clonidine thus resemble those of volatile anesthetics, opioids, and propofol. These data suggest that the antishivering effect of clonidine results from central thermoregulatory inhibition rather than a specific peripheral action on thermogenic muscular activity. Unlike other sedatives and anesthetics, the concentration-dependence of clonidine demonstrates a ceiling beyond which the administration of an additional drug fails to enhance the effect, suggesting that the thermoregulatory effect of clonidine may be limited, even at high plasma concentrations. The gain of sweating was well preserved indicating that this response remains effective in the presence of sedatives and anesthetics.

Adrenergic alpha-Agonists↗
PubMed1996

Prediction of movement during propofol/nitrous oxide anesthesia. Performance of concentration, electroencephalographic, pupillary, and hemodynamic indicators.

BACKGROUND: Movement in response to painful stimulation is the end point classically used to assess the potency of anesthetic agents. In this study, the ability of modeled propofol effect-site concentration to predict movement in volunteers during propofol/nitrous oxide anesthesia was tested, then it was compared with the predictive abilities of the Bispectral Index and 95% spectral edge frequency of the electroencephalogram, pupillary reflex amplitude, and systolic arterial blood pressure. In addition, the relationships between simple end points of loss and recovery of consciousness, and pupillary, hemodynamic, and propofol concentration indicators were studied. METHODS: Ten healthy volunteers were anesthetized with an infusion of propofol, which was increased in three equal steps to 21 mg.kg lean body mass-1.h-1. After loss of the ability to hold a syringe and of the eyelash reflex, 60% nitrous oxide was introduced and the trachea was intubated without the use of muscle relaxants. The propofol infusion rate then was decreased to 15.4 mg.kg lean body mass-1.h-1. Ten minutes later, tetanic electrical stimulation was administered to the thigh via needle electrodes: if movement was observed within 1 min, the propofol infusion rate was increased by 1.75 mg.kg lean body mass-1.h-1 5 min after the stimulus; if not, it was similarly decreased. This 15-min sequence was repeated until volunteers "crossed over" from movement to no movement (or vice versa) four times. The propofol infusion rate then was increased to 21 mg.kg lean body mass-1.h-1, nitrous oxide was discontinued, the trachea was extubated, and the infusion rate was decreased in five equal steps over 50 min. The times at which the eyelash reflex returned and the birth date was recalled were recorded. The electroencephalogram was monitored continuously (FP1, FP2, ref: nasion, ground: mastoid). Measurements of the pupillary response, arterial blood pressure, and heart rate were recorded during induction and awakening, just before and for 5 min after each stimulation. Arterial blood samples were obtained for propofol assay, and propofol effect-site concentrations were calculated at each time. The predictive value of indicators was compared using a new static, the prediction probability (PK). RESULTS: Loss and return of the eyelash reflex occurred at greater propofol effect-site concentrations than either dropping the syringe or recall of the birthday. The propofol effect-site concentration (in the presence of 60% nitrous oxide) predicted to prevent movement after a supramaximal stimulus in 50% of volunteers was 1.80 micrograms/ml (95% confidence limits: 1.40-2.34 micrograms/ml). The Bispectral Index (PK = 0.86), 95% spectral edge frequency (PK = 0.81), pupillary reflex amplitude (PK = 0.74), and systolic arterial blood pressure (PK = 0.78) did not differ significantly from modeled propofol effect-site concentration (PK = 0.76) in their ability to predict movement. CONCLUSIONS: Indicators of pharmacodynamic effect, such as the electroencephalogram, pupillary light reflex, and systolic arterial blood pressure, predict movement as well as effect-site concentration during propofol/nitrous oxide anesthesia. Loss and return of the eyelash reflex correspond to a deeper level of anesthesia than syringe-dropping or recall of the birth date.

Adult↗
PubMed1996

Reduction in the shivering threshold is proportional to spinal block height.

BACKGROUND: Hypothermia is nearly as common, and may be as severe, during spinal and epidural anesthesia as during general anesthesia. The authors have proposed that thermoregulatory failure results when regional anesthesia increases apparent leg skin temperature to a level far exceeding actual leg skin temperature. Extensive dermatomal blocks will alter thermal input to the hypothalamus from a greater skin-surface area more than less extensive ones and thus might be expected to impair central thermoregulatory control more. Accordingly, they tested the hypothesis that reduction in the shivering threshold is directly related to the number of dermatomes blocked during spinal anesthesia. METHODS: Eleven men, aged 62 +/- 6 yr (mean +/- SD), undergoing urologic surgery were studied. Ice-cold lactated Ringer's solution was administered intravenously before spinal blockade and the shivering threshold (triggering core temperature) was established. Spinal anesthesia then was induced using a randomly assigned dose of 0.5% bupivacaine (2-4 ml). Again, sufficient cold lactated Ringer's solution was given to induce shivering. Tympanic membrane, ambient and skin temperatures were measured, and extent of block was defined by loss of temperature discrimination. Presence of shivering was evaluated by a blinded observer. Mean upper-body skin and ambient temperatures, cooling rates and intravenous fluid volumes at the two thresholds were compared using paired, two-tailed t tests (P < 0.05). Linear regression defined the relationship between reduction in shivering threshold and the number of dermatomes blocked. RESULTS: There were no significant differences between mean upper-body skin and ambient temperatures, cooling rates or intravenous fluid volumes at the control and spinal shivering thresholds. Spinal anesthesia reduced the shivering threshold in direct relation to the number of dermatomes blocked: delta threshold = 0.74 - 0.06 (dermatomes blocked); r2 = 0.58, P < 0.006. CONCLUSIONS: Extensive spinal blockade impairs central thermoregulatory control more than less extensive blockade. Clinicians can thus anticipate more core hypothermia during extensive than during restricted spinal blockade.

Aged↗
PubMed1996

Isoflurane produces marked and nonlinear decreases in the vasoconstriction and shivering thresholds.

BACKGROUND: Desflurane decreases the vasoconstriction and shivering thresholds disproportionately at high anesthetic concentrations. This result contrasts with the authors' previous report that isoflurane decreases the vasoconstriction threshold linearly. It is surprising that the basic shape of the concentration-response curve should differ with these two otherwise similar anesthetics. Therefore, the hypothesis that isoflurane produces a nonlinear reduction in the vasoconstriction threshold was tested. Because the effect of isoflurane on shivering remains unknown, the extent to which isoflurane reduces the shivering threshold also was determined. METHODS: Eight men volunteered to be studied on four randomly ordered days: (1) a target end-tidal isoflurane concentration of 0.55%, (2) a target concentration of 0.7%, (3) control (no anesthesia) and a target end-tidal concentration of 0.85%, and (4) a target end-tidal concentration of 1.0%. Volunteers were surface-cooled until peripheral vasoconstriction and shivering were observed. We arithmetically compensated for changes in skin temperature using the established linear cutaneous contributions to control for each response. From the calculated thresholds (core temperatures triggering responses at a designated skin temperature of 34 degrees C), the concentration-response relation was determined. RESULTS: Isoflurane administration produced a dose-dependent reduction in the vasoconstriction and shivering thresholds, decreasing each approximately 4.6 degrees C at an end-tidal concentration of 1%. Residual analysis indicated that the vasoconstriction and shivering thresholds were decreased in a nonlinear fashion during isoflurane administration. The vasoconstriction-to-shivering range was 1.5 +/- 0.8 degree C without isoflurane, and did not change significantly during isoflurane administration. CONCLUSIONS: The vasoconstriction-to-shivering range remained unchanged by isoflurane administration. In this regard, the effects of isoflurane are similar to those of desflurane, propofol, and alfentanil. The current data differ from the authors' previous report, in that the dose-dependence for vasoconstriction was nonlinear, with isoflurane reducing the threshold disproportionately at higher anesthetic concentrations. Differing dose-dependence in the two studies may result either because the current study's volunteers were not exposed to surgical stimulation and were given less isoflurane, or because of design limitations in the previous protocol.

Adult↗
PubMed1996

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 C/h). CONCLUSIONS: The authors failed to confirm their hypothesis that thermoregulatory vasoconstriction decreases cutaneous transfer of applied heat and restricts peripheral-to-core flow of heat in anesthetized subjects. The reported difference between intraoperative and postoperative rewarming efficacy may result from nonthermoregulatory anesthetic-induced vasodilation.

Adult↗
PubMed1996

Sympathetic nervous system does not mediate reflex pupillary dilation during desflurane anesthesia.

BACKGROUND: Pupil size is determined by an interaction between the sympathetic and parasympathetic divisions of the autonomic nervous system. Noxious stimulation dilates the pupil in both unanesthetized and anesthetized humans. In the absence of anesthesia, dilation is primarily mediated by the sympathetic nervous system. In contrast, pupillary dilation in cats given barbiturate or cloralose anesthesia is mediated solely by inhibition of the midbrain parasympathetic nucleus. The mechanism by which noxious stimuli dilate pupils during anesthesia in humans remains unknown. Accordingly, the authors tested the hypothesis that the pupillary dilation in response to noxious stimulation during desflurane anesthesia is primarily a parasympathetic reflex. METHODS: In six volunteers, the alpha-I adrenergic receptors of the iris musculature were blocked by unilateral administration of topical dapiprazole; six other volunteers were given unilateral topical tropicamide to block the muscarinic receptors in the iris. Desflurane anesthesia was subsequently induced in all volunteers. Sympathetic nervous system activation, with reflex dilation of the pupil, was produced by noxious electrical stimulation during 4% and 8% end-tidal desflurane, and by a rapid 4%-to-8% step-up in the desflurane concentration. Pupil diameter and the change in pupil size induced by a light stimulus (light reflex amplitude) were measured with infrared pupillometry. RESULTS: Dapiprazole drops produced a Horner's miosis, but pupils were equally small after induction of anesthesia. Pupillary dilation after noxious stimulation and desflurane step-up was identical in the unblocked and dapiprazole-blocked pupils. After tropicamide administration, the pupil was dilated and the light reflex was completely inhibited. Noxious stimulation nonetheless produced a slight additional dilation. CONCLUSIONS: During desflurane anesthesia, pupillary dilation in response to noxious stimulation or desflurane step-up is not mediated by the sympathetic nervous system (as it is in unanesthetized persons). Although inhibition of the pupillo-constrictor nucleus may be the cause of this dilation, the mechanism remains unknown.

Administration, Topical↗
PubMed1996

First and second phases of biphasic fever: two sequential stages of the sickness syndrome?

We hypothesized that the systemic inflammatory response undergoes two consecutive stages, each characterized by different nonspecific sickness patterns. To test this hypothesis, we studied thermal, nociceptive, and motor responses to lipopolysaccharide (LPS) in 43 unanesthetized, habituated, and lightly restrained male Wistar rats previously implanted with a catheter in the jugular vein. Escherichia coli LPS was injected intravenously in a dose of 0, 0.1, 1, 10, 100, or 1,000 micrograms/kg. Colonic temperature (Tc) was measured with a thermocouple. Changes in nociception were assessed by tail flick latency (TFL) to a noxious heat stimulus. Motor activity was evaluated using an observation-based activity score (AS). The two lowest doses were apyrogenic. The next dose induced a monophasic fever with a maximal Tc rise of 0.9 +/- 0.2 degrees C at 108 +/- 11 min post-LPS. The next two higher doses caused biphasic fevers with the first and second peaks of 0.7 +/- 0.1 and 1.4 +/- 0.1 degrees C (10 micrograms/kg) and 0.7 +/- 0.1 and 1.4 +/- 0.2 degrees C (100 micrograms/kg) occurring at 60 +/- 6 and 165 +/- 17 min and at 45 +/- 3 and 141 +/- 6 min, respectively. The highest dose of LPS resulted in a Tc fall (nadir, -0.6 +/- 0.1 degree C at 83 +/- 6 min). Two different sickness patterns were exhibited. The first (high Tc, low TFL and high AS) occurred during the monophasic fever and the first (early) phase of the biphasic fevers, and it was termed the early phase syndrome. The second pattern (high or low Tc, high TFL, and low AS) developed during the second (late) phase of the biphasic fevers and LPS-hypothermia (endotoxin shock), and it was termed the late phase syndrome. Occurring at different stages of the systemic inflammatory response and developing through different coping patterns [fight/flight (energy expenditure) vs. depression/withdrawal (energy conservation)], the two syndromes represent two different types of adaptation to infection and have different biological significance. Viewing sickness as a dynamic entity is justified clinically. Such a dynamic approach to the problem resolves several contradictions in the current concept of sickness.

Animals↗
PubMed1996

Thermoregulatory vasoconstriction and perianesthetic heat transfer.

Heat transfer between the core and its environment in normothermic and slightly hypothermic situations is determined largely by the influence of vasomotion on convection. Tonic vasoconstriction, the normal barrier to heat loss from the core, is impaired upon induction of anesthesia. The resulting dilation of the arteriovenous shunts leads to redistribution of heat from the core to the periphery, diminishing the temperature gradient between the two compartments. With reemergence of thermoregulatory vasoconstriction at core temperatures near 34 degrees C, the core and the periphery are again separated, with metabolic heat being largely constrained to the core. Under normal conditions of mild thermal stress, thermoregulatory vasoconstriction is thus able to protect core temperature by reducing cutaneous heat transfer and functionally isolating the peripheral and core thermal compartments. Consequently, anesthetic-induced alterations in vasomotor tone is one of the major factors influencing core temperature in patients who are not actively cooled or warmed. In contrast, thermoregulatory tone is insufficient to prevent core temperature perturbations in patients undergoing vigorous cutaneous cooling or warming.

Anesthesia, General↗
PubMed1996

Thermoregulation and hyperthermia.

Despite minor daily and monthly cyclical variations, body temperature remains relatively constant. Core temperature is maintained by thermoregulatory responses such as sweating, vasoconstriction and shivering, which are largely controlled by the hypothalamus. Within the hierarchy of neural structures regulating autonomic thermoregulatory responses, the preoptic area of the anterior hypothalamus plays a dominant role. In contrast, the posterior hypothalamus mediates behavioral defenses. Neurons in both regions sense core temperature and integrate central and peripheral thermal information. The setpoint temperature is then determined by relative synaptic inputs to warm-sensitive, cold-sensitive, and temperature-insensitive neurons. Fever is a regulated elevation in the preoptic setpoint temperature. Endogenous pyrogens and other fever mediators inhibit preoptic warm-sensitive neurons that normally facilitate heat loss and suppress heat production. This elevates the setpoint temperature for all thermoregulatory responses and activates cold-defenses such as vasoconstriction (which decreases heat loss) and shivering (which increases metabolic heat production). When pyrogen concentrations decrease, the setpoint temperature returns towards normal, triggering active vasodilation and sweating, which increases heat loss from the skin surface. The increasing phase of fever is often associated with shivering, which can markedly increase heart rate and cardiac output. Defervescence (and passive hyperthermia) is also often accompanied by tachycardia resulting from active precapillary vasodilation. Thus, cardiovascular complications are common throughout the febrile course and constitute the major clinical consequence of fever.

Body Temperature↗
PubMed1995

Localized or systemic in vivo heat inactivation of human immunodeficiency virus (HIV): a mathematical analysis.

Temperatures > or = 42 degrees C, maintained for > or = 25 min, inactivate approximately 25% of human immunodeficiency virus (HIV). HIV-infected T cells are more sensitive to heat than healthy lymphocytes, and susceptibility increases when the cells are presensitized by exposure to tumor necrosis factor. Thus, induction of a whole-body hyperthermia or hyperthermia specifically limited to tissues having a high viral load is a potential antiviral therapy for acquired immunodeficiency syndrome (AIDS). Accordingly, we incorporated therapeutic hyperthermia into an existing mathematical model that evaluates the interaction between HIV and CD4+ T cells. Given the assumptions and limitations of this model, the results indicate that a daily therapy lowering the population of actively infected cells by 40% or infectious virus by 40% would effectively reverse the depletion of T cells. In contrast, a daily decline of 20% of either actively infected cells or infectious virus would have a marginal effect. However, daily reduction by 20% of both actively infected cells and infectious virus could restore T-cell numbers, assuming that permanent damage had not been inflicted on the thymus. Since daily treatments would probably be excessively stressful, whole-body hyperthermia seems unlikely to be clinically useful. In contrast, heating directed specifically to areas of viral concentration may be effective and have a suitable risk/benefit ratio.

CD4 Lymphocyte Count↗
PubMed1995

Postoperative hemodynamic and thermoregulatory consequences of intraoperative core hypothermia.

STUDY OBJECTIVE: To evaluate the postoperative hemodynamic and thermoregulatory consequences of intraoperative core hypothermia. DESIGN: Prospective, randomized clinical trial. SETTING: Operating room and postanesthesia care unit of a university hospital. PATIENTS: 74 healthy, ASA status I, II, and III patients (average age 58 yrs) undergoing elective colon surgery. INTERVENTIONS: Patients were randomly assigned to be kept normothermic or approximately 2.5 degrees C hypothermic during surgery. Anesthesia was maintained with isoflurane, nitrous oxide, and fentanyl. Postoperatively, surgical pain was treated with patient-controlled analgesia (PCA) opioid. MEASUREMENTS AND MAIN RESULTS: An observer blinded to group assignment and core temperatures evaluated shivering, thermal comfort, surgical pain, heart rates (HRs), and blood pressures (BPs) during the first six postoperative hours. Morphometric characteristics, oxygen saturation, fluid balance, PCA-administered opioid, and visual analog pain scores were comparable in the two groups. Hypothermic patients felt uncomfortably cold during recovery, and their postoperative core temperatures remained significantly less than in the normothermic patients for more than four hours. Peripheral vasoconstriction and shivering were common in the hypothermic patients but rare in those kept normothermic. HRs and BPs were comparable in the two groups. CONCLUSIONS: These data confirm that the effects of intraoperative hypothermia on postoperative HR and BP are modest in relatively young, generally healthy patients. In contrast, intraoperative hypothermia caused substantial postoperative thermal discomfort, and full recovery from hypothermia required many hours. Delayed return to care normothermia apparently resulted largely from postoperative thermoregulatory impairment.

Analgesia, Patient-Controlled↗
PubMed1995

Pre-induction skin-surface warming minimizes intraoperative core hypothermia.

STUDY OBJECTIVE: To test the hypothesis that only one hour of preinduction skin-surface warming decreases the rate at which core hypothermia develops during the first hour of anesthesia. DESIGN: Randomized, prospective study. SETTING: Operating theater of a university hospital. PATIENTS: 16 ASA status I and II adult patients scheduled for laparoscopic cholecystectomy under general anesthesia. INTERVENTIONS: Eight patients were assigned to receive forced-air warming for one hour before induction of anesthesia (prewarmed group); the other eight patients were covered only with a wool blanket during a similar preinduction period (control group). MEASUREMENTS AND MAIN RESULTS: Tympanic membrane (core) and mean skin-surface temperatures were measured at 15-minutes intervals, starting one hour before induction of anesthesia. Mean skin temperature increased from 34.0 +/- 0.1 C to 37.0 +/- 0.2 degrees C in the pre-warmed group (p < 0.05), but remained unchanged at 34.7 +/- 0.3 degrees C in the control group. Core temperature during the preinduction period did not change significantly in either group. Following induction of anesthesia, core temperature decreased at a rate of 1.1 +/- 0.1 degrees C/hr in the control group, but only 0.6 +/- 0.1 degrees C/hr in the pre-warmed group (p < 0.05). After one hour of anesthesia, six of eight pre-warmed patients had core temperatures of at least 36.5 degrees C, whereas only one of the eight control patients did (p < 0.05). CONCLUSIONS: A single hour of preoperative skin-surface warming reduced the rate at which core hypothermia developed during the first hour of anesthesia. Preoperative skin surface warming is particularly helpful during short procedures because redistribution hypothermia is otherwise difficult to treat.

Adult↗
PubMed1995

Morphometric influences on intraoperative core temperature changes.

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

Adult↗