Thermoregulatory vasoconstriction impairs active core cooling

BACKGROUND: Many clinicians now consider hypothermia indicated during neurosurgery. Active cooling often will be required to reach target temperatures < 34 degrees C sufficiently rapidly and nearly always will be required if the target temperature is 32 degrees C. However, the efficacy even of active cooling might be impaired by thermoregulatory vasoconstriction, which reduces cutaneous heat loss and constrains metabolic heat to the core thermal compartment. The authors therefore tested the hypothesis that the efficacy of active cooling is reduced by thermoregulatory vasoconstriction. METHODS: Patients undergoing neurosurgical procedures with hypothermia were anesthetized with either isoflurane/nitrous oxide (n = 13) or propofol/fentanyl (n = 13) anesthesia. All were cooled using a prototype forced-air cooling device until core temperature reached 32 degrees C. Core temperature was measured in the distal esophagus. Vasoconstriction was evaluated using forearm minus fingertip skin-temperature gradients. The core temperature triggering a gradient of 0 degree C identified the vasoconstriction threshold. RESULTS: In 6 of the 13 patients given isoflurane, vasoconstriction (skin-temperature gradient = 0 degrees C) occurred at a core temperature of 34.4 +/- 0.9 degree C, 1.7 +/- 0.58 h after induction of anesthesia. Similarly, in 7 of the 13 patients given propofol, vasoconstriction occurred at a core temperature of 34.5 +/- 0.9 degree C, 1.6 +/- 0.6 h after induction of anesthesia. In the remaining patients, vasodilation continued even at core temperatures of 32 degrees C. Core cooling rates were comparable in each anesthetic group. However, patients in whom vasodilation was maintained cooled fastest. Patients in whom vasoconstriction occurred required nearly an hour longer to reach core temperatures of 33 degrees C and 32 degrees C than did those in whom vasodilation was maintained (P < 0.01). CONCLUSIONS: Vasoconstriction did not produce a full core temperature "plateau," because of the extreme microenvironment provided by forced-air cooling. However, it markedly decreased the rate at which hypothermia developed. The approximately 1-h delay in reaching core temperatures of 33 degrees C and 32 degrees C could be clinically important, depending on the target temperature and the time required to reach critical portions of the operation.     

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.     

Desflurane reduces the febrile response to administration of interleukin-2

BACKGROUND: Intraoperative fever is relatively rare considering how often pyrogenic causes are likely to be present and how common fever is postoperatively. This low incidence suggests that general anesthesia per se inhibits the normal response to pyrogenic stimulation. The authors therefore tested the hypothesis that desflurane-induced anesthesia produces a dose-dependent inhibition of the febrile response. METHODS: Eight volunteers were studied, each on 3 study days. Each was given an intravenous injection of 50,000 IU/ kg of interleukin-2 (elapsed time, 0 h), followed 2 h later by 100,000 IU/kg. One hour after the second dose, the volunteers were assigned randomly to three doses of desflurane to induce anesthesia: (1) 0.0 minimum alveolar concentration (MAC; control), (2) 0.6 MAC, and (3) 1.0 MAC. Anesthesia continued for 5 h. Core temperatures were recorded from the tympanic membrane. Thermoregulatory vasoconstriction was evaluated using forearm-minus-fingertip skin temperature gradients; shivering was evaluated with electromyography. Integrated and peak temperatures during anesthesia were compared with repeated-measures analysis of variance and Scheffé's F tests. RESULTS: Values are presented as mean +/- SD. Desflurane reduced the integrated (area under the curve) febrile response to pyrogen, from 7.7 +/- 2.0 degrees C x h on the control day to 2.1 +/- 2.3 degrees C x h during 0.6 MAC and to -1.4 +/- 3.1 degrees C x h during 1.0 MAC desflurane-induced anesthesia. Peak core temperature (elapsed time, 5-8 h) decreased in a dose-dependent fashion: 38.6 +/- 0.5 degrees C on the control day, 37.7 +/- 0.7 degrees C during 0.6 MAC and 37.2 +/- 1.0 degrees C during 1.0 MAC desflurane anesthesia. Rising core temperature was always associated with fingertip vasoconstriction and often with shivering. CONCLUSIONS: Desflurane-induced anesthesia produced a dose-dependent decrease in integrated and peak core temperatures after administration of pyrogen, with 1.0 MAC essentially obliterating fever. Anesthetic-induced inhibition of the pyrogenic response is therefore one reason that fever is an inconsistent clinical response to inflammation during surgery.     

Shivering threshold during spinal anesthesia is reduced in elderly patients

BACKGROUND: Both accidental and perioperative hypothermia are common in the elderly. The elderly are at risk because their responses to hypothermia may be delayed or less efficient than in those of younger subjects. For example, the vasoconstriction threshold during isoflurane anesthesia is approximately 1 degree C less in elderly than younger patients. However, the extent to which other cold defenses are impaired in the elderly remains unclear, especially in those older than 80 yr. Operations suitable for spinal anesthesia provided an opportunity to quantify shivering thresholds in patients of varying ages. Accordingly, the hypothesis that the shivering threshold is reduced as a function of age during spinal anesthesia was tested. METHODS: Twenty-eight ASA Physical Status 1-3 patients undergoing lower extremity orthopedic procedures were studied. Spinal anesthesia was induced without preanesthetic medication, using bupivacaine sufficient to produce a dermatomal level near T9. Electrocardiogram signals were recorded at 10-min intervals. Subsequently, an observer masked to patient age and core temperature identified the onset of sustained electromyographic artifact consistent with shivering. The tympanic membrane temperature triggering shivering identified the threshold. RESULTS: Three patients did not shiver at minimum core temperatures exceeding 36.2 degrees C. Fifteen patients aged < 80 yr (58 +/- 10 yr) shivered at 36.1 +/- 0.6 degrees C; in contrast, ten patients aged > or = 80 yr (89 +/- 7 yr) shivered at a significantly lower mean temperature, 35.2 +/- 0.7 degrees C (P = 0.002). The shivering thresholds in seven of the ten patients older than 80 yr was less than 35.5 degrees C, whereas the threshold equaled or exceeded this value in all younger patients (P = 0.0002). CONCLUSIONS: Age-dependent inhibition of autonomic thermoregulatory control in the elderly might be expected to result in hypothermia. That it usually does not suggests that behavioral regulation (e.g., increasing ambient temperature, dressing warmly) compensates for impaired autonomic control. Elderly patients undergoing spinal anesthesia, however, may be especially at risk of hypothermia because low core temperatures may not trigger protective autonomic responses. Furthermore, hypothermia in the elderly given regional anesthesia may not be perceived by the patient (who typically feels less cold after induction of the block), or by the anesthesiologist (who does not observe shivering). Consequently, temperature monitoring and management usually is indicated in these patients.     

Alfentanil slightly increases the sweating threshold and markedly reduces the vasoconstriction and shivering thresholds

BACKGROUND: Hypothermia is common in surgical patients and victims of major trauma; it also results from environmental exposure and drug abuse. In most cases, hypothermia results largely from drug-induced inhibition of normal thermoregulatory control. Although opioids are given to a variety of patients, the thermoregulatory effects of opioids in humans remain unknown. Accordingly, the hypothesis that opioid administration impairs thermoregulatory control was tested. METHODS: Eight volunteers were studied, each on 3 days: (1) a target total plasma alfentanil concentration of 100 ng/ml, (2) control (no drug), and (3) a target alfentanil concentration of 300 ng/ml. Each day, skin and core temperatures were increased sufficiently to provoke sweating. Temperatures subsequently were reduced to elicit peripheral vasoconstriction and shivering. Mathematical compensations were made for changes in skin temperature using the established linear cutaneous contributions to control of sweating (10%) and to vasoconstriction and shivering (20%). From the calculated thresholds (core temperatures triggering responses at a designated skin temperature of 34 degrees C) and unbound plasma alfentanil concentrations, the individual concentration-response relationship was determined. The concentration-response relationship for all the volunteers was determined similarly using total alfentanil concentrations. RESULTS: In terms of unbound concentration, alfentanil increased the sweating threshold (slope = 0.021 +/- 0.016 degrees C.ng-1.ml; r2 = 0.92 +/- 0.06). Alfentanil also significantly decreased the vasoconstriction (slope = -0.075 +/- 0.067 degrees C.ng-1.ml; r2 = 0.92 +/- 0.07) and shivering thresholds (slope = -0.063 +/- -0.037 degrees C.ng-1.ml; r2 = 0.98 +/- 0.04). In terms of total alfentanil concentration (degrees C.ng-1.ml), the sweating threshold increased according to the equation: threshold (degrees C) = 0.0014[alfentanil] + 37.2 (r2 = 0.33). In contrast, alfentanil produced a linear decrease in the core temperature, triggering vasoconstriction: threshold (degrees C) = -0.0049[alfentanil] + 36.7 (r2 = 0.64). Similarly, alfentanil linearly decreased the shivering threshold: threshold (degrees C) = -0.0057[alfentanil] + 35.9 (r2 = 0.70). CONCLUSIONS: The observed pattern of thermoregulatory impairment is similar to that produced by most general anesthetics: a slight increase in the sweating threshold and a substantial, linear decrease in the vasoconstriction and shivering thresholds.     

Selective deimination of vimentin in calcium ionophore-induced apoptosis of mouse peritoneal macrophages

Amino acid infusions during general anesthesia induce thermogenesis and prevent postoperative hypothermia. The effects of increased heat production during anesthesia on postoperative nitrogen balance have not been examined. Therefore, we studied the effect of perioperative amino acid infusions on postoperative nitrogen excretion in 24 patients scheduled for hysterectomy. Seven volunteers not subjected to anesthesia or surgery were used as awake controls. During isoflurane anesthesia, 8 patients received acetated Ringer's solution, and 16 patients received an IV amino acid mixture, 240 kJ/h, before and during anesthesia. Rectal temperature and energy expenditure were measured. The urinary nitrogen content was calculated from urea, creatinine, and urate the day before surgery and for 4 days postoperatively. Diets were recorded. In anesthetized control patients, postoperative nitrogen excretion was less than preoperative levels. Those patients also experienced the largest decrease in core body temperature during anesthesia (1.7+/-0.1 degrees C). All had postoperative shivering. In the amino acid-treated patients, the temperature decrease during anesthesia was less pronounced (1.0+/-0.1 degrees C; P < 0.001) and postoperative shivering disappeared. In addition, the nitrogen excretion was unchanged postoperatively, perhaps indicating an increase in protein turnover known to generate heat. In conclusion, the increase in heat production induced by amino acids reduced hypothermia, abolished shivering, and attenuated/normalized the postoperative nitrogen saving that occurred in patients who did not receive amino acids. IMPLICATIONS: We compared nitrogen excretion before and after surgery in patients who received a saline or amino acid infusion during isoflurane anesthesia. The increase in heat production induced by amino acids reduced hypothermia, abolished shivering, and attenuated/normalized the postoperative nitrogen saving that occurred in patients who did not receive amino acids.     

Inorganic fluoride nephrotoxicity: prolonged enflurane and halothane anesthesia in volunteers

The effects of prolonged enflurane and halothane administration on urine-concentrating ability were determined in volunteers by examining their responses to vasopressin before anesthesia and on days 1 and 5 after anesthesia. A significant decrease in maximum urinary osmolality of 264 +/- 34 mOsm/kg (26 per cent of the preanesthetic value) was present on day 1 after enflurane anesthesia, whereas subjects anesthetized with halothane had a significant increase in maximum urinary osmolality of 120 +/- 44 mOsm/kg. Serum inorganic fluoride level peaked at 33.6 muM and remained above 20 muM for approximately 18 hours. Thus, the threshold level for inorganic fluoride nephrotoxicity is lower than previously suspected.     

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

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

The effects of sevoflurane, isoflurane, halothane, and enflurane on hemodynamic responses during an inhaled induction of anesthesia via a mask in humans

A rapid increase in isoflurane or desflurane concentration induces tachycardia and hypertension and increases-plasma catecholamine concentration. Little information is available as to whether sevoflurane, halothane, and enflurane induce similar responses during anesthesia induction via mask. Fifty ASA physical status I patients, aged 20-40 yr, and scheduled for elective minor surgery, received one of four volatile anesthetics: sevoflurane, isoflurane, halothane, or enflurane. Anesthesia was induced with thiamylal, followed by inhalation of 0.9 minimum alveolar anesthetic concentration (MAC) of the anesthetic in 100% oxygen via mask. The inspired concentration of anesthetic was increased by 0.9 MAC every 5 min to a maximum of 2.7 MAC. Heart rate (HR) and systolic blood pressure (SBP) were measured before and every minute for 15 min during anesthetic inhalation. In the sevoflurane and isoflurane groups, venous blood samples were drawn to determine the concentrations of plasma epinephrine and norepinephrine 3 min after each increase in anesthetic concentration. Sustained increments in HR were observed after increases in inspired isoflurane concentration to 1.8 MAC and 2.7 MAC (peak changes of 15 +/- 3 and 17 +/- 3 bpm, respectively). Isoflurane also increased SBP transiently after the inspired concentration was increased to 2.7 MAC (peak change of 10 +/- 4 mm Hg). Enflurane increased HR after the inspired concentration was increased to 2.7 MAC (peak change of 9 +/- 2 bpm). In contrast, changes in sevoflurane and halothane concentrations did not induce hyperdynamic responses. Plasma norepinephrine concentration in the isoflurane group was significantly higher than that in the sevoflurane group during 2.7 MAC (P = 0.022). We propose that there is a direct relationship between airway irritation of the anesthetic and immediate cardiovascular change during an inhaled induction of anesthesia.     

Multicomponent intravenous and epidural anesthesia in aorto-coronary bypass surgery

The influence of epidural anesthesia (CEA) on clinical manifestations, cortisole and adrenocorticotropic hormone (ACTH) level, central hemodynamic values during aorto-coronary bypass surgery (ACBS) in 56 patients aged 42-68 years with preserved functional capacity of the myocardium was studied. Catheterisation of the epidural space was carried out in the evening before the operation according to the standard method at the level of T4-T5 with the use of disposable epidural set. During the procedure before perfusion 2% solution of lidocaine 3.8 +/- 0.2 mg/kg was introduced in epidural space (taking into account test-dose) as a bolus in 3-4 motions. The dose of local anesthetics for infusion was selected separately for each individual case with due regard for hemodynamic values. During artificial circulation additionally local anesthetic was introduced as a bolus, the dose being 4.7 +/- 0.8 mg/kg. At the end of the operation morphine (0.061 +/- 0.001 mg/kg) was introduced. It was established that combined application of intravenous and epidural anesthesia represents highly effective method of anesthesia in aorto-coronary bypass surgery. According to clinical course data, cortisone and ACTH blood contents and hemodynamic parameters, EA provides adequate anesthesia, promotes stabilization of hemodynamic values and creates functionally more advantageous conditions for the myocardium in patients with CHD during aorto-coronary bypass operation. Anesthesiologic aid with the use of EA promotes reduction of intravenous anesthetics expenditure, earlier waking up of the patients in postoperative period and decrease in duration of postoperative artificial lung ventilation.     

Hypothermia eliminates isoflurane requirements at 20 degrees C

BACKGROUND: Hypothermia decreases anesthetic requirements, but the temperature that completely eliminates anesthetic needs has not been previously determined. METHODS: Eight female goats were anesthetized with isoflurane and catheters were placed in the femoral artery and cranial vena cava, after which the right carotid artery and external jugular vein were dissected free. Peripheral temperature was monitored in the rectum and core temperature in the vena cava. A thermistor was placed in the epidural space via a small burr hole to monitor brain temperature. Minimum alveolar concentration (MAC) for isoflurane was determined by eliciting gross, purposeful movement with a tail clamp. Cardiopulmonary bypass (CPB) was established using bubble oxygenators with venous blood drained from a jugular vein and arterial blood infused with a roller pump into the carotid artery. The animals were cooled to approximately 29 degrees C, and MAC redetermined, after which further cooling to 20 degrees C was accomplished. Isoflurane was eliminated, core and brain temperature adjusted in 2-3 degrees C increments, and the tail clamp applied until two temperatures were found that just permitted and just prevented movement. The animals were rewarmed, isoflurane added, and post-CPB MAC determined. RESULTS: At 38.5 degrees C, pre-CPB MAC was 1.3 +/- 0.1% (mean +/- SEM). At 29.0 degrees C, MAC was 0.7 +/- 0.1%, and the anesthetizing temperature was 20.1 +/- 0.6 degrees C. At 37.3 degrees C, post-CPB MAC was 1.0 +/- 0.1% (P < 0.05 vs. pre-CPB). CONCLUSIONS: These results confirm the rectilinear decrease in MAC seen in previous studies and establishes the anesthetizing temperature at 20 degrees C.     

PCL reconstruction. In vitro biomechanical comparison of ''isometric'' versus single and double-bundled ''anatomic'' grafts

The analgesic tramadol inhibits the neuronal reuptake of norepinephrine and 5-hydroxytryptamine, facilitates 5-hydroxytryptamine release, and activates mu-opioid receptors. Each of these actions is likely to influence thermoregulatory control. We therefore tested the hypothesis that tramadol inhibits thermoregulatory control. Eight volunteers were evaluated on four study days, on which they received no drugs, tramadol 125 mg, tramadol 250 mg, and tramadol 250 mg with naloxone, respectively. Skin and core temperatures were gradually increased until sweating was observed and then decreased until vasoconstriction and shivering were detected. The core temperature triggering each response defined its threshold. Tramadol decreased the sweating threshold by -1.03 +/- 0.67 degrees C microgram-1.mL (r2 = 0.90 +/- 0.12). Tramadol also decreased the vasoconstriction threshold by -3.0 +/- 4.0 degrees C microgram-1.mL (r2 = 0.94 +/- 0.98) and the shivering threshold by -4.2 +/- 4.0 degrees C microgram-1.mL(r2 = 0.98 +/- 0.98). The sweating to vasoconstriction interthreshold range nearly doubled from 0.3 +/- 0.4 degree C to 0.7 +/- 0.6 degree C during the administration of large-dose tramadol (P = 0.04). The addition of naloxone only partially reversed the thermoregulatory effects of tramadol. The thermoregulatory effects of tramadol thus most resemble those of midazolam, another drug that slightly decreases the thresholds triggering all three major autonomic thermoregulatory defenses. In this respect, both drugs reduce the "setpoint" rather than produce a generalized impairment of thermoregulatory control. Nonetheless, tramadol nearly doubled the interthreshold range at a concentration near 200 ng/mL. This indicates that tramadol slightly decreases the precision of thermoregulatory control in addition to reducing the setpoint. IMPLICATIONS: The authors evaluated the effects of the analgesic tramadol on the three major thermoregulatory responses: sweating, vasoconstriction, and shivering. Tramadol had only slight thermoregulatory effects. Its use is thus unlikely to provoke hypothermia or to facilitate fever.     

Reducing lipid peroxidation stress of erythrocyte membrane by alpha-tocopherol nicotinate plays an important role in improving blood rheological properties in type 2 diabetic patients with retinopathy

STUDY OBJECTIVE: To test the hypothesis that warming intravenous (i.v.) fluids in conjunction with convective warming results in less intraoperative hypothermia (core temperature < 36.0 degrees C) than that seen with convective warming alone. DESIGN: Prospective, randomized study. SETTING: University affiliated tertiary care teaching hospital. PATIENTS: 61 ASA physical status, I, II, and III adults undergoing major surgery and general anesthesia with isoflurane. INTERVENTIONS: All patients received convective warming. Group 1 patients received warmed fluids (setpoint 42 degrees C). Group 2 patients received room temperature fluids (approximately 21 degrees C). MEASUREMENTS AND MAIN RESULTS: Lowest and final intraoperative distal esophageal temperatures were higher (p < 0.05) in Group 1 (mean +/- SEM: 35.8 +/- 0.1 degrees C and 36.6 +/- 0.1 degrees C) versus Group 2 (35.4 +/- 0.1 degrees C and 36.1 +/- 0.1 degrees C, respectively). Compared with Group 1, more Group 2 patients were hypothermic at the end of anesthesia (10 of 26 patients, or 38.5% vs. 4 of 30 patients, or 13%; p < 0.05). After 30 minutes in the recovery room, there were no differences in temperature between groups (36.7 +/- 0.1 degrees C and 36.5 +/- 0.1 degrees C in Groups 1 and 2, respectively). Intraoperative cessation of convective warming because of core temperature greater than 37 degrees C was required in 33% of Group 1 patients (vs. 11.5% in Group 2; p = 0.052). CONCLUSIONS: The combination of convective and fluid warming was associated with a decreased likelihood of patients leaving the operating room hypothermic. However, average final temperatures were greater than 36 degrees C in both groups, and intergroup differences were small. Care must be taken to avoid overheating the patient when both warming modalities are employed together.     

Hypoxemia decreases the shivering threshold in rabbits anesthetized with 0.2 minimum alveolar anesthetic concentration isoflurane

Shivering has been proposed as an etiology of postoperative hypoxemia. The difficulty with this theory is that hypoxemia inhibits shivering in unanesthetized cats, rats, and humans. However, anesthesia inhibits many protective reflexes, including the ventilatory response to hypoxemia. We therefore tested the hypothesis that arterial hypoxemia fails to inhibit shivering in lightly anesthetized rabbits. Rabbits were intubated and instrumented during exposure to surgical concentrations of anesthesia, and anesthesia was then maintained with 0.2 minimum alveolar anesthetic concentration isoflurane. The core was cooled at a rate of 2-3 degrees C/h by perfusing water at 10 degrees C through a colonic thermode. Core temperatures were recorded from the distal esophagus. Sustained, vigorous shivering was considered physiologically significant. The core temperature that triggering significant shivering identified the thermoregulatory threshold for this response. Arterial blood was sampled for gas analysis at the shivering threshold in each rabbit. Hypoxemia linearly reduced the shivering threshold from 36.7 degrees C at 130 mm Hg to 35.4 degrees C at 50 mm Hg (threshold = PaO2.0.019 + 34.3; r2 = 0.49). We failed to confirm our hypothesis: instead, even mild hypoxemia reduced the shivering threshold >1 C. A 1 C decrease in the shivering threshold is likely to prevent or stop most postoperative shivering because it exceeds the reduction produced by many effective anti-shivering drugs. These data do not support the theory that shivering causes postoperative hypoxemia. IMPLICATIONS: Shivering has been proposed as an etiology of postoperative hypoxemia. Our data, in contrast, show that mild hypoxemia inhibits shivering. Shivering is thus unlikely to be a cause of postoperative hypoxemia.     

Changing from isoflurane to desflurane toward the end of anesthesia does not accelerate recovery in humans

BACKGROUND: In an attempt to combine the advantage of the lower solubilities of new inhaled anesthetics with the lesser cost of older anesthetics, some clinicians substitute the former for the latter toward the end of anesthesia. The authors tried to determine whether substituting desflurane for isoflurane in the last 30 min of a 120-min anesthetic would accelerate recovery. METHODS: Five volunteers were anesthetized three times for 2 h using a fresh gas inflow of 2 l/min: 1.25 minimum alveolar concentration (MAC) desflurane, 1.25 MAC isoflurane, and 1.25 MAC isoflurane for 90 min followed by 30 min of desflurane concentrations sufficient to achieve a total of 1.25 MAC equivalent ("crossover"). Recovery from anesthesia was assessed by the time to respond to commands, by orientation, and by tests of cognitive function. RESULTS: Compared with isoflurane, the crossover technique did not accelerate early or late recovery (P > 0.05). Recovery from isoflurane or the crossover anesthetic was significantly longer than after desflurane (P < 0.05). Times to response to commands for isoflurane, the crossover anesthetic, and desflurane were 23 +/- 5 min (mean +/- SD), 21 +/- 5 min, and 11 +/- 1 min, respectively, and to orientation the times were 27 +/- 7 min, 25 +/- 5 min, and 13 +/- 2 min, respectively. Cognitive test performance returned to reference values 15-30 min sooner after desflurane than after isoflurane or the crossover anesthetic. Isoflurane cognitive test performance did not differ from that with the crossover anesthetic at any time. CONCLUSIONS: Substituting desflurane for isoflurane during the latter part of anesthesia does not improve recovery, in part because partial rebreathing through a semiclosed circuit limits elimination of isoflurane during the crossover period. Although higher fresh gas flow during the crossover period would speed isoflurane elimination, the amount of desflurane used and, therefore, the cost would increase.     

Identification of entero-aggregative Escherichia coli based on surface properties

OBJECTIVES: Afterdrop in core temperatures after discontinuation of cardiopulmonary bypass (CPB) is reported to be a sign of inadequate total body rewarming on CPB. The purpose of this study was to compare the effects of three different drug regimens on hemodynamic stability and the uniformity of rewarming during the rewarming period of CPB. DESIGN: This prospective randomized study was performed in the Anesthesiology Department of the University of Istanbul. PARTICIPANTS: Sixty-six patients undergoing uncomplicated valve replacement and aortocoronary bypass grafting surgery were studied. INTERVENTIONS: Anesthesia was maintained with isoflurane and fentanyl infusion during the prebypass and the postbypass periods. Patients were allocated into three groups by the initiation of CPB. Group 1 (n = 22): fentanyl infusion + diazepam + sodium nitroprusside (SNP) in the rewarming period), group 2 (n = 22): fentanyl infusion + isoflurane, group 3, control (n = 22): fentanyl infusion + diazepam. Rectal, esophageal, and forearm temperatures were monitored throughout the study. MEASUREMENTS AND MAIN RESULTS: None of the durational and temperature data showed significant differences between groups 1 and 2. In the control group, afterdrop in esophageal temperature was significantly higher than groups 1 and 2 (group 1: -1.4 +/- 0.9 degrees C, group 2: -1.44 +/- 0.8 degrees C, group 3: -2.1 +/- 0.65 degrees C). In group 1, the number of patients whose mean arterial pressure (MAP) decreased below 45 mmHg was significantly higher than group 2 (p = 0.002). Mean SNP infusion rate and mean isoflurane concentration during the rewarming period were calculated as 1.55 +/- 0.8 micrograms/kg/min and 0.775 +/- 0.27%, respectively. CONCLUSIONS: Isoflurane produced more stable hemodynamic conditions than SNP during the rewarming period, improved the uniformity of rewarming, and permitted earlier extubation in the intensive care unit (ICU). It is concluded that isoflurane alone is capable of fulfilling the anesthesia needs during hypothermia and the rewarming period of CPB.     

Selective convective brain cooling during normothermic cardiopulmonary bypass in dogs

BACKGROUND: Neurologic complications, primarily resulting from ischemic insults, represent the leading cause of morbidity and disability, and the second most common source of death, after cardiac operations. Previous studies have reported that increases (as occur during the rewarming phase of cardiopulmonary bypass [CPB]) or decreases in brain temperature of a mere 0.5 degrees to 2 degrees C can significantly worsen or improve, respectively, postischemic neurologic outcome. The purpose of the present study was to evaluate a novel approach of selectively cooling the brain during hypothermic CPB and subsequent rewarming. METHODS: Sixteen dogs were anesthetized with either intravenous pentobarbital or inhaled halothane (n = 8 per group). Normocapnia (alpha stat technique) and a blood pressure near 75 mm Hg were maintained. Temperatures were monitored by placing thermistors in the esophagus (i.e., core), parietal epidural space, and brain parenchyma at depths of 1 and 2 cm beneath the dura. During CPB, core temperature was actively cycled from 38 degrees C to 28 degrees C, and then returned to 38 degrees C. Forced air pericranial cooling (air temperature of approximately 13 degrees C) was initiated simultaneous with the onset of CPB, and maintained throughout the bypass period. Brain-to-core temperature gradients were calculated by subtracting the core temperature from regional brain temperatures. RESULTS: In halothane-anesthetized dogs, brain temperatures at all monitoring sites were significantly less than core during all phases of CPB, with one exception (2 cm during systemic cooling). Brain cooling was most prominent during and after systemic rewarming. For example, during systemic rewarming, average temperatures in the parietal epidural space, and 1 and 2 cm beneath the dura, were 3.3 degrees +/- 1.3 degrees C (mean +/- standard deviation), 3.2+/-1.4 degrees C, and 1.6 degrees +/-1.0 degrees C, cooler than the core, respectively. Similar trends, but of a greater magnitude, were noted in pentobarbital-anesthetized dogs. For example, during systemic rewarming, corresponding brain temperatures were 6.5 degrees +/-1.7 degrees C, 6.3 degrees +/-1.6 degrees C, and 4.2+/-1.3 degrees C cooler than the core, respectively. CONCLUSIONS: The magnitude of selective brain cooling observed in both study groups typically exceeded the 0.5 degrees to 2.0 degrees C change previously reported to modulate ischemic injury, and was most prominent during the latter phases of CPB. When compared with previous research from our laboratory, application of cold forced air to the cranial surface resulted in brain temperatures that were cooler than those observed during hypothermic CPB without pericranial cooling. On the basis of the assumption that similar beneficial brain temperature changes can be induced in humans, we speculate that selective convective brain cooling may enable clinicians to improve neurologic outcome after hypothermic CPB.     

Eucapnic hypoxia lowers human cold thermoregulatory response thresholds and accelerates core cooling

Hypoxia lowers the basic thermoregulatory responses of animals and humans. In cold-exposed animals, hypoxia increases core temperature (Tco) cooling rate and suppresses shivering thermogenesis. In humans, the experimental effects of hypoxia on thermoregulation are equivocal. Also, the effect of hypoxia has not been separated from that of hypocapnia consequent to hypoxic hyperventilation. To determine the isolated effects of hypoxia on warm and cold thermoregulatory responses and core cooling during mild cold stress, we examined the Tco thresholds for sweating, vasoconstriction, and shivering as well as the core cooling rates of eight subjects immersed in 28 degrees C water under eucapnic conditions. On 2 separate days, subjects exercised on an underwater cycle ergometer to elevate Tco above the sweating threshold. They then rested and cooled until they shivered vigorously. Subjects inspired humidified room air during the control trial. For the eucapnic hypoxia trial, they inspired 12% O2-balance N2 with CO2 added to maintain eucapnia. Eucapnic hypoxia lowered the Tco thresholds for vasoconstriction and shivering by 0.14 and 0.19 degrees C, respectively, and increased core cooling rate by 33% (1.83 vs. 1.38 degrees C/h). These results demonstrate that eucapnic hypoxia enhances the core cooling rate in humans during mild cold stress. This may be attributed in part to a delay in the onset of vasoconstriction and shivering as well as increased respiratory heat loss during hypoxic hyperventilation.     

Alteration of renal blood flow during epidural anesthesia in normal subjects

The cardiovascular consequences of epidural anesthesia secondary to sympathetic blockade are well documented; however, their repercussions on renal hemodynamics in humans have not been reported. We investigated the effect of epidural anesthesia on renal blood flow (RBF) in 13 healthy volunteers 18-45 yr of age. RBF was measured using paraaminohippurate clearance before and after bilateral T6 epidural sensory block (to ensure adequate sympathetic renal nerve blockade). Epidural anesthesia was established using 22 +/- 3 mL of 2% plain lidocaine (without epinephrine) via L1-L2 epidural catheter; urine output was measured using a three-way Foley catheter. Mean arterial pressure remained > or = 70 mm Hg in all subjects without any pharmacologic intervention. Mean RBF before epidural anesthesia was 16.1 +/- 6.8 mL.kg-1.min-1 and 14.3 +/- 2.9 mL.kg-1.min-1 after bilateral T6 epidural blockade. We conclude that the institution of epidural anesthesia in healthy subjects does not result in a significant change in RBF (P > 0.25).     

Autoregulation of human inner ear blood flow during middle ear surgery with propofol or isoflurane anesthesia during controlled hypotension

We used controlled hypotension to obtain a bloodless cavity during middle ear surgery under an optical microscope. No previous study has assessed the effect of controlled hypotension on inner ear blood flow (IEF) autoregulation in humans receiving propofol or isoflurane anesthesia. In the present study, the IEF autoregulation was determined using laser Doppler flowmetry in combination with transient evoked otoacoustic emissions (TEOAEs) during controlled hypotension with sodium nitroprusside in 20 patients randomly anesthetized with propofol or isoflurane. A coefficient of IEF autoregulation (Ga) was determined during controlled hypotension, with a Ga value ranging between 0 (no autoregulation) and 1 (perfect autoregulation). During controlled hypotension with propofol, IEF remained stable (1%+/-6%; P > 0.05) but decreased by 25%+/-8% with isoflurane (P < 0.05). The Ga was higher during propofol anesthesia (0.62+/-0.03) than during isoflurane anesthesia (0.22+/-0.03; P < 0.0001). Under propofol anesthesia, there were individual relationships between TEOAE amplitude and change in IEF in four patients. Such a correlation was not observed under isoflurane anesthesia. These results suggest that human IEF is autoregulated in response to decreased systemic pressure. Furthermore, isoflurane has a greater propensity to decrease cochlear autoregulation and function than propofol. IMPLICATIONS: The present study shows that inner ear blood flow is autoregulated under propofol, but not isoflurane, anesthesia during controlled hypotension in humans during middle ear surgery. Further studies are needed to explore the postoperative auditory functional consequences of the choice of the anesthetic drug used in middle ear surgery.