James M. Hynson

Intraoperative Warming Therapies: A Comparison of Three Devices

STUDY OBJECTIVE To compare the effectiveness of three commonly used intraoperative warming devices. DESIGN A randomized, prospective clinical trial. SETTING The surgical suite of a university medical center. PATIENTS Twenty adult patients undergoing kidney transplantation for end-stage renal disease. INTERVENTIONS Patients were assigned to one of four warming therapy groups: circulating-water blanket (40 degrees C), heated humidifier (40 degrees C), forced-air warmer (43 degrees C, blanket covering legs), or control (no extra warming). Intravenous fluids were warmed (37 degrees C), and fresh gas flow was 5 L/min for all groups. No passive heat and moisture exchangers were used. MEASUREMENTS AND MAIN RESULTS The central temperature (tympanic membrane thermocouple) decreased approximately 1 degree C during the first hour of anesthesia in all groups. After three hours of anesthesia, the decrease in the tympanic membrane temperature from baseline (preinduction) was least in the forced-air warmer group (-0.5 degrees C +/- 0.4 degrees C), intermediate in the circulating-water blanket group (-1.2 degrees C +/- 0.4 degrees C), and greatest in the heated humidifier and control groups (-2.0 degrees C +/- 0.5 degrees C and -2.0 degrees C +/- 0.7 degrees C, respectively). Total cutaneous heat loss measured with distributed thermal flux transducers was approximately 35W (watts = joules/sec) less in the forced-air warmer group than in the others. Heat gain across the back from the circulating-water blanket was approximately 7W versus a loss of approximately 3W in patients lying on a standard foam mattress. CONCLUSION The forced-air warmer applied to only a limited skin surface area transferred more heat and was clinically more effective (at maintaining central body temperature) than were the other devices. The characteristic early decrease in central temperature observed in all groups regardless of warming therapy is consistent with the theory of anesthetic-induced heat redistribution within the body.

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° C when volunteers were not warmed and 36.7 ± 0.6° C when volunteers were warmed. Tympanic membrane temperature did not change during the preinduction period without warming but increased slightly (ΔT = 0.4 ± 0.2° C) during warming. After induction of anesthesia, core temperatures decreased to 36.1 ± 0.4° C over 1 h when volunteers were prewarmed but decreased to 34.9 ± 0.4° 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 ≈17 mmHg. Warming was associated with a reversal of the systolic pressure difference to ≈−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 radial 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.

Isoflurane-induced Vasodilation Minimally Increases Cutaneous Heat Loss

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

Thermoregulatory vasoconstriction decreases cutaneous heat loss

To determine the extent to which thermoregulatory vasoconstriction decreases heat loss to the environment, we measured regional heat flux, average skin temperature, and tympanic membrane temperature before and after thermoregulatory vasoconstriction in five minimally clothed volunteers maintained in a 30.8 +/- 0.1 degrees C environment. Thermoregulatory vasoconstriction was induced by central venous infusion of cooled fluid. Peripheral cutaneous blood flow was evaluated with venous-occlusion volume plethysmography and skin-surface temperature gradients. Laser Doppler flowmetry was used to measure vasoconstriction in centrally located skin. This model mimics the common clinical situation in which patients in a warm environment are centrally cooled by administration of cold intravenous fluids or by lavage of internal cavities with cold fluids. Tympanic membrane temperature decreased 1.5 +/- 0.3 degrees C in the first 15 min after the cold fluid infusion was started and remained approximately 1 degrees C below control values during the rest of the study. Average skin-surface temperature decreased slowly to approximately 0.7 degrees C below control. Flow in capillaries of centrally distributed skin, determined with laser Doppler flowmetry, decreased only approximately 40%. Total heat flux, and flux from the arms and legs decreased approximately 25% (15.5 +/- 0.3 W). Heat loss from the trunk and head decreased only 17%, whereas, loss from the hands and feet (10.5% of the body surface area) decreased approximately 50%. All measured values decreased significantly following vasoconstriction (P less than 0.01). Therefore, thermoregulatory vasoconstriction in a thermoneutral environment appears to decrease cutaneous loss of metabolic heat approximately 25%.

Nausea and vomiting following thyroid and parathyroid surgery

STUDY OBJECTIVES To determine the incidence of postoperative nausea and vomiting (PONV) following thyroid and parathyroid surgery. To determine whether PONV is reduced when propofol is used for maintenance of anesthesia as compared to isoflurane and to evaluate the costs and resource consumption associated with these two anesthetic regimens. DESIGN Randomized, prospective study. SETTING University-affiliated hospital--a referral center for endocrinologic surgery. PATIENTS 118 ASA physical status I and II patients, aged 18 years and older, undergoing elective thyroid or parathyroid surgery. INTERVENTIONS Patients received either isoflurane (0.5 to 1.3% end-tidal) or propofol (50 to 200 micrograms/kg/min) for maintenance of anesthesia. All patients received propofol for induction of anesthesia, succinylcholine or vecuronium, nitrous oxide, and fentanyl. Prophylactic antiemetics were not administered. Postoperative pain was treated with ketorolac, fentanyl, or acetaminophen. MEASUREMENTS AND MAIN RESULTS Signs and symptoms of nausea and vomiting were graded on a four point scale as 1 = no nausea; 2 = mild nausea; 3 = severe nausea; 4 = retching and/or vomiting. Grades 3 and 4 were grouped together as PONV. The combined incidence of PONV was 54% over the 24-hour postoperative evaluation period. PONV was significantly more common in patients receiving isoflurane than propofol for maintenance of anesthesia (64% vs. 44%). In women (n = 87), the incidence of PONV was significantly greater in those patients who received isoflurane than those who received propofol for maintenance (71% vs. 42%). However, in men (n = 31), there was no significant difference in PONV between anesthetic regimens (47% with isoflurane vs. 50% with propofol). There were no differences in the duration of stay in the postanesthesia care unit, time to discharge from the hospital, or local wound complications (hematomas) between groups. The use of propofol for maintenance of anesthesia was associated with an additional cost, relative to the isoflurane group, of

A new noninvasive method to measure blood pressure: results of a multicenter trial.

54.26 per patient. CONCLUSION Patients undergoing thyroid or parathyroid surgery are at high risk for the development of PONV. Propofol for maintenance of anesthesia, although more expensive than isoflurane, reduces the rate of PONV in women.

Thermoregulatory vasoconstriction during isoflurane anesthesia minimally decreases cutaneous heat loss.

BACKGROUND Blood pressure (BP) monitoring with arterial waveform display requires an arterial cannula. We evaluated a new noninvasive device, Vasotrac (Medwave, Arden Hills, MN) that provides BP measurements approximately every 12-15 beats and displays pulse rate and a calibrated arterial waveform for each BP measurement. METHODS Surgical and critically ill patients (n = 80) served as subjects for the study. BPs, pulse waveforms, and pulse rates measured via a radial artery catheter were compared with those obtained by the Vasotrac from the opposite radial artery. Data were analyzed to determine agreement between the two systems of measurement. RESULTS Blood pressure measured noninvasively by the Vasotrac demonstrated excellent correlation (P<0.01) with BP measured via a radial arterial catheter (systolic r2 = 0.93; diastolic r2 = 0.89; mean r2 = 0.95). Differences in BP measured by the Vasotrac versus the radial arterial catheter were small. The mean+/-SD bias and precision were as follows: systolic BP 0.02+/-5.4 mm Hg and 3.9+/-3.7 mm Hg; diastolic BP -0.39+/-3.9 mm Hg and 2.7+/-2.8 mm Hg; mean BP -0.21+/-3.0 mm Hg and 2.1+/-2.2 mm Hg compared with radial artery measurements. The Vasotrac pulse rates were almost identical to those measured directly (r2 = 0.95). The Vasotrac BP waveform resembled those directly obtained radial artery pulsatile waveforms. CONCLUSIONS In surgical and critically ill patients, the Vasotrac measured BP, pulse rate, and displayed radial artery waveform, which was similar to direct radial arterial measurements. It should be a suitable device to measure BP frequently in a noninvasive fashion.

THERMAL BALANCE AND TREMOR PATTERNS DURING EPIDURAL ANESTHESIA

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

Absence of Nonshivering Thermogenesis in Anesthetized Adult Humans

Five healthy, nonpregnant volunteers were studied before and after induction of lumbar epidural anesthesia to determine the cause of central hypothermia during epidural anesthesia. Cutaneous heat loss was measured from 10 area-weighted sites using thermal flux transducers. Oxygen consumption was measured and converted to heat production in watts (W). After a 2-h control period at approximately 20 degrees C, epidural anesthesia was induced by injection of 30-50 ml 3% chloroprocaine. Additional boluses were given to extend the sensory blockade to at least the T5 dermatome. Tremor during epidural anesthesia was compared with normal shivering induced by rapid central venous infusion of approximately 4 l iced saline in six unanesthetized volunteers. Average skin temperature and cutaneous heat loss decreased during the control period, while tympanic membrane temperature remained stable. During the 1st h of epidural blockade, tympanic membrane temperature decreased 1.1 +/- 0.3 degrees C, and average skin temperature increased 0.9 +/- 0.5 degrees C. Cutaneous heat loss increased 16 +/- 6% (15 +/- 5 W), but metabolic heat production increased even more (and was associated with a shivering-like tremor). Tremor during epidural anesthesia and shivering induced by iced saline infusion had similar synchronous waxing-and-waning patterns. No abnormal EMG patterns were detected during epidural anesthesia. We conclude that central hypothermia during the 1st h of epidural anesthesia does not result from heat loss to the environment in excess of metabolic heat production, but results primarily from redistribution of body heat from central to peripheral tissues. Analysis of the tremor patterns suggests that oscillations recorded during epidural anesthesia in nonpregnant individuals is normal thermoregulatory shivering. Shivering occurred sooner and was more intense during iced saline infusion than during epidural anesthesia, despite comparable central hypothermia. The low intensity of shivering during epidural anesthesia, and in some individuals the delay in onset, may result from blockade of afferent cutaneous cold signals.

Painful Stimulation Minimally Increases the Thermoregulatory Threshold for Vasoconstriction during Enflurane Anesthesia in Humans

BackgroundTypically, 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. MethodsFive volunteers were anesthetized with isoflurane and paralyzed with vecuronium. Oxygen consumption was measured during cooling to a core temperature at least 1° 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. ResultsThe core temperature threshold for vasoconstriction was 35.2 ± 0.8 ° C. Oxygen consumption decreased 9 ± 5%/° C during active cooling before vasoconstriction and 9 ± 3%/° 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° 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. ConclusionsThe 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.