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Anesth Analg 2001;92:261-266
© 2001 International Anesthesia Research Society

GENERAL ARTICLES

Negative Pressure Rewarming vs. Forced Air Warming in Hypothermic Postanesthetic Volunteers

Akiko Taguchi, MD*, Cem F. Arkilic, MD*, Arundhathi Ahluwalia, MD*, Daniel I. Sessler, MD{dagger}, and Andrea Kurz, MD{dagger}

*Department of Anesthesiology, Washington University, St. Louis, St. Louis, Missouri, {dagger}OUTCOMES RESEARCHTM Institute, Department of Anesthesiology, University of Louisville, Louisville, Kentucky, and Ludwig Boltzmann Institute for Clinical Anesthesia and Intensive Care, University of Vienna, Vienna, Austria; and {ddagger}Department of Anesthesiology, Washington University, St. Louis, and the Department of Anesthesiology and Intensive Care Medicine, University of Vienna, Vienna, Austria

Address correspondence to Andrea Kurz, MD, Department of Anesthesiology, Washington University, 660 S. Euclid Avenue, St. Louis, MO, 63110. Address e-mail to kurza{at}msnotes.wustl.edu


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
We compared changes in core temperature and systemic heat balance with a new negative pressure/warming device (Vital Heat® ) that uses negative pressure combined with heat to facilitate warming in vasoconstricted postoperative patients to those resulting from passive insulation or forced air. Seven healthy volunteers were anesthetized and cooled to a tympanic membrane temperature near 34°C. Anesthesia was discontinued and shivering was prevented by using meperidine. The vasoconstricted volunteers were rewarmed for 2 h using three randomly assigned methods: 1) Vital Heat® plus cotton blanket; 2) one layer of cotton blanket; 3) forced-air warming. Thermal flux was recorded from 15 skin-surface sites; metabolic heat production was estimated from total body oxygen consumption. Metabolic heat production remained constant throughout the study. Systemic heat loss remained constant during warming with cotton blankets but decreased significantly during the other treatments. Systemic heat balance increased significantly more with forced air (140 ± 21 kcal) than with Vital Heat® (66 ± 19 kcal) or cotton blankets (47 ± 18 kcal). Core temperature increased no faster with Vital Heat® warming (1.3 ± 0.4°C) than with a cotton blanket (1.2 ± 0.4°C). In contrast, core temperature increased more rapidly with forced air warming (2.6 ± 0.6°C). In this study we show that calories from a negative pressure rewarming device are largely constrained to the forearm and that heat does not flow to the core thermal compartment.

Implications: In this study we show that calories from a negative pressure rewarming device are largely constrained to the forearm, and that heat does not flow to the core thermal compartment. Consequently, this warming concept is not more effective than passive insulation in hypothermic postanesthetic subjects. In contrast, rewarming is very effective with convective warming.


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
Perioperative hypothermia causes numerous adverse outcomes (1–4). Most are initiated intraoperatively, although they are generally manifested or detected later. Consequently, many anesthesiologists try to maintain intraoperative normothermia (i.e., core temperature >36°C). Nonetheless, occasional patients unavoidably become hypothermic or are cooled therapeutically. These patients will presumably benefit from postoperative rewarming.

Hypothermic postoperative patients are invariably vasoconstricted (5,6). A difficulty with rewarming postoperative patients is that thermoregulatory vasoconstriction restricts peripheral-to-core flow of heat (7). In contrast, heat flows easily between the core and peripheral compartments during anesthesia (8) or when postoperative vasodilation is maintained by spinal anesthesia (9).

The Food and Drug Administration certified a technology designed to facilitate rapid warming in vasoconstricted postoperative patients. It uses negative pressure applied to one arm, which is thought to dilate the arteriovenous shunts and to increase arm blood flow. In theory, this allows rapid transfer of applied heat from the arm to the core. The efficacy of this new warming technique, now called Vital Heat® (formerly called Thermostat® ), has been described. Grahn et al. (10) showed with a preliminary version of this device that application of heat (45–46°C) increases core temperature at a rate of 1.4 ± 0.1°C/h. However, core rewarming rate increased 10-fold to 13.6 ± 2.1°C/h when heat was combined with negative pressure. The plausibility of this remarkable rewarming rate was disputed by Oakley in a Letter-to-the-Editor (11) because it suggested an extraordinary heat-transfer rate.

A recent article about a commercially available negative pressure rewarming device (Thermostat®) showed that it was not effective in accelerating rewarming in postoperative hypothermic surgical patients after general anesthesia when compared with passive insulation (12). Although the authors measured core temperatures during the postoperative period, they did not evaluate heat balance or heat transfer from the periphery to the core.

Additionally the clinical question is not simply whether this technology works better for hypothermia than no treatment, but whether it works better than currently available treatments. We thus tested the hypothesis that Vital Heat® Warming is less effective than forced-air warming in transferring heat from the peripheral to the core compartment.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
With IRB approval and informed consent, we studied seven healthy volunteers (3 male, 4 female). Each was evaluated on three randomly assigned study days. None was obese, pregnant, taking any medication, or had a history of infection, recent fever, diabetes, problem with general anesthesia, or neuromuscular disease. The subjects were minimally clothed and reclined on a padded table in the Anesthesia Clinical Research Area during the study.

Studies started at approximately 9:30 AM, and volunteers fasted during the 8 h preceding each study. A catheter was inserted into the left antecubital vein. Anesthesia was induced with propofol 2–3 mg/kg, and maintained with sevoflurane at a relatively large dose designed to prevent thermoregulatory vasoconstriction (2.0–2.5%, end-tidal). A laryngeal mask airway was inserted, and ventilation assisted as necessary to maintain end-tidal PCO2 near 40 mm Hg. Anesthesia was supplemented with meperidine 0.5 mg · kg-1 · h-1. The subjects were actively cooled with forced air (10°C) until tympanic membrane temperature reached 34 ± 0.2°C. Anesthesia was subsequently discontinued.

After spontaneous ventilation was reestablished, the laryngeal mask was removed. The volunteers were observed for a minimum of 30 min, or until they were intensely vasoconstricted. Intense vasoconstriction was then maintained for an additional 30 min. Meperidine was given in 10-mg boluses as necessary to prevent shivering, as detected by visual inspection and an increase in oxygen consumption.

The subjects were then warmed for 2 h using one of three randomly assigned methods. Each volunteer was rewarmed with one of the following methods each day, for a total of three study days: 1) forced air warming (Bair Hugger® ; Augustine Medical, Inc.) set to 43°C via a full-length postanesthesia care unit cover; 2) passive insulation with a single layer of cotton blanket; or 3) a single layer of cotton blanket, supplemented by Vital Heat® warming (Aquarius Medical Corp., Phoenix, AZ) applied to one forearm.

The Vital Heat® device was applied contralateral to the IV catheter. The system consists of a reusable thermal exchange chamber that provides the negative pressure (-40 mm Hg) when air is manually exhausted from the chamber. A disposable hypothermia warming mitt/seal provides heat by activating exothermic crystallization in a supersaturated solution of sodium acetate. Because the disposable Vital Heat® chemical pack is designed to last only 1 h, we inserted a new chemical pack after the first hour of warming.

Routine morphometric and demographic characteristics were recorded. All routine anesthetic, respiratory, and hemodynamic variables were recorded at 10-min intervals.

Core temperature was recorded from the tympanic membrane. The aural probe was inserted by volunteers until they felt the thermocouple touch the tympanic membrane; appropriate placement was confirmed when volunteers easily detected a gentle rubbing of the attached wire. The aural canal was occluded with cotton, the probe securely taped in place, and a gauze bandage positioned over the external ear. Mean skin-surface temperature and cutaneous heat transfer were calculated from measurements at 15 area-weighted sites (13). Skin temperature within the Vital Heat® negative-pressure apparatus was calculated from the average of the three forearm, finger, and hand thermocouples. Temperatures were recorded at 5-min intervals from thermocouples connected to Iso-Thermex® thermometers having an accuracy of 0.1°C (Columbus Instruments, Corp., Columbus, OH).

Forearm minus fingertip skin-surface temperature gradients were measured on both arms and used as an index of arteriovenous shunt perfusion (14). A gradient exceeding 4°C indicated intense vasoconstriction and a negative gradient indicated vasodilation (15).

Heat flux from 15 area-weighted cutaneous sites was measured in W/m2 using thermal flux transducers (Concept Engineering, Old Saybrook, CT) (16). These values were converted into watts/site by multiplying by the calculated body surface area (17) and the appropriate regional percentages (13). Three of these transducers were located within the Vital Heat® device: finger, hand, and forearm. The sum of these three sites was considered to be heat transfer from the Vital Heat® system.

We defined flux as positive when heat traversed skin to the environment. As in previous studies, measured cutaneous heat loss was augmented by 10% to account for insensible transcutaneous evaporative loss (18) and reduced 3% to compensate for the skin covered by the volunteers’ shorts. We further augmented cutaneous loss by 5% of the metabolic rate (as determined from oxygen consumption) to account for respiratory loss (19).

Oxygen consumption was measured using a metabolic monitor ( VmaxTM , SensorMedics Corp., Yorba Linda, CA). The system was calibrated daily using a known mixture of gases. Measurements were averaged over 1-min intervals and recorded every 5 min. Oxygen consumption (mL/min) was converted to equivalent metabolic heat production (kcal/h) assuming the caloric value of oxygen to be 4.82 kcal/L (respiratory quotient = 0.82) (20). We choose a standard value for the respiratory quotient because the caloric value of oxygen varies only slightly over the full range of respiratory quotients (20).

Oxygen consumption was used to document absence of shivering and comparable metabolic heat production during each treatment. Thermal flux was used to quantify the efficacy of each treatment. The change in systemic heat content was determined by integrating the difference between cutaneous heat loss and metabolic heat production over the 2-h warming period. We have used this method in numerous previous studies and shown that it correlates well with direct measurements of tissue heat (5,16).

Morphometric characteristics, ambient conditions, anesthetic management were compared with a one-way analysis of variance. Time-dependent changes were evaluated using repeated-measures analysis of variance and the Scheffé F test. Results are expressed as means ± SD; differences were considered statistically significant when P < 0.05.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
The mean age of the volunteers was 28 ± 8 yr, weight was 67 ± 8.5 kg, and height was 167 ± 6 cm. Ambient temperatures were similar on each of the three study days. In contrast, significantly less meperidine was required to prevent shivering during forced air warming than with the other two treatments. All volunteers were vasoconstricted throughout the control period, 30 min before start of treatment ( Table 1). It took 90 ± 17 min for the subjects to cool to 34°C. Core temperature, which was nearly constant during the control period, increased significantly more with forced air warming (2.6 ± 0.6°C) than with Vital Heat® warming (1.3 ± 0.4°C) or the cotton blanket alone (1.2 ± 0.4°C) ( Fig. 1).


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  		Table 1. Temperatures, Hemodynamic Responses, and Meperidine Doses
 


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  		Figure 1. Core temperatures before and after treatment. Warming with Vital Heat®, cotton blankets, or forced air warming began at elapsed time zero and lasted for 120 min. At all times after 50 min of treatment forced air warming differed significantly from the other two treatments (as indicated by the asterisk). Vital Heat® and cotton blankets were virtually identical. Results are presented as mean ± SD.

 
Temperature of the heating element within the Vital Heat® device increased to 45.6 ± 1.8°C within 5 min of being activated. Subsequently the temperature decreased gradually ( Fig. 2). Finger temperature inside the Vital Heat® device increased from 28.7 ± 1.0°C to a maximum temperature of 41.4 ± 1.2°C during the first hour of warming, and from 38.7 ± 1.3°C up to a maximum finger temperature of 42.2 ± 1.4°C during the second hour of warming (Fig. 2). Negative pressure was kept constant throughout the treatment period. Forearm-fingertip gradients demonstrated vasodilation in the treated arm and vasoconstriction in the other arm throughout the treatment period. Average temperature of the three skin monitoring sites within the Vital Heat® device during the 2 h of treatment period was 37.8 ± 2.2, and the average maximum skin temperature within the device was 39.8 ± 1.0°C.



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  		Figure 2. Finger temperature and temperature of the heating element in the Vital Heat® device. Elapsed time zero is the beginning of rewarming. Results are presented as mean ± SD. Temperature of the heating element within the Vital Heat® negative pressure apparatus increased to 45.6 ± 1.8°C within 5 min of being activated.

 
Cutaneous heat loss during the control period was similar for the three treatments, near 30 kcal/h. The Vital Heat® system transferred considerable heat across the skin surface of the lower arm ( Fig. 3). Systemic heat loss remained constant during warming with cotton blankets but decreased significantly during the other warming treatments ( Fig. 4). The respiratory quotient was 0.8 ± 0.1 and did not change significantly during the study period. Metabolic heat production, which was nearly constant before start of treatment, remained constant throughout the warming period ( Fig. 5). Systemic heat balance thus increased significantly more with forced air (140 ± 21 kcal) than with Vital Heat® (66 ± 19 kcal) or a cotton blanket (47 ± 18 kcal, P < 0.001) ( Fig. 6).



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  		Figure 3. Finger, hand, and forearm heat loss during treatment with the Vital Heat® device. Elapsed time zero is the beginning of rewarming. The arrow indicates reinsertion of the second warming pad. Results are presented as mean ± SD.

 


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  		Figure 4. Cutaneous heat loss before and after start of treatment. Warming with Vital Heat®, cotton blankets, or forced air warming began at elapsed time zero and lasted for 120 min. Cutaneous heat loss during forced air warming differed significantly from the other two treatments at any time during the treatment period (as indicated by one asterisk). Cotton blanket and Vital Heat® differed significantly at 0, 10, 20 minutes (as indicated by two asterisks). Results are presented as mean ± SD.

 


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  		Figure 5. Heat production before and after start of treatment. Warming with Vital Heat®, cotton blankets, or forced air warming began at elapsed time zero and lasted for 120 min. Results are presented as mean ± SD.

 


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  		Figure 6. Change in body heat content as determined by systemic heat balance. Warming with Vital Heat®, cotton blankets, or forced air warming began at elapsed time zero and lasted for 120 min. At all times during the warming period forced air warming differed significantly from the other two treatments (as indicated by the asterisk). Vital Heat® and cotton blankets were virtually identical. Results are presented as mean ± SD.

 

   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
Arteriovenous shunt vasoconstriction is among the primary defenses against hypothermia (6). The primary purpose of vasoconstriction is to constrain metabolic heat to the core thermal compartment. Vasoconstriction is effective and maintains the normal core-to-peripheral tissue temperature gradient. Conversely, anesthetic-induced inhibition of tonic thermoregulatory vasoconstriction causes redistribution hypothermia, which is the primary cause of core cooling after the induction of general anesthesia (16,21). Reemergence of vasoconstriction, inpatients becoming sufficiently hypothermic, produces a core temperature plateau that prevents further hypothermia—even during very large and long procedures (5).

Thermoregulatory vasoconstriction is remarkably effective in constraining metabolic heat to the core. This response, though, can be dysfunctional in the context of external heating because vasoconstriction then restricts peripheral-to-core transfer of applied heat. Vasoconstriction thus decreases rewarming rates in postanesthetic patients (7), whereas maintaining dilation improves rewarming (9). The negative pressure aspect of the Vital Heat® system was designed to overcome peripheral thermoregulatory vasoconstriction and thus permit rapid transfer of applied heat from the arm to the core.

Analysis of the heat flow data is revealing. The Vital Heat® device transferred considerable amounts of heat into the forearm. Consequently, total cutaneous heat loss was reduced with this treatment and systemic heat balance improved slightly. However, our results do not support the theory that negative pressure improves peripheral-to-core heat transfer. Vital Heat® warming, combined with passive insulation, increased core temperature no more than passive insulation alone. Virtually all heat transferred into the forearm thus remained in the forearm and was not transferred to the core. These data suggest that to the extent that negative pressure mechanically distended vessels, it did not actually augment flow. Consequently, rewarming rates with negative pressure rewarming were similar to passive insulation. Rewarming rates were twice as much with forced air than Vital Heat® warming, presumably because much of the heat was applied to the trunk, where it could easily reach the core.

Our results are consistent with a recent report by Smith et al. (12) They showed that the rewarming rate in hypothermic postoperative surgical patients was approximately 0.8°C over 90–120 minutes with the Thermostat® device, and that negative pressure rewarming was no better than passive insulation. The Thermostat® was a preliminary version of the Vital Heat® device, which uses a chemical heating pad. Our study extends their work by evaluating regional and systemic heat transfer as well as body heat content. Furthermore, the Vital Heat® device used in our study has been modified and now includes a different heating element that operates at a higher temperature. However, our results and those of Smith et al. (12) are notable in their similarity, suggesting that interim changes in the product design have not improved efficacy.

We, as well as Smith et al. (12), failed to replicate the remarkable rewarming rate of 13.6°C/h reported by Grahn et al. (10). It is thus worth considering potential limitations of their study. Important limitations include the use of external auditory meatus temperature as measure of core temperature; this site is not generally considered sufficient for thermoregulatory studies. There is no mention in the article of shivering or whether the degree of shivering was comparable in the two groups. Finally, the rewarming rates are based on the very highest rates observed during the study and do not represent the average rate at which core temperature increased over the study period.

A difference between our study (as well as Smith’s study) and the one reported previously by Grahn et al. (10) is that the Vital Heat® device is now formulated with a sodium acetate chemical heat source. In the initial study, the heat source was a water-perfused blanket adjusted to maintain a temperature of 44–46°C. The chemical heat source was not as hot as the water blanket and of course did not keep the temperature of the pad as constant as the circulating water. Nonetheless, it averaged {approx}42°C throughout warming, which should have been sufficient and is probably the highest temperature that is safe in a broad range of surgical patients.

The optimal temperature at which the Vital Heat® source needs to be maintained is unknown, but it cannot be much more than 42°C without risking tissue injury. Our measured finger temperature was near 42°C throughout much of the study period. Considering that the core temperature of our subjects was approximately 34°C, a peripheral tissue temperature near 42°C should have provided a sufficient temperature gradient to facilitate heat flow from the periphery to the core of the body, although heat flow, of course, depends critically on peripheral blood flow.

A limitation of our study is that we did not measure blood flow within the negative pressure device, as most of the commonly used techniques for measurement of blood flow are not useful under the condition of negative pressure. However, our main interest was to test two different warming concepts, negative pressure rewarming versus convective warming, and to determine heat balance and heat transfer from the periphery to the core. We clearly demonstrated that heat was not transferred from the peripheral to the core compartment. The mechanisms of heat transfer, blood flow, were not subjects of this study. However, our data raises the question why heat was not transferred from the peripheral to the core compartment, and implies the assumption that blood flow actually decreases with negative pressure.

In summary, systemic heat balance measurements indicate that calories from the Vital Heat® device are largely constrained to the forearm and do not rapidly flow to the core thermal compartment. Consequently, core rewarming rates in nonshivering hypothermic subjects were virtually identical with passive insulation alone or passive insulation combined with Vital Heat® warming. In contrast, rewarming was rapid with forced-air. We cannot explain why the rewarming rates we observed with the Vital Heat® device were an order of magnitude less than reported previously.


   Acknowledgments
 
Supported by National Institutes of Health Grant GM58273, the Joseph Drown Foundation (Los Angeles, CA), Baxter, Inc. (Round Lake, IL), Aquarius Medical Corporation (Scottsdale, AZ), and Augustine Medical, Inc. (Eden, Prairie, MN).


   Footnotes
 
Mallinckrodt Anesthesiology Products, Inc. (St. Louis, MO) donated the thermocouples used.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

  1. Frank SM, Fleisher LA, Breslow MJ, et al. Perioperative maintenance of normothermia reduces the incidence of morbid cardiac events: a randomized clinical trial. JAMA 1997; 277: 1127–34.[Abstract]
  2. Kurz A, Sessler DI, Lenhardt RA, et al. Perioperative normothermia to reduce the incidence of surgical-wound infection and shorten hospitalization. N Engl J Med 1996; 334: 1209–15.[Abstract/Free Full Text]
  3. Schmied H, Kurz A, Sessler DI, et al. Mild intraoperative hypothermia increases blood loss and allogeneic transfusion requirements during total hip arthroplasty. Lancet 1996; 347: 289–92.[ISI][Medline]
  4. Lenhardt R, Marker E, Goll V, et al. Mild intraoperative hypothermia prolongs postoperative recovery. Anesthesiology 1997; 87: 1318–23.[ISI][Medline]
  5. Kurz A, Sessler DI, Christensen R, et al. Heat balance and distribution during the core-temperature plateau in anesthetized humans. Anesthesiology 1995; 83: 491–9.[ISI][Medline]
  6. Lopez M, Sessler DI, Walter K, et al. Rate and gender dependence of the sweating, vasoconstriction, and shivering thresholds in humans. Anesthesiology 1994; 80: 780–8.[ISI][Medline]
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  8. Clough D, Kurz A, Sessler DI, et al. Thermoregulatory vasoconstriction does not impede core warming during cutaneous heating. Anesthesiology 1996; 85: 281–8.[ISI][Medline]
  9. Szmuk P, Ezri T, Sessler DI, et al. Spinal anesthesia only minimally increases the efficacy of postoperative forced-air rewarming. Anesthesiology 1997; 87: 1050–4.[ISI][Medline]
  10. Grahn D, Brock-Utne JG, Watenpaugh DE, et al. Recovery from mild hypothermia can be accelerated by mechanically distending blood vessels in the hand. J Appl Physiol 1998; 85: 1643–8.[Abstract/Free Full Text]
  11. Oakley EHN. Can recovery from mild hypothermia be accelerated so much by mechanically distending locally heated blood vessels? J Appl Physiol 1999; 87: 867–8.[Free Full Text]
  12. Smith CE, Parand A, Pinchak AC, et al. The failure of negative pressure rewarming (Thermostat) to accelerate recovery from mild hypothermia in postoperative surgical patients. Anesth Analg 1999; 89: 1541–5.[Abstract/Free Full Text]
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Accepted for publication September 19, 2000.




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press