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Vol. 83, Issue 5, 1635-1640, 1997
1 Laboratory for Exercise and Environmental Medicine, Health, Leisure, and Human Performance Research Institute, and Department of Anesthesia, Faculty of Medicine, University of Manitoba, Manitoba R3T 2N2; and 2 Defense and Civil Institute of Environmental Medicine, North York, Ontario, Canada, M3M 3B9
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
FOOTNOTES
REFERENCES
ABSTRACT 
Goheen, M. S. L., M. B. Ducharme, G. P. Kenny, C. E. Johnston, John Frim, Gerald K. Bristow, and Gordon G. Giesbrecht. Efficacy of forced-air and inhalation rewarming by using a human
model for severe hypothermia. J. Appl.
Physiol. 83(5): 1635-1640, 1997.
We recently
developed a nonshivering human model for severe hypothermia by using
meperidine to inhibit shivering in mildly hypothermic subjects. This
thermal model was used to evaluate warming techniques. On three
occasions, eight subjects were immersed for ~25 min in 9°C water.
Meperidine (1.5 mg/kg) was injected before the subjects exited the
water. Subjects were then removed, insulated, and rewarmed in an
ambient temperature of 
20°C with either
1) spontaneous rewarming (control),
2) inhalation rewarming with
saturated air at ~43°C, or 3)
forced-air warming. Additional meperidine (to a maximum
cumulative dose of 2.5 mg/kg) was given to maintain shivering
inhibition. The core temperature afterdrop was 30-40% less during
forced-air warming (0.9°C) than during control (1.4°C) and
inhalation rewarming (1.2°C) (P < 0.05). Rewarming rate was 6- to 10-fold greater during forced-air
warming (2.40°C/h) than during control (0.41°C/h) and
inhalation rewarming (0.23°C/h) (P < 0.05). In nonshivering hypothermic subjects, forced-air warming provided a rewarming advantage, but inhalation rewarming did not.
afterdrop; cold stress; heat production; shivering thermogenesis; treatment
INTRODUCTION IT IS GENERALLY AGREED that treatment of the
hypothermic victim should minimize the postexposure afterdrop in core
temperature (Tco) and promote a
steady, continuous rate of rewarming to a level where physiological
homeostasis can be maintained. To date, laboratory research on field
treatment for hypothermia has been limited to mild hypothermic
conditions (i.e., Tco
>33.0°C) in which subjects shiver vigorously. Because skin
warming inhibits shivering thermogenesis, external application of
moderate sources of exogenous heat provides little rewarming advantage
if vigorous shivering is present (3, 5). External warming will only provide a benefit to shivering patients if the amount of heat donated
exceeds the amount of shivering heat production that is inhibited.
Warm-water immersion is one method of donating a high amount of heat
and promoting a rapid rate of rewarming (24), but it may also increase
the afterdrop in Tco
(11). Forced-air warming has also been used to donate a
considerable amount of heat (~200 W). Although the rewarming rate was
not increased, Tco afterdrop was
decreased by 30% (8). Whereas warm-water immersion is impractical in
the field, forced-air warming systems could be adapted for field use.
Inhalation of warm, humidified air or
O2 has also been used extensively
as a noninvasive internal application of exogenous heat (17).
Comparative studies have shown little (12, 23, 24) or no (3, 4)
rewarming benefit over shivering thermogenesis alone in mildly
hypothermic subjects. This is not surprising given the limited
calculated heat transfer capabilities of this method (29), the probable
inhibitory effect of inhalation rewarming on shivering, and the small
temperature differences between inspired gas and the body core of only
5-10°C at relatively high
Tco values (i.e., >33°C).
Despite the equivocal results in shivering subjects, exogenous heat is
likely beneficial for victims of severe hypothermia (i.e.,
Tco <30°C) in whom shivering
is impaired or absent (1). For obvious ethical reasons, it is
impossible to lower human Tco values to below 30°C, where the shivering response is naturally suppressed. However, we have recently developed a human model for
severe hypothermia in which meperidine (1.5 mg/kg iv) was administered
to inhibit shivering in mildly hypothermic subjects (7). During
rewarming under these nonshivering conditions, the afterdrop in
esophageal temperature (Tes)
reached values as great as 2.5°C compared with 0.4°C with
shivering intact. Without the endogenous heat production of shivering,
Tes remained at or near nadir
values for up to 150 min postimmersion.
This new protocol was used to evaluate
Tco during recovery in fieldlike
conditions [ambient temperature
(Ta) = METHODS With approval from our Faculty Human Ethics Committee, eight healthy
subjects (2 women, 6 men) were studied after giving informed consent.
The subjects were without allergy history or adverse reactions to or
chronic use of narcotics. The eight subjects were 30 ± 5 (SD) yr
old, had a mass of 74 ± 7 kg, were 177 ± 8 cm tall, had a sum
of 4 skinfolds (biceps, triceps, suprailiac, and subscapularis) of 54 ± 10 mm, and had 18 ± 6% body fat.
Subjects were studied on three occasions. During cold-water immersion
they received injections of meperidine to inhibit shivering thermogenesis. They then exited the water and lay in an insulated enclosure (see Warming systems) for
potential rewarming by means of endogenous heat production only,
inhalation rewarming, or forced-air warming.
20°C]
during 1) spontaneous rewarming with
no exogenous heat donation (control), 2) inhalation rewarming with
saturated air heated to ~43°C, and 3) forced-air warming with a newly
developed system. We hypothesized that, compared with spontaneous
nonshivering conditions, forced-air warming would decrease the
afterdrop and enhance rewarming, whereas inhalation rewarming would
provide a smaller but significant rewarming advantage.
O2) and
cutaneous heat flux and temperatures were measured according to methods
described previously (8, 9).
O2 was determined by an
open-circuit method from measurements of expired minute ventilation
(E) and inspired and mixed
expired gas concentrations sampled from a 10-liter fluted mixing box.
Subjects wore a snugly fitting face mask with a one-way valve that was
connected to the appropriate instrumentation by a suitable length of
corrugated plastic tubing. The corrugated tubing that was exposed to
20°C air was insulated to prevent condensation within the
tubing. A thermocouple was attached to the inflow side of the one-way
valve on the face mask to measure inspired air temperature. During the
inhalation rewarming condition, the entire one-way valve was insulated
to maximize temperature of the inspirate.
Cutaneous heat flux and temperature were measured from 12 sites by
thermal flux transducers (Concept Engineering, Old Saybrook, CT). Flux
was defined as positive when heat traversed the skin toward the
environment (6). Body surface area (BSA) was calculated [BSA
(m2) = weight0.425
(kg) · height0.725
(cm) · 0.007184], and the following regional
percents were assigned based on those of Layton et al. (15): forehead,
7%; upper chest, 8.8%; abdomen, 8.7%; scapula, 8.8%, lower back,
8.7%, anterior thigh, 9.5%, posterior thigh, 9.5%; shin, 6.5%;
calf, 6.5%; dorsum of the foot, 7%; dorsum of the hand 5.0%; and
arm, 14%. Flux values from each transducer
(W/m2) were then converted into
watts per region [flux at region (W) = transducer flux
(W/m2) · BSA
(m2) · regional
percentage · 0.01]. Temperature was also
measured on the plantar surface of the left great toe and the ventral
surface of the third right fingertip to monitor calf-to-toe and
forearm-to-finger skin temperature
(Tsk) gradients for indications
of peripheral vasodilation during rewarming. Rapid rises in finger
temperature and decreases in forearm-to-finger temperature gradients
below 4°C have been used to signify cutaneous vasodilation
(25). At 30-s intervals, thermal, HR, and metabolic data
were averaged for the preceding 30-s period, displayed graphically on
the computer screen, and recorded in spreadsheet format on a hard disk.
Warming systems.
The new forced-air warming system consisted of a mobile insulated
wooden warming box (1.6 m long × 0.725 m wide × 0.33 m
high) that supported a nylon webbed stretcher (2.14 m long). With the subject lying on the stretcher, a wire frame (curved side to side) was
placed over the subject. The rostral portion of the box was hollow and
contained two 1,200-W electric heaters and six circulating fans below
the webbed stretcher. Two more 1,200-W heaters and three fans were
contained in an enclosed section on top of the wire frame just above
the subject's chest. A down sleeping bag (13 clo) was then placed over
the wire frame and attached securely to the wooden box via Velcro
strips. The head of the subject (which was exterior to the insulated
enclosure) was covered with a down hood. The enclosure allowed exposure
to air of all anterior and posterior skin surfaces from midthigh to the
shoulders. Thermocouples were used to measure
Ta values above and below the
torso. During forced-air warming, the circulating fans were activated
and the heaters were thermostatically controlled to maintain
Ta within the enclosure at
~46-48°C with a maximum local
Tsk of 43°C. For consistency,
subjects were placed in the warming enclosure for all trials, with the
fans and heaters turned off during the control and inhalation rewarming
trials.
In the inhalation rewarming trials, a Res-Q-Air inhalate delivery
system (model HT 1000, CF Electronics, Comack, NY) was used. A 12-V
marine battery provides power to heat water in the system reservoir.
Inspired air is first drawn through the water where it is heated and
saturated, thus providing humidified inspirate at the mouth at
~43°C.
Protocol.
Each subject was cooled on three occasions separated by at least 3 days. Trials were conducted at the same time of day. Subjects were
instructed to abstain from alcohol and medications for a period of 24 h
before each study. They were also asked to fast for 8 h
before coming to the laboratory to minimize any potential nausea caused
by meperidine infusion. The subjects, who were dressed in swimsuits,
were instrumented and sat quietly, covered by a blanket, at a
Ta of ~22°C for 10 min of
baseline data collection. Before immersion they were
dressed in a thin plastic body suit. Removal of this suit after
immersion allowed a rapid transition to the rewarming phase and ensured
that the subject was completely dry after immersion (minimizing
evaporative heat loss during rewarming without the time consuming, and
mechanically stimulating, process of towel drying).
Subjects were then immersed to the shoulders in a stirred water bath in
which the water temperature was lowered from 20 to 9°C within 10 min by the addition of ice. For comparative purposes, the immersion
time and removal Tes for each
subject were kept similar for all trials. Ten minutes before the end of
immersion the subjects were given 1.5 mg/kg of meperidine iv (diluted
in 10 ml of saline) injected in five 2-ml aliquots in successive 2-min
intervals. They were then hoisted out of the water, and the body suit
was removed. Subjects were fitted with an insulated hood, and a pulse
oximeter was placed on the middle finger to monitor arterial oxygen
saturation as an indication of adequate oxygenation. During the
forced-air condition, insulated mitts (up to the level of the elbow)
and boots (up to the level of the knee) were placed over the distal
limbs to minimize peripheral warming and consequent vasodilation, which
could exaggerate afterdrop through redistribution of heat from the core
to the periphery. For consistency, this procedure was also followed in
the control and inhalation rewarming protocols.
Subjects were then placed supine in the rewarming enclosure. An
airtight neck seal was accomplished by insulating the subject's head
and neck area. The rewarming enclosure was then rolled into an
environmental chamber where Ta = 20°C. No exogenous heat source was used in the control
trials. In the inhalation rewarming trials, the Res-Q-Air inhalate
delivery system was placed in the rewarming enclosure and connected to
the input valve of the face mask, providing humidified inspirate at
~43°C. During the forced-air warming trials, the heaters and
circulating fans were activated just before the rewarming enclosure was
transported into the environmental chamber. Treatment continued until
either Tes increased to 36.8°C
or 150 min had elapsed. In the latter situation, subjects were then
immersed in 40°C water until
Tes increased to a normothermic
level.
In our previous study (7) subjects were cooled for an average of 52 min
to an average Tes of
35.9°C. This cold stimulus was sufficient to cause a
slight disinhibition of shivering during rewarming. To eliminate this
effect, we decided to shorten immersion times and provide supplemental
injections of meperidine (to a cumulative maximum dose of 2.5 mg/kg) as
required to maintain shivering suppression and reverse any increases in
O2. Therefore, spontaneous
rewarming (i.e., control) trials were performed first in all subjects.
In six of the eight subjects, shivering resumed during rewarming, and
the immersion time and/or meperidine dose were adjusted for a
second control trial. In the other two subjects, the immersion time and
meperidine dose in the initial trial were sufficient to completely
eliminate shivering throughout rewarming. Inhalation rewarming and
forced-air warming trials then followed control trials in a balanced
design, with the immersion time and supplemental meperidine dosing
schedule for each subject following that established during their
control trials.
Data analysis.
All data were averaged for the baseline period (10 min) and for
subsequent 5-min intervals during immersion and postimmersion. The
following variables were calculated for each trial: the afterdrop (difference between Tes on exit
from cold water and its nadir), the length of the afterdrop period
(time between exit from cold water until
Tes returned to original exit
Tes), the rate of rewarming (calculated by linear regression for
Tes data during the linear increase after the Tes nadir),
total net cutaneous heat transfer, and area-weighted mean
Tsk
(Tsk avg).
O2 was used as an indicator of metabolic heat production, and values greater than baseline were
attributed to shivering thermogenesis (2). Data for the three trials
were compared by using an analysis of variance for repeated measures
with Tukey's post hoc test used to identify significant differences.
Results are reported as means ± SD.
P < 0.05 identified statistically
significant differences.
RESULTS
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O2 increased during cooling
until meperidine infusion (Fig. 2).
Postimmersion in both the control and forced-air warming conditions,
O2 continued to drop to or
below baseline levels and remained at these low levels for the
remainder of the trials. During inhalation rewarming,
O2 was
significantly higher at 30 min postimmersion
(P < 0.05).
E was similar in all conditions, increasing from ~13 l/min during baseline to ~22 l/min before meperidine injection and then decreasing to ~13 l/min just before the
subjects exited the cold water and to ~9 l/min postimmersion.
Inhalation
rewarming significantly greater than control only,
P < 0.05.
HR increased from baseline values of ~74 beats/min to a maximum of ~81 beats/min just before meperidine infusion. Postimmersion HR declined and stabilized below baseline values, being significantly greater during forced-air warming (~67 beats/min) than in the other two conditions (~53 beats/min) after 10 min postimmersion (P < 0.05). Mean blood pressure rose from ~92 to ~114 mmHg during cooling and subsequently decreased to ~106 mmHg after meperidine injection. Postimmersion blood pressure varied slightly, with the only significant difference occurring between inhalation rewarming (97 ± 8 mmHg) and forced-air warming (90 ± 6 mmHg) after 35 min of treatment (P < 0.05). Tsk and heat flux responses. Enclosure Ta increased to ~48.0°C within 5 min of forced-air warming (Table 1). This resulted in a significantly higher Tsk avg during forced-air warming than during the other two conditions (P < 0.0001). Postimmersion heat was continually lost throughout control and inhalation rewarming (Fig. 3). In comparison, forced-air warming provided a total heat gain. At the period of maximum heat gain, all but 30 W was gained through the anterior torso and thigh (132 W) and the back and posterior thigh (110 W).
During baseline, all subjects were vasoconstricted in the lower extremities, and six were vasoconstricted in the upper extremities. After 30 min postimmersion, extremities were vasoconstricted in all subjects during the control and inhalation rewarming trials (Table 1). During forced-air warming, peripheral vasodilation occurred after 30 min in the fingers of three subjects and by the end of warming in six of the subjects. Only one subject showed evidence of vasodilation in the toes.
DISCUSSION
This study is the first to pharmacologically inhibit shivering and create a human model for severe hypothermia to evaluate relative efficacy of emergency field rewarming techniques. Inhalation rewarming did not significantly lower the magnitude of afterdrop, shorten the rewarming period, or improve the rate of rewarming compared with spontaneous rewarming. Forced-air warming with a high source of heat (up to 270 W) reduced the afterdrop by 30-40% and resulted in a 6- to 10-fold increase in rewarming rate.
During inhalation rewarming, our nonshivering subjects rewarmed at slightly lower rates than those reported by Lloyd (16) (0.5°C/h) in unconscious victims, with Tco values below 30°C, who were probably not shivering. The slightly higher rewarming rates in the report by Lloyd may be due to the higher inspired air temperatures used (50-80°C) vs. 43°C in the present study. In comparison, studies employing inhalation rewarming in shivering subjects report much higher rates of rewarming of between 0.8 and 1.4°C/h (10, 12, 18, 22-24, 28). This is consistent with data demonstrating that, with shivering intact, both metabolic heat production and rewarming rates increase as initial Tco and Tsk decrease (22).
Our lack of difference between rewarming rates for control and
inhalation rewarming trials is consistent with other studies in which
inhalation rewarming rates were between 63 and 133% of spontaneous
(shivering-intact) rewarming rates (3, 10, 18, 24). Although Hayward
et. al (11) reported an 80% increase in rewarming rate with inhalation
rewarming, only one subject was studied, and these results may not be
generalizable. In the present study, rewarming was conducted at a
Ta of 20°C to maximize the difference in inspired air temperature between control
(20°C) and inhalation rewarming (43°C) trials. Two other
studies have conducted rewarming at a
Ta of 20°C with
shivering subjects at average Tco
values of 35.4°C (19) and 33.9°C (4). In both cases,
spontaneous and inhalation rewarming rates were similar.
The proposed advantages of inhalation rewarming are a decrease in respiratory heat loss and an increase in heat donation through the respiratory tract. Some authors have calculated that inhalation rewarming can improve heat balance by only 23 kcal/h (26) or 17.1 kcal/h (29), of which only 6.0 kcal/h are actually due to heat donation itself with the rest due to prevention of heat loss (29). These are relatively small values considering they are only ~16-22% of resting metabolic heat production observed during our inhalation rewarming trials and that humans can increase heat production by a factor of 5 during vigorous shivering. Also, for every 1 kJ of respiratory heat added via inhalation rewarming, shivering metabolic heat production has been shown to decrease by 1.4 kJ (21) and 1.95 kJ (24). In contrast, when shivering was suppressed in our hypothermic subjects, metabolic heat production was slightly increased during inhalation rewarming. This increase may be at least partly explained by added work of breathing introduced by the apparatus itself.
Hayward and Steinman (12) have suggested other benefits of inhalation rewarming, including rehydration, stimulation of respiratory mucociliary activity, and direct heat transfer from the upper airways to the hypothalamus, brain stem, and other brain structures. Warming of the respiratory and cardiovascular centers could help stabilize cardiorespiratory parameters even if total body heat content was not increased significantly. Also, central thermoregulatory control may be reinstated in a severely hypothermic victim. There are numerous anecdotal reports where application of inhalation rewarming significantly improved the hypothermic patient's pulse rate and mental state within 20-40 min (R. Douwens, personal communication). This is consistent with inhalation therapy warming the brain stem and/or other brain structures without significantly increasing core body heat content.
It may be difficult to demonstrate a thermal advantage with inhalation rewarming in the present laboratory study because of inherent limitations. Clinically, a moderately to severely hypothermic patient would have depressed ventilation, thus minimizing respiratory heat transfer. Also, the airway warming system used in this study may not represent all inhalation therapy systems because other devices may deliver hotter air with greater saturation (i.e., slightly cooled steam).
Forced-air warming systems have generally been used for prevention or reversal of hypothermia in surgical patients (14), but the potential value for prehospital stabilization for accidental hypothermia has also been suggested (8, 27). We have previously demonstrated that a conventional forced-air warming system (Bair Hugger, Augustine Medical) transfers a moderate amount of heat (~100 W) to the body surface in normothermic subjects (6) and a greater amount of heat transfer in hypothermic subjects who had much lower Tsk values (237 W initially, falling to 163 W after 30 min) (8).
We expected that the newly designed forced-air warming system would transfer even more heat to our subjects. Although total heat transfer to the body was only moderately greater, the new system redistributed heat away from the extremities toward the torso, including the back. As expected, afterdrop was decreased and rewarming rate was increased significantly. The decreased afterdrop was likely a result of decreased thermal gradients for conductive heat loss through direct warming of peripheral tissue. This protective effect may prevent a victim's Tco from dropping below the threshold for cold-induced ventricular fibrillation (1). The high amount of heat transfer during forced-air warming (average >200 W) facilitated more rapid rewarming than did spontaneous rewarming. In severely hypothermic nonshivering victims, endogenous heat production is likely below 50 W at a Tco of 27°C (1). Therefore, forced-air warming could be beneficial for severe hypothermia during transport.
The main safety concern with forced-air warming is burn prevention. At the end of 30 min of forced-air warming Tsk avg was only 35.5°C, and local Tsk did not exceed 43°C in any area. Under these conditions the risk of burns is likely minimal (13).
To maintain shivering suppression throughout the rewarming periods, the decrease in Tes was necessarily small. Despite the relatively high Tes, peripheral tissues were cooled sufficiently to produce temperature gradients resulting in larger afterdrops (0.9-1.4°C) than reported in other studies with shivering subjects at lower Tco values (3, 5). The comparative results in this study are qualitatively valid, although the absolute changes would likely be even greater at lower Tco values.
In summary, Tco did not increase significantly in nonshivering, mildly hypothermic subjects even after 150 min of spontaneous or inhalation rewarming. However, external heat delivery with forced-air warming decreased Tco afterdrop by 30-40% and increased the rewarming rate by 6- to 10-fold. These data indicate that exogenous heat is likely beneficial to a severely hypothermic nonshivering patient. A portable forced-air warming system holds considerable promise for field use because of the rapid reversal of core cooling, the high rate of rewarming, and overall comfort provided to the victim. Finally, our new human model for severe hypothermia will allow the study of other rewarming methods, without the complicating factor of shivering thermogenesis.
ACKNOWLEDGEMENTS
We thank Andrew Chen for assistance in data analysis. We also thank RES-Q Products, Inc., for the use of the Res-Q-Air inhalate delivery system.
FOOTNOTES
Address for reprint requests: G. G. Giesbrecht, Univ. of Manitoba, Faculty of Physical Education and Recreation Studies, 102 Frank Kennedy Bldg., Winnipeg, MB, Canada R3T 2N2 (E-mail: Giesbrec{at}cc.umanitoba.ca).
Received 29 October 1996; accepted in final form 26 June 1997.
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