Recovery from mild hypothermia can be accelerated
by mechanically distending blood vessels in the hand
DENNIS GRAHN,1 JOHN G. BROCK-UTNE,2
DONALD E. WATENPAUGH,3 AND H. CRAIG HELLER1
Departments of 1Biological Sciences and 2Anesthesiology, School of Medicine, Stanford University,
Stanford, California 94305; and 3Department of Integrative Physiology,
University of North Texas Health Science Center, Fort Worth, Texas 76107
follows that removal of the vasoconstrictive blockade to
heat exchange would facilitate transfer of heat from the
skin to the body core in hypothermic individuals. The
purpose of this study was to determine to what extent
heat transfer to the thermal core of a hypothermic
individual could be enhanced by increasing blood flow
through the skin area to which exogenous heat is
applied.
Blood volume and blood flow in an appendage can be
altered by placing the appendage in a sealed enclosure
and manipulating the local atmospheric pressure. Blood
vessels in the hand can be distended by exposing the
distal portion of the limb to subatmospheric pressures
(14). The application of superficial heat to the mechanically distended tissues increases blood flow through the
hand (4). Therefore, we hypothesized that the combined
application of subatmospheric pressure and heat to the
hand of a hypothermic individual would increase subcutaneous blood flow and thus be an effective noninvasive
technique for rapidly transferring heat from the skin
surface to the body core.
core temperature; heat transfer; negative pressure; subatmospheric pressure; vasomotor tone
MATERIALS AND METHODS
LIKE ALL HOMEOTHERMIC MAMMALS,
humans maintain a
relatively constant core body temperature (Tc ). Mammals minimize the energy costs of homeothermy by
selecting thermal environments in which Tc can be
maintained with minimal metabolic effort. Within this
thermoneutral environment, Tc is regulated by vasomotor adjustments that control heat transfer between the
body core and the skin (2). Vasoconstriction reduces
heat transfer; vasodilation increases heat transfer.
Vasomotor tone is centrally regulated and determined
primarily by Tc (33, 34). When vasomotor responses are
not sufficient to maintain a desired Tc, metabolically
more expensive thermogenic or thermolytic mechanisms are activated.
Hypothermia occurs when the capacity to conserve
and produce heat is overwhelmed by environmental
cold or is compromised (e.g., by anesthesia) (19). Because vasoconstriction occurs before the activation of
thermogenic mechanisms, hypothermia in conscious
individuals is always associated with maximal vasoconstriction. Whereas vasoconstriction is an appropriate
response to prevent heat loss from the thermal core, it
also slows the transfer of exogenous heat from the body
surface to the body core (5). Thus application of heat to
the skin of a hypothermic individual affects Tc slowly. It
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Subjects. This study was conducted in the Post Anesthetic
Care Unit (PACU) of Stanford University Hospital and followed a protocol approved by the Human Subjects Committee
of Stanford University. Informed consent for participation in
this study was obtained from 32 patients undergoing a
variety of surgical procedures, before the induction of anesthesia. The axillary temperature of the potential subjects was
measured on admission to the PACU. Sixteen subjects (age
range 21–77 yr, mean age 46.7 yr; 9 men, 7 women) qualified
as mildly hypothermic (33.5°C , axillary temperature ,
35.5°C) and were randomly assigned to either the experimental or control group.
Equipment. The experimental device consisted of a circulating water bath, a vacuum pump, and a sealed chamber that
housed a water-perfusion blanket. The chamber was constructed from a 35-cm length of acrylic tubing (15.25 cm ID, 3
mm thick) capped at one end with an acrylic plate. A conical
neoprene collar (15 cm long, 16–8 cm OD, 6 mm thick) created
a seal around the subject’s forearm. An acrylic adapter ring (7
cm long, 16 cm OD, 5 mm thick) connected the chamber body
to the neoprene collar. The chamber was connected to the
vacuum pump via a port in the chamber wall and polyethylene tubing (1/4 in. ID, 1/8-in. wall). Water lines (polyethylene
tubing, 1/4 in. ID, 1/16-in. wall) connecting the water bath to
the water-perfusion blanket were attached by means of
compression fittings through holes in the adapter ring. Chamber pressure was measured with an analog pressure gauge
(range 0 to 2100 mmHg). Chamber pressure was controlled
by adjusting a needle valve mounted in the vacuum line.
Temperatures were measured with copper-constantan thermo-
8750-7587/98 $5.00 Copyright r 1998 the American Physiological Society
1643
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Grahn, Dennis, John G. Brock-Utne, Donald E. Watenpaugh, and H. Craig Heller. Recovery from mild hypothermia can be accelerated by mechanically distending blood
vessels in the hand. J. Appl. Physiol. 85(5): 1643–1648,
1998.—Peripheral vasoconstriction decreases thermal conductance of hypothermic individuals, making it difficult to transfer externally applied heat to the body core. We hypothesized
that increasing blood flow to the skin of a hypothermic
individual would enhance the transfer of exogenous heat to
the body core, thereby increasing the rate of rewarming.
External auditory meatus temperature (TEAM ) was monitored
in hypothermic subjects during recovery from general anesthesia. In 10 subjects, heat (45–46°C, water-perfused blanket)
was applied to a single forearm and hand that had been
placed in a subatmospheric pressure environment (230 to
240 mmHg) to distend the blood vessels. Heat alone was
applied to control subjects (n 5 6). The application of subatmospheric pressure resulted in a 10-fold increase in rewarming
rates as determined by changes in TEAM [13.6 6 2.1 (SE) °C/h
in the experimental group vs. 1.4 6 0.1°C/h in the control
group; P , 0.001]. In the experimental subjects, the rate of
change of TEAM decreased sharply as TEAM neared the normothermic range.
1644
ACCELERATED RECOVERY FROM MILD HYPOTHERMIA
RESULTS
All subjects were hypothermic (TEAM , 35.5°C) at the
onset of treatment [34.6 6 0.8 (SE) °C] (Table 1). The
initial TEAM of the experimental group was not significantly different from that of the control group (34.3 6
0.9 vs. 34.8 6 0.3°C). Final temperatures were also not
statistically different (36.0 6 0.5 vs. 36.2 6 0.4°C,
respectively). However, the time required to achieve
the final stable TEAM was significantly reduced in the
experimental group (8.1 6 2.3 vs. 59.0 6 14.3 min,
respectively).
The combined application of heat and subatmospheric pressure to a single forearm, hand, and fingers
accelerated recovery from hypothermia (Fig. 1). In the
experimental subjects, there was an upward inflection
of TEAM on application of heat and subatmospheric
pressure, but as TEAM approached normal, the rate of
change in TEAM decreased. In all of the experimental
subjects, the changes in TEAM were complete within 15
min of application of subatmospheric pressure and heat
(Fig. 2, top). In contrast, none of the control subjects
exhibited an abrupt increase in TEAM (Fig. 2, bottom).
Within the treatment groups, the changes in TEAM
over time of the individual subjects were similar.
Standardized rewarming curves were generated for the
experimental and control groups (Fig. 3). The maximum rate of change of TEAM (the steepest portion of the
rewarming curve) of the experimental group was 13.6 6
2.1°C/h, 10 times faster than that of the control group
(1.4 6 0.1°C/h). The rewarming rates determined in
this study are compared with those from comparable
studies reported in the literature (see Table 2).
DISCUSSION
A criterion for an effective heating device is that the
heat generated by the device reach the desired target.
Table 1. Effect on recovery time of mechanically
distending subcutaneous vasculature
during application of heat to the hand
of mildly hypothermic individuals
Treatment Group
n
Initial TEAM , °C
Final TEAM , °C
Time to final TEAM , min
Experimental
Control
10
34.3 6 0.9
36.0 6 0.5
8.1 6 2.3*
6
34.8 6 0.3
36.2 6 0.4
59.0 6 14.3
Values are means 6 SE for n subjects. Experimental subjects were
treated with subatmospheric pressure and heat, whereas control
group subjects were treated with conventional noninvasive rewarming techniques or with heat but not with subatmospheric pressure.
Experimental subjects received heat applied directly to the skin of a
single forearm and hand of an appendage placed in a subatmospheric
pressure environment. Subjects were patients recovering from general anesthesia in the Post Anesthetic Care Unit (PACU) and deemed
by the PACU nursing staff to be suffering from anesthesia-induced
hypothermia. TEAM , external auditory meatus temperature. Initial
TEAM , TEAM at the initiation of treatment, ,20 min after admission to
the PACU; final TEAM , TEAM at which patients stabilized; time to final
TEAM , time from initiation of treatment to attainment of a stable
TEAM . * Significantly different from control group (P , 0.001).
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couples connected to custom-made signal-conditioning units
with digital temperature displays. Water-perfusion blanket
temperature was monitored by measuring the temperature in
the water-perfusion line where it entered the vacuum chamber and was controlled by adjusting the temperature of the
water bath.
A temperature probe, similar in design to that described by
Sato et al. (27) for measuring tympanic membrane temperature in unanesthetized individuals, was used in this study.
However, because the temperature probe was placed on our
subjects as they were emerging from a surgical plane of
anesthesia and there is a substantial risk of perforating the
tympanic membrane when a temperature probe is placed
directly on the tympanic membrane of an anesthetized individual, tympanic membrane temperature itself was not measured in this study (31). Instead, external auditory meatus
temperature (TEAM ) was monitored throughout the experiments. The thermocouple used to measure TEAM was inserted
through the center of a sound-attenuation ear plug (Bilsom
Perfit, Billesholm, Sweden) so that the tip of the thermocouple extended 5 mm past the end of the ear plug. The ear
plug was positioned so that the tip of the thermocouple
penetrated ,7 mm into the external auditory meatus. TEAM
was recorded at ,1-min intervals, and the data were manually entered into a computer for subsequent analyses.
Experimental procedure. Each experiment was initiated
after the patient had been admitted to the PACU and the
PACU nursing staff had determined that, aside from being
hypothermic, the patient was in stable condition (generally
15–30 min after admission to the PACU). The subject was
fitted with the device so that the water-perfusion blanket
surrounded the forearm, hand, and fingers of a single appendage. For the experimental group (n 5 10), the water blanket
was maintained at 44–46°C, and the chamber was evacuated
to a pressure of 230 to 240 mmHg. For two of the six control
subjects, the water-perfusion blanket was maintained at
44–46°C, but the chamber was not evacuated. The other four
subjects included in the control group received conventional
PACU treatment (two were wrapped in warm blankets and
two were subjected to forced-air rewarming techniques).
Data analysis. TEAM vs. time graphs were generated for
each subject. Visual inspection of the graphs determined that
the experimental subjects’ plots were exponentially saturating, whereas those of the control subjects were linear. Because the objective of this study was to determine the effect of
treatment on the rate of recovery from hypothermia, the rates
of change in TEAM over time, rather than the absolute
temperatures, were the relevant measurements. For each
subject, the stable TEAM after rewarming served as a baseline.
The recorded TEAM values were subtracted from the baseline
TEAM to generate return to baseline curves. These curves were
then aligned by visually adjusting the time-axis location of
the individual plots to maximize the overlap between the
individual records. Mean and SE values for the aligned data
sets were then calculated at 2-min intervals for the experimental group and at 5-min intervals for the control group.
Maximum rewarming rate, the slope of the steepest portion of
the TEAM vs. time curves, was calculated for each individual.
Mean and SE values for maximum rewarming rates were
then calculated for the experimental and control groups. The
maximum rewarming rates, initial TEAM, final TEAM, and
rewarming time were statistically analyzed by using Student’s t-test (P , 0.001). The results from this study were
compared with results from previously published studies that
assessed the efficacy of other noninvasive rewarming techniques for the treatment of hypothermia.
ACCELERATED RECOVERY FROM MILD HYPOTHERMIA
Because hypothermia is a condition in which the thermal core of the body falls below the desired temperature range, the thermal core (rather than the peripheral tissues) must be heated to reverse hypothermia.
The thermal core is defined as the internal regions of
the body having temperatures that are not changed in
their relationship to each other by circulatory adjustments or changes in heat dissipation to the environment that affect the thermal shell of the body (19). The
thermal core comprises ,8% of the total body mass (1).
This small central portion of the total body mass needs
to be warmed to reverse hypothermia. Thus, to rapidly
treat hypothermia, it is necessary to maximize the
transfer of heat from the body surface into the thermal
core. Blood flow between the body surface and the
thermal core is the normal modality for heat transfer
between the environment and the body core. However,
in hypothermic individuals, vasoconstriction suppresses peripheral blood flow and slows heat transfer
between the skin surface and the thermal core. To
utilize the circulatory system of a hypothermic individual as a heat-transfer medium, two factors must be
considered: 1) peripheral vasoconstriction is centrally
mediated, and thus local application of heat to the skin
surface will have little effect on vasomotor tone when Tc
is below the desired range; and 2) only limited areas of
the skin surface are specialized for heat transfer between the body core and the environment.
Thermoregulation is under central nervous system
control. The central nervous system receives inputs
from temperature sensors located in the body core as
well as on the skin surface. A hierarchy of the thermal
inputs to the thermoregulatory control system can be
determined based on the response to local temperature
manipulations. The temperature of the preoptic/
anterior hypothalamic region of the brain stem (POAH)
is known to provide potent input to the mammalian
thermoregulatory system, whereas local skin temperatures provide a relatively low-priority input (28). Local
manipulations of POAH temperature (TPOAH ) in experimental mammals activate appropriate thermoregulatory-effector mechanisms: increases in TPOAH elicit peripheral vasodilation and active thermolytic responses
such as panting and sweating, which decrease Tc,
whereas decreases in TPOAH elicit peripheral vasoconstriction and active thermogenic responses (e.g., shivering), which increase Tc (16). Skin temperature, although important for behavioral thermoregulatory
responses, has little impact on autonomic thermoregulatory function (17, 21). Cutaneous thermal input can
alter the TPOAH thresholds for eliciting metabolic thermoregulatory responses but does not affect the relationship between the displacement of TPOAH from the
threshold temperature and the magnitude of the thermoregulatory response (17). In fact, eliminating input
from the trunk and face cutaneous thermoreceptors (by
sectioning nerves supplying the cutaneous receptors)
Fig. 2. Subatmospheric pressure enhanced heat transfer and sped
recovery from anesthesia-induced hypothermia. Top: experimental
subjects (n 5 10). Each symbol represents a different subject (not all
symbols are visible). Both heat and subatmospheric pressure were
applied to a single forearm and hand. Bottom: control subjects (n 5 6).
Each symbol represents a different subject. n, Subjects were fitted
with the rewarming device, but chamber was not evacuated; k,
subjects treated with cotton blankets; s, subjects treated with forced
warm air devices. Although individual subjects in control group
received different rewarming procedures, different methods of treatment had no effect on rate of rewarming. Time is referenced to
initiation of treatment. Data presented in Fig. 1 are included;
however, data points before initiation of treatment are not included.
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Fig. 1. Rewarming curves of 2 subjects, each using 1 rewarming
technique, demonstrate effect of subatmospheric pressure on rewarming during recovery from hypothermia. Subjects were recorded in
Post Anesthetic Care Unit (PACU) during recovery from anesthesiainduced hypothermia after general surgical procedures. Changes in
condition of thermal core were determined by measuring external
auditory meatus temperature (TEAM ). Time is referenced to initiation
of treatment, ,20 min after admission to PACU. r, Experimental
subject. One forearm was wrapped in a 45°C water-perfusion blanket
and placed in a sealed chamber. Chamber was evacuated to 240
mmHg at time 5 0 min. k, Control subject. One forearm was
wrapped in a 45°C water-perfusion blanket and placed in a sealed
chamber, but chamber was not evacuated.
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ACCELERATED RECOVERY FROM MILD HYPOTHERMIA
does not substantially interfere with an animal’s ability
to regulate its body temperature (17). When Tc of intact
animals is in the hypothermic range, warming of the
skin is relatively ineffective in reducing shivering or
vasoconstriction (21). The cold inputs from core and
brain to the thermoregulatory system take priority
over warm input from skin sensors, thus preserving the
vasoconstrictive blockade to heat transfer.
Under normal conditions, a constant Tc is maintained by balancing heat production and heat loss. In a
thermoneutral environment, heat production is relatively constant, and Tc is regulated by controlling heat
loss. Over 70% of the total heat produced by a resting
human is generated in the body core (1). The excess
heat generated in the body core is transferred directly
to the environment through specialized subcutaneous
heat-exchange vasculature. The heat-exchange vasculature is limited to the hairless regions of the face, ears,
hands, and feet (13). The heat-transfer structures
consist of subcutaneous venous plexuses (dense networks of thin-walled, large-diameter venules) and arteriovenous anastomoses (AVAs) (vascular communications directly between the arteries and the venous
plexuses). Where found, these exchange structures are
dense, e.g., .500 AVAs/cm2 in the nail beds of the
fingers and toes (13). The dimensions of venous plexuses determine the blood volume capacity of a heatexchange region, and the AVAs control the blood flow
through the venous plexuses. The blood-flow velocities
through the venous plexuses can range from ,0.1 to .1
m/s (3). It has been estimated that, with maximum
vasodilation, blood flow into the subcutaneous venous
plexuses can be as great as 30% of the total cardiac
output (15). Thus when these structures are vasodilated, there is a free exchange of heat between the body
core and the environment. We speculate that, in this
study, the mechanical distension of the heat-exchange
structures filled the venous plexuses to near capacity so
that, when the AVAs opened, there was an extremely
Table 2. Comparison of rewarming rates of
hypothermic subjects with noninvasive rewarming
methods: subatmospheric pressure and
heat vs. standard methods
Rewarming
Rates, °C/h
References
Present study
Subatmospheric pressure and heat
Standard methods
13.6 6 2.1
1.4 6 0.1
Previous studies using standard methods
Anesthesia-induced hypothermia
Clinical patients
Volunteers
Cold-exposure hypothermia
Clinical patients
Volunteers
0.2–1.4
1.0–1.5
5, 18, 20, 23,
24, 26, 30
25
1.0–2.4
0.4–3.3
22, 29
8–12
Values for present study are rate of change in TEAM (means 6 SE).
Values for previous studies are range of rewarming rate means
reported in cited references. In studies with clinical patients, temperature recording sites varied considerably. One or more of the following
temperatures were measured in the clinical studies: tympanic membrane, oral, pulmonary artery, bladder, nasopharynx, or rectal.
Tympanic membrane temperatures were measured in anesthesiainduced hypothermia volunteers. Esophageal temperatures were
measured in cold-exposure hypothermia volunteers. Standard rewarming methods included forcing heated air onto exposed surfaces
of the patient, covering patient in warm cotton blankets, patient
inhaling heated humidified gases, and application of radiant heat to
patient. Forced warm air devices used in the clinical studies delivered air to less than one-half of total body surface. Cold-exposed
volunteer subject studies conducted by Giesbrecht and colleagues
(8–11) utilized a variety of perturbations during rewarming, including exercise, shivering, inhibition of shivering, and placing the
hypothermic individual in an air-circulating chamber in which warm
air (46–48°C) was passed over entire body surface.
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Fig. 3. TEAM (relative to stable TEAM ) during recovery from mild
hypothermia: effect of subatmospheric pressure applied to a forearm
and hand on rewarming rates. Standardized rewarming curves for
experimental and control groups (means 6 SE). r, Experimental
subjects (n 5 10); k, control subjects (n 5 6). See MATERIALS AND
METHODS for a detailed description of standardization procedure.
high blood flow through the venous plexuses in the
hand. The heated blood then was returned directly to
the thermal core, providing for rapid heat exchange
between the treated skin surface and the body core.
The rewarming rates reported here for the control
subjects are consistent with the values reported by
others using noninvasive rewarming techniques to
reverse hypothermia, such as immersing the subject in
warm water, wrapping the subject in warmed cotton or
water-perfusion blankets, radiant heating, or forcing
warm air over the skin surface (see Table 2). These
conventional techniques are effective for heating the
skin. Unfortunately, because hypothermic individuals
are also vasoconstricted, the heat applied to the skin is
slow to penetrate into the body core (5). In contrast, by
applying heat to mechanically distended heat-exchange vasculature, the applied heat goes directly to
the heart, where it is distributed to tissues based on the
priority determined by the individual’s thermoregulatory system. By accessing the thermal core through the
heat-exchange vasculature, the critical core regions
(which are normally protected by vasomotor tone) are
the first, rather than the last, to receive the superficially applied heat. Because the peripheral thermoregulatory vasoconstriction is reversed when the thermal
core, hence the POAH, reaches normothermia, the
ACCELERATED RECOVERY FROM MILD HYPOTHERMIA
and tympanic membrane temperature was virtually
indistinguishable from esophageal temperatures (27).
When both feet were heated in a water bath, esophageal and tympanic membrane temperatures responded
in a similar manner. Actually, the appearance of a
temperature transient on foot warming was slightly
faster in tympanic membrane than in esophageal temperature (27). Esophageal temperature was not measured in this study for practical reasons: under the best
conditions, most patients refuse placement of an esophageal probe, and it was unreasonable to expect our
patient subject population to accept placement of an
esophageal probe as they were emerging from anesthesia after an invasive surgical procedure. However, we
can see no reason to doubt that the same close correlation between tympanic membrane and esophageal temperatures as reported by Sato et al. (27) would be seen
under the conditions of our study. Deviations between
esophageal and tympanic membrane temperatures are
more commonly seen in studies involving exercise or
exposure to thermal transients (6), neither of which
were characteristics of our study.
In the present study, relative change in the recorded
temperature was the relevant measurement. The thermocouple was placed in the external auditory meatus
internal to the body surface and isolated from ambienttemperature influences by the ear plug. The skull and
overlying tissues serve as an insulation barrier between the brain and the environment, and thus a
thermal gradient exists along the external auditory
meatus in which temperatures range from close to
ambient temperature at the ear pinna to near the
temperature of the thermal core at the tympanic membrane. The position of the tip of the thermocouple in the
ear canal determined the extent to which changes in
local ambient temperature could have influenced the
measured temperature. However, because ambient temperature remained constant, the ear plug isolated the
tip of the temperature probe from the external environment, and the recording site was fixed, the relative
changes in the measured temperatures reflected
changes in the subjects’ internal thermal milieu rather
than the effect of changes in local external thermal
conditions. It may be that, because tympanic membrane temperature itself was not measured, the observed changes in the measured temperature underestimated the true Tc response, but they are still accurate
reflections of rates of change of Tc.
The authors express gratitude to the PACU nursing staff and the
operating room personnel whose cooperation made this project
possible, to James Roundy for assistance in data collection, and to
Grace Hagiwara for critical input during the preparation of this
manuscript.
A patent has been issued for a device [D. Grahn (Inventor);
Stanford University (Assignee). Apparatus and Method for Core
Rewarming of Mammals Experiencing Hypothermia. US Patent
5,683,438. 4 Nov. 1997.], and Stanford Univ. has entered into a
licensing agreement with Aquarius Medical Corp., Scottsdale, AZ, for
the commercialization of the technology. Included in the license is a
royalties agreement that grants Stanford Univ. a percentage of the
net sales of the technology, which will be shared by the University
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rapid rise in Tc effected by the method described in this
paper is self-regulating and presents little danger of
inducing hyperthermia.
Afterdrop, when deep Tc continues to decrease despite the application of heat to the skin surface, is
commonly observed during the treatment of hypothermia (7, 32). However, no afterdrop was observed in any
of our study subjects. Two factors that determine the
incidence and severity of afterdrop are 1) the pattern of
cooling and 2) the time delay between cooling and
rewarming. Afterdrop is more common after abruptly
acquired hypothermia (e.g., accidental immersion in
very cold water) than after slowly acquired hypothermia (prolonged exposure to mild cold) (32). Increasing
the delay between cooling and treatment onset decreases the incidence of afterdrop observed during
treatment (32). The absence of afterdrop in our study is
not surprising because the hypothermia was slowly
acquired in our subjects and there was a considerable
lag between the time when the subjects began to lose
heat and when rewarming treatment was commenced.
Conventional wisdom suggests that afterdrop is the
result of cold blood returning to the core from the arms
and legs where surface rewarming has caused peripheral vasodilation. However, this circulatory explanation of afterdrop is unlikely because peripheral blood
flow remains low during afterdrop (32). An alternative
explanation of the afterdrop phenomenon is based on
physical conduction of heat through tissue. When the
surface of a mass of tissue is cooled, a thermal gradient
is established between the surface and the deep core of
the mass, with each layer of the tissue cooling as the
layer exterior to it extracts heat from it. Once a thermal
gradient has been established and a direction of temperature change has been initiated, a reversal of the
heat flux through the surface does not immediately
affect the deeper layers of tissue, and the established
cooling pattern continues. Webb (32) states: ‘‘To avoid
afterdrop, one must heat the core organs first: e.g., by
heating the blood in an extracorporeal circuit or by
using peritoneal lavage or diathermy.’’ The device used
in the present study simulates an extracorporeal heating circuit except that it heats the blood in a noninvasive manner. It is anticipated that, if a device similar to
that described here were applied to victims of rapidly
acquired hypothermia immediately after cold exposure,
afterdrop would be either eliminated or greatly attenuated.
A controversy in thermoregulatory physiology is
whether tympanic membrane temperature is an accurate measurement of Tc in humans. The argument
against tympanic membrane temperature as a measurement of Tc is that tympanic membrane temperature in
part measures skin TEAM and thus, because tympanic
membrane temperature can be influenced by the skin
temperature of the face and neck, it is in fact a
measurement of peripheral temperature. However,
when the external auditory meatus was sealed, insulating the internal portion of the meatus from ambient
conditions, thermal manipulations of the scalp and face
had little effect on tympanic membrane temperature,
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ACCELERATED RECOVERY FROM MILD HYPOTHERMIA
and the inventor. D. Grahn is also serving as a consultant to Aquarius
Medical Corp. to assist in the development of the technology.
Address for reprint requests: D. Grahn, Dept. of Biological
Sciences, Stanford Univ., Stanford, CA 94305 (E-mail: dagrahn@
leland.stanford.edu).
Received 17 December 1997; accepted in final form 6 July 1998.
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