Background

Hypothermia describes a state in which the body's mechanism for temperature regulation is
overwhelmed in the face of a cold stressor. Hypothermia is classified as accidental or
intentional, primary or secondary, and by the degree of hypothermia.
Accidental hypothermia generally results from unanticipated exposure in an inadequately
prepared person; examples include inadequate shelter for a homeless person, someone caught
in a winter storm or motor vehicle accident, or an outdoor sport enthusiast caught off guard
by the elements. Intentional hypothermia is an induced state generally directed at
neuroprotection after an at-risk situation (usually after cardiac arrest, see Therapeutic
Hypothermia).
[1]
Primary hypothermia is due to environmental exposure, with no underlying
medical condition causing disruption of temperature regulation.
[2]
Secondary hypothermia is
low body temperature resulting from a medical illness lowering the temperature set-point.
Many patients have recovered from severe hypothermia, so early recognition and prompt
initiation of optimal treatment is paramount.
Systemic hypothermia may also be accompanied by localized cold injury (seeFrostbite). See
the image below.
Osborne (J) waves (V3) in a patient with a rectal core
temperature of 26.7C (80.1F). ECG courtesy of Heather Murphy-Lavoie of Charity
Hospital, New Orleans.
Pathophysiology
The body's core temperature is tightly regulated in the "thermoneutral zone" between 36.5C
and 37.5C, outside of which thermoregulatory responses are usually activated. The body
maintains a stable core temperature through balancing heat production and heat loss. At rest,
humans produce 40-60 kilocalories (kcal) of heat per square meter of body surface area
through generation by cellular metabolism, most prominently in the liver and the heart. Heat
production increases with striated muscle contraction; shivering increases the rate of heat
production 2-5 times.
Heat loss occurs via several mechanisms, the most significant of which, under dry conditions,
is radiation (55-65% of heat loss). Conduction and convection account for about 15% of
additional heat loss, and respiration and evaporation account for the remainder. Conductive
and convective heat loss, or direct transfer of heat to another object or circulating air,
respectively, are the most common causes of accidental hypothermia. Conduction is a
particularly significant mechanism of heat loss in drowning/immersion accidents as thermal
conductivity of water is up to 30 times that of air.
The hypothalamus controls thermoregulation via increased heat conservation (peripheral
vasoconstriction and behavior responses) and heat production (shivering and increasing levels
of thyroxine and epinephrine). Alterations of the CNS may impair these mechanisms. The
threshold for shivering is 1 degree lower than that of vasoconstriction and is considered a last
resort mechanism by the body to maintain temperature.
[3]
The mechanisms for heat
preservation may be overwhelmed in the face of cold stress and core temperature can drop
secondary to fatigue or glycogen depletion.
Hypothermia affects virtually all organ systems. Perhaps the most significant effects are seen
in the cardiovascular system and the CNS. Hypothermia results in decreased depolarization
of cardiac pacemaker cells, causing bradycardia. Since this bradycardia is not vagally
mediated, it can be refractory to standard therapies such as atropine. Mean arterial pressure
and cardiac output decrease, and an electrocardiogram (ECG) may show characteristic J or
Osborne waves (see the image below). While generally associated with hypothermia, the J
wave may be a normal variant and is seen occasionally in sepsis and myocardial ischemia.
Osborne (J) waves (V3) in a patient with a rectal core
temperature of 26.7C (80.1F). ECG courtesy of Heather Murphy-Lavoie of Charity
Hospital, New Orleans.
Atrial and ventricular arrhythmias can result from hypothermia; asystole and ventricular
fibrillation have been noted to begin spontaneously at core temperatures below 25-28C.
Hypothermia progressively depresses the CNS, decreasing CNS metabolism in a linear
fashion as the core temperature drops. At core temperatures less than 33C, brain electrical
activity becomes abnormal; between 19C and 20C, an electroencephalogram (EEG) may
appear consistent with brain death. Tissues have decreased oxygen consumption at lower
temperatures; it is not clear whether this is due to decreases in metabolic rate at lower
temperatures or a greater hemoglobin affinity for oxygen coupled with impaired oxygen
extraction of hypothermic tissues.
The term "core temperature after drop" refers to a further decrease in core temperature and
associated clinical deterioration of a patient after rewarming has been initiated. The current
theory of this documented phenomenon is that as peripheral tissues are warmed, vasodilation
allows cooler blood in the extremities to circulate back into the body core. Other mechanisms
may be in operation as well. Some believe that after drop is most likely to occur in patients
with frostbite or long-standing hypothermia.
Epidemiology
Frequency
United States
Accurately estimating the incidence of hypothermia is impossible, as hospital encounters only
represent the "tip of the iceberg" in that they reflect the more severe cases. Even so, the
number of emergency department encounters for hypothermia is growing, as ever-growing
numbers of people take to the outdoors in search of adventure. Hypothermia is also a disease
of urban settings. Societal problems with alcoholism, mental illness, and homelessness create
a steady stream of these cases to inner-city hospitals. Although most cases occur in regions of
the country with severe winter weather, other areas with milder climates also experience
cases on a regular basis. This is especially true in milder climates that experience rapid
climate changes either due to seasonal changes or day-to-night changes secondary to altitude.
According to current data, states with the highest overall death rates for hypothermia are
Alaska, New Mexico, North Dakota, and Montana.
The greatest number of cases of hypothermia occur in an urban setting and are related to
environmental exposure attributed to alcoholism, illicit drug use, or mental illness, often
exacerbated by concurrent homelessness. This is simply due to the fact that more people are
found in the urban regions rather than rural areas.
A second affected group includes people in an outdoor setting for work or pleasure, including
hunters, skiers, climbers, boaters/rafters, and swimmers.
Mortality/Morbidity
According to one study, overall in-patient mortality in hypothermic patients was 12%. Most
people tolerate mild hypothermia (32-35C body temperature) fairly well, which is not
associated with significant morbidity or mortality. In contrast, a multicenter survey found a
21% mortality rate for patients with moderate hypothermia (28-32C body temperature).
Mortality is even higher in severe hypothermia (core temperature below 28C). Despite
hospital-based treatment, mortality from moderate or severe hypothermia approaches 40%.
Patients experiencing concurrent infection account for most deaths due to hypothermia. Other
comorbidities associated with higher mortality rates include homelessness, alcoholism,
psychiatric disease, and advanced age.
"Indoor hypothermia" is more likely to occur in patients with significant medical
comorbidities (alcoholism, sepsis, hypothyroidism/hypopituitarism) and tends to carry worse
outcomes than exposure hypothermia.
According to current records, approximately 700 people die in the United States from
accidental primary hypothermia each year.
Sex
The overall mortality rate from hypothermia is similar between men and women. Because of
a higher incidence of exposure among males, men account for 65% of hypothermia-related
deaths.
Age
Very young and elderly persons are at increased risk and may present to the emergency
department with symptoms that are not clinically obvious or specific for hypothermia, such as
altered mental status.
Older patients appear to be more likely to present with chronic or secondary hypothermia.
Half of the recorded deaths from accidental hypothermia occurred in individuals older than
65 years.
History
Hypothermia is usually readily apparent in the setting of severe environmental exposure. In
elderly patients or "indoor" patients, or for a patientparticularly a wet patient, with
exposure to less extreme cold, the history may be subtle and less obvious. These patients may
have a higher mortality rate secondary to a longer time to diagnosis and increased age and
fragility. Mild or moderate hypothermia can present with misleading symptoms, such as
confusion, dizziness, chills, or dyspnea.
A patient's companions often note initial symptoms in the field. Symptoms can include mood
change, irritability, poor judgment, and lassitude. Companions may note the patient to
demonstrate paradoxical undressing (a severely hypothermic person removes clothing in
response to prolonged cold stress) or rhythmic or repeated motions such as rocking. Slurred
speech and ataxia may mimic a stroke, alcohol intoxication, or high-altitude cerebral edema.
Similarly, profound hypothermia may present as coma or cardiac arrest.
In an urban environment, the use of alcohol or illicit drugs, overdose, psychiatric emergency,
and major trauma all are associated with an increased risk of hypothermia.
Physical
The key to establishing a diagnosis of hypothermia is rapid determination of true core
temperature. In the emergency department, core temperature is best measured using a low-
reading temperature probe in the bladder or rectum or an esophageal probe. In the field, core
temperature may be more difficult to establish reliably. A special low-reading thermometer
can be used orally or rectally, but it may not reflect a true core temperature. Care should be
taken not to rely on a temperature from a rectal thermometer lodged in stool because an
inaccurately low core temperature can be recorded; the probe's reading will also lag behind
the core temperature during rewarming. Additionally, a thermometer may become dislodged;
be suspicious if a core temperature reading is identical to the room temperature.
Obtaining a core temperature may help prevent erroneous diagnosis for patients with an
altered mental status due to stroke, drug overdose, alcohol intoxication, or mental illness.
Standard temperature measuring devices commonly used for triage may lack the capability to
report unusually low temperature; obtain a core temperature reading for any patient suspected
of being significantly hypothermic.
At a given temperature, specific physical examination findings vary among patients.
However, an examination does provide a frame of reference for dividing presenting
symptoms into mild, moderate, and severe hypothermic signs.
[4]

Mild hypothermia (32-35C)
Between 34C and 35C, most people shiver vigorously, usually in all extremities.
As the temperature drops below 34C, a patient may develop altered judgment, amnesia, and
dysarthria. Respiratory rate may increase.
At approximately 33C, ataxia and apathy may be seen. Patients generally are stable
hemodynamically and able to compensate for the symptoms.
In this temperature range, the following may also be observed: hyperventilation, tachypnea,
tachycardia, and cold diuresis as renal concentrating ability is compromised.
Moderate hypothermia (28-32C)
Oxygen consumption decreases, and the CNS depresses further; hypoventilation,
hyporeflexia, decreased renal flow, and paradoxical undressing may be noted.
Most patients with temperatures of 32C or lower present in stupor.
As the core reaches temperatures of 31C or below, the body loses its ability to generate heat
by shivering.
At 30C, patients develop a higher risk for arrhythmias. Atrial fibrillation and other atrial and
ventricular rhythms become more likely. The pulse continues to slow progressively, and
cardiac output is reduced. J wave may be seen on ECG in moderate hypothermia.
Between 28C and 30C, pupils may become markedly dilated and minimally responsive to
light, a condition that can mimic brain death.
Severe hypothermia (< 28C)
At 28C, the body becomes markedly susceptible to ventricular fibrillation and further
depression of myocardial contractility.
Below 27C, 83% of patients are comatose.
Pulmonary edema, oliguria, coma, hypotension, rigidity, apnea, pulselessness, areflexia,
unresponsiveness, fixed pupils, and decreased or absent activity on EEG are all seen.
Causes
Decreased heat production
Several etiologies related to endocrine derangements may cause decreased heat production.
These include hypopituitarism, hypoadrenalism, and hypothyroidism. Consider all these
conditions in patients presenting with unexplained hypothermia who fail to rewarm with
standard therapy.
Other causes include severe malnutrition or hypoglycemia and neuromuscular inefficiencies
seen in the extremes of age.
Increased heat loss
This category includes accidental hypothermia due to both immersion etiologies and
nonimmersion etiologies and is the most common form of hypothermia encountered in the
emergency department.
Patients may present with induced vasodilatation from pharmacologic or toxicologic agents.
Erythrodermas, such as burns or psoriasis, that decrease the body's ability to preserve heat, or
iatrogenic etiologies, such as cold infusions, overenthusiastic treatment of heatstroke, or
emergency deliveries, may cause hypothermia due to increased heat loss.
Impaired thermoregulation
A variety of causes may be associated with impaired thermoregulation, but, generally, it is
associated with failure of the hypothalamus to regulate core body temperature.
This may occur with CNS trauma, strokes, toxicologic and metabolic derangements,
intracranial bleeding, Parkinson disease, CNS tumors, Wernicke disease, and multiple
sclerosis.
Other causes
Miscellaneous causes include sepsis, multiple trauma, pancreatitis, prolonged cardiac arrest,
and uremia.
Hypothermia may be related to drug administration; such medications include beta-blockers,
clonidine, meperidine, neuroleptics, and general anesthetic agents. Ethanol, phenothiazines,
and sedative-hypnotics also reduce the bodys ability to respond to low ambient temperatures.
Laboratory Studies
Arterial blood gas determination includes the following:
Blood gas analyzers warm blood to 37C.
Because gasses are less soluble in hypothermic plasma, arterial blood gas (ABG) level may
show higher oxygen and carbon dioxide levels and a lower pH than a patient's actual values
as the blood is warmed in the ABG machinery.
The best approach is to expect uncorrected ABG values compared with the normal values at
37C.
An uncorrected pH at 7.4 and pCO
2
at 40 mm Hg reflect acid-base balance.
Many hypothermic patients are volume contracted because of cold diuresis. As a result,
hematocrit level may be deceptively high. Hematocrit levels may increase 2% for each 1C
drop in core temperature.
Hypothermia may present with wide fluctuations in electrolytes, and no clear trend or
predictability exists as to when a patient's electrolytes will be abnormal or how large swings
may be. Plasma potassium levels can be useful in evaluating prognosis. A level of 10 mmol/L
or greater is associated with a very low likelihood of recovery. Classic ECG changes of
hyperkalemia may be absent or diminished. Chronic hypothermia occasionally can lead to
hypokalemia.
Acute hypothermia can result in hyperglycemia, while chronic hypothermia or secondary
hypothermia may present with low blood glucose level.
The body's coagulation mechanism is often disrupted in moderate or severe hypothermia, and
a disseminated intervascular coagulationtype syndrome can be present.
Coagulopathy has several causes. The primary issue is disruption of enzymatic reactions of
the clotting cascade caused by protein denaturization at decreased temperature.
Because the kinetic tests of coagulation are performed at 37C in the laboratory, a clinically
evident coagulopathy may not be reflected by deceptively normal laboratory values.
Imaging Studies
A chest radiograph is indicated in patients with hypoxia. Aspiration pneumonia and
pulmonary edema are common findings.
Patients with trauma or altered mental status of indeterminate cause may need a noncontrast
head CT scan and further imaging for a standard trauma evaluation.
Other Tests
The ECG may show prolonged PR, QRS, and QT intervals, and atrial or ventricular
arrhythmias. The length and height of the respective QT-interval prolongation and
characteristic J (Osborne) waves are often proportional to the degree of hypothermia.

Prehospital Care
Prehospital management focuses on preventing further heat loss, rewarming the body core
temperature, and avoiding precipitating ventricular fibrillation or another malignant cardiac
rhythm. This should be the preeminent concern. Conscious patients can develop ventricular
fibrillation suddenly; prehospital workers, particularly those operating in remote search-and-
rescue operations, should avoid inadvertent jerky movement of severely hypothermic
patients. Patients who develop hypothermia-induced dysrhythmia in the field may be beyond
resuscitation. How the hypothermic heart deteriorates into the rhythm of ventricular
fibrillation remains under debate.
Patients developing hypothermia from cold-water immersion appear to be at high risk of
fibrillation; rescuers probably are justified in instructing such patients to minimize motion
and to await careful extrication.
Anecdotal reports of sudden cardiac death associated with tracheal intubation appear to be
exaggerated, particularly if a patient is adequately preoxygenated.
Both cardiac pacing and atropine are generally ineffective for bradyarrhythmia.
Lidocaine is ineffective in preventing hypothermia-induced ventricular dysrhythmias.
Many authors have advocated prophylactic bretylium in cases of severe hypothermia when
spontaneous conversion to ventricular fibrillation is possible. This recommendation is due to
the success of such therapy both in controlled animal studies and in anecdotal human reports.
Cardiac dysrhythmias begin to develop at a core temperature of 30C.
Ventricular fibrillation susceptibility is greatest below the core temperature of 22C.
Bretylium (5 mg/kg initially) is recommended for any hypothermic patient manifesting
significant new ventricular ectopy or frank dysrhythmia. However, bretylium has been
discontinued by all manufacturers resulting in a worldwide shortage and has been
unavailable to many centers since 1999.
Although the optimal dosage and ideal infusion rate for bretylium are unknown, consider
prophylactic bretylium for patients with core temperatures below 30C.
To prevent cardiac dysrhythmia with continued hypothermia, rescuers or paramedics should
attempt rewarming in the field. (A notable exception would be isolated frostbite injury in
which limb rewarming would preclude self-rescue because of pain.)
Gently place patients in an environment most favorable to reducing further heat loss from
evaporation, radiation, conduction, or convection.
Remove wet clothing, and replace it with dry blankets or sleeping bags.
Initiate active external rewarming with heat packs (eg, hot water bottles, chemical packs)
placed in the axillae, on the groin, and on the abdomen.
Be aware of the risk of causing body surface burns from exuberant active external
rewarming.
In dire circumstances, when heat packs are unavailable, rescuers can provide skin-to-skin
contact with patients.
Ventricular fibrillation in a cold patient is a desperate event. Generally, defibrillation is
ineffective at hypothermic core temperatures and when equipment for heroic attempts at
resuscitation is unavailable. In such circumstances, attempt a round of chemical conversion
with intravenous bretylium (if available), followed by extended cardiopulmonary
resuscitation (CPR) until rescuers can begin active rewarming and perform successful
defibrillation.
Emergency Department Care
Patients with respiratory failure should be endotracheally intubated and placed on a
mechanical ventilator. Intubation and insertion of vascular catheters should not be delayed
but performed gently while closely monitoring cardiac rhythm for ventricular fibrillation.
Measure core temperatures using a low-reading esophageal, rectal, or bladder thermometer.
Tympanic thermometers are unreliable in a setting of profound hypothermia and should not
be used. If using a rectal probe, be careful not to insert it into stool.
Determine whether a cold patient is profoundly or mildly hypothermic. Profoundly
hypothermic patients present with stupor or cardiac dysrhythmia (regardless of the recorded
temperature) and a core temperature of 30C or lower. Mildly hypothermic patients may be
rewarmed in any available manner (eg, warm blankets, removal of cold, wet clothing) since
their risk for cardiac dysrhythmia is low. Surface rewarming is adequate in these cases, but it
is ineffective in very low body temperatures and carries an additional risk of temperature
after drops and shock secondary to peripheral vasodilation.
Remove any wet clothing, and replace it with warm, dry materials.
Profound hypothermia is a true emergency, warranting the same resource-intensive
resuscitation as myocardial infarction. Direct treatment at maintaining or restoring cardiac
perfusion; maximizing oxygenation is indicated for a prolonged period of time until the core
temperature is at least 32C.
Do not attempt resuscitation on the patient with a frozen chest where compressions are not
possible.
Gingerly handle patients identified with profound hypothermia, and take immediate measures
to prevent degeneration of cardiac activity into malignant dysrhythmia.
Profoundly hypothermic patients who demonstrate cardiac ectopy may be ideal candidates for
bretylium, if available. Administer an initial dose of 5 mg/kg IV (repeated at 10 mg/kg, as
needed) to prevent ventricular fibrillation. Lidocaine is ineffective for treatment of
hypothermia-induced dysrhythmias. While no randomized human trials have been reported,
at least 4 animal trials and 2 human case reports support using bretylium for any patient with
profound hypothermia. Based on such evidence, the US Wilderness Emergency Medical
Services Institute recommends using empiric bretylium for profound hypothermia.
Initiate warmed, humidified oxygen; provide heated intravenous saline; and place warmed
blankets or heat lamps around a hypothermic patient.
Although many texts suggest that intravenous fluids be heated to 45C, this temperature
choice is based on convenience of previous study designs rather than any hard evidence. A
trial using fluids heated to 65C demonstrated more efficacy in treating severe hypothermia.
Emergency departments that routinely treat hypothermia can keep blankets and intravenous
fluid bags in a shared heater. In urgent situations, intravenous fluids that contain no dextrose
or blood can be heated in a microwave oven. Once these simple measures have been applied,
consider more difficult rewarming therapies.
Optimal rewarming techniques depend upon a patient's condition. Treatment is often limited
by hospital availability and physician inexperience with rewarming approaches. If core body
temperature does not respond to warming efforts, underlying infection or endocrine
derangements must be considered.
A patient who is not becoming progressively colder, is conscious, and has a perfusing cardiac
rhythm may not require intensive intervention beyond the methods already discussed.
Debate centers on interventions for patients who are worsening, are comatose, have
nonperfusing rhythms, or appear dead. Most texts advocate aggressive therapy for severely
hypothermic patients, basing the recommendation on anecdotal reports of success.
Researchers recently confirmed justification for aggressive treatment in a 16-year
longitudinal review of profound hypothermia. In this series of 32 Swiss patients presenting
with hypothermia and cardiac arrest, 15 patients were resuscitated with aggressive
techniques, and all 15 patients showed full neurologic recovery.
In an older review, rewarming at rates faster than 2C/h was noted to reduce mortality when
compared with slower rates.
An optimal warming strategy is elusive. Some have postulated that rapidly warming a patient
to 33C and maintaining him or her at that temperature, using hypothermia therapeutically as
though he or she was a cardiac arrest patient might be beneficial.
For simplicity, aggressive rewarming methods can be categorized as slow, moderate, or rapid.
Slow rewarming provides heat from 17-30 kcal/h, corresponding to increasing temperature by
0.3-1.2C/h. (Comparisons are somewhat difficult since different study groups used different
measurements of heat gain.) Slow rewarming methods include IV solutions heated to 45C
(17 kcal/h); heated, humidified oxygen by mask (30 kcal/h or 0.7C/h); warmed blankets
(0.9C/h); and heated, humidified oxygen via endotracheal tube (1.2C/h). If intact, a patient's
endogenous physiologic mechanisms (other than shivering) provide similar rates of
rewarming (30 kcal/h).
Moderate rewarming methods provide heat at approximately 3C/h. Methods include warmed
gastric lavage (2.8C/h), intravenous solutions heated to 65C (2.9C/h), and peritoneal
lavage with 45C fluid at 4 L/h (70 kcal/h or 3C/h).
Rapid rewarming methods provide heat at levels higher than 100 kcal/h. Methods include
thoracic lavage at 500 mL/min (6.1C/h), cardiopulmonary bypass (400 kcal/h or 18C/h),
thoracic lavage at 2 L/min (19.7C/h), ECMO, and AV dialysis (1-4 degrees per hour, and
warm-water immersion [1500 kcal/h]).
In comparison, endogenous shivering provides rewarming at a rate of 300 kcal/h. No
noninvasive technique rewarms as rapidly as full-body immersion in warm water. Known as
the Hubbard tank technique, immersion has successfully rewarmed humans with severe
hypothermia. Unfortunately, patients who require rapid rewarming in the emergency
department also need cardiac monitoring and intravenous therapy, both of which are difficult
to manage under water.
Defibrillation also is difficult; however, defibrillation is likely futile once a patient's core
temperature falls below 30C.
Initiate CPR for hypothermic patients who deteriorate into ventricular fibrillation. These
patients also warrant immediate weight-based defibrillation (2 J/kg), along with prompt
administration of high-dose bretylium (10 mg/kg).
Consider initiating cardiopulmonary bypass for any case of ventricular fibrillation or
profound hypothermia with deterioration. Patients with this degree of hypothermia have
optimized outcomes with procedures such as cardiopulmonary bypass and pleural lavage.
However, these methods are invasive, often unavailable, and infrequently used and as such
are subject to user-inexperience.
Ventricular fibrillation should be treated immediately with defibrillation, despite the fact that
most other dysrhythmias will correct with warming alone. If initial attempts at defibrillation
are unsuccessful, further attempts at defibrillation and antiarrhythmic intravenous
medications should be held until the patient is warmed to above 30C. During this interval,
basic life support is continued. If ventricular fibrillation persists despite rewarming, current
AHA guidelines recommend administration of amiodarone.
Although studies in emergency medicine are lacking, cardiothoracic surgeons who induce
hypothermia to perform open-heart procedures rewarm patients on a daily basis using open
cardiac massage with warmed saline solution. Therefore, a desperate case of severe
hypothermia may warrant consideration of direct cardiac rewarming via open emergency
department thoracotomy with open cardiac massage.
Cardiothoracic bypass has been successful for treating cases of accidental hypothermia with
prolonged cardiac arrest. To be successful, bypass must be performed rapidly. If a delay is
expected, the physician can expedite bypass during an interim period by placing cordis
catheters in the patient's femoral vein and artery. Groin cutdowns may be necessary to
facilitate such placement; if cutdowns are needed, perform them without hesitation. If bypass
is unavailable or delayed, 2 previously described methods of internal rewarming are
available: heated thoracic lavage and arteriovenous (AV) heated countercurrent exchange.
The literature describes 2 methods of thoracic lavage; the simplest method uses available
equipment and provides rewarming rates equivalent to cardiopulmonary bypass.
The technique involves placing 2 left-sided, 38 French chest tubes (third intercostal space
midclavicular line and sixth intercostal space midaxillary line). Isotonic saline, in 3-liter bags
heated to at least 41C, is infused through the anterior tube at 2 L/min, then drained by
gravity via the posterior tube. When warmed saline was not available, physicians successfully
infused warmed tap water.
The AV heating method, developed at the University of Washington, uses a modified bypass
technique for rapid blood rewarming using a level one fluid warmer that is familiar to
physicians experienced in trauma resuscitation. The treatment is preferred for patients with
profound hypothermia and markedly depressed hemodynamic status or cardiac arrest. AV
heating requires a spontaneous pulse, since the patient's intrinsic blood pressure drives flow
through the countercurrent module. (In true cardiothoracic bypass, an external pump is built
into the machine.) Catheters are placed into the femoral artery and venous cordis.
Once catheters are placed, the arterial output is connected to the inflow port of a level one
countercurrent warmer, where intravenous fluids are connected. The outflow port is
connected to the femoral venous catheter. Water is circulated, at a temperature preset on the
level one device, around the blood-containing tubing; the blood warms as it flows through the
countercurrent module. The AV method has rewarmed profoundly hypothermic patients 5
times more rapidly (39 min vs 199 min) than standard methods and was demonstrated to
decrease the mortality rate.
In an alternative endovascular warming technique,
[5]
a catheter is advanced into the inferior
vena cava and circulates warmed fluids. The catheter acts as indwelling radiator as it is
connected to an esophageal temperature probe and uses a feedback loop to attain and
maintain programmed patient temperature. By this method, the core body temperature may be
elevated at a rate of 3 degrees an hour. Additionally, it is an invasive technique to raise core
temperature that utilizes skills that emergency physicians are already well trained and
comfortable with.
Vasodilation increases the vascular space; consequently, patients that have been hypothermic
for more than 45-60 minutes often require fluid administration. Hypotension should be
addressed with volume resuscitation; inotropic agents, such as dopamine, should be avoided
unless the hypotension is refractory to intravenous fluids due to the possible cardiac
stimulation/ectopy that pressors may induce.
Probes for pulse oximetry placed on the ears or the forehead appear to be less influenced by
the peripheral vasoconstriction of the digits associated with decreased body temperature.
Assessment should include a total body survey to exclude local cold-induced injuries.