Hypothermia is a core temperature of <35°C
(<95°F). Although most commonly seen in cold climates, it may
develop without exposure to extreme environmental conditions. Hypothermia
is not uncommon in temperate regions and may even develop indoors
during the summer. In the U.S., an average of 700 people die of
hypothermia each year. Half of those who die of hypothermia are
>65 years of age.1
Body temperature may fall due to heat loss by conduction, convection,
radiation, or evaporation. Conduction is the transfer
of heat by direct contact down a temperature gradient, such as from
a warm body to the cold environment. When immersed in water, the
body loses heat rapidly, which results in a swift decline in body
temperature, because the thermal conductivity of water is approximately
30 times that of air. Convection is the transfer
of heat by the actual movement of heated material, such as the wind’s
disrupting the layer of warm air surrounding the body. Convective
heat loss increases markedly in windy conditions. Heat also may
be lost by radiation to the environment (primarily
from noninsulated body areas) and by evaporation of water.
Evaporation of the water contained in exhaled, water-saturated air
occurs over a wide range of ambient temperatures and may be prevented
by inhalation of warmed, humidified air.
Opposing the loss of body heat are the mechanisms of heat conservation
and gain. In general, these are controlled by the hypothalamus;
thus hypothalamic dysfunction may cause impairment in temperature
homeostasis. Heat is conserved by peripheral vasoconstriction and,
importantly, by behavioral responses. If behavioral responses such
as putting on clothing or coming indoors from a cold environment
are impaired for any reason (e.g., dementia, drug intoxication,
or trauma), the risk of hypothermia is increased.
Heat gain is effected by shivering and by nonshivering thermogenesis.
The nonshivering component of heat production consists of an increase
in metabolic rate brought about by increased output from the thyroid
and adrenal glands.
The most important causes of hypothermia are listed in Table 203-1. Accidental (environmental) hypothermia
can be divided into immersion and nonimmersion cold exposure. Exposure
to cold environmental conditions may lead to hypothermia even in healthy
individuals, especially in wind and rain, and cold swimming water.
Inadequate clothing and physical exhaustion contribute to the loss
of body heat. The high thermal conductivity of water leads to the
rapid development of hypothermia during immersion. The rate of heat
loss is determined by water temperature, and immersion in any water
colder than 16°C to 21°C (60.8°F to 69.8°F) can lead to severe hypothermia.
Table 203-1 Causes
| Save Table
Table 203-1 Causes
|Accidental (environmental) exposure|
|Hypothalamic and central nervous system dysfunction|
|Acute incapacitating illness|
|Massive fluid or blood resuscitation|
The response of various organ systems to lowered temperature varies
widely among individuals.2–4 In general, body
temperatures of 32°C to 35°C (89.6°F to 95.0°F)
constitute “mild” hypothermia. In this temperature
range, the patient is in an excitation (responsive) stage, in which
the body makes physiologic adjustments in an attempt to retain and
generate heat. In the initial excitation phase, heart rate, cardiac
output, and blood pressure all rise. With decreasing temperature,
these all decline. When temperature drops below 32°C (89.6°F), general
excitation gives way to the slowing (adynamic) stage, in which there
is a progressive slowdown of bodily functions and metabolism, causing
a decrease in both oxygen utilization and carbon dioxide production.
Shivering ceases when body temperature falls below 30°C to
32°C (86.0°F to 89.6°F), which removes a major source of heat production.
Cardiac output and blood pressure may be markedly depressed by the
negative inotropic and chronotropic effects of hypothermia and further
depressed by concomitant hypovolemia. Circulating volume can decrease
by up to one third of the normal blood volume.
Metabolic causes of hypothermia
include various hypoendocrine states that lead to a decrease in
metabolic rate (hypothyroidism, hypoadrenalism, hypopituitarism).
Hypoglycemia also may lead to hypothermia; the probable mechanism
is hypothalamic dysfunction secondary to glucopenia. Other causes
of hypothalamic and central nervous system (CNS) dysfunction (e.g.,
head trauma, tumor, stroke) may interfere with mechanisms of temperature
regulation. Wernicke disease may involve the hypothalamus; this
is a rare but important cause of hypothermia, because it is potentially
reversible with parenteral thiamine administration.
U.S., ethanol or drug intoxication is frequently noted in hypothermic
patients. Ethanol is a vasodilator, and because of its anesthetic
and CNS depressant effects, intoxicated individuals neither feel
the cold nor respond to it appropriately. Other sedative-hypnotic
and vasodilating drugs also may be implicated in the development
of hypothermia, as may insulin and other hypoglycemic agents.
may alter the hypothalamic temperature set point and is a well-known
cause of hypothermia. Subnormal body temperature is a poor prognostic
factor in patients with bacteremia. Severe dermal disease, significant
burns, or severe exfoliative dermatitis may prevent cutaneous vasoconstriction
and increase transcutaneous water loss, predisposing to the development
of hypothermia. Hypothermia may develop in anyone with an acute incapacitating
illness. Thus patients with severe infections, diabetic ketoacidosis,
immobilizing injuries, and various other conditions may have hypothermia
due to impaired thermoregulatory function, including altered behavioral
responses. Hypothermia is a particular risk in patients undergoing
massive volume replacement with room-temperature fluid or cold blood.
Hypothermia causes characteristic ECG changes and may induce
life-threatening dysrhythmias5 (Table
203-2). The Osborn or J wave—a slow, positive deflection
at the end of the QRS complex—is characteristic, though
not pathognomonic, of hypothermia (Figure 203-1).
Table 203-2 ECG Changes
| Save Table
Table 203-2 ECG Changes
|PR, QRS, QT prolongation|
|Muscle tremor artifact|
|Osborn (J) wave|
|Atrial fibrillation or flutter|
|Premature ventricular contractions|
ECG strip from a patient with a temperature of 25°C (77°F) showing
atrial fibrillation with a slow ...
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