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Chapter 16
Heat Exhaustion and Heat Stroke
Heat exhaustion
is a state of collapse, often taking the form
of fainting, due to hypotension brought on by (1) depletion
of plasma volume secondary to sweating, and (2) extreme
dilation of skin blood vessels. Recall from Chapter 12 that
blood pressure, cardiac output, and total peripheral resistance
are related according to the equation MAP
=
CO
×
TPR.
Thus, decreases in both cardiac output (due to the decreased
plasma volume) and peripheral resistance (due to the
vasodilation) contribute to the hypotension. Heat exhaustion
occurs as a direct consequence of the activity of heat-loss
mechanisms. Because these mechanisms have been so active,
the body temperature is only modestly elevated. In a sense,
heat exhaustion is a safety valve that, by forcing a cessation
of work in a hot environment when heat-loss mechanisms are
overtaxed, prevents the larger rise in body temperature that
would cause the far more serious condition of heat stroke.
In contrast to heat exhaustion,
heat stroke
represents
a complete breakdown in heat-regulating systems so that
body temperature keeps going up and up. It is an extremely
dangerous situation characterized by collapse, delirium,
seizures, or prolonged unconsciousness—all due to greatly
elevated body temperature. It almost always occurs in
association with exposure to or overexertion in hot and
humid environments. In some individuals, particularly the
elderly, heat stroke may appear with no apparent prior period
of severe sweating, but in most cases, it comes on as the end
stage of prolonged untreated heat exhaustion. Exactly what
triggers the transition to heat stroke is not clear, although
impaired circulation to the brain due to dehydration is one
factor. The striking fi nding, however, is that even in the
face of a rapidly rising body temperature, the person fails to
sweat. Heat stroke is a positive-feedback situation in which
the rising body temperature directly stimulates metabolism—
that is, heat production—which further raises body
temperature. For both heat exhaustion and heat stroke, the
remedy is external cooling, fl uid replacement, and cessation
of activity.
SECTION B SUMMARY
Basic Concepts of Energy Expenditure
I. The energy liberated during a chemical reaction appears either
as heat or work.
II. Total energy expenditure = heat produced + external work
done + energy stored.
III. Metabolic rate is infl uenced by the many factors summarized in
Table 16–5.
IV. Metabolic rate is increased by the thyroid hormones and
epinephrine. The other functions of the thyroid hormones are
summarized in Table 16–6.
Regulation of Total-Body Energy Stores
I. Energy storage as fat can be positive when the metabolic rate
is less than, or negative when the metabolic rate is greater than
the energy content of ingested food.
a. Energy storage is regulated mainly by refl ex adjustment of
food intake.
b. In addition, the metabolic rate increases or decreases to
some extent when food intake is chronically increased or
decreased, respectively.
II. Food intake is controlled by leptin, which is secreted by
adipose tissue cells, and a variety of satiety factors, as
summarized in Figure 16–15.
III. Being overweight or obese, the result of an imbalance between
food intake and metabolic rate, increases the risk of many
diseases.
Regulation of Body Temperature
I. Core body temperature shows a circadian rhythm, with
temperature highest during the day and lowest at night.
II. The body exchanges heat with the external environment by
radiation, conduction, convection, and evaporation of water
from the body surface.
III. The hypothalamus and other brain areas contain the
integrating centers for temperature-regulating refl exes, and
both peripheral and central thermoreceptors participate in
these refl exes.
IV. Body temperature is regulated by altering heat production
and/or heat loss so as to change total-body heat content.
a. Heat production is altered by increasing muscle tone,
shivering, and voluntary activity.
b. Heat loss by radiation, conduction, and convection depends
on the temperature difference between the skin surface and
the environment.
c. In response to cold, skin temperature is decreased by
decreasing skin blood fl ow through refl ex stimulation of
the sympathetic nerves to the skin. In response to heat,
skin temperature is increased by inhibiting these nerves.
d. Behavioral responses such as putting on more clothes also
infl uence heat loss.
e. Evaporation of water occurs all the time as insensible loss
from the skin and respiratory lining. Additional water
for evaporation is supplied by sweat, stimulated by the
sympathetic nerves to the sweat glands.
f. Increased heat production is essential for temperature
regulation at environmental temperatures below
the thermoneutral zone, and sweating is essential at
temperatures above this zone.
V. Temperature acclimatization to heat is achieved by an earlier
onset of sweating, an increased volume of sweat, and a
decreased sodium concentration of the sweat.
Additional Clinical Examples
I. Fever is due to a resetting of the temperature set point so
that heat production is increased and heat loss is decreased in
order to raise body temperature to the new set point and keep
it there. The stimulus is endogenous pyrogen, in the form of
interleukin 1 and other peptides as well.
II. The hyperthermia of exercise is due to the increased heat
produced by the muscles, and it is partially offset by skin
vasodilation.
III. Extreme increases in body temperature can result in heat
exhaustion or heat stroke. In heat exhaustion, blood pressure
decreases due to vasodilation. In heat stroke, the normal
thermoregulatory mechanisms fail, and thus heat stroke can
be fatal.
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