Page 32 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)
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Hyperthermia, Heat Injuries
       On severe physical effort (increased heat pro-  ment and/or submerging them into cool water.
       duction) and/or in a hot environment (de-  However, the body surface must not be al-
       creased net heat loss) the thermoregulatory  lowed to get too cold, because the resulting va-
       mechanisms of the organism are overtasked,  soconstriction would delay the reduction in
       especially when there is a lack of water and at  core temperature. Even successfully treated
       high ambient humidity. In contrast to the sit-  heat stroke may leave lasting damage in the
       uation in fever (→ p. 20), the body’s core tem-  thermoregulatory centers. This restricts future
       perature can no longer be kept at the (un-  tolerance to extreme ambient temperatures.
       changed) set level of ca. 378C and hyperther-  Malignant hyperthermia (→ B) is the poten-
       mia results (→ A, top). On standing upright,  tially lethal result of heterogeneous genetic
       heat-induced vasodilation causes some of the  defects of sarcoplasmic Ca 2+  transport, in
                                               2+
       blood to pool in the legs, and the extracellular  which the Ca -releasing channel (ryanodine
    Temperature, Energy  particularly because vasodilation in the skin  depolarizing muscle relaxants (suxametho-
       volume is reduced by sweating. As a result,
                                       receptor) is affected. Some inhalation anes-
                                       thetics (halothane, enflurane, isoflurane) and
       cardiac output (CO) and blood pressure fall,
                                       nium chloride) cause the sudden and excessive
       reduces peripheral vascular resistance. Even
                                               2+
                                                from the sarcoplasmic reticu-
       at a core temperature below 398C, weakness,
                                       release of Ca
                                       lum, so that generalized, uncoordinated mus-
       dizziness, nausea, and loss of consciousness
                                       tion and enormous heat production. The result
       pressure (heat collapse; → A1). Blood pressure
                                       is acidosis, hyperkalemia, tachycardia, ar-
       will again rise on lying down and after taking
    2  may occur as a consequence of reduced blood  cle twitches occur with high oxygen consump-
       fluids.                         rhythmia, and rapidly rising hyperthermia. If
         A much greater danger arises when the core  recognized in time, malignant hyperthermia
       temperature reaches 40.58C, because the brain  can be successfully treated by discontinuing
       cannot tolerate such temperatures. To protect  the anesthetics and/or muscle relaxants, ad-
       itself against heat stroke the brain can tem-  ministering dantrolene, which blocks Ca 2+  re-
       porarily be kept cooler than the rest of the  lease in skeletal muscle cells, as well as cooling
       body because a rising core temperature causes  the body.
       profuse sweating of the head (even with dehy-  Heat cramps occur with strenuous physical
       dration), especially the face (→ A2). Blood that  work in high ambient temperature (e.g., at a
       has been cooled in this way reaches the endo-  furnace) if only the loss of water, but not of
       cranial venous system and the sinus caverno-  salt, is replaced.
       sus, where it lowers the temperature of the  Sun stroke must be distinguished from hy-
       neighboring arteries. This would seem to be  perthermia. It is caused by direct sun radiation
       the only explanation for the fact that a mara-  on head and neck and causes nausea, dizzi-
       thon runner in whom a transient rise in core  ness, severe headache, cerebral hyperemia,
       temperature to 41.98C had been measured did  and serous meningitis and may end fatally.
       not suffer from heat stroke.     Contact or radiant heat may cause first de-
         If there is a prolonged rise in core tempera-  gree, second degree, or third degree burns
       ture to between 40.5 and 438C, the thermoreg-  (reddening, blisters, or necroses, respectively)
       ulatory center in the midbrain fails (→ p. 20)  to the skin. Frequent and intense exposure to
       and sweating ceases. Disorientation, apathy,  the sun also increases the risk of melanoma.
       and loss of consciousness result (heat stroke).
       Cerebral edema with accompanying damage to
       the central nervous system will, without rapid
       help, lead to death; children are especially at
       risk because their surface area to body mass
       ratio is larger than adults’, and they produce
   22  less sweat. Treatment of heat stroke consists
       of bringing the person into a cooler environ-
       Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
       All rights reserved. Usage subject to terms and conditions of license.
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