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Chapter 020. Hypothermia and Frostbite (Part 2) pot

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Hypothermia and Frostbite Part 2 Thermoregulation Heat loss occurs through five mechanisms: radiation 55–65% of heat loss, conduction 10–15% of heat loss, but much greater in cold wate

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Chapter 020 Hypothermia and Frostbite

(Part 2)

Thermoregulation

Heat loss occurs through five mechanisms: radiation (55–65% of heat loss), conduction (10–15% of heat loss, but much greater in cold water), convection (increased in the wind), respiration, and evaporation (which are affected by the ambient temperature and the relative humidity)

The preoptic anterior hypothalamus normally orchestrates thermoregulation (Chap 17) The immediate defense of thermoneutrality is via the autonomic nervous system, whereas delayed control is mediated by the endocrine system Autonomic nervous system responses include the release of norepinephrine, increased muscle tone, and shivering, leading to thermogenesis and an increase in the basal metabolic rate Cutaneous cold thermoreception causes direct reflex vasoconstriction to conserve heat Prolonged exposure to cold also stimulates the thyroid axis, leading to an increased metabolic rate

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Clinical Presentation

In most cases of hypothermia, the history of exposure to environmental factors, such as prolonged exposure to the outdoors without adequate clothing, makes the diagnosis straightforward In urban settings, however, the presentation

is often more subtle and other disease processes, toxin exposures, or psychiatric diagnoses should be considered

After initial stimulation by hypothermia, there is progressive depression of all organ systems The timing of the appearance of these clinical manifestations varies widely (Table 20-2) Without knowing the core temperature, it can be difficult to interpret other vital signs For example, a tachycardia disproportionate

to the core temperature suggests secondary hypothermia resulting from hypoglycemia, hypovolemia, or a toxin overdose Because carbon dioxide production declines progressively, the respiratory rate should be low; persistent hyperventilation suggests a central nervous system (CNS) lesion or one of the organic acidoses A markedly depressed level of consciousness in a patient with mild hypothermia should raise suspicion of an overdose or CNS dysfunction due

to infection or trauma

Table 20-2 Physiologic Changes Associated with Accidental Hypothermia

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everity

B ody

Tempe

rature

C entral Nervou

s System

Car diovascula

r

Resp iratory

R enal and Endocr ine

Neur omuscular

M

ild

3 5°C

(95°F)–

32.2°C

(90°F)

L inear depressi

on of cerebral metabol ism;

amnesia

; apathy;

dysarthr ia;

impaire

d judgme

Tach ycardia, then progressive bradycardia

; cardiac-cycle prolongatio n;

vasoconstri ction;

increase in cardiac output and blood

Tach ypnea, then progressive decrease in respiratory minute volume;

declining oxygen consumptio n;

bronchorrhe a;

bronchospa

D iuresis;

increase

in catechol amines, adrenal steroids, triiodot hyronin

e and thyroxin e;

increase

in

Incre ased

preshiverin

g muscle tone, then fatiguing

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nt;

malada ptive behavio

r

pressure sm metabol

ism with shiverin

g

M

oderate

<

32.2°C

(90°F)–

28°C

(82.4°F

)

E

EG abnorm alities;

progres sive depressi

on of level of conscio usness;

pupillar

y dilatatio n;

Prog ressive decrease in pulse and cardiac output;

increased atrial and ventricular arrhythmias

; suggestive (J- wave) ECG

changes

Hypo ventilation;

50%

decrease in carbon dioxide production per 8°C drop in temperature

; absence of protective airway reflexes

5 0%

increase

in renal blood flow;

renal autoreg ulation intact;

impaire

d insulin action

Hyp oreflexia; diminishing shivering-induced thermogene sis; rigidity

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paradox ical undress ing;

hallucin ations

S

evere

<

28°C

(82.4°F

)

L oss of cerebro vascula

r autoreg ulation;

decline

in cerebral blood flow;

coma;

loss of

Prog ressive decrease in blood

pressure, heart rate, and cardiac output; re-entrant dysrhythmi as;

maximum risk of ventricular

Pulm onic

congestion and edema;

75%

decrease in oxygen consumptio n; apnea

D ecrease

in renal blood flow parallels decreas

e in cardiac output;

extreme oliguria;

poikilot hermia;

No motion; decreased nerve- conduction velocity; peripheral areflexia;

no corneal

or oculocephal

ic reflexes

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ocular reflexes

; progres sive decreas

e in EEG

fibrillation;

asystole

80% decreas

e in basal metabol ism

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