Etiology
The underlying mechanism of hypothermia is an imbalance between heat production and heat loss.[18] Primary hypothermia is caused by cold exposure, while secondary hypothermia is caused by reduced physiologic reserve as a result of illness or other external causes.[19][20] Primary hypothermia is more common in homeless or intoxicated people, athletes, and people who get lost outdoors as a result of impaired cognition (e.g., stroke or Parkinson disease).[19][20] Conditions associated with secondary hypothermia can be grouped into those causing impaired thermoregulation, decreased heat production, or increased heat loss.[18][19]
Impaired thermoregulation[19]
Central nervous system failure
Anorexia nervosa
Traumatic brain injury
Hypothalamic dysfunction
Metabolic failure
Neoplasm
Parkinson disease
Pharmacologic effects (general anesthetics)
Stroke (hemorrhagic or ischemic)
Toxins
Peripheral failure
Acute spinal cord transection
Peripheral neuropathy
Decreased heat production[19]
Endocrine failure
Alcoholic or diabetic ketoacidosis
Hypoadrenalism
Hypopituitarism
Lactic acidosis
Insufficient fuel
Extreme physical exertion
Hypoglycemia
Malnutrition
Neuromuscular compromise
Extremes of age
Impaired shivering
Inactivity
Increased heat loss[19]
Dermatologic illness
Burns
Induced vasodilation
Drugs and toxins
Iatrogenic
Emergency childbirth
Cold infusions
Heat-stroke treatment
Other associated clinical states
Carcinomatosis
Cardiopulmonary disease
Major infections
Multiple trauma
Shock
Pathophysiology
Hypothermia occurs because of a lowering of the core temperature. Core temperature is a reflection of the balance between heat production and heat loss.[18] Heat is produced during the breakdown of high-energy phosphate bonds, and heat is lost through the lungs and skin. Radiation heat loss from the body occurs primarily from infrared emission.[21]
In the initial stages of hypothermia, thermoreceptors situated in the skin and subcutaneous tissues sense the low ambient temperature and cause a regional vasoconstriction. This causes the hypothalamus to stimulate the release of thyroid-stimulating hormone and adrenocorticotropic hormone, leading to stimulation of the thyroid and adrenal glands. The hypothalamus also stimulates heat production by promoting shivering, typically occurring between 93.2°F and 96.8°F (34°C and 36°C). Owing to the effects of prolonged vasoconstriction, acidosis may occur, which may blunt the response to catecholamine production.
Continuous ECG monitoring demonstrates progressive bradycardia. J waves (Osborn waves) may occur at temperatures below 86°F (30°C) and are usually best seen in the lateral precordial leads.[22] Broad QRS complexes, ST elevation or depression, and T wave inversion may also occur as myocardial conduction slows.[11] PR, QT, and QTc intervals are prolonged. Some patients develop atrial fibrillation or junctional rhythms.[23]
Early on, the respiratory center is stimulated, but as time passes, the respiratory rate and tidal volume become depressed. Anatomic and physiologic dead space increases, as does bronchiolar and alveolar edema.[24] The body begins to limit energy-producing functions.
The renal blood flow and glomerular filtration rate decrease as well. Tubular reabsorption decreases as this is an energy-requiring process. As a result, cold-induced natriuresis and diuresis occur.[11]
Hypothermia is also associated with insulin resistance and hyperglycemia. Platelet dysfunction commonly occurs and may lead to a bleeding disorder. Vasoconstriction may lead to tissue hypoxia.[25]
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