Abstract
BackgroundAccidental hypothermia (AH) is an unintended decrease in body core temperature (BCT) to below 35°C. We present an update on physiological/pathophysiological changes associated with AH and rewarming from hypothermic cardiac arrest (HCA).Temperature Regulation and MetabolismTriggered by falling skin temperature, Thyrotropin-Releasing Hormone (TRH) from hypothalamus induces release of Thyroid-Stimulating Hormone (TSH) and Prolactin from pituitary gland anterior lobe that stimulate thyroid generation of triiodothyronine and thyroxine (T4). The latter act together with noradrenaline to induce heat production by binding to adrenergic β3-receptors in fat cells. Exposed to cold, noradrenaline prompts degradation of triglycerides from brown adipose tissue (BAT) into free fatty acids that uncouple metabolism to heat production, rather than generating adenosine triphosphate. If BAT is lacking, AH occurs more readily.Cardiac OutputAssuming a 7% drop in metabolism per °C, a BCT decrease of 10°C can reduce metabolism by 70% paralleled by a corresponding decline in CO. Consequently, it is possible to maintain adequate oxygen delivery provided correctly performed cardiopulmonary resuscitation (CPR), which might result in approximately 30% of CO generated at normal BCT.Liver and CoagulationAH promotes coagulation disturbances following trauma and acidosis by reducing coagulation and platelet functions. Mean prothrombin and partial thromboplastin times might increase by 40–60% in moderate hypothermia. Rewarming might release tissue factor from damaged tissues, that triggers disseminated intravascular coagulation. Hypothermia might inhibit platelet aggregation and coagulation.KidneysRenal blood flow decreases due to vasoconstriction of afferent arterioles, electrolyte and fluid disturbances and increasing blood viscosity. Severely deranged renal function occurs particularly in the presence of rhabdomyolysis induced by severe AH combined with trauma.ConclusionMetabolism drops 7% per °C fall in BCT, reducing CO correspondingly. Therefore, it is possible to maintain adequate oxygen delivery after 10°C drop in BCT provided correctly performed CPR. Hypothermia may facilitate rhabdomyolysis in traumatized patients. Victims suspected of HCA should be rewarmed before being pronounced dead. Rewarming avalanche victims of HCA with serum potassium > 12 mmol/L and a burial time >30 min with no air pocket, most probably be futile.
Highlights
Accidental hypothermia (AH) is a fall in body core temperature (BCT) to below 35◦C after exposure to cold or decrease in metabolic rate [1, 2]
Adjustment of acid-base balance in hypothermic children should follow the “pH-stat strategy”, i.e., correcting pH and blood gases analyzed at 37◦C back to the patient’s BCT
Adjustment of acid-base balance in hypothermic adults with hypothermic cardiac arrest (HCA) should follow the “alpha-stat strategy,” i.e., employing the values measured at 37◦C directly without correcting to the actual BCT
Summary
Accidental hypothermia (AH) is an unintended decrease in body core temperature (BCT) to below 35◦C. Temperature Regulation and Metabolism: Triggered by falling skin temperature, Thyrotropin-Releasing Hormone (TRH) from hypothalamus induces release of Thyroid-Stimulating Hormone (TSH) and Prolactin from pituitary gland anterior lobe that stimulate thyroid generation of triiodothyronine and thyroxine (T4). The latter act together with noradrenaline to induce heat production by binding to adrenergic β3-receptors in fat cells. Cardiac Output: Assuming a 7% drop in metabolism per ◦C, a BCT decrease of 10◦C can reduce metabolism by 70% paralleled by a corresponding decline in CO. Deranged renal function occurs in the presence of rhabdomyolysis induced by severe AH combined with trauma
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