Physiological Changes in Subjects Exposed to Accidental Hypothermia: An Update

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.

Mild Therapeutic Hypothermia Reduces Ischemia-Reperfusion Injury After Zone 1 Reboa in a Swine Hemorrhagic Shock Model

“…However, the core temperature of the hypothermia group in this study significantly decreased after balloon deflation, and that was maintained at 34°C to 36°C. Studies have shown that hypothermia can affect the hemodynamics, CO decreased considerably (17,24), and SVR increased significantly (25), and circulatory failure may occur with deep or prolonged cooling, which may limit the chances of safe survival of the cooled patient (17,18). This study found that the CO reduced significantly and the SVR increased significantly during the whole cooling.…”

Pharmacodynamic properties for inhibition of cAMP- and cGMP elimination by pentoxifylline remain unaltered in vitro during hypothermia

“…The same decrease in blood viscosity caused by pentoxifylline might also be useful for hypothermic patients. During hypothermia, blood viscosity increases and decreased organ specific blood flow is observed [29]. By lowering the blood viscosity, organ specific blood perfusion may increase as the erythrocytes become more flexible and increases the ability to reach organs throughout the body [30].…”

“…Pentoxyfilline could however cause adverse effects, such as arrythmias and altered blood pressure [31]. Such complications are not uncommon in hypothermia per se [29], and it is possible that administering pentoxifylline to hypothermic patients, could lead to increased risk. Both in vivo, ex vivo and human data show that there is an increased risk of ventricular fibrillation (VF) in hypothermia, when the core temperature is around 30 °C [32][33][34].…”