Bjertnæs Lars J, Næsheim Torvind O, Reierth Eirik, Suborov Evgeny V, Kirov Mikhail Y, Lebedinskii Konstantin M, Tveita Torkjel
Department of Clinical Medicine, Faculty of Health Sciences, Anesthesia and Critical Care Research Group, University of Tromsø, UiT The Arctic University of Norway, Tromsø, Norway.
Division of Surgical Medicine and Intensive Care, University Hospital of North Norway, Tromsø, Norway.
Front Med (Lausanne). 2022 Feb 23;9:824395. doi: 10.3389/fmed.2022.824395. eCollection 2022.
Accidental 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).
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. 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.
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. 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.
AH 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.
Renal 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.
Metabolism 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.
意外低温(AH)是指人体核心体温(BCT)意外降至35°C以下。我们提供了与AH以及低温心脏骤停(HCA)复温相关的生理/病理生理变化的最新信息。
由皮肤温度下降触发,下丘脑分泌的促甲状腺激素释放激素(TRH)诱导垂体前叶释放促甲状腺激素(TSH)和催乳素,刺激甲状腺生成三碘甲状腺原氨酸和甲状腺素(T4)。后者与去甲肾上腺素共同作用,通过与脂肪细胞中的肾上腺素能β3受体结合来诱导产热。暴露于寒冷环境时,去甲肾上腺素促使棕色脂肪组织(BAT)中的甘油三酯降解为游离脂肪酸,使代谢与产热解偶联,而不是生成三磷酸腺苷。如果缺乏BAT,更容易发生AH。
假设代谢每降低1°C下降7%,BCT下降10°C可使代谢降低70%,同时心输出量(CO)相应下降。因此,如果正确进行心肺复苏(CPR),有可能维持足够的氧输送,这可能导致在正常BCT时产生约30%的CO。
AH通过降低凝血和血小板功能,促进创伤和酸中毒后的凝血紊乱。在中度低温时,平均凝血酶原时间和部分凝血活酶时间可能增加40 - 60%。复温可能从受损组织中释放组织因子,引发弥散性血管内凝血。低温可能抑制血小板聚集和凝血。
由于入球小动脉血管收缩、电解质和液体紊乱以及血液粘度增加,肾血流量减少。严重的肾功能紊乱尤其发生在严重AH合并创伤引起横纹肌溶解的情况下。
BCT每下降1°C,代谢下降7%,相应降低CO。因此,如果正确进行CPR,BCT下降10°C后有可能维持足够的氧输送。低温可能促进创伤患者的横纹肌溶解。疑似HCA的受害者在被宣布死亡前应进行复温。对于血清钾>12 mmol/L且掩埋时间>30分钟且无气腔的HCA雪崩受害者进行复温很可能是徒劳的。