Abstract：
Blood potassium is the main prognostic biomarker used for triage in hypothermic cardiac arrest. The aim of this review was to assess the impact of hypothermia on blood potassium levels and compare the underlying pathophysiological theories.
The Medline electronic database was searched via PubMed for articles published from January 1970 to December 2016. The search strategy included studies related to hypothermia and potassium levels. The relevant literature on clinical studies and experimental studies was reviewed by the authors.
Among the 50 studies included in the review, 39 (78%) reported a decrease in blood potassium levels upon hypothermia onset. Hypothermic hypokalaemia is linked to an intracellular shift rather than an actual net loss. The intracellular shift is caused by a variety of factors such as enhanced functioning of Na+K+ATPase, beta-adrenergic stimulation, pH and membrane stabilisation in deep hypothermia. In contrast, hypothermia can act as an aggravating factor in severe trauma with hyperkalaemia being an indicator of an irreversible state of cell death. An increase in the blood potassium level during hypothermia may result from a lack of enzyme functioning at cold temperatures and blocked active transport.
Hypothermia causes an initial decrease of potassium levels; however, the final stage of hypothermic cardiac arrest can induce hyperkalaemia due to cell lysis and final depolarisation. Better understanding the physiopathology of potassium levels during accidental hypothermia could be critically important to better select patients who could benefit from aggressive resuscitation therapy such as extracorporeal cardiopulmonary resuscitation.
The Medline electronic database was searched via PubMed for articles published from January 1970 to December 2016. The search strategy included studies related to hypothermia and potassium levels. The relevant literature on clinical studies and experimental studies was reviewed by the authors.
Among the 50 studies included in the review, 39 (78%) reported a decrease in blood potassium levels upon hypothermia onset. Hypothermic hypokalaemia is linked to an intracellular shift rather than an actual net loss. The intracellular shift is caused by a variety of factors such as enhanced functioning of Na+K+ATPase, beta-adrenergic stimulation, pH and membrane stabilisation in deep hypothermia. In contrast, hypothermia can act as an aggravating factor in severe trauma with hyperkalaemia being an indicator of an irreversible state of cell death. An increase in the blood potassium level during hypothermia may result from a lack of enzyme functioning at cold temperatures and blocked active transport.
Hypothermia causes an initial decrease of potassium levels; however, the final stage of hypothermic cardiac arrest can induce hyperkalaemia due to cell lysis and final depolarisation. Better understanding the physiopathology of potassium levels during accidental hypothermia could be critically important to better select patients who could benefit from aggressive resuscitation therapy such as extracorporeal cardiopulmonary resuscitation.
摘要：
血钾是用于低温心脏骤停的主要预后生物标志物。这篇综述的目的是评估低温对血钾水平的影响，并比较潜在的病理生理学理论。
Medline电子数据库通过PubMed搜索了1970年1月至2016年12月发表的文章。搜索策略包括与低温和钾水平相关的研究。作者对临床研究和实验研究的相关文献进行了综述。
在纳入综述的50项研究中，39例（78％）报告了低温发作时血钾水平降低。低温低钾血症与细胞内转移有关，而不是与实际的净损失有关。细胞内移位是由多种因素引起的，如Na+K+ATPase的功能增强，β-肾上腺素能刺激,深低温中的pH和膜稳定。相比之下,低温可作为严重创伤的加重因素，高钾血症是细胞死亡不可逆状态的指标。低温期间血钾水平的增加可能是由于在低温下缺乏酶功能和阻断主动运输所致。
体温过低导致钾水平的初始降低；然而，由于细胞溶解和最终的去极化，低温心脏骤停的最后阶段可以诱导高钾血症。更好地了解意外低温期间钾水平的病理生理学对于更好地选择可以从积极复苏治疗（例如体外心肺复苏）中受益的患者至关重要。
Medline电子数据库通过PubMed搜索了1970年1月至2016年12月发表的文章。搜索策略包括与低温和钾水平相关的研究。作者对临床研究和实验研究的相关文献进行了综述。
在纳入综述的50项研究中，39例（78％）报告了低温发作时血钾水平降低。低温低钾血症与细胞内转移有关，而不是与实际的净损失有关。细胞内移位是由多种因素引起的，如Na+K+ATPase的功能增强，β-肾上腺素能刺激,深低温中的pH和膜稳定。相比之下,低温可作为严重创伤的加重因素，高钾血症是细胞死亡不可逆状态的指标。低温期间血钾水平的增加可能是由于在低温下缺乏酶功能和阻断主动运输所致。
体温过低导致钾水平的初始降低；然而，由于细胞溶解和最终的去极化，低温心脏骤停的最后阶段可以诱导高钾血症。更好地了解意外低温期间钾水平的病理生理学对于更好地选择可以从积极复苏治疗（例如体外心肺复苏）中受益的患者至关重要。
