Long Brit, Warix Justin R, Koyfman Alex
Department of Emergency Medicine, San Antonio Military Medical Center, Fort Sam Houston, Texas.
Central Peninsula Hospital, Soldotna, Alaska.
J Emerg Med. 2018 Aug;55(2):192-205. doi: 10.1016/j.jemermed.2018.04.004. Epub 2018 May 3.
Hyperkalemia is a common electrolyte disorder that can result in morbidity and mortality if not managed appropriately.
This review evaluates the classic treatments of hyperkalemia and discusses controversies and new medications for management.
Potassium (K+) plays a key role in determining the transmembrane potentials of "excitable membranes" present in nerve and muscle cells. K+ is the predominant intracellular cation, and clinical deterioration typically ensues when patients develop sufficiently marked elevation in extracellular fluid concentrations of K+ (hyperkalemia). Hyperkalemia is usually detected via serum clinical laboratory measurement. The most severe effect of hyperkalemia includes various cardiac dysrhythmias, which may result in cardiac arrest and death. Treatment includes measures to "stabilize" cardiac membranes, to shift K+ from extracellular to intracellular stores, and to promote K+ excretion. Calcium gluconate 10% dosed 10 mL intravenously should be provided for membrane stabilization, unless the patient is in cardiac arrest, in which case 10 mL calcium chloride is warranted. Beta-agonists and intravenous insulin should be given, and some experts recommend the use of synthetic short-acting insulins rather than regular insulin. Dextrose should also be administered, as indicated by initial and serial serum glucose measurements. Dialysis is the most efficient means to enable removal of excess K+. Loop and thiazide diuretics can also be useful. Sodium polystyrene sulfonate is not efficacious. New medications to promote gastrointestinal K+ excretion, which include patiromer and sodium zirconium cyclosilicate, hold promise.
Hyperkalemia can be deadly, and treatment requires specific measures including membrane stabilization, cellular shift, and excretion.
高钾血症是一种常见的电解质紊乱疾病，如果处理不当可导致发病和死亡。
本综述评估高钾血症的经典治疗方法，并讨论治疗中的争议问题和新药物。
钾（K+）在决定神经和肌肉细胞中“可兴奋膜”的跨膜电位方面起关键作用。K+是细胞内主要阳离子，当患者细胞外液中K+浓度显著升高（高钾血症）时，通常会出现临床病情恶化。高钾血症通常通过血清临床实验室检测发现。高钾血症最严重的影响包括各种心律失常，可能导致心脏骤停和死亡。治疗措施包括“稳定”心脏膜、将K+从细胞外转移至细胞内储存以及促进K+排泄。应静脉注射10%葡萄糖酸钙10 mL以稳定细胞膜，除非患者心脏骤停，此时应使用10 mL氯化钙。应给予β受体激动剂和静脉胰岛素，一些专家建议使用合成短效胰岛素而非普通胰岛素。应根据初始和系列血清葡萄糖测量结果给予葡萄糖。透析是清除多余K+的最有效方法。袢利尿剂和噻嗪类利尿剂也可能有用。聚苯乙烯磺酸钠无效。促进胃肠道K+排泄的新药物，包括帕替罗姆和环硅锆酸钠，前景良好。
高钾血症可能致命，治疗需要采取包括稳定细胞膜、细胞内转移和排泄等具体措施。
