Mattu Amal, Hayes Bryan D, Martinez Joseph P, Brady William J, Greenwood John C
University of Maryland School of Medicine Department of Emergency Medicine Baltimore, MD USA.
Harvard Medical School Department of Emergency Medicine Boston, MA USA.
J Acute Med. 2025 Jun 1;15(2):43-51. doi: 10.6705/j.jacme.202506_15(2).0001.
Hyperkalemia is an acute life-threatening metabolic imbalance that is commonly seen in emergency departments. The primary cause is renal disease, but it also results from increased potassium intake in the diet, severe volume contraction, some medications, and other metabolic disturbances. Signs and symptoms suggestive of hyperkalemia must be recognized early so that life-saving interventions can be initiated. Rapid acquisition of an electrocardiogram (ECG) is important for making an early diagnosis because it can provide clues to the diagnosis long before laboratory results become available. Acute care providers are trained in the progression of alterations on the ECG tracings that occur as serum potassium levels rise. The earliest signs of mild hyperkalemia (5.5-6.5 mmol/L) are tall, narrow-based T waves, best seen in the precordial leads. As the potassium level becomes moderately elevated (6.5-8.0 mmol/L), the PR and QRS intervals become progressively longer, and the P waves might be lost. Severe hyperkalemia (> 8.0 mmol/L) often produces fascicular and intraventricular blocks and an eventual "sine wave" appearance which leads to ventricular fibrillation or asystole if immediate treatment is not provided. Hyperkalemia also often produces bradycardic rhythms along the progression of ECG findings, but this manifestation is not well-known or commonly taught. As a result, life-threatening hyperkalemia may be easily missed until laboratory results reveal the diagnosis. Additionally, standard treatments for bradydysrhythmias, such as atropine and electrical pacing, are often ineffective in treating this life-threatening cause of bradycardia. With early recognition of bradyarrhythmia caused by hyperkalemia, however, the proper treatment can be expedited and clinical decline can be averted.
高钾血症是一种急性的、危及生命的代谢失衡,在急诊科很常见。主要病因是肾脏疾病,但也可由饮食中钾摄入增加、严重的血容量减少、某些药物以及其他代谢紊乱引起。必须尽早识别提示高钾血症的体征和症状,以便启动挽救生命的干预措施。快速获取心电图(ECG)对于早期诊断很重要,因为在实验室结果出来之前很久,它就能为诊断提供线索。急症护理人员接受过关于随着血清钾水平升高心电图描记图变化进展的培训。轻度高钾血症(5.5 - 6.5 mmol/L)最早的体征是高耸、基底部狭窄的T波,在前胸导联最明显。随着钾水平中度升高(6.5 - 8.0 mmol/L),PR间期和QRS间期逐渐延长,P波可能消失。严重高钾血症(> 8.0 mmol/L)常产生束支传导阻滞和室内传导阻滞,并最终出现“正弦波”表现,如果不立即治疗,会导致心室颤动或心搏停止。在心电图表现进展过程中,高钾血症还常产生心动过缓节律,但这种表现并不广为人知或普遍讲授。因此,在实验室结果揭示诊断之前,可能很容易漏诊危及生命的高钾血症。此外,用于治疗缓慢性心律失常的标准疗法,如阿托品和电起搏,通常对治疗这种危及生命的心动过缓病因无效。然而,如果能早期识别高钾血症引起的缓慢性心律失常,就可以加快采取适当治疗措施,避免病情恶化。