Montague Brian T, Ouellette Jason R, Buller Gregory K
Department of Medicine, Saint Mary's Hospital, 56 Franklin Street, Waterbury, CT 06706, USA.
Clin J Am Soc Nephrol. 2008 Mar;3(2):324-30. doi: 10.2215/CJN.04611007. Epub 2008 Jan 30.
Experimentally elevated potassium causes a clear pattern of electrocardiographic changes, but, clinically, the reliability of this pattern is unclear. Case reports suggest patients with renal insufficiency may have no electrocardiographic changes despite markedly elevated serum potassium. In a prospective series, 46% of patients with hyperkalemia were noted to have electrocardiographic changes, but no clear criteria were presented.
DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Charts were reviewed for patients who were admitted to a community-based hospital with a diagnosis of hyperkalemia. Inclusion criteria were potassium >/=6 with a concurrent electrocardiogram. Data were abstracted regarding comorbid diagnoses, medications, and treatment. Potassium concentrations were documented along with other electrolytes, pH, creatinine, and biomarkers of cardiac injury. Coincident, baseline, and follow-up electrocardiograms were examined for quantitative and qualitative changes in the QRS and T waves as well as the official cardiology readings.
Ninety patients met criteria; two thirds were older than 65, and 48% presented with renal failure. Common medications included beta blockers, insulin, and aspirin; 80% had potassium <7.2. The electrocardiogram was insensitive for diagnosing hyperkalemia. Quantitative assessments of T-wave amplitude corroborated subjective assessments of T-wave peaking; however, no diagnostic threshold could be established. The probability of electrocardiographic changes increased with increasing potassium. The correlation between readers was moderate.
Given the poor sensitivity and specificity of electrocardiogram changes, there is no support for their use in guiding treatment of stable patients. Without identifiable electrocardiographic markers of the risk for complications, management of hyperkalemia should be guided by the clinical scenario and serial potassium measurements.
实验性高钾血症会引起明确的心电图变化模式，但在临床中，这种模式的可靠性尚不清楚。病例报告表明，尽管血清钾显著升高，但肾功能不全患者可能没有心电图变化。在一项前瞻性研究系列中，46%的高钾血症患者有心电图变化，但未给出明确标准。
设计、地点、参与者及测量：回顾了一家社区医院收治的诊断为高钾血症患者的病历。纳入标准为血钾≥6.0且同时进行了心电图检查。提取了关于合并诊断、用药及治疗的数据。记录了血钾浓度以及其他电解质、pH值、肌酐和心脏损伤生物标志物。检查了同时期、基线及随访心电图的QRS波和T波的定量及定性变化以及心脏病学的正式读数。
90例患者符合标准；三分之二年龄超过65岁，48%有肾衰竭表现。常用药物包括β受体阻滞剂、胰岛素和阿司匹林；80%的患者血钾<7.2。心电图对诊断高钾血症不敏感。T波振幅的定量评估证实了对T波高耸的主观评估；然而，无法确定诊断阈值。心电图变化的可能性随血钾升高而增加。读者之间的相关性中等。
鉴于心电图变化的敏感性和特异性较差，不支持将其用于指导稳定患者的治疗。由于缺乏可识别的并发症风险心电图标志物，高钾血症的管理应以临床情况和系列血钾测量为指导。
