ArticleCritical care medicine2024
Beneficial Effect of Calcium Treatment for Hyperkalemia Is Not Due to "Membrane Stabilization".
Article in Critical care medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Singapore Paediatric Life Support Guidelines 2026.Singapore medical journal · 2026Guideline
- Clinical impact of an EHR-integrated hyperkalemia management system: a real-world study of 10,934 episodes.Renal failure · 2026Article
- Do Magnesium Ions Have Similar Effects as Calcium Ions on Resting Membrane Potential?Membranes · 2026Article
- [Consensus recommendations on the diagnosis and treatment of hyperkalemia of the Austrian Society of Nephrology 2026].Wiener klinische Wochenschrift · 2026Review
- Cardiac Arrest Pharmacopeia: A Personalized Approach to Drug Administration During Cardiopulmonary Resuscitation.Critical care clinics · 2026Review
- A Case of Acute Hyperkalaemia of Unknown Origin During General Anaesthesia in a Rottweiler.Animals : an open access journal from MDPI · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
objectivesHyperkalemia is a common life-threatening condition causing severe electrophysiologic derangements and arrhythmias. The beneficial effects of calcium (Ca 2+ ) treatment for hyperkalemia have been attributed to "membrane stabilization," by restoration of resting membrane potential (RMP). However, the underlying mechanisms remain poorly understood. Our objective was to investigate the mechanisms underlying adverse electrophysiologic effects of hyperkalemia and the therapeutic effects of Ca 2+ treatment.
designControlled experimental trial.
settingLaboratory investigation. SUBJECTS: Canine myocytes and tissue preparations. INTERVENTIONS AND MEASUREMENTS: Optical action potentials and volume averaged electrocardiograms were recorded from the transmural wall of ventricular wedge preparations ( n = 7) at baseline (4 mM potassium), hyperkalemia (8-12 mM), and hyperkalemia + Ca 2+ (3.6 mM). Isolated myocytes were studied during hyperkalemia (8 mM) and after Ca 2+ treatment (6 mM) to determine cellular RMP. MAIN
resultsHyperkalemia markedly slowed conduction velocity (CV, by 67% ± 7%; p < 0.001) and homogeneously shortened action potential duration (APD, by 20% ± 10%; p < 0.002). In all preparations, this resulted in QRS widening and the "sine wave" pattern observed in severe hyperkalemia. Ca 2+ treatment restored CV (increase by 44% ± 18%; p < 0.02), resulting in narrowing of the QRS and normalization of the electrocardiogram, but did not restore APD. RMP was significantly elevated by hyperkalemia; however, it was not restored with Ca 2+ treatment suggesting a mechanism unrelated to "membrane stabilization." In addition, the effect of Ca 2+ was attenuated during L-type Ca 2+ channel blockade, suggesting a mechanism related to Ca 2+ -dependent (rather than normally sodium-dependent) conduction.
conclusionsThese data suggest that Ca 2+ treatment for hyperkalemia restores conduction through Ca 2+ -dependent propagation, rather than restoration of membrane potential or "membrane stabilization." Our findings provide a mechanistic rationale for Ca 2+ treatment when hyperkalemia produces abnormalities of conduction (i.e., QRS prolongation).
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