Hypokalemic weakness in hyperaldosteronism: activity-dependent conduction block
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Updated: Aug 15, 2026

Voltage-Dependent Potassium Current Recording on H9c2 Cardiomyocytes via the Whole-Cell Patch-Clamp Technique
Published on: November 11, 2022
Arun V Krishnan1, James G Colebatch, Matthew C Kiernan
1The Institute of Neurological Sciences, Prince of Wales Hospital, University of New South Wales, Randwick, Sydney, NSW, Australia.
Abstract:
The authors describe a 48-year-old man who presented with acute weakness. Serum K+ was 1.7 mmol/L, and investigations established hyperaldosteronism. Nerve excitability studies during hypokalemia demonstrated that axons were of high threshold with a fanning out of threshold electrotonus, consistent with hyperpolarization. Activity-dependent conduction block was induced by voluntary contraction. Excitability abnormalities resolved with K+ replacement. Activity-dependent conduction block induced by normal activity may contribute to weakness and paralysis developing with hypokalemia.
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