Hypokalemia and arrhythmias

  • Richard H. Helfant
    Request for reprints should be addressed to Dr. Richard H. Helfant, Presbyterian University of Pennsylvania Medical School, 39th and Market Streets, Philadelphia, Pennsylvania 19104.
    Department of Medicine, Mid-Atlantic Heart and Vascular Institute, Presbyterian University of Pennsylvania Medical School, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania USA
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      The focus of this article is hypokalemia, its electrophysiologic properties, and clinical arrhythmias. The effects of potassium on the electrophysiologic properties of the heart have been extensively studied and clearly are arrhythmogenic. Hypokalemia increases resting membrane potential and increases both the duration of the action potential and the duration of the refractory period, the latter to a greater degree than the former. This combination is conducive to the genesis of reentrant arrhythmias. Hypokalemia also increases threshold potential as well as automaticity, thus providing the context for automatic arrhythmias as well. Lastly, hypokalemia decreases conductivity, which also predisposes to arrhythmias of the reentrant type. The electrocardiographic criteria for hypokalemia include the presence of U waves greater than 1 mm and U waves larger than the T wave in the same lead (with associated ST-segment depression). Other criteria have been a T:U ratio of 1 or less and a U wave greater than 0.5 mm in electrocardiographic lead II or greater than 1.0 mm in lead V3. The relationship between hypokalemia and clinical arrhythmias has long been recognized. In 1949, Bellet et al [1] reported extrasystoles with hypokalemic alkalosis that decreased with potassium administration. These observations were confirmed by several groups in the early 1950s. In 1953, Surawicz and Lepeschkin [2] described a series of patients with hypokalemia and frequent junctional and ventricular premature beats; in all cases the arrhythmias disappeared with administration of potassium. These clinical observations were strengthened by the 1962 findings of Gettes et al [3], who employed microelectrode techniques to show that perfusion of low potassium solutions resulted in ventricular ectopic beats, ventricular tachycardia, and ventricular fibrillation. In more recent years, several studies have evaluated the relationship between potassium levels and arrhythmias in patients with and without hypertension who were receiving diuretic therapy. These studies have demonstrated that there is an increased incidence of ventricular arrhythmias associated with the hypokalemia induced by diuretic therapy, an observation with obvious clinical implications.
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