Abnormalities in serum electrolyte levels and impaired electrolyte homeostasis may aberrate cardiac conduction by altering cardiac ion current kinetics. Oftentimes, the bedside electrocardiogram (ECG) can render expeditious insight and prompt emergency therapy while laboratory investigations of fluid, acid-base and electrolyte imbalances are underway for establishing a definitive diagnosis. The most frequent electrolyte aberrations affecting the ECG include disturbances of potassium, calcium, and magnesium concentrations. Electrolyte dyshomeostasis impacts the depolarization and repolarization phases of action potential in cardiomyocytes by modifying potentials across their cell membranes. Further, individual electrolyte disturbances often have wide-ranging consequences due to their effect on one another. Serum potassium concentration changes can cause considerable repercussions on myocyte conduction and potentially resulting in ECG changes. The ECG changes in hypokalemia mimic those of myocardial ischemia. With severe hypokalemia, the telltale ECG change is the development of U waves. In hyperkalemia, the primary ECG manifestation is T wave tenting, that is seen as a symmetrical narrowing or peaking but with oftentimes a wide deflection and high amplitude. With very severe hyperkalemia, a slurring “sine-wave” appearance may be observed on the ECG due to significant prolongation and widening of QRS complex and subsequent fusion with the T wave. Hyper-and hypo-calcemia mainly change the action potential span (phase 2), which causes either shrinking (in hypercalcemia) or extension (in hypocalcemia) of the QT interval. The effect on the QT interval is mainly the result of an alteration of the ST-segment time span. Both situations can impact T wave structure. No classic ECG presentation is observed in hypo-or hyper-states of magnesium. Bedside electrocardiography serves as an important aid in forming diagnoses and managing patients presenting with electrolytic dyshomeostasis.

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