Hypokalemia on ECG

What it looks like on ECG

Changes develop gradually and are generally related to the degree of blood potassium reduction, although there is no exact parallelism between the potassium level and the severity of the ECG pattern — patient sensitivity varies, and the grading below is approximate and non-validated.

T-wave inversion and the degree of ST depression do not allow for a reliable determination of hypokalaemia severity — these are guides rather than a rigid grading scale.

Changes are best visualized in chest leads V2–V4, where the U wave is physiologically more prominent. It is important to distinguish true QT interval prolongation from QU prolongation caused by fusion of the T wave with an enlarged U wave — for this, look for a separate peak or notch between T and U across multiple leads.

In severe hypokalaemia (laboratory potassium typically under 2.5 mmol/L), ventricular extrasystoles, paroxysms of ventricular tachycardia, including polymorphic VT such as torsades de pointes, may occur, especially in the presence of concurrent QT-prolonging medications or coexisting hypomagnesaemia.

Mechanism

Potassium is the primary ion determining the resting membrane potential and cardiomyocyte repolarization. In hypokalaemia, repolarization potassium currents are altered, particularly the rapid delayed rectifier current ($I_{Kr}$), which prolongs and heterogeneously changes late repolarization, primarily phase 3 of the action potential. Repolarization becomes heterogeneous across myocardial layers (endocardium–epicardium, Purkinje system), causing the T wave to flatten and the U wave to increase. The mechanism of U-wave origin is not fully established; it is likely related to late repolarization components, including Purkinje fibers and papillary muscles. Repolarization delay and heterogeneity also increase the risk of triggered activity in the form of early afterdepolarizations — hence the increased tendency toward ventricular arrhythmias.

Causes

• Gastrointestinal potassium losses: vomiting, diarrhea, laxative abuse
• Renal losses: diuretics (loop, thiazide), hyperaldosteronism, Cushing's syndrome, renal tubular acidosis
• Intracellular potassium shift: insulin, beta-agonists, alkalosis, thyrotoxic periodic paralysis; hypothermia can transiently promote potassium redistribution and requires separate clinical evaluation
• Inadequate dietary potassium intake (rarely isolated)
• Magnesium deficiency (hypomagnesaemia exacerbates and maintains hypokalaemia)
• Use of certain medications (glucocorticoids, amphotericin B)

Differential diagnosis

• True QT prolongation (long QT syndrome, drugs) — T-U fusion is characteristic of hypokalemia, but is non-specific and also occurs in congenital long QT; differentiation by morphology on a single ECG may be impossible, requiring serial tracings, medication review, and electrolyte assessment
• Hypocalcemia — usually prolongs QT predominantly at the expense of the ST segment; the T wave is generally preserved, though changes are possible, and a prominent U wave is uncharacteristic of hypocalcemia
• Normal physiological U wave — in healthy individuals, the U wave is small, with an amplitude noticeably less than the T wave; in hypokalemia, the U wave is pathologically prominent and may approach or exceed the amplitude of the T wave
• Ischemic ST-T changes — isolated or localized ST-T changes are possible without obligatory reciprocal changes; clinical presentation, localization, ECG dynamics, and troponins are decisive in differential diagnosis
• Digoxin effect on ECG — produces a scooping (hammock-shaped) ST depression, but without a marked increase in the U wave

Clinical significance and management

ECG changes in hypokalemia are an indication to immediately check blood potassium and magnesium levels, especially in patients on diuretics, with vomiting/diarrhea, or in the presence of other risk factors. Severe hypokalemia is dangerous due to ventricular arrhythmias, including torsades de pointes, particularly in combination with QT-prolonging drugs and hypomagnesemia.

What is important for a physician on an ECG: assess the degree of T/U changes; if the end of the T wave is clearly distinguishable, measure QT up to it, excluding the U wave. With T-U fusion, reliable measurement of QT/QTc may be impossible — in this case, select the lead with the most distinguishable T-wave end, compare serial ECGs, and do not calculate QTc using the QU interval. It is also necessary to check for extrasystoles and signs of AV slowing. The decision on rhythm monitoring and potassium correction is made based on laboratory data and the clinical picture, rather than the ECG alone. In suspected drug-induced repolarization toxicity, monitoring and correction of potassium and magnesium levels are necessary. When cardiac glycosides are taken concomitantly, hypokalemia increases the risk of their toxic effects.

Common interpretation errors

• Mistaking a fused T+U wave for true QT prolongation and overestimating the risk using Bazett's formula without accounting for the U wave
• Failing to look for the U wave separately — at a paper speed of 25 mm/s, it easily merges with the T wave upon a cursory glance
• Measuring QT as QU and interpreting the result using standard QTc thresholds
• Ignoring ST depression as "non-specific" without linking it to the electrolyte profile
• Forgetting to check magnesium — hypomagnesemia frequently accompanies and exacerbates the ECG manifestations of hypokalemia

Frequently asked questions

Related terms

More in "Electrolytes and Metabolism"

Entire section

Sources

• Surawicz B., Knilans T. Chou's Electrocardiography in Clinical Practice, 6th ed.
• Hampton J. The ECG Made Easy
• Orlov V.N. Guide to Electrocardiography
• AHA/ACCF/HRS Recommendations for the Standardization of the Electrocardiogram, 2009

Educational material for medical students and physicians. Does not replace clinical guidelines and physical examination; the ECG must always be interpreted in conjunction with the clinical picture.