QT Interval on ECG: Norms, Measurement, and Prolongation

What it looks like on ECG

The QT interval begins at the point where QRS crosses the isoelectric line (onset of Q or R wave) and ends at the point where the T wave returns to the isoelectric line. Visually, this is the distance from the first significant deflection of the ventricular complex to the complete return of the repolarization wave to the baseline.

Measurement is performed in the lead where the end of the T wave is most clearly defined — most often lead II or V5. There is no fixed rule of "only these leads": if the T-wave end is unclear in one lead, evaluate multiple leads and take the longest reliably measurable QT. In low-voltage leads (aVR, aVL, III) and with biphasic T waves, measurement is difficult and such leads are usually avoided.

The absolute QT value strongly depends on heart rate: it is shorter during tachycardia and longer during bradycardia, so relying on absolute QT without accounting for rate is incorrect. Any individual QT value should be evaluated only after calculating QTc, taking into account heart rate, sex, age, and clinical context. A separate rule applies to QRS width: with QRS ≥ 0.12 s (bundle branch block, ventricular pacing), QT increases not only due to repolarization but also due to depolarization itself, so standard QTc in this situation may be falsely elevated. It is preferable to evaluate the JT interval (JTc) — from the end of QRS to the end of T — or use a validated correction formula that accounts for QRS duration; a diagnosis of LQTS should not be made based on a single QTc value uncorrected for QRS width.

Corrected QTc normalizes the dependence of QT on heart rate and allows comparison of patients with different heart rhythms. Bazett's formula (QTc = QT / √RR) is the most widespread clinically, but is known to overestimate QTc during tachycardia and underestimate it during bradycardia; at extreme heart rates, Fridericia's or Framingham's formulas are preferred.

Norm and variants

Corrected QTc (approximate reference limits, varying by formula, source, sex, and age):

• Men: upper limit is cited in various guidelines from approximately 0.44 s (stricter reference point) to approximately 0.45 s
• Women, children, young adults: up to approximately 0.46 s

These are upper reference benchmarks rather than a rigid boundary between health and disease: when using Bazett's formula at extreme heart rates, the result may be skewed, and sources lack a single consensus value — the choice of threshold depends on the correction formula and clinical context.

Borderline zone: QTc values within 10–20 ms above the specified reference points (e.g., approximately 0.45–0.47 s in men, 0.46–0.48 s in women) require reassessment, exclusion of acquired causes (electrolytes, medications), and consideration of the clinical context, rather than a definitive interpretation as pathology.

Prolongation: exceeding the upper reference limit raises suspicion, but diagnosing congenital long QT syndrome (LQTS) typically requires a stricter, repeatedly confirmed threshold — a QTc of about 0.48 s and above, or about 0.46 s in the presence of typical syncope, after excluding acquired causes.

Shortening: in modern diagnostic criteria for short QT syndrome, a repeatedly measured QTc ≤ 0.34 s is considered highly suspicious for the diagnosis after excluding secondary causes; a QTc of 0.34–0.36 s is evaluated alongside additional features — syncope, atrial fibrillation, family history, cardiac arrest, or a pathogenic genetic variant. The stricter 0.33 s threshold found in some older sources is not used independently in modern criteria. Acquired causes of shortening include hypercalcemia, acidosis, and digoxin therapy.

Reference limits in clinical practice are typically not adjusted for race; population studies describe potential racial and ethnic differences in QTc, but this does not alter standard evaluation by formula, sex, age, and clinical context. Women have a longer QTc on average, especially at low heart rates. In atrial fibrillation and frequent extrasystoles, QTc measurement and interpretation are more complex.

Mechanism

The QT interval reflects the temporal sequence of ventricular depolarization and complete repolarization: QT = QRS + JT, where the QRS complex entirely represents ventricular depolarization and typically lasts about 0.08–0.12 s, and the JT interval (predominantly the T wave) reflects repolarization; the specific duration of JT depends on heart rate and measurement conditions. QT duration is determined by the duration of the cardiomyocyte action potential. The rapid inward sodium current provides phase 0 — depolarization itself and the formation of QRS — and is not in itself a typical cause of QT prolongation. Action potential duration and repolarization are influenced by other currents: outward potassium currents (primarily IKr and IKs) ensure repolarization and limit action potential duration; their reduction or blockade prolongs the action potential and QT; enhancement of the late (rather than rapid) sodium current and changes in the calcium current can also prolong the action potential. As heart rate increases, RR shortens and the action potential reflexively shortens (adaptation); conversely, bradycardia prolongs the action potential. Blockade of potassium channels (medications, congenital syndromes), enhancement of late sodium current, or alterations in calcium current prolong QT and increase the risk of early afterdepolarizations and torsades de pointes.

Causes of QT prolongation

Congenital syndromes:

• Romano–Ward syndrome — typically autosomal dominant LQTS (most commonly KCNQ1, KCNH2, SCN5A mutations)
• Jervell and Lange-Nielsen syndrome — autosomal recessive, usually associated with biallelic KCNQ1 or KCNE1 variants, accompanied by congenital deafness
• Other genetic ion channel variants

Electrolyte disturbances:

• Hypokalemia (< 3.5 mmol/L)
• Hypocalcemia: evaluate total calcium adjusted for albumin or ionized calcium against laboratory reference ranges (typically below approx. 2 mmol/L for total calcium, but the exact threshold depends on the laboratory)
• Hypomagnesemia: laboratory reference ranges vary across labs; values near or below the lower limit of normal increase risk, with precise interpretation (normal/borderline/hypomagnesemia) provided based on the specific laboratory's reference range

QT-prolonging drugs:

• Direct potassium channel blockers (hERG): antiarrhythmics — amiodarone, sotalol, dofetilide, ibutilide; antipsychotics — haloperidol, quetiapine; macrolides — azithromycin, erythromycin; fluconazole; methadone
• Drugs that increase the risk predominantly indirectly (via hypokalemia/hypomagnesemia or other mechanisms of cardiotoxicity): amphotericin B, certain antineoplastic agents (e.g., cisplatin, anthracyclines), protease inhibitors, tricyclic antidepressants
• The risk depends on the dose, drug interactions, and individual factors; the current status of the drug regarding QT risk should be verified using the active prescribing information or specialized lists (e.g., CredibleMeds)

Cardiac diseases:

• Myocarditis, cardiomyopathy
• Myocardial infarction (acute phase)
• Left ventricular hypertrophy
• Bundle branch block and ventricular pacing (increase the measured QT due to QRS widening; interpretation requires assessing JT/JTc or correcting for QRS width)

Systemic and neurological:

• Subarachnoid haemorrhage
• Hypothyroidism
• Sepsis
• Hypothermia
• Female sex (physiologically longer QTc)

Clinical significance and management

Diagnostic significance: A prolonged QTc is a marker of delayed repolarization and an increased risk of life-threatening arrhythmias, especially torsades de pointes; the underlying mechanisms are early afterdepolarizations and spatial-temporal repolarization heterogeneity. Particularly dangerous thresholds are considered to be QTc ≥ 0.50 s or a QTc increase of ≥ 60 ms from baseline, especially when combined with bradycardia, electrolyte disturbances, or the use of ECG-active drugs.

When urgent action is required:

• QTc ≥ 0.50 s or an increase in QTc of ≥ 60 ms from baseline
• History of or monitored torsades de pointes
• Syncope of unclear etiology in the setting of a known prolonged QT
• Use of two or more QT-prolonging drugs combined with electrolyte disturbances

Emergency management of torsades de pointes: Discontinue the offending drug, administer intravenous magnesium regardless of baseline blood levels, correct potassium (target level typically in the upper half of the normal range), eliminate bradycardia and pauses in rhythm (temporary overdrive pacing, or sometimes isoproterenol for acquired forms until a pacemaker is placed); in case of hemodynamic instability, perform emergency electrical cardioversion.

Further physician management:

1. Measure QTc on a resting ECG, repeating at different heart rates if possible
2. Check potassium, magnesium, calcium, and thyroid function
3. Review the medication list; discontinue or replace QT-prolonging agents considering indications and alternatives
4. Correct electrolyte disturbances under laboratory monitoring
5. If congenital LQTS is clinically likely (repeated QTc around 0.48 s and higher, typical syncope, family history of sudden death), refer for inherited arrhythmia consultation and genetic testing
6. If LQTS is confirmed, recommend genotype-based restrictions (e.g., avoiding unsupervised swimming in LQT1, sudden loud noises in LQT2) and individualize them with a specialist
7. Consider beta-blockers (propranolol, nadolol) to prevent arrhythmic events in congenital LQTS; their main goal is not QT shortening, but reducing the risk of events
8. Implantable cardioverter-defibrillator (ICD) placement is considered after cardiac arrest or in patients at high risk for events despite optimal therapy; left cardiac sympathetic denervation is discussed in selected cases of congenital LQTS. Catheter ablation is not a standard treatment for LQTS

Common interpretation errors

1. Failing to correct QT for heart rate. Absolute QT should be interpreted only after calculating QTc: the same QT value can be normal during bradycardia and pathological during tachycardia. Bazett's formula is particularly unreliable at extreme heart rates — Fredericia's or Framingham's formulas are preferred in these cases.

1. Mistaking the end of U for the end of T. The U wave often superimposes on or merges with the T wave. When T and U fuse, the end of T is determined by the tangent to the terminal portion of the descending limb of T, rather than mechanically by the first return to the isoelectric line; when in doubt, select the lead with a more clearly separated T wave (often II or V5) and repeat the measurement.

1. Measuring QT in leads with a biphasic T wave. In aVR, III, and V1, the T wave is frequently biphasic or negative, leading to errors in determining the end of T. Leads with a distinct monophasic T wave, such as II or V5, are preferred.

1. Applying sex- and age-specific thresholds too rigidly. Approximate upper limits of QTc (ranging in different sources from approximately 0.44 to 0.45 s in men, to about 0.46 s in women) are not rigid disease boundaries. A borderline value in a man requires confirmation and evaluation of causes rather than an automatic diagnosis; in a woman, the same value may fall within the reference range.

1. Failing to account for QRS width. In bundle branch block or ventricular pacing (QRS ≥ 0.12 s), the standard QTc is falsely elevated due to prolonged depolarization. In this situation, a diagnosis of LQTS should not be made based on a single uncorrected QTc alone — assess JT/JTc or apply correction for QRS duration.

1. Failing to account for arrhythmia when calculating QTc. In atrial fibrillation, there are no sinus RR intervals; QT is measured across multiple complexes by averaging the preceding RR intervals using an accepted method, avoiding extrasystoles and post-extrasystolic complexes, rather than relying on a single "correct" RR.

Frequently asked questions

Related terms

More in the section «Basics: waves, intervals, axes»

Entire section

Sources

• Goldberger AL. Clinical Electrocardiography: A Simplified Approach. 9th ed. Elsevier, 2018
• Surawicz B, Knilans TK. Chou's Electrocardiography in Clinical Practice: Adult and Pediatric. 6th ed. Saunders, 2008
• AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the Electrocardiogram, 2009
• Orlov VN. Guidelines for Electrocardiography. 9th ed. Medpress-inform, 2017

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.