Also known as: QTc, Corrected QT Interval, QT/QTc Interval
Measurement
| Normal Range | QTc less than 450 ms in males, less than 460 ms in females. Values of 450–500 ms (males) or 460–500 ms (females) are borderline prolonged. QTc greater than 500 ms carries a substantially increased risk of Torsades de Pointes and sudden cardiac death. Normal QT without rate correction is approximately 0.36–0.44 seconds at 60 bpm. |
| Measurement | Measure from the beginning of the QRS complex to the end of the T wave (where the T wave returns to the isoelectric baseline). Use the lead with the longest QT interval, typically V5 or V6, and avoid leads with prominent U waves that may be mistaken for T wave endings. Apply the Bazett formula (QTc = QT / √RR, with RR in seconds) or Fridericia formula (QTc = QT / ∛RR) for rate correction. Average at least three to five consecutive beats. |
Clinical Significance
The QT interval reflects the duration of ventricular action potentials. Prolongation creates a window of vulnerability during which early afterdepolarizations can trigger polymorphic ventricular tachycardia (Torsades de Pointes), which may degenerate into ventricular fibrillation. Congenital long QT syndromes (LQTS types 1–17) and numerous medications, electrolyte abnormalities, and structural heart disease can all prolong the QT interval. QT shortening, while less common, is associated with hypercalcemia, digitalis toxicity, and short QT syndrome, also carrying arrhythmia risk.
Abnormalities
Congenital Long QT Syndrome (LQTS)
Inherited channelopathies affecting cardiac ion channels (most commonly KCNQ1 in LQT1, HERG in LQT2, and SCN5A in LQT3) that prolong ventricular repolarization. Patients are at risk for syncope, Torsades de Pointes, and sudden cardiac death, often triggered by exercise, auditory stimuli, or sleep depending on the genotype. Management includes beta-blockers, avoidance of QT-prolonging medications, and implantable cardioverter-defibrillator placement in high-risk patients.
Acquired QT Prolongation (Drug-Induced)
Many medications prolong the QT interval by blocking cardiac potassium channels (IKr/hERG channel), including antiarrhythmics (sotalol, amiodarone, quinidine), antibiotics (fluoroquinolones, macrolides), antipsychotics (haloperidol, ziprasidone), and antidepressants. Risk is amplified by hypokalemia, hypomagnesemia, bradycardia, female sex, and underlying structural heart disease.
Torsades de Pointes
A polymorphic ventricular tachycardia characterized by QRS complexes that appear to twist around the isoelectric baseline, occurring on the background of a prolonged QT interval. It is often initiated by a long-short RR sequence. Treatment of the acute episode includes IV magnesium sulfate; the underlying QT-prolonging cause must be identified and corrected.
Hypokalemia and Hypomagnesemia
Low serum potassium prolongs the QT interval by impairing repolarizing potassium currents. Hypomagnesemia has a similar effect and often coexists with hypokalemia. Both electrolyte deficiencies increase the risk of Torsades de Pointes, particularly in the setting of concurrent QT-prolonging medications.
Short QT Syndrome
A rare inherited channelopathy with QTc less than 360 ms associated with gain-of-function mutations in potassium channels or loss-of-function in calcium channels. Accelerated repolarization shortens the refractory period and predisposes to atrial fibrillation, ventricular fibrillation, and sudden cardiac death in otherwise young, healthy individuals.
Frequently Asked Questions
Why do we correct the QT interval for heart rate?
The QT interval naturally shortens at faster heart rates and lengthens at slower rates because faster rates leave less time for each complete cardiac cycle, compressing the repolarization phase. Without rate correction, a QT interval of 0.44 seconds would appear normal at 60 bpm but inappropriately long at 100 bpm. The Bazett formula (QTc = QT / √RR) corrects this by normalizing the measured QT interval to what it would be at a heart rate of 60 bpm, allowing meaningful comparisons across different heart rates and patients.
What medications commonly prolong the QT interval?
A large and diverse group of medications can prolong QT, most commonly by blocking the hERG potassium channel responsible for rapid repolarization. Major categories include: antiarrhythmics (amiodarone, sotalol, dofetilide, quinidine), antibiotics (azithromycin, ciprofloxacin, clarithromycin), antipsychotics (haloperidol, thioridazine, quetiapine), antidepressants (citalopram at high doses, tricyclics), and antiemetics (ondansetron, domperidone). Resources like CredibleMeds maintain updated lists of QT risk by drug category.
What is the difference between long QT syndrome types 1, 2, and 3?
LQT1 involves a mutation in KCNQ1, which encodes the slow delayed rectifier potassium channel (IKs). It is the most common type, triggers typically occur with exercise (especially swimming), and beta-blockers are highly protective. LQT2 involves HERG (IKr channel), triggers include auditory stimuli and emotional stress, and patients should avoid loud noises and QT-prolonging drugs. LQT3 involves SCN5A (the cardiac sodium channel), events typically occur at rest or during sleep, and beta-blockers are less effective; sodium channel blockers like mexiletine may help. Each genotype has distinct risk profiles and treatment nuances.
How does gender affect the QT interval?
Women have longer QTc intervals than men by approximately 10–20 ms on average, a difference that emerges after puberty and is attributed to androgens shortening and estrogens lengthening repolarization. This biologic difference means women have a narrower safety margin before reaching pathological QT prolongation and are two to three times more likely than men to develop Torsades de Pointes in the setting of QT-prolonging drugs or electrolyte abnormalities. Sex-specific QTc cutoffs (450 ms for males, 460 ms for females) are used in clinical practice to account for this difference.
See QT Interval in 3D
Explore ECG rhythms interactively with our simulator and 3D heart visualization synced beat-for-beat. See how electrical activity produces every wave on the tracing.
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