Vol IX · Chapter 1
Volume IX · Chapter 1 · 12 min read

The QT Interval

Measurement, correction, and the link between prolonged repolarization and sudden death.

The QT interval is the surface ECG reflection of ventricular repolarization. It measures the time from the start of the QRS complex (when depolarization begins) to the end of the T wave (when repolarization ends).

When the QT is prolonged, the ventricle stays electrically vulnerable for longer. Cells that should have fully recovered remain partially depolarized, and the membrane potential hovers in a range where L-type calcium channels can reactivate. This creates the conditions for early afterdepolarizations. If those EADs trigger propagated impulses in the setting of transmural dispersion, the result is Torsades de Pointes.

Understanding QT measurement is foundational. Every drug safety decision, every inherited arrhythmia evaluation, and every post-syncope workup depends on accurate QT assessment.

Measuring the QT Interval

The QT is measured from the earliest deflection of the QRS complex to the point where the T wave returns to baseline. Lead II or V5/V6 typically gives the clearest T-wave termination.

The tangent method improves reproducibility: draw a tangent along the steepest part of the T-wave downslope, then mark where that tangent crosses the isoelectric baseline. This defines the T-wave end more consistently than trying to identify where the signal "disappears" into noise.

U waves create a common pitfall. If a distinct U wave separates from the T wave with a clear return to baseline between them, exclude it from the QT measurement. If the U wave merges with the T wave without a clear nadir, include it. The merged T-U complex reflects prolonged repolarization and should be captured.

The QT interval varies with heart rate. At faster rates, action potential duration shortens, and the QT shortens with it. At slower rates, the QT lengthens. A raw QT of 480 ms means something very different at a heart rate of 50 than at a rate of 100. This rate-dependence means we need correction formulas.

Correcting for Heart Rate

Bazett's formula (QTc = QT / √RR) is the most widely used correction. It was derived in 1920 from a small dataset and remains the default in most automated ECG reports. Its limitation: it overcorrects at fast heart rates (making the QTc appear longer than it truly is) and undercorrects at slow rates (making the QTc appear shorter). At rates between 60 and 90 bpm, Bazett performs reasonably well.

Fridericia's formula (QTc = QT / RR1/3) uses a cube-root correction that handles rate extremes more accurately. Drug trials and regulatory agencies increasingly prefer Fridericia because it reduces the false positives that Bazett generates in tachycardic patients and the false negatives it generates in bradycardic ones.

Hodges' formula applies a linear correction (QTc = QT + 1.75 × (HR − 60)). It avoids the nonlinear distortions of Bazett and Fridericia entirely, though it is less commonly encountered in clinical practice.

When to use which? For routine clinical screening at normal heart rates, Bazett is adequate and universally understood. For patients with rates below 50 or above 90, Fridericia gives a more reliable answer. For research protocols evaluating drug-induced QT prolongation, Fridericia is the standard.

Transmural Dispersion of Repolarization

The ventricular wall is not electrically uniform. Three distinct cell populations repolarize at different rates. Epicardial cells repolarize first (their prominent Ito current gives them the shortest action potential). Endocardial cells repolarize next. Sandwiched between them, M-cells have the longest action potential duration and repolarize last.

The T wave on the surface ECG reflects the voltage gradient created by these different repolarization times. The peak of the T wave corresponds roughly to epicardial repolarization. The end of the T wave corresponds to M-cell repolarization. The interval from T-peak to T-end (Tp-Te) is a surrogate for transmural dispersion.

When the QT prolongs, M-cell action potentials lengthen disproportionately compared to epicardial and endocardial layers. This widens the temporal window during which adjacent cells exist in different refractory states: one layer fully recovered and excitable, the neighboring layer still refractory or partially refractory.

This dispersion is the substrate. A premature impulse arriving during this heterogeneous recovery can propagate through recovered tissue while blocking in refractory tissue. The result is unidirectional block and Phase 2 reentry, the cellular mechanism that initiates Torsades de Pointes.

QT Interval and Vulnerable Window
Normal QT QT = 380 ms Prolonged QT QT = 540 ms Vulnerable Window QRS T wave tangent

Left: normal QT interval. Right: prolonged QT with a widened vulnerable window (shaded) where early afterdepolarizations can trigger Torsades de Pointes. The tangent method defines T-wave offset.

Normal Values and Thresholds

QTc thresholds differ by sex because women have slightly longer baseline QT intervals, likely due to hormonal effects on repolarizing potassium currents.

Normal
Men: < 450 ms
Women: < 460 ms
Borderline
Men: 450–470 ms
Women: 460–480 ms
Prolonged
Men: > 470 ms
Women: > 480 ms

Key Takeaways

  • The QT interval measures total ventricular repolarization time, from the earliest QRS deflection to the end of the T wave.
  • Use the tangent method in lead II or V5/V6 for consistent measurement; include merged U waves but exclude discrete ones.
  • Bazett's correction works at normal rates but distorts at extremes; Fridericia is more reliable for tachycardia, bradycardia, and drug trials.
  • Prolonged QT widens transmural dispersion of repolarization, creating the substrate for early afterdepolarizations and Torsades de Pointes.
  • QTc thresholds are sex-specific: prolonged is above 470 ms in men and above 480 ms in women.
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