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.
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.
Try It Yourself: From Long QT to Torsades
This is a single ventricular action potential. Block the repolarizing potassium current (IKr), lower the serum potassium, or add a pause. Watch repolarization stretch, an early afterdepolarization rise on the downslope, and, once it reaches threshold, fire a triggered beat: the pathway to Torsades.
How the EP Lab Tests It
The surface QT is a summed shadow of ventricular repolarization, so it cannot show us the membrane events that matter. A monophasic action potential (MAP) catheter, a contact electrode pressed against the endocardium, records the local repolarization waveform directly. On a prolonged-QT substrate the MAP shows a stretched Phase 3, and we can watch the early afterdepolarizations ride on that slow downslope: a small hump of reactivated inward current at the moment the T wave is inscribed on the 12-lead.
Dispersion has been demonstrated the same way. Recording MAPs across the ventricular wall, or arterially perfused wedge preparations with electrodes at epicardium, midmyocardium, and endocardium, confirms that M cells repolarize latest and that their action potential lengthens disproportionately when the QT prolongs. The T-peak marks epicardial recovery and the T-end marks M-cell recovery, which is why we read the Tp-Te interval on the surface tracing as a surrogate for that transmural spread.
At the bedside the unstable substrate announces itself on telemetry. T-wave alternans, a beat-to-beat swing in T-wave amplitude, signals that repolarization is dispersing enough to alternate. A premature beat followed by a compensatory pause lengthens the QT of the next beat, and the short-long-short sequence that lands a beat on that pause-prolonged T wave is the classic setup for Torsades. QTc by Bazett or Fridericia normalizes the QT to a standard rate so the corrected value is comparable across heart rates; a QTc of 500 ms flags the same risk at 50 bpm and at 100. Bazett overcorrects at fast rates and undercorrects at slow ones, so we often prefer Fridericia at the extremes.
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.
Quick Reference
Key Terms
Time from QRS onset to T-wave end; reflects total ventricular repolarization duration.
QTc = QT / √RR. Simple but overcorrects at fast rates and undercorrects at slow rates.
Mid-myocardial cells with the longest action potential duration; primary source of transmural dispersion.
Differences in repolarization timing across the ventricular wall that create the substrate for reentry.
Core Insight
The QT interval is a single number, but the danger it reflects is spatial. Prolonged QT means adjacent cells recover at different times, and that temporal heterogeneity is what allows wavefronts to find excitable pathways next to refractory ones.