The QT interval is the duration of time from the beginning of the QRS complex to the end of the T wave. This correlates to the summated action potential duration of all ventricular cardiomyocytes.

Measurement of the QT Interval

In order to accurately measure the QT interval, we have to try to omit the U wave from the QT interval, as it does not correlate with the picture of ventricular repolarization we are trying to attain with the QT interval. However, because U waves have low prominence or may fuse with the T wave, we may unintentionally incorporate them in our QT interval measurement.

We can do this using the maximum slope intercept method to measure the QT interval.

When measuring QT, ignore small U waves that are fused to the T wave.

Ignore all U waves, regardless of size, if they are separate from the T wave.

If there is a tall U wave fused with the T wave, as shown, you do include it. This is equivalent to choosing the tangent line with the maximum downward slope.

Rate Correction of the QT Interval

Action Potential Restitution

The QT interval changes with heart rate. The faster the heart rate, the shorter the QT interval (and hence, the action potential duration). This is known as action potential restitution, wherein the action potential duration is affected by the preceding diastolic interval (a.k.a. the time during which the heart is completely repolarized and relaxed). 

It is thought to be an adaptive mechanism to preserve diastolic filling times at faster heart rates. The action potential duration is essentially the time it takes the heart to fully relax. With a faster heart rate, the goal is to relax quicker (i.e. the action potential duration) so we allow more time for diastolic filling, which improves cardiac output as well as coronary perfusion.

On the ECG, we can think of the QT interval being related to the preceding R-R interval. The longer the R-R interval preceding the QT interval, the longer the QT interval will be. This is demonstrated in the diagram below, where you can see the QT interval shortens after a short preceding R-R interval (in green) caused by a premature atrial beat.

There is no strong evidence suggesting the superiority of one formula over another. None of the formulas have shown a strong correlation to mortality.

That being said, here are some rules of thumb that may be useful in determining which formula to use:

• If HR 60-100: use Bazett’s.

• If HR >100 or <60: use Fredericia’s, Framingham’s, or Hodge's formula. Bazett’s overestimates if HR>100 and underestimates if HR < 60.

• If HR exactly 60: just use the absolute QT interval – no need for correction.

Note: These formulas can be found on MDCalc.

When is Absolute QT Better than Corrected QT?

In the context of drug-induced QT prolongation, the absolute QT value is more useful than the corrected QT.

This is because there’s an evidence-based tool, the QT nomogram developed by Chan et al, to better predict the risk of deadly arrhythmia (Torsades de pointes). This tool requires the absolute QT interval as an input. Note that the nomogram essentially does the rate correction for you.

The Significance of Long QT Intervals

The reason QTc is measured is because an aberration in this value can suggest an elevated risk of potentially fatal ventricular arrhythmias. A deeper dive is taken in the Torsades de pointes section, but the basics will be covered here.

As mentioned in the section on The T and U Waves, ventricular repolarization happens in a very organized fashion from epicardium to endocardium, due to the normal transmural dispersion of repolarization.

A prolonged QTc signifies an extended action potential duration, which may result in prolonged repolarization (I use "may" as this can, in some cases, be associated with prolonged depolarization, discussed below). Lengthened repolarization implies a longer relative refractory period for the ventricular cardiomyocytes. Moreover, the action potential prolongation during long QT may not affect all cardiomyocytes uniformly – certain cells may become absolutely refractory while others are simultaneously in a relatively refractory state. This phenomenon disrupts the usual transmural dispersion of repolarization, creating a myocardial landscape of varied refractoriness. Within this landscape, "islands" of absolute refractoriness can exist within "seas" of relative refractoriness, elevating the risk of arrhythmogenic reentrant circuits (discussed in the Mechanisms of Arrhythmogenesis section). This is known as the vulnerable period of the heart.

Take notice of the animation above on the right ("Prolonged QT"). Because repolarization is occurring slower, patches of absolutely refractory tissue (in blue) start forming with the backdrop of relatively refractory tissue (in red). This heterogeneity juxtaposes with the uniform pattern of repolarization observed in the animation on the left ("Normal QT"). This heterogeneity of repolarization that is evoked by long QT can increase the risk of deadly reentrant rhythms.

Correcting for QRS Width

Because it is prolonged repolarization that leads to the heterogeneous excitability amenable to arrhythmias, any long QT related primarily to a wide QRS is less worrisome.

Short QT

Similarly, short QTc <350 ms is also associated with an increased risk of mortality due to increased arrhythmogenicity (propensity to allow arrhythmias). 

The mechanism of arrhythmias is not as well understood as that for long QT. However, this mechanism is explored further in the Short QT Syndrome section.