QTc Calculator

Why the QT interval needs correcting

The QT interval on an electrocardiogram represents ventricular depolarisation and repolarisation. It shortens as heart rate rises and lengthens as it falls, which makes a raw measurement uninterpretable without knowing the rate.

Correction formulas normalise the interval to a heart rate of 60 beats per minute, producing QTc, so that measurements at different rates can be compared against a single threshold.

The correction is what makes the number usable and it is also where much of the error enters, because the formulas disagree substantially outside normal heart rates.

The formulas and where each fails

Bazett, from 1920, divides QT by the square root of the RR interval in seconds. It is the most widely used and it over-corrects at high heart rates and under-corrects at low ones.

Fridericia uses the cube root and performs better at extremes of heart rate. Framingham and Hodges use linear corrections and also outperform Bazett outside the normal range.

Bazett persists largely through inertia and because most reference thresholds were established using it. In tachycardia it can produce alarming QTc values that Fridericia does not, which is a recognised source of unnecessary concern.

The thresholds

Prolongation is generally defined as a QTc above 450 milliseconds in men and 460 in women. Above 500 is associated with substantially increased risk of torsades de pointes regardless of sex.

Short QT syndrome exists at the other end, with a QTc below about 340 milliseconds, and is a rare inherited arrhythmia syndrome.

The risk relationship is continuous rather than stepped. A QTc of 480 is not safe and 500 dangerous; risk rises progressively, and the thresholds mark where clinical action is generally warranted.

What prolongs it

A large number of drugs do, across many classes: several antiarrhythmics, antipsychotics, some antibiotics including macrolides and fluoroquinolones, antifungals, methadone and ondansetron among others.

Electrolyte disturbance is the other major cause: hypokalaemia, hypomagnesaemia and hypocalcaemia all prolong the interval, and they frequently coexist with the drugs.

Congenital long QT syndrome, bradycardia, myocardial ischaemia and hypothermia complete the common list. The risk is multiplicative rather than additive: a patient on two QT-prolonging drugs with a low potassium is in a considerably worse position than any one factor suggests.

Measuring it correctly

The QT interval is measured from the start of the QRS complex to the end of the T wave, using the lead where the T wave ends latest, conventionally lead II or V5.

Determining where the T wave ends is the difficult part, particularly where a U wave follows. The tangent method, drawing a tangent to the steepest downslope of the T wave and taking its intersection with the baseline, is the standard approach.

Automated measurements from ECG machines are reasonable and are wrong often enough that any clinically significant value should be measured manually. This page corrects a QT interval that someone else has measured, and the measurement is where most of the error lives.

Bundle branch block complicates the measurement in a way worth knowing about. Where the QRS is widened, part of the QT interval reflects delayed depolarisation rather than repolarisation, so the raw QT overstates the repolarisation time. Several correction approaches exist for this, commonly subtracting the excess QRS duration, and none is universally agreed. A prolonged QTc in the presence of a wide QRS should be interpreted with that in mind rather than taken at face value.