QT Interval

  • The QT interval is the time from the start of the Q wave to the end of the T wave.
  • It represents the time taken for ventricular depolarisation and repolarisation.

waves of the ecg

The QT interval is inversely proportional to heart rate:

  • The QT shortens at faster heart rates
  • The QT lengthens at slower heart rates
  • An abnormally prolonged QT is associated with an increased risk of ventricular arrhythmias, especially Torsades de Pointes.
  • The recently described congenital short QT syndrome has been found to be associated with an increased risk of paroxysmal atrial and ventricular fibrillation and sudden cardiac death.

How to measure QT

  • The QT interval should be measured in either lead II or V5-6
  • Several successive beats should be measured, with the maximum interval taken
  • Large U waves (> 1mm) that are fused to the T wave should be included in the measurement
  • Smaller U waves and those that are separate from the T wave should be excluded
  • The maximum slope intercept method is used to define the end of the T wave (see below)

The QT interval is defined from the beginning of the QRS complex to the end of the T wave. The maximum slope intercept method defines the end of the T wave as the intercept between the isoelectric line with the tangent drawn through the maximum down slope of the T wave (left). When notched T waves are present (right), the QT interval is measured from the beginning of the QRS complex extending to the intersection point between the isoelectric line and the tangent drawn from the maximum down slope of the second notch, T2

Corrected QT

  • The corrected QT interval (QTc) estimates the QT interval at a heart rate of 60 bpm.
  • This allows comparison of QT values over time at different heart rates and improves detection of patients at increased risk of arrhythmias.

There are multiple formulas used to estimate QTc (see below). It is not clear which formula is the most useful.

  • Bazett’s formula: QTC = QT / √ RR
  • Fredericia’s formula: QTC = QT / RR 1/3
  • Framingham formula: QTC = QT + 0.154 (1 – RR)
  • Hodges formula: QTC = QT + 1.75 (heart rate – 60)

NB. The RR interval is given in seconds (RR interval = 60 / heart rate).

  • Bazett’s formula is the most commonly used due to its simplicity. It over-corrects at heart rates > 100 bpm and under-corrects at heart rates < 60 bpm, but provides an adequate correction for heart rates ranging from 60 – 100 bpm.
  • At heart rates outside of the 60 – 100 bpm range, the Fredericia or Framingham corrections are more accurate and should be used instead.
  • If an ECG is fortuitously captured while the patient’s heart rate is 60 bpm, the absolute QT interval should be used instead!

There are now multiple i-phone apps that will calculate QTc for you (e.g. MedCalc), and the website MDCalc.com has a quick and easy QTc calculator that is free to use.

Normal QTc values

  • QTc is prolonged if > 440ms in men or > 460ms in women
  • QTc > 500 is associated with increased risk of torsades de pointes
  • QTc is abnormally short if < 350ms
  • A useful rule of thumb is that a normal QT is less than half the preceding RR interval

Causes of a prolonged QTc (>440ms)


Hypokalaemia causes apparent QTc prolongation in the limb leads (due to T-U fusion) with prominent U waves in the precordial leads.

Apparent QTc 500ms – prominent U waves in precordial leads (hypokalaemia (K+ 1.9))


QTc 510 ms secondary to hypomagnesaemia


Hypocalcaemia typically prolongs the ST segment, leaving the T wave unchanged.

QTc 510ms due to hypocalcaemia


Severe hypothermia can cause marked QTc prolongation, often in association with bradyarrhythmias (especially slow AF), Osborne waves and shivering artifact.

QTc 620 ms due to severe hypothermia

Myocardial Ischaemia

Myocardial ischemia tends to produce a modest increase in the QTc, in the 450-500 ms range. This may be useful in distinguishing hyperacute MI from benign early repolarization (both may produce similar hyperacute T waves, but BER will usually have a normal QTc).

QTc 495 ms due to hyperacute MI

Raised ICP

A sudden rise in intracranial pressure (e.g. due to subarachnoid haemorrhage) may produce characteristic T wave changes (‘cerebral T waves’): widespread, deep T wave inversions with a prolonged QTc.

QTc 630ms with widespread T wave inversion due to subarachnoid haemorrhage

Congenital Long QT Syndrome

There are several congenital disorders of ion channels that produce a long QT syndrome and are associated with increased risk of torsades de pointes and sudden cardiac death.

QTc 550ms due to congenital long QT syndrome

Causes of a short QTc (<350ms)


Hypercalcaemia leads to shortening of the ST segment and may be associated with the appearance of Osborne waves.

Marked shortening of the QTc (260ms) due to hypercalcaemia

Congenital short QT syndrome

  • Congenital short QT syndrome (SQTS) is an autosomal-dominant inherited disorder of potassium channels associated with an increased risk of paroxysmal atrial and ventricular fibrillation and sudden cardiac death.
  • The main ECG changes are very short QTc (<300-350ms) with tall, peaked T waves.

Very short QTc (280ms) with tall, peaked T waves due to congenital short QT syndrome

Short QT syndrome may be suggested by the presence of:

  • Lone atrial fibrillation in young adults
  • Family member with a short QT interval
  • Family history of sudden cardiac death
  • ECG showing QTc < 350 ms with tall, peaked T waves
  • Failure of the QT interval to increase as the heart rate slows

Very short QT (< 300ms) with peaked T waves in two patients with SQTS


Digoxin produces a relative shortening of the QT interval, along with downward sloping ST segment depression in the lateral leads (‘reverse tick’ appearance), widespread T-wave flattening and inversion, and a multitude of arrhythmias (ventricular ectopy, atrial tachycardia with block, sinus bradycardia, regularized AF, any type of AV block).

Short QT interval due to digoxin (QT 260 ms, QTc 320ms approx)

QT interval scale

Viskin (2009) proposes the use of a ‘QT interval scale’ to aid diagnosis of patients with short and long QT syndromes (once reversible causes have been excluded):

QT interval scale

Drug-induced QT-Prolongation and Torsades

  • In the context of acute poisoning with QT-prolonging agents, the risk of TdP is better described by the absolute rather than corrected QT.
  • More precisely, the risk of TdP is determined by considering both the absolute QT interval and the simultaneous heart rate (i.e. on the same ECG tracing).
  • These values are then plotted on the QT nomogram (below) to determine whether the patient is at risk of TdP.
  • A QT interval-heart rate pair that plots above the line indicates that the patient is at risk of TdP.
  • From the nomogram, you can see that QTc-prolonging drugs that are associated with a relative tachycardia (e.g. quetiapine) are much less likely to cause TdP than those that are associated with a relative bradycardia (e.g. amisulpride).
QT nomogram Polymorphic VT & Torsades de Pointes

Further Reading


  • Surawicz B, Knilans T. Chou’s Electrocardiography in Clinical Practice (6th edition), Saunders 2008.
  • Viskin S. The QT interval: too long, too short or just right. Heart Rhythm. 2009 May;6(5):711-5. Epub 2009 Mar 3. [PMID: 19389656] [Full text]
  • Wagner, GS. Marriott’s Practical Electrocardiography (11th edition), Lippincott Williams & Wilkins 2007.
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