The QT interval indicates of the time from ventricular depolarisation (phase 0) to ventricular repolarisation (phases 1-3). It is the duration of activation and recovery of the ventricular myocardium.
The QT interval is best measured on lead II, V5 or V6. Measure the distance between the start of the Q wave and the end of the T wave.
Compare QT intervals between sequential ECGs in order to determine change in QT.The QT interval shortens with rapid heart rates and lengthens at slower heart rates, as a compensatory mechanism. In order to truly estimate risk it is important to correct for the heart rate, i.e. estimatinng what the QT interval would be at 60 beats per minute.
Adjust the QT interval according the to heart rate using the Bazett, Fridericia or Framingham method. The Bazett formula is the most commonly used, and is validated for heart rates between 60-100bpm. In the presence of tachycardia or bradycardia, one of the other two formulae should be used.
A prolonged QT interval represents delayed ventricular repolarisation, and increases the risk of a re-entry circuit from forming (i.e. Torsade de Pointes).
The QT interval is prolonged if it is >450ms in men, >460ms in women, or if there is an increase of >30ms in sequential ECG recordings.
The congenital long QT syndromes are a diverse group of diseases that predispose to ventricular tachyarrhythmias. The three most common are LQTS1, in which events are triggered by exercise; LQTS2, in which events are triggered by stress and loud noises; and LQTS3, in which events often occur during sleep. Other congenital causes are much rarer.
Many drugs can cause a prolonged QT interval; particularly certain antiarrhythmics, many antimicrobials, and many psychoactive drugs.
Electrolyte disturbances can cause prolonged QT intervals, as can severe hypothermia, sevre bradycardia, cardiovascular stress and cerebrovascular pathology.