The long QT interval

What it is

The QT interval runs from the start of the QRS to the end of the T wave and measures ventricular depolarisation plus repolarisation. Because it shortens as the heart rate rises, it is corrected for rate (QTc); Bazett's formula divides the QT by the square root of the RR interval in seconds, but it overcorrects at fast rates and undercorrects at slow ones, where Fridericia's cube-root formula is more accurate. A QTc above about 450 ms in men and 460 to 470 ms in women is prolonged, and above 500 ms the risk of torsades de pointes rises sharply. A quick check at normal heart rates: a QT longer than half the preceding RR interval is probably prolonged. The QT is measured in the lead where it is longest, usually II or V2–V3, from the QRS onset to where a tangent to the steepest down-slope of the T meets the baseline, leaving out any separate U wave. Long QT is either congenital or acquired. Congenital long QT syndrome comes from mutations in ion channels: type 1 (KCNQ1) with broad T waves and events during exercise, especially swimming; type 2 (KCNH2) with notched or bifid T waves and events triggered by sudden noise or emotion and in the postpartum period; and type 3 (SCN5A) with a long flat ST segment, a late T wave and events at rest or during sleep. Acquired prolongation is far more common: drugs (macrolides, fluoroquinolones, antipsychotics, methadone, ondansetron, tricyclic antidepressants, class IA and III antiarrhythmics), low potassium, magnesium or calcium, bradycardia, hypothermia, ischaemia and intracranial bleeding, and the causes often add up. The feared rhythm is torsades de pointes: a polymorphic ventricular tachycardia whose QRS axis twists around the baseline, often started by a short-long-short sequence of beats.

How to recognise it

• Measure from QRS onset to the end of T in the lead with the longest QT (often II or V2–V3); use the tangent method and exclude a separate U wave.
• Correct for rate: QTc by Bazett (QT divided by the square root of RR in seconds); prefer Fridericia below 60 or above 100 bpm.
• Prolonged: QTc above about 450 ms (men) or 460 to 470 ms (women); 500 ms or more, or a rise of more than 60 ms on a drug, is high risk.
• Quick screen at normal rates: QT longer than half the preceding RR interval is probably prolonged.
• T-wave clues: LQT1 broad-based T; LQT2 low, notched or bifid T; LQT3 long isoelectric ST with a late, narrow T.
• Warning signs on the tracing: T-wave alternans, pauses, ventricular ectopics landing on the T wave, runs of polymorphic VT.
• In bundle branch block or pacing the wide QRS lengthens the QT; use the JT interval or a QRS-adjusted method.

Why it happens

• The QT reflects the ventricular action potential; fewer outward potassium currents (IKr, IKs) or a late inward sodium current prolong repolarisation.
• A long repolarisation lets calcium channels reopen and cause early afterdepolarisations, which can trigger extra beats.
• Repolarisation becomes uneven across the ventricular wall, providing the substrate for re-entry and torsades de pointes.
• Most QT-prolonging drugs block the IKr (hERG) channel; low potassium makes that channel work less, so drugs and electrolytes add up.

Step by step

1. Find the lead with the longest QT and a clear T end, usually II or V2–V3 — the QT varies between leads.
2. Mark the T end with a tangent on its steepest down-slope — this avoids including a U wave.
3. Measure the RR interval and correct the QT for rate — the raw QT misleads at fast or slow rates.
4. Check the QRS width — a wide QRS adds to the QT without abnormal repolarisation.
5. Look at the T and U morphology — notched T, U waves or a long flat ST point to the cause.
6. Review drugs, electrolytes, heart rate and temperature — acquired causes are common and add up.

Congenital long QT: the three main types

Differential and pitfalls

• Measurement errors: counting the U wave as part of the T, using a lead with a flat T, and machine readings in noisy or wide-QRS tracings.
• Wide QRS (bundle branch block, pacing, hyperkalaemia) lengthens the QT without abnormal repolarisation.
• Hypocalcaemia lengthens the ST segment with a normal T; hypokalaemia gives T-U fusion.
• Torsades versus other polymorphic VT: polymorphic VT with a normal QT suggests acute ischaemia, not torsades, and is treated differently.
• Pitfall: one normal QTc does not exclude congenital long QT; repeat ECGs, exercise testing and family history help.
• Short QT (QTc under about 340 to 360 ms) is a separate rare channelopathy; also consider hypercalcaemia and digoxin.

Next step

• Torsades de pointes or QTc of 500 ms or more: continuous monitoring, defibrillator at hand, and call a senior.
• Torsades: IV magnesium sulfate as protocol sets; defibrillate if pulseless; overdrive pacing or isoprenaline for pause-dependent torsades with specialist advice.
• Stop every QT-prolonging drug and keep potassium and magnesium in the high-normal range; repeat the ECG.
• Suspected congenital long QT: cardiology review, beta-blockers as the specialist decides, family screening, and a list of drugs to avoid.
• Before starting a QT-prolonging drug in a patient at risk: baseline ECG, electrolytes and a repeat ECG after starting it.

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Elsewhere in DurgiPedia

• The ventricular action potential
• How arrhythmias arise
• ECG basics: waves, intervals and leads
• The ECG in potassium and calcium disorders
• Arrhythmias and sudden cardiac death

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Educational content; it does not replace supervised hands-on training, your institution's protocols or a prescriber's order. A procedure is learnt with a teacher and done only once you are trained to do it.

Sources: Long QT Syndrome (StatPearls (NCBI Bookshelf), 2022).

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