Overview
The QT interval extends from the start of ventricular depolarisation to the end of repolarisation. It varies with heart rate, so clinicians use a corrected value, QTc, to support comparison and risk assessment. QTc prolongation can reflect congenital channel disease, medicines, electrolyte disturbance, bradycardia, structural heart disease or acute illness. It is associated with risk of torsades de pointes, but QTc alone does not determine whether an individual patient will develop an arrhythmia.
Historical development
Early electrocardiographers recognised that QT duration shortened as heart rate increased. Bazett proposed a square-root correction in the 1920s, and it became embedded in ECG machines and clinical practice. Subsequent formulas, including Fridericia, Framingham and Hodges, were developed to reduce systematic error at very high or low heart rates. The persistence of several formulas reflects the absence of one correction that performs perfectly across every rhythm, rate and population.
How to measure the QT interval
Measure from the beginning of the QRS complex to the end of the T wave in a lead with a clear termination, commonly lead II or V5/V6. The tangent method can help identify the end of the T wave. Exclude a separate U wave, but recognise that T–U fusion can make measurement uncertain. Average several beats when rhythm is regular. In atrial fibrillation, variability complicates assessment and several beats at different cycle lengths may be needed.
Correction formulas
Bazett divides QT by the square root of the RR interval and tends to overcorrect during tachycardia and undercorrect during bradycardia. Fridericia uses the cube root and often performs better across a wider rate range. Framingham and Hodges use linear approaches. The chosen formula should be documented when it matters. Comparing serial ECGs is most meaningful when the same method is used and the underlying rhythm and QRS duration are considered.
Automated versus manual measurement
Automated ECG values are convenient but can be wrong when T waves are flat, notched or merged with U waves; when there is artefact; or when the rhythm or QRS is abnormal. A value that will change medication or trigger escalation should be checked manually. Computer algorithms may also apply different correction formulas. Review the tracing itself rather than relying solely on the printed QTc.
What constitutes prolongation
Thresholds vary by sex, age, method and guideline. Risk is continuous rather than binary. A QTc above about 500 ms is commonly associated with a pronounced increase in torsades risk, and a substantial rise from baseline can also be important. Borderline values should be interpreted with symptoms, family history, medication exposure and reversible risk factors. Congenital long-QT syndrome cannot be diagnosed from a single automated value alone.
Torsades de pointes
Torsades is a polymorphic ventricular tachycardia associated with prolonged repolarisation. It may terminate spontaneously, recur or deteriorate into ventricular fibrillation. Typical triggers involve early afterdepolarisations in a vulnerable myocardium. Risk is greatest when QT prolongation coexists with bradycardia or pauses, hypokalaemia, hypomagnesaemia, structural heart disease, female sex, advanced age, renal or hepatic impairment and multiple QT-prolonging medicines.
Drug-induced QT prolongation
Medicines can block cardiac potassium currents or alter exposure to other QT-prolonging drugs through pharmacokinetic interactions. Risk depends on dose, concentration, renal and hepatic clearance, electrolyte state and patient susceptibility. Review prescription, over-the-counter and recently stopped medicines. Use a recognised, actively maintained drug-risk resource rather than memory alone. Avoid combining several risk drugs where alternatives exist and monitor when treatment is necessary.
Electrolytes and reversible factors
Low potassium and magnesium increase arrhythmic risk, and hypocalcaemia can prolong repolarisation. Correct abnormalities promptly, especially in symptomatic patients or when QTc is markedly prolonged. Review vomiting, diarrhoea, diuretic use, refeeding, insulin therapy and other causes. Treat bradycardia, ischaemia and acute neurological or systemic illness where relevant. Correction of the QTc number is not the goal; correction of the arrhythmogenic environment is.
Wide QRS and paced rhythms
Bundle branch block and ventricular pacing lengthen the QT because depolarisation is prolonged. Standard QTc may therefore overstate repolarisation abnormality. The JT interval or adjusted approaches may be considered, but methods vary and specialist interpretation is often appropriate. Do not apply ordinary narrow-QRS thresholds mechanically. Compare with previous ECGs and assess the reason for QRS widening.
Clinical assessment pathway
For an unexpected prolonged QTc, verify the measurement and formula, review prior ECGs, check electrolytes and renal function, and assess medicines and interactions. Ask about syncope, seizures, palpitations, sudden deaths and known long-QT syndrome in relatives. Marked prolongation, ventricular arrhythmia, exertional or emotional syncope, or strong family history warrants urgent cardiology input. Genetic evaluation may be appropriate when congenital disease is suspected.
Management of severe prolongation
Stop or substitute non-essential offending medicines, correct electrolytes and provide monitoring according to risk. Torsades with instability requires immediate resuscitation and defibrillation as appropriate. Intravenous magnesium is commonly used, and recurrent pause-dependent torsades may require increasing heart rate through pacing or pharmacological measures under specialist direction. Management must follow emergency protocols and local guidance.
Monitoring and communication
Document the measured QT, QTc, formula, heart rate, rhythm, QRS duration, relevant drugs and electrolytes. Communicate clearly at transitions of care. Patients with significant drug-related prolongation should understand which medicine was implicated and when reassessment is needed. Avoid labelling a patient with congenital long-QT syndrome without adequate evaluation, because the diagnosis has long-term implications for treatment and relatives.
Frequently asked questions
Which QT correction formula is best?
No formula is universally best. Fridericia often behaves better than Bazett at rate extremes, but context and consistency matter.
Does QTc above 500 ms guarantee torsades?
No, but it is a widely recognised high-risk marker that warrants urgent review.
Can a normal QTc exclude congenital long-QT syndrome?
No. Intermittent or concealed disease can occur.
Should automated QTc always be accepted?
No. Manually verify values that influence management.
Key points for practice
- Inspect the ECG and verify important automated measurements.
- Document the correction formula and heart rate.
- Review all medicines, interactions and electrolytes.
- Recognise the importance of QTc above 500 ms and major change from baseline.
- Interpret wide-QRS rhythms differently.
- Escalate syncope, arrhythmia or suspected congenital disease.
Clinical pearls and professional practice
Use the result to answer a clearly defined clinical question. Calculations and thresholds are most useful when they are embedded in a structured assessment that includes history, examination, baseline risk, time course and response to treatment. A result should change a decision, refine a differential diagnosis or prompt monitoring; otherwise, repeating it without a plan may add noise rather than value.
When handing over care, communicate the actual value, the relevant reference interval or threshold, the trend and the interpretation. Avoid shorthand that can be misunderstood by another team. Where local protocols differ from a general reference, the local validated pathway takes precedence. Document uncertainty explicitly and identify what subsequent finding would confirm or refute the working diagnosis.
Equity and population context also matter. Diagnostic equations and thresholds may perform differently at age extremes, in pregnancy, in people with unusual body composition and in populations under-represented in validation studies. Clinicians should recognise these limitations without withholding appropriate investigation. Specialist or laboratory advice is valuable when a result does not fit the clinical picture.
Quality and safety checklist
- Confirm patient identity, sample timing and measurement method.
- Check units and the local reference interval.
- Compare with previous values and the clinical trajectory.
- Review medicines, comorbidities and reversible factors.
- Look for conditions in which the test or equation is unreliable.
- Record the interpretation, action and follow-up plan.
- Escalate immediately when the patient is unstable, regardless of a reassuring calculation.
Clinical interpretation should remain proportionate to the decision being made. Reassess when new information becomes available, and avoid allowing a single numerical result to outweigh clear evidence of deterioration or an alternative diagnosis. Multidisciplinary discussion improves safety when treatment carries substantial benefit and risk.
Manual verification of the QT interval
Automated ECG measurements are useful screening tools but may be unreliable with abnormal T-wave morphology, U waves, bundle branch block, pacing, atrial fibrillation or artefact. When the result affects treatment, inspect the tracing and measure in a lead with a clear T-wave end, often lead II or V5. Use a consistent method and average several beats when rhythm varies. The QT should be measured from the start of the QRS complex to the end of ventricular repolarisation.
Choosing a correction formula
Bazett correction is widely reported but tends to overcorrect at faster heart rates and undercorrect at slower rates. Fridericia often performs better across a broader range and is commonly preferred in drug-safety work, while Framingham and Hodges are alternatives. The formula, heart rate and raw QT should be documented. Apparent change can reflect a change in rate or formula rather than a true alteration in repolarisation.
Assessing risk rather than a single threshold
Risk of torsades de pointes rises with greater QT prolongation, but no threshold perfectly separates safe from unsafe. A QTc above 500 ms or an increase of around 60 ms from baseline is generally concerning, especially with bradycardia, hypokalaemia, hypomagnesaemia, structural heart disease, female sex, congenital long-QT syndrome or multiple QT-prolonging medicines. Clinical urgency depends on symptoms, ventricular ectopy and the modifiability of risk factors.
Medication review
Review all prescribed, over-the-counter and recently stopped medicines, including pharmacokinetic interactions that increase exposure. Correct potassium, magnesium and calcium abnormalities, address bradycardia and discontinue non-essential QT-prolonging agents where safe. A specialist drug-risk resource can help classify medicines, but individual susceptibility and combinations remain important. Decisions should balance arrhythmic risk against the benefit of treating the underlying condition.
Wide QRS complexes and pacing
Bundle branch block and ventricular pacing lengthen the QT partly because depolarisation is prolonged. Direct QTc interpretation can therefore exaggerate repolarisation delay. Approaches using the JT interval or adjusted formulas may be considered, ideally with cardiology or electrophysiology input when the decision is consequential. Serial comparison using the same method is often more informative than a single automated value.
Escalation and follow-up
Syncope, documented ventricular arrhythmia, marked QT prolongation or suspected congenital long-QT syndrome warrants urgent assessment. Continuous monitoring may be needed during correction of reversible factors or initiation of high-risk therapy. After recovery, record the suspected cause, offending medicines and follow-up plan so that the risk is visible to future prescribers.