Corrected QT and Torsades Risk

Evidence & Pearls

1. The Measurement Is Where Most of the Error Lives

The arithmetic is exact and the measurement is not, so the corrected value can never be better than the QT that went into it.

• Measure from the first deflection of the QRS to where the T wave returns to the isoelectric line, in the lead where the T wave ends latest and is clearest, conventionally lead II or V5.
• Where the downslope is gradual, take the point at which a tangent to its steepest part crosses the baseline. Average three consecutive beats if the rhythm is regular.
• Exclude the U wave: a low, late, rounded deflection after the T wave belongs to the next part of repolarisation.
• The machine's reading is a screening figure: automated algorithms are reliable when the T wave is tall and clean and unreliable when it is flat, notched, biphasic or merged with a U wave, which is when the number matters. Do not stop a drug on an unconfirmed automated reading.

2. Why the Interval Has to Be Corrected

Repolarisation shortens as the rate rises, so the raw QT falls with tachycardia and lengthens with bradycardia in every normal heart. Correction restates the interval as what it would have been at 60 beats per minute, the only form in which two ECGs, or one ECG before and after a drug, can be set beside each other.

It is an empirical fit to population data, not a physiological law, so five formulas exist and none is right for everybody. All five agree exactly at a rate of 60, where the RR interval is one second, and diverge either side of it, differing by more than 50 ms at the extremes, which is the width of the whole decision.

3. The Five Formulas, and Which the Heart Rate Allows

This tool prints all five and leads with Fridericia. A single number invites the reader to treat it as the answer, when the formulas disagree and the heart rate decides whether the disagreement matters. Between 60 and 100 beats/min they converge; outside that, the gap between Bazett and Fridericia is the error you would have carried had you read the machine.

4. Where the Thresholds Come From, and Where They Disagree

Three conventions are in circulation. This tool uses the first and prints the rest rather than settling between them: the primary 2009 standardisation statement could not be read directly while this tool was built.

Above 500 ms every convention agrees, and that is where the weight lies: the risk of torsades de pointes rises steeply there. The 2010 American Heart Association statement on preventing torsades in hospital reviews the drug list at a QTc above 500 ms or a rise of more than 60 ms from the patient's own baseline. The disagreement bites only on women with a QTc between 461 and 470, prolonged here and borderline on the second convention.

A QTc below 350 ms is worth a second look rather than a diagnosis. The 2022 European Society of Cardiology guideline considers short QT syndrome at 320 ms or less, and diagnoses it at 360 ms or less with a pathogenic variant, a family history or a survived arrest. Hypercalcaemia, digoxin effect and hyperthermia shorten the interval far more often than the syndrome does.

5. The Wide QRS Problem

When the QRS is wide, part of the measured QT is the extra time the ventricles took to depolarise, and the interval is long without repolarisation being abnormal. Read as drug-induced prolongation, that stops a drug the patient needed.

• The Bogossian correction: subtract 48.5 per cent of the QRS duration from the measured QT, close enough at the bedside to half the QRS, then rate-correct as usual. Derived in left bundle branch block and validated again in right ventricular pacing.
• Applied here in left bundle branch block and ventricular pacing.
• Not applied in right bundle branch block or non-specific intraventricular conduction delay, where it has not been established. There the corrected interval cannot be read reliably: use the JT interval, the QT minus the QRS, or a cardiology opinion.

6. The Drug List, and the Indian Prescribing Reality

CredibleMeds, maintained by AZCERT, is the reference list. Its four categories:

• Known risk: prolongs the QT and has caused torsades even when taken as directed.
• Possible risk: prolongs the QT, with no established evidence of torsades on ordinary use.
• Conditional risk: torsades only in defined circumstances, such as overdose, an interaction, hypokalaemia or an inherited long QT.
• Special risk: to be avoided in congenital long QT syndrome for other reasons, largely the sympathomimetics.

The table is a working subset of agents in common Indian use, from the list revised on 12 December 2023. It is a teaching aid with a date on it, not a live register: crediblemeds.org is the authority and the categories move.

Three are prescribed here at a volume with no parallel elsewhere, and a patient can arrive on all three without any single prescriber having considered the QT.

• Levosulpiride, known risk, sold for functional dyspepsia and often continued for months.
• Domperidone, known risk, dispensed for nausea with very little scrutiny, and restricted in Europe for this reason.
• Ondansetron, given almost reflexively for vomiting, including to patients vomiting because they are hypokalaemic, which stacks the two mechanisms.

Amiodarone is the recognised exception. It prolongs the QT in almost everyone, yet torsades on it is uncommon: it blocks several currents rather than the rapid potassium current alone and produces little transmural dispersion of repolarisation. A long QTc on amiodarone is expected and is not by itself a reason to stop it. It remains on the Known Risk of TdP list revised on 12 December 2023 and sits in the known-risk row above. Until 24 August 2026 this table gave it no category at all. That was our error.

7. The Electrolytes, and Torsades in Progress

Hypokalaemia, hypomagnesaemia and hypocalcaemia each prolong repolarisation and travel together: diarrhoeal illness, diuretics, alcohol use and refeeding produce all three at once. Correcting potassium without magnesium fails, because magnesium is required for the cell to retain potassium, so a resistant hypokalaemia is a magnesium problem until proved otherwise. Hypocalcaemia is the exception. It lengthens the ST segment and leaves the T wave much as it was.

If torsades de pointes occurs:

• Magnesium sulphate whether or not the serum magnesium is low: the action here is on the membrane, not on a deficiency. The Indian ampoule is usually 50 per cent magnesium sulphate, in which 2 g is 4 mL, intravenously over 10 to 15 minutes, repeated once if the rhythm returns.
• Stop every contributing drug and replace potassium to the upper half of the normal range.
• Treat the pause-dependence. Torsades is characteristically initiated after a pause, so raise the rate with isoprenaline or temporary pacing to about 90 to 110 beats per minute where magnesium alone has not worked.
• Defibrillate a sustained, haemodynamically unstable episode as ventricular fibrillation.

8. QT Monitoring Under the National Tuberculosis Elimination Programme

Drug-resistant regimens stack QT-prolonging agents for months: bedaquiline and delamanid at possible risk, moxifloxacin at known risk, clofazimine at conditional risk. The guidance specifies Fridericia, not the Bazett value the machine prints, the formula used in the phase II studies of bedaquiline and delamanid and in the STREAM trial.

• Where ECGs are available often: baseline, week 2, week 4, then every 4 weeks.
• Where they are not: baseline, week 4, week 8, week 24, with additional ECGs whenever clinically indicated.

ECG monitoring is not critical for levofloxacin, whose effect on the QT is small; moxifloxacin's larger effect does warrant monitoring alongside other QT-prolonging agents. In a regimen that already holds bedaquiline and clofazimine, that is a real choice of fluoroquinolone.

Indian data. Among 70 patients in Mumbai given bedaquiline and delamanid concomitantly under programmatic conditions, QTcF prolongation was recorded in about 7 per cent and only two exceeded 500 ms, both within the first month and neither subsequently. The rate was lower than in comparable series, and it argues for concentrating a district programme's scarce ECG capacity in the first four to eight weeks.

9. The Poisoned Patient

Here the QT marks both the poison's effect on repolarisation and the severity. In organophosphorus poisoning, among the commonest reasons for an intensive care admission in rural southern India, a prolonged QTc at presentation has repeatedly been associated with respiratory failure, the need for ventilation and mortality. It costs one ECG and arrives before any cholinesterase assay.

The formulas are least reliable here, because poisoned patients are frequently tachycardic and Bazett over-corrects hardest there. The toxicological literature prefers the Chan and Isbister nomogram, which plots the uncorrected QT against the heart rate and treats a point above the boundary line as at risk. This tool does not implement it: the coordinates of the line could not be obtained from a primary source, and a boundary reconstructed from a picture would be a confident wrong number where the decision is time-critical. Plot it from the published figure. Rautaharju is the closest of the five to usable at a high heart rate.

10. What This Tool Does Not Print

• A diagnosis of congenital long QT syndrome. That needs repeated ECGs, a family and syncope history and often genetic testing, and the Schwartz score which formalises it is not reproduced here.
• A recommendation to stop any named drug, because the decision depends on what the drug is treating.
• A reading of an ECG image.
• The Chan and Isbister nomogram, for the reason given in section 9.

The Tisdale score beside the interval answers a different question: the interval says whether repolarisation is prolonged on this ECG, the score says how likely this patient is to develop prolongation during the admission. A patient can score high with a normal QTc today, which is what the score was built to find.