Corrected QT (QTc) Calculator
Calculates the heart-rate-corrected QT interval using Bazett, Fridericia, and Framingham formulas. Essential for identifying prolonged QT — a risk factor for Torsades de Pointes and sudden cardiac death — and for monitoring QT-prolonging medications.
Calculate QTc
Enter the measured QT interval (in milliseconds) and heart rate (in bpm) from the patient’s ECG. All three correction formulas are calculated simultaneously. The Bazett formula is most widely used; Fridericia is preferred at heart rates outside the 60–100 bpm range.
Measure the QT interval from the onset of the QRS complex to the end of the T wave, ideally in leads II or V5–V6 where the T wave is usually best defined. Avoid leads where the T wave is flat, biphasic, or merged with a U wave. If U waves are present, measure to the nadir between the T and U waves, not the end of the U wave. Use the longest QT across multiple leads.
Understanding QTc
The QT interval on an ECG represents the total duration of ventricular depolarisation and repolarisation — from the start of the QRS complex to the end of the T wave. It is the electrical correlate of the ventricular action potential. A prolonged QT interval indicates delayed repolarisation, which creates a vulnerable window for early afterdepolarisations and the potentially fatal polymorphic ventricular tachycardia known as Torsades de Pointes (TdP).
Because the QT interval shortens physiologically with faster heart rates, a raw QT measurement cannot be compared against a single threshold. The corrected QT (QTc) adjusts the measured QT for heart rate, allowing comparison against standardised normal values regardless of the patient’s heart rate at the time of the ECG.
Bazett (1920)
QTc = QT / √RR
The most widely used formula. Tends to overcorrect at high HR (overestimates QTc) and undercorrect at low HR. Best accuracy at HR 60–100 bpm.
Fridericia (1920)
QTc = QT / ∘RR
Uses the cube root of RR. More accurate than Bazett at heart rates outside 60–100 bpm. Increasingly recommended by guidelines and the FDA for drug safety studies.
Framingham (1992)
QTc = QT + 0.154 × (1 − RR) × 1000
A linear correction derived from the Framingham Heart Study cohort. Avoids the overcorrection problem at high HR. Less commonly used but provides a useful comparator.
Key distinction: All three formulas use the RR interval (in seconds), derived as RR = 60 / Heart Rate. The Bazett formula dominates clinical practice and drug labelling, but its accuracy degrades outside normal heart rate ranges. For tachycardic or bradycardic patients, Fridericia is generally preferred. Providing all three values allows clinicians to make a balanced assessment.
Interpreting QTc Values
Normal QTc thresholds differ by sex. Women have a physiologically longer QT interval than men, and sex-specific cut-offs should always be applied. The values below apply to adults using the Bazett formula — other formulas may yield slightly different absolute values, but the clinical thresholds remain the same.
| QTc (ms) | Males | Females | Clinical Significance |
|---|---|---|---|
| < 390 | Normal | Normal | Within normal limits. No action needed. |
| 390 – 450 | Normal | Normal (up to 460) | Normal range. Upper limit is 450 ms for males, 460 ms for females. |
| 450 – 470 | Borderline / Prolonged | Borderline (460–470) | Borderline prolongation. Review medications. Repeat ECG. Check electrolytes (K⁺, Mg²⁺, Ca²⁺). |
| 470 – 500 | Prolonged | Prolonged | Clinically significant prolongation. Increased TdP risk. Discontinue offending drugs. Correct electrolytes. Cardiology review. |
| > 500 | Markedly Prolonged | Markedly Prolonged | High risk of TdP and sudden cardiac death. Urgent action needed. Consider cardiac monitoring, IV magnesium, and temporary pacing if symptomatic. |
| < 340 | Short QT | Short QT | May indicate short QT syndrome — a rare channelopathy associated with atrial fibrillation and sudden cardiac death. Cardiology referral warranted. |
A QTc > 500 ms is the most widely cited threshold for high risk of TdP. However, the absolute risk per patient depends on additional factors: rate of QT prolongation, presence of bradycardia, hypokalaemia, hypomagnesaemia, female sex, structural heart disease, and the number of QT-prolonging drugs. A QTc of 480 ms in a patient on three QT-prolonging drugs with K⁺ of 3.0 may carry more risk than a QTc of 510 ms in an otherwise healthy patient with congenital long QT.
Causes of QT Prolongation & Clinical Approach
QT prolongation may be congenital (channelopathies) or acquired (drugs, electrolyte disturbances, structural heart disease). Acquired causes are far more common and are usually reversible. Identifying and addressing the cause is the cornerstone of management.
Acquired Causes
Drug-induced QT prolongation is the most common acquired cause and the leading reason for post-marketing drug withdrawals. Drugs prolong the QT by blocking the hERG (IKr) potassium channel, delaying ventricular repolarisation. The risk is dose-dependent and compounded by drug interactions, hepatic/renal impairment, and pharmacogenomic variation.
High-risk drug classes:
- Antiarrhythmics: Sotalol, amiodarone, dofetilide, procainamide, quinidine — highest risk class. Amiodarone paradoxically causes QT prolongation but has a lower TdP rate than other Class III agents due to its multi-channel effects.
- Antibiotics: Macrolides (erythromycin, azithromycin, clarithromycin), fluoroquinolones (moxifloxacin > levofloxacin > ciprofloxacin), pentamidine, hydroxychloroquine.
- Antipsychotics: Haloperidol (especially IV), thioridazine, ziprasidone, pimozide. Most atypical antipsychotics carry some QT risk.
- Antiemetics: Ondansetron (dose-dependent, particularly IV > 16 mg), domperidone, droperidol.
- Antidepressants: Citalopram, escitalopram (dose caps exist specifically for QT risk), tricyclic antidepressants in overdose.
- Others: Methadone, sumatriptan, some antihistamines (terfenadine — withdrawn), antifungals (ketoconazole, fluconazole).
Always check CredibleMeds (crediblemeds.org) for the most current QT risk classification of any medication.
Electrolyte abnormalities directly affect cardiac ion channel function and are among the most important — and most correctable — causes of QT prolongation.
- Hypokalaemia: Low extracellular K⁺ reduces IKr channel conductance, prolonging repolarisation. Even mild hypokalaemia (3.0–3.5 mEq/L) can significantly prolong the QT, especially in patients on QT-prolonging drugs. Target K⁺ > 4.0 mEq/L in patients at risk of TdP.
- Hypomagnesaemia: Magnesium is a cofactor for multiple cardiac ion channels. Low Mg²⁺ predisposes to TdP even when the QTc is only modestly prolonged. IV magnesium is the first-line treatment for TdP regardless of the serum magnesium level. Target Mg²⁺ > 2.0 mg/dL in at-risk patients.
- Hypocalcaemia: Prolongs the ST segment and therefore the overall QT interval. Seen in hypoparathyroidism, vitamin D deficiency, pancreatitis, and massive transfusion. Correct calcium alongside other electrolytes.
Structural and systemic conditions can prolong the QT through myocardial remodelling, ischaemia, or autonomic dysfunction.
- Acute myocardial ischaemia/infarction: Ischaemia disrupts repolarisation and can transiently or persistently prolong QT. A new QT prolongation in the context of chest pain should raise suspicion for ACS.
- Cardiomyopathy and heart failure: Myocardial fibrosis and remodelling alter conduction pathways and repolarisation. Patients with reduced LVEF are at increased risk of TdP when exposed to QT-prolonging drugs.
- Bradycardia: Slower heart rates are independently associated with longer QT intervals and increased TdP risk. Complete heart block with QT prolongation is a high-risk scenario.
- Hypothyroidism: Slows cardiac conduction and prolongs repolarisation. QT normalises with thyroid replacement. Severe hypothyroidism may also cause bradycardia, compounding the risk.
- Hypothermia: Prolongs all ECG intervals including the QT. Osborn (J) waves are a classic finding. QT normalises with rewarming.
- Raised intracranial pressure: Subarachnoid haemorrhage in particular can cause dramatic QT prolongation and T-wave changes (cerebral T waves) via sympathetic surge.
Congenital Long QT Syndromes
Congenital long QT syndrome encompasses a group of inherited channelopathies with characteristic ECG patterns and distinct arrhythmia triggers. The three most common types account for approximately 90% of genotyped cases.
- LQT1 (KCNQ1 — IKs channel): The most common type (~35%). Events are typically triggered by exercise, especially swimming. ECG shows broad-based T waves. Beta-blockers are highly effective. Avoid competitive sports.
- LQT2 (KCNH2/hERG — IKr channel): Second most common (~30%). Events triggered by auditory stimuli (alarm clocks, phone ringing) and emotional stress. ECG shows low-amplitude, notched, or bifid T waves. Beta-blockers are effective but less so than in LQT1. Avoid sudden loud noises during sleep.
- LQT3 (SCN5A — sodium channel): Less common (~10%). Events occur at rest or during sleep. ECG shows late-onset, peaked T waves with a long isoelectric ST segment. Beta-blockers are less effective; mexiletine (sodium channel blocker) may shorten the QT. ICD is often recommended.
Diagnosis is supported by the Schwartz score (clinical criteria) and confirmed by genetic testing. Family screening with ECG is recommended for all first-degree relatives of affected individuals.
Short QT syndrome (SQTS) is a rare congenital channelopathy characterised by a QTc < 340 ms, tall peaked T waves, and a propensity for atrial fibrillation, ventricular fibrillation, and sudden cardiac death. It was first described in 2000. Unlike LQTS, there is no effective pharmacological therapy — ICD implantation is the primary treatment. Quinidine has shown some benefit in prolonging the QT in SQTS but evidence is limited. Consider SQTS when the QTc is persistently < 340 ms without a clear secondary cause (e.g., hypercalcaemia, digoxin, acidosis).
Step 1: Calculate QTc (use Fridericia if HR is < 60 or > 100). Step 2: If prolonged, check K⁺, Mg²⁺, Ca²⁺ and correct aggressively (target K⁺ > 4.0, Mg²⁺ > 2.0). Step 3: Review all medications against a QT drug list (CredibleMeds). Step 4: Discontinue or substitute any offending agent. Step 5: If QTc > 500 ms, institute cardiac monitoring and consider IV magnesium prophylactically.
Common Pitfalls & Limitations
The Bazett formula was derived from data at normal resting heart rates and uses a square-root correction that becomes increasingly inaccurate outside the 60–100 bpm range. At heart rates above 100 bpm, Bazett systematically overestimates the QTc — potentially flagging a normal QT as prolonged and leading to unnecessary drug discontinuation or clinical concern. Conversely, at heart rates below 60 bpm, Bazett underestimates the QTc and may miss genuinely prolonged values. The Fridericia (cube-root) correction is less affected by heart rate extremes and is now recommended by the FDA and EMA for clinical drug trials. When the heart rate is tachycardic or bradycardic, always compare the Bazett and Fridericia values — a large discrepancy suggests Bazett is unreliable.
QTc calculation is only as good as the QT measurement it is based on, and accurate QT measurement is one of the most difficult tasks in ECG interpretation. Common errors include: measuring in a lead where the T wave is poorly defined (leads aVR, V1 are often poor choices), including U waves in the measurement (which overestimates QT — the end of the T wave, not the U wave, should be used), and automated ECG machine readings that are frequently inaccurate (manual verification is always recommended, especially when the QTc result will influence drug decisions). Measuring the QT in multiple leads and using the longest value is recommended. The “teach-the-tangent” method — drawing a tangent to the steepest part of the T-wave downslope and measuring to where it intersects the baseline — can improve consistency.
A prolonged QTc in a hospitalised patient is frequently attributed to medications alone, but electrolyte disturbances are often the precipitant — or the factor that tips a borderline QTc into a dangerous range. Hypokalaemia and hypomagnesaemia are especially common in patients on diuretics, those with poor oral intake, or those with gastrointestinal losses. Correcting K⁺ to > 4.0 mEq/L and Mg²⁺ to > 2.0 mg/dL should be the first intervention, not an afterthought. Many cases of drug-associated QT prolongation are actually drug-plus-electrolyte events. IV magnesium (2 g over 15 minutes) is also the first-line treatment for active Torsades de Pointes, regardless of the serum magnesium level.
In atrial fibrillation and other irregular rhythms, the RR interval varies beat-to-beat. Using a single RR interval to calculate QTc produces unreliable results — a short RR interval (fast rate) will make the QTc appear longer (via Bazett), while a long RR will make it appear shorter. The recommended approach is to average the QT and RR intervals over multiple beats (typically 3–5 consecutive cycles) and use the averaged values for correction. Some sources recommend using the QT interval that follows the RR interval closest to 1 second (i.e., HR ~60 bpm), as this requires the least correction. In any case, QTc values in irregular rhythms should be interpreted with caution.
In patients with bundle branch block (BBB) or any wide QRS complex (> 120 ms), the QT interval is inherently prolonged because part of the QT duration reflects delayed depolarisation (the wide QRS), not delayed repolarisation. Using the uncorrected QT in these patients will overestimate the true repolarisation time. One practical approach is to subtract the excess QRS duration: QT adjusted = QT – (QRS – 120) when the QRS is > 120 ms. This “JT interval” approach focuses on the repolarisation component. However, this adjustment is not universally validated, and expert opinion or cardiology input should be sought when interpreting QT prolongation in the context of wide QRS complexes or ventricular pacing.
Quick Reference Summary
| Clinical Scenario | Action |
|---|---|
| QTc 450–470 ms (male) or 460–470 ms (female) | Borderline. Check K⁺, Mg²⁺, Ca²⁺. Review drug list. Repeat ECG. Monitor if starting QT-prolonging drug. |
| QTc 470–500 ms | Prolonged. Correct electrolytes aggressively. Discontinue or substitute QT-prolonging drugs. Cardiology review. |
| QTc > 500 ms | High risk. Continuous cardiac monitoring. IV Mg²⁺ 2 g. Stop all QT-prolonging drugs. Cardiology consultation. |
| Active Torsades de Pointes | IV Mg²⁺ 2 g bolus. Overdrive pacing (temporary or isoproterenol) to shorten QT. Avoid further antiarrhythmics except for lidocaine if needed. |
| HR > 100 or < 60 bpm | Prefer Fridericia over Bazett. Compare both. Large discrepancy = Bazett is unreliable at this HR. |
The Golden Rule: A QTc value is only as reliable as the QT measurement and the heart rate. Always manually verify the QT, use Fridericia at extreme heart rates, correct electrolytes before blaming drugs, and remember that a QTc > 500 ms demands urgent action — not just documentation.
Disclaimer & References
For Educational Purposes Only. This calculator and the accompanying clinical information are intended as educational tools for healthcare professionals. They do not replace clinical judgement. Results should be interpreted in the full clinical context. Lab reference ranges vary by institution — verify with your own laboratory. Drug dosages should be confirmed against current prescribing information.
References
- Bazett HC. An analysis of the time-relations of electrocardiograms. Heart. 1920;7:353–370. (Republished: Annals of Noninvasive Electrocardiology. 1997;2(2):177–194. DOI: 10.1111/j.1542-474X.1997.tb00325.x)
- Fridericia LS. Die Systolendauer im Elektrokardiogramm bei normalen Menschen und bei Herzkranken. Acta Medica Scandinavica. 1920;53(1):469–486. DOI: 10.1111/j.0954-6820.1920.tb18266.x
- Sagie A, Larson MG, Goldberg RJ, Bengtson JR, Levy D. An improved method for adjusting the QT interval for heart rate (the Framingham Heart Study). The American Journal of Cardiology. 1992;70(7):797–801. DOI: 10.1016/0002-9149(92)90562-D
- Rautaharju PM, Surawicz B, Gettes LS, et al. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part IV. Journal of the American College of Cardiology. 2009;53(11):982–991. DOI: 10.1016/j.jacc.2008.12.014
- Drew BJ, Ackerman MJ, Funk M, et al. Prevention of Torsade de Pointes in hospital settings: a scientific statement from the AHA and ACCP. Circulation. 2010;121(8):1047–1060. DOI: 10.1161/CIRCULATIONAHA.109.192704
- Schwartz PJ, Crotti L, Insolia R. Long-QT syndrome: from genetics to management. Circulation: Arrhythmia and Electrophysiology. 2012;5(4):868–877. DOI: 10.1161/CIRCEP.111.962019
- Viskin S, Rosovski U, Sands AJ, et al. Inaccurate electrocardiographic interpretation of long QT: the majority of physicians cannot recognize a long QT when they see one. Heart Rhythm. 2005;2(6):569–574. DOI: 10.1016/j.hrthm.2005.02.011
- Vandenberk B, Vandael E, Roez T, Jasber M, Nackaerts M, Willems R. Which QT correction formulae to use for QT monitoring? Journal of the American Heart Association. 2016;5(6):e003264. DOI: 10.1161/JAHA.116.003264