What rate correction of the QT interval is for
The QT interval spans ventricular depolarisation and repolarisation, from the earliest onset of the QRS to the end of the T wave. It shortens as the heart speeds up, which makes the raw measurement almost useless for comparison: a QT of 400 ms is unremarkable at 60 bpm and distinctly abnormal at 100 bpm. Rate correction rescales the measurement to what it would be at a reference rate of 60 bpm, so that two ECGs taken at different rates, or the same patient before and after a drug, can be put side by side.
The number matters because a long QT is the electrocardiographic signature of delayed repolarisation, and delayed repolarisation is the substrate for torsades de pointes. Every regulatory drug-safety programme, every antiarrhythmic protocol and every methadone or antipsychotic monitoring pathway is built around a QTc threshold. Yet the correction itself is an empirical curve fit, not a law of physiology, and the four formulas here disagree by tens of milliseconds at the rates where the decision is hardest.
All four share one property worth fixing in your mind: at exactly 60 bpm, RR is 1.000 s, and every formula returns the measured QT unchanged. Every difference between them is a difference in how quickly they diverge from that anchor.
The four corrections and how they differ
Bazett (1920) divides QT by the square root of RR in seconds. It is the oldest, the one built into most ECG machines, and the one nearly all published cut-points and drug labels are written against. Its weakness is well documented: because the square root curve is steep, it over-corrects at fast rates and under-corrects at slow ones. At 100 bpm a QT of 400 ms becomes 516 ms by Bazett and 474 ms by Fridericia — the difference between a red flag and a borderline result.
Fridericia (1920) divides by the cube root of RR instead. The gentler exponent makes it markedly more stable across rate, and it is the correction preferred in thorough QT studies and in tachycardia. ICH E14 requires a sponsor to justify the correction method used, and its question-and-answer guidance singles out Bazett's correction as generally inadequate, which is why Fridericia's is the usual choice in a thorough QT study.
Framingham (Sagie and colleagues, 1992) is linear in RR: QTc = QT + 154 × (1 − RR), fitted to a large community cohort. Being linear, it cannot blow up at extreme rates the way a root-based correction can, and it tends to sit between the others.
Hodges (1983) is linear in heart rate rather than in RR: QTc = QT + 1.75 × (HR − 60). It adds 1.75 ms for every beat per minute above 60 and subtracts the same below. It is the easiest of the four to do in your head at the bedside.
No single correction is right for all patients, which is the reason this calculator shows all four rather than picking one. The practical rule is to name the formula whenever you quote a QTc, and to use the same formula on the follow-up ECG that you used on the first one.
Worked example: a woman at 96 bpm starting an antiemetic
A woman is prescribed a QT-prolonging antiemetic. The 12-lead ECG shows a QT of 400 ms at a rate of 96 bpm with a QRS of 100 ms.
- RR interval. 60 ÷ 96 = 0.625 s.
- Bazett. √0.625 = 0.790569, so QTc = 400 ÷ 0.790569 = 506 ms.
- Fridericia. 0.6251/3 = 0.854988, so QTc = 400 ÷ 0.854988 = 468 ms.
- Framingham. 400 + 154 × (1 − 0.625) = 400 + 57.75 = 458 ms.
- Hodges. 400 + 1.75 × (96 − 60) = 400 + 63 = 463 ms.
- JT interval. 400 − 100 = 300 ms, and JTc = 300 ÷ 0.790569 = 379 ms.
Bazett places this patient above 500 ms, the threshold at which most protocols stop the drug. The other three place her between 458 and 468 ms, which is above the 460 ms female cut-point only by the Fridericia and Hodges values and below it by Framingham. The spread across formulas here is 48 ms, and the entire disagreement comes from the tachycardia — repeat the ECG when the rate has settled and much of it disappears.
That is the practical lesson: before you stop a drug on a Bazett QTc measured at 96 bpm, ask why the patient is tachycardic. Pain, fever, hypovolaemia and anxiety all inflate a Bazett correction without changing repolarisation at all.
Reading the result against real thresholds
The AHA/ACCF/HRS 2009 recommendations for ECG interpretation give 450 ms in men and 460 ms in women as the cut-points above which the rate-corrected QT is considered prolonged. Those values sit behind the comparison column in the results table.
Three further thresholds are worth carrying:
480 ms. The HRS/EHRA/APHRS expert consensus on inherited arrhythmia syndromes treats a QTc at or above 480 ms on repeated 12-lead ECGs as diagnostic of long QT syndrome in the absence of a secondary cause. Below that, diagnosis rests on the full clinical score rather than a single number.
500 ms. The value above which proarrhythmic risk is treated as substantial in drug-safety practice, irrespective of sex. Most institutional protocols for methadone, antipsychotics, fluoroquinolones and class III antiarrhythmics use it as a stopping rule.
A rise of 60 ms from baseline. ICH E14, the international guideline governing QT assessment of new drugs, treats a change from baseline of this size as a signal in its own right, even when the absolute QTc stays under 500 ms. Enter a pre-treatment QTc above and the calculator reports that change.
At the other end, a QTc at or below about 330 to 340 ms raises short QT syndrome, and more commonly hypercalcaemia or digoxin effect. Verify a short interval by hand before you act on it; automated algorithms measure T-wave offset poorly when the T wave is tall and peaked.
The measurement itself is the largest source of error in everything above. Use the tangent method — extend the steepest tangent to the T-wave downslope until it crosses the isoelectric line — measure in the lead with the longest clearly defined interval, conventionally lead II or V5, and exclude a U wave unless it merges with the T. A 20 ms measurement disagreement between two clinicians is ordinary, and under Bazett at 100 bpm it moves the QTc by 20 ÷ √0.6 = 26 ms.
How the four formulas diverge across heart rate
| Heart rate (bpm) | RR (s) | Bazett | Fridericia | Framingham | Hodges |
|---|---|---|---|---|---|
| 40 | 1.500 | 327 | 349 | 323 | 365 |
| 50 | 1.200 | 365 | 376 | 369 | 383 |
| 60 | 1.000 | 400 | 400 | 400 | 400 |
| 70 | 0.857 | 432 | 421 | 422 | 418 |
| 80 | 0.750 | 462 | 440 | 439 | 435 |
| 100 | 0.600 | 516 | 474 | 462 | 470 |
| 120 | 0.500 | 566 | 504 | 477 | 505 |
| 150 | 0.400 | 632 | 543 | 492 | 558 |
Bazett exceeds Fridericia at every rate above 60 bpm and falls below it at every rate under 60, because √RR and RR^⅓ cross at RR = 1. The spread across all four widens with distance from 60 bpm: 42 ms at 40 bpm, 14 ms at 70 bpm, 140 ms at 150 bpm.
A wide QRS inflates the QT without delaying repolarisation
The QT interval contains the QRS. In left bundle branch block, ventricular pacing or a wide-complex rhythm, a QRS of 160 ms is 70 ms longer than a normal 90 ms complex, and that 70 ms sits inside the QT as depolarisation rather than repolarisation. Applying a standard cut-point to that QTc labels conduction disease as a repolarisation abnormality. The JT interval — QT minus QRS, rate-corrected the same way — isolates repolarisation and is reported above whenever the QRS is shorter than the QT. Published JTc cut-points are less well established than QTc cut-points, so use JTc for trend and comparison within a patient rather than as a stand-alone threshold.
Pitfalls that produce a wrong QTc
- Measuring the wrong beat. The RR interval must be the one preceding the beat whose QT you measured. Using the machine's average rate against a hand-measured QT mixes two different beats.
- Atrial fibrillation. With beat-to-beat variation in RR there is no single rate to correct to. The usual approach is to measure several beats across the range of RR intervals and average the resulting QTc values, or to average the RR over ten beats and apply the correction once; state which you did.
- Including the U wave. A separate U wave is not part of the QT. When T and U merge — classically in hypokalaemia — the interval genuinely cannot be measured reliably, and that limitation belongs in the report.
- Trusting the machine at extremes of rate. Automated QT algorithms are accurate in the middle of the range and degrade with tachycardia, low T-wave amplitude, and pacing artefact. Confirm any result near a decision threshold by hand.
- Switching formulas between ECGs. A patient who moves from 458 ms to 471 ms has not necessarily changed if the first number was Fridericia and the second Bazett.
- Ignoring the reversible causes. Hypokalaemia, hypomagnesaemia and hypocalcaemia all prolong repolarisation, and all are correctable in minutes. Check the electrolytes before you attribute a long QTc to a drug.
Where QTc fits in a drug-safety and critical-care workflow
QTc is a screening measurement embedded in a larger assessment. On the ward it usually arrives with a question attached: can this patient start, or continue, a QT-prolonging drug? Answering it means combining the corrected interval with the electrolytes, the renal function that governs clearance of many of those drugs, and the other agents already on the chart, since risk from two QT-prolonging drugs is greater than either alone.
Calcium is the electrolyte most directly tied to the interval, and the number you should be reading is the albumin-adjusted one rather than the total — the corrected calcium calculator handles that adjustment. Renal clearance of sotalol, dofetilide and several fluoroquinolones is the constraint that decides dose, so an estimated GFR or a Cockcroft–Gault creatinine clearance belongs alongside this result; dofetilide dosing in particular is written against creatinine clearance, not eGFR. When the dose itself is weight-based, the weight-based dosage calculator closes the loop, and in a haemodynamically unstable patient the mean arterial pressure often decides whether a rate-slowing strategy is even available.
For regulatory work the framework is ICH E14, which sets out how a new drug's effect on the QT interval is characterised: a dedicated thorough QT study, correction by Fridericia or by a study-specific method rather than by Bazett alone, and attention to change from baseline as well as absolute value. For inherited long QT syndrome the framework is different again — the diagnostic score weighs the QTc alongside syncope history, T-wave morphology and family history, and no single interval confirms or excludes the diagnosis.
Use this calculator to get four defensible numbers and the spread between them. Use the spread itself as information: a large disagreement between formulas is a signal that the heart rate, not the repolarisation, is driving the result.
Key terms
- QT interval
- The time from the earliest onset of the QRS complex to the end of the T wave, covering both ventricular depolarisation and repolarisation.
- RR interval
- The time between consecutive R-wave peaks, expressed in seconds for the Bazett and Fridericia formulas. RR in seconds equals 60 divided by the heart rate.
- JT interval
- QT minus QRS duration — the repolarisation portion of the interval on its own. It is the more interpretable measurement when the QRS is wide.
- Torsades de pointes
- A polymorphic ventricular tachycardia with a characteristic twisting axis that arises on a substrate of delayed repolarisation. It is the arrhythmia that QT monitoring exists to prevent.
- Tangent method
- The standard technique for locating the end of the T wave: extend the steepest tangent to the T-wave downslope and take the point where it crosses the isoelectric baseline.