ECG Basic – QT Interval
QT Interval
Learn how to identify and measure the QT interval, correct it for heart rate, recognize abnormal QT values, and understand the clinical implications of prolonged and shortened ventricular repolarization.
Learning Objectives
1. What Is the QT Interval?
The QT interval is measured from the beginning of the QRS complex to the end of the T wave. It represents the total duration of ventricular electrical depolarization and repolarization. It therefore spans most of the ventricular electrical systole.
QT duration is dependent on heart rate:
- At faster heart rates, the QT interval normally becomes shorter.
- At slower heart rates, the QT interval normally becomes longer.
Marked QT prolongation is associated with an increased risk of ventricular arrhythmias, particularly torsades de pointes (TdP). Congenital short QT syndrome is also associated with atrial and ventricular arrhythmias and sudden cardiac death.
2. How to Measure the QT Interval
QT measurement should be performed on a clear ECG tracing, with attention to T-wave morphology and the lead in which the T-wave termination can be identified most reliably.
- Select the lead. Lead II or V5–V6 is commonly used. Compare suitable leads and use the lead with the longest clearly measurable QT interval.
- Measure several consecutive beats. Record multiple cycles and use the maximum reliable QT measurement, avoiding ectopic or distorted beats when possible.
- Identify QRS onset. Start at the earliest beginning of the QRS complex.
- Identify T-wave termination. Use the maximum-slope tangent method when the end of the T wave is indistinct.
- Assess U waves. A large U wave (greater than 1 mm) fused with the T wave is included in the measurement. A small or clearly separate U wave is excluded.
Maximum-slope tangent method
Draw a tangent along the steepest descending limb of the T wave. The point where this tangent intersects the isoelectric baseline is taken as the end of the T wave. If the T wave is notched, the tangent is drawn from the steepest downslope of the second notch, as described in the supplied ECG reference.
Prominent U waves, particularly in hypokalaemia, may merge with the T wave and create apparent QT prolongation. Decide whether the deflection is a fused T–U complex or a separate U wave before recording the QT.
3. Corrected QT Interval (QTc)
Because the measured QT changes with heart rate, the corrected QT (QTc) estimates the QT duration at a standardized heart rate of 60 beats/min. QTc allows comparison across different heart rates and during serial ECG assessment.
Common correction formulas
QTc = QT / √RRQTc = QT / ∛RRQTc = QT + 154 × (1 − RR)QTc = QT + 1.75 × (HR − 60)Units: QT and QTc are expressed in milliseconds (ms), RR in seconds, and heart rate (HR) in beats/min. For the Framingham and Hodges equations, the QT input is in milliseconds.
RR (seconds) = 60 ÷ heart rate (beats/min). For example, at 75 beats/min, RR = 0.80 seconds.
Choosing a correction formula
Bazett is widely used because it is simple, but it tends to overcorrect at faster rates and undercorrect at slower rates. The supplied reference notes that Fridericia or Framingham correction may be more appropriate when the heart rate is outside approximately 60–100 beats/min. No single formula is universally optimal in every clinical setting.
When the heart rate is exactly 60 beats/min, the measured QT can be considered directly because RR is one second.
QTc formulas are estimates. Marked bradycardia or tachycardia, irregular RR intervals, broad QRS complexes, pacing, and uncertain T-wave termination can reduce reliability. Use a consistent lead, measurement method, device, and correction formula when following an individual over time.
Interactive QTc Calculator
Enter the measured QT and heart rate to compare four correction methods.
RR is calculated as 60 ÷ heart rate. Results are rounded to the nearest millisecond.
These calculations support learning and do not establish a diagnosis. Interpret the QTc alongside the ECG, clinical history, medications, electrolytes, and the selected reference standard.
4. QTc Interpretation: Prolonged and Short QT
The supplied ECG reference gives the following practical thresholds. Values should be interpreted with the measurement method, heart rate, clinical context, and applicable diagnostic criteria in mind.
| Finding | QTc threshold in the supplied reference | Clinical context |
|---|---|---|
| Prolonged QTc | >440 ms in men; >460 ms in women | Consider acquired and congenital causes. |
| Marked QTc prolongation | >500 ms | Associated with increased risk of torsades de pointes. |
| Short QTc | <350 ms | Consider hypercalcaemia, digoxin effect, and congenital short QT syndrome. |
| Quick visual estimate | QT less than half of the preceding RR interval | A rough rule of thumb, not a substitute for measuring QT and calculating QTc. |
The 2022 ESC ventricular arrhythmia guideline uses a QTc ≥480 ms or a diagnostic score >3 for clinical diagnosis of long QT syndrome; in a patient with arrhythmic syncope or cardiac arrest, QTc ≥460 ms is sufficient to consider the diagnosis. These diagnostic criteria are distinct from the simpler reference thresholds above.
Why QTc above 500 ms is important
A QTc above 500 ms is a high-risk finding in the appropriate clinical setting, particularly with QT-prolonging drugs, bradycardia, electrolyte disturbance, or other predisposing factors. The AHA/ACCF scientific statement advises prompt evaluation when QTc exceeds 500 ms or rises by at least 60 ms from baseline during treatment with a QT-prolonging drug.
5. Causes of QTc Prolongation
Acquired causes
- Hypokalaemia
- Hypomagnesaemia
- Hypocalcaemia
- Hypothermia
- Myocardial ischaemia
- Post-resuscitation state (after return of spontaneous circulation)
- Raised intracranial pressure
- Medications and drugs that prolong repolarization
Congenital long QT syndrome
Inherited cardiac ion-channel disorders can prolong ventricular repolarization and increase the risk of torsades de pointes and sudden cardiac death. A family history of unexplained sudden death, syncope, or a known long QT diagnosis should prompt careful assessment.
Hypokalaemia may produce prominent U waves and T–U fusion, making the QT appear prolonged. Hypocalcaemia typically prolongs the ST segment while leaving the T wave relatively unchanged.
Severe hypothermia can cause marked QTc prolongation and may coexist with bradyarrhythmias, slow atrial fibrillation, Osborn waves, and shivering artefact.
Myocardial ischaemia may cause a modest QTc increase. Raised intracranial pressure, including subarachnoid haemorrhage, may be associated with widespread deep T-wave inversion (“cerebral T waves”) and QTc prolongation.
Medication-related QT prolongation
Review prescribed, over-the-counter, and recently administered drugs when QTc is prolonged. Assess combinations of QT-prolonging agents, drug interactions, bradycardia, and electrolyte abnormalities. In patients receiving high-risk drugs, serial QT assessment should use a consistent measurement approach.
6. Causes of a Short QTc
- Hypercalcaemia
- Congenital short QT syndrome
- Digoxin effect
Hypercalcaemia
Hypercalcaemia shortens the ST segment and can markedly shorten the QT interval. The supplied source also notes that Osborn waves may be seen.
Congenital short QT syndrome
Short QT syndrome is a rare inherited channelopathy associated with atrial fibrillation, ventricular fibrillation, and sudden cardiac death. The supplied ECG reference describes very short QTc values (often below 300–350 ms) and tall, peaked T waves.
Features that may raise suspicion include atrial fibrillation at a young age without structural heart disease, a family member with a short QT interval, a family history of sudden cardiac death, and failure of the QT interval to lengthen appropriately as the heart rate slows.
The 2022 ESC guideline proposes QTc ≤320 ms as a diagnostic threshold on its own, or QTc ≤360 ms together with a family history of short QT syndrome, aborted cardiac arrest in the absence of heart disease, or a pathogenic mutation. This is more specific than using QTc <350 ms as a screening flag.
Digoxin effect
Digoxin can shorten the QT interval and produce characteristic downsloping ST-segment depression (“reverse tick” appearance), T-wave flattening or inversion, and a range of rhythm and conduction disturbances. A short QT in a patient taking digoxin should be interpreted with the clinical context and other ECG findings.
7. Drug-Induced QT Prolongation and the QT Nomogram
In acute poisoning with QT-prolonging agents, the supplied source emphasizes assessment of the absolute QT interval together with the simultaneous heart rate, rather than relying only on a corrected QT value.
- Measure the absolute QT interval on the ECG.
- Determine the heart rate from the same tracing.
- Plot the QT–heart-rate pair on the QT nomogram described by Chan and colleagues.
- A point above the nomogram line indicates a potentially increased risk of torsades de pointes.
The QT nomogram is intended for risk assessment in drug-induced QT prolongation, particularly overdose. It is not interchangeable with routine QTc interpretation or diagnostic criteria for congenital long QT syndrome. Use the validated nomogram and local toxicology protocols rather than estimating a threshold from memory.
8. Practical ECG Interpretation Workflow
- Confirm the ECG calibration and identify a representative sinus beat.
- Inspect leads II and V5–V6, then select the lead with the clearest T-wave end and longest reliable QT.
- Measure multiple consecutive beats and document the lead and method.
- Check for T–U fusion, notched T waves, baseline instability, ectopy, and broad QRS complexes.
- Calculate QTc and state which formula was used.
- Review medications, potassium, magnesium, calcium, temperature, ischaemia, and relevant neurological or post-arrest context.
- If markedly abnormal, assess symptoms, family history, serial ECGs, and the need for monitored evaluation or specialist input.
For comparisons before and after a medication change, keep the ECG device, lead, measurement technique, and QT correction formula consistent whenever possible.
Key Takeaways
- The QT interval runs from the beginning of the QRS complex to the end of the T wave.
- QT shortens as heart rate increases and lengthens as heart rate decreases; QTc adjusts for this relationship.
- Measure the longest clearly interpretable QT, using a consistent method and careful T-wave endpoint identification.
- Bazett is common but may overcorrect at faster rates and undercorrect at slower rates; compare alternative formulas when appropriate.
- QTc >500 ms is associated with increased torsades risk, especially in the presence of additional risk factors.
- Electrolyte abnormalities, hypothermia, ischaemia, drugs, and inherited channelopathies can alter QT duration.
- In drug overdose, the absolute QT and simultaneous heart rate may be assessed using the QT nomogram.
References
Related ECG Academy Lessons
Continue with the ECG components that define repolarization and adjacent waveform morphology:
- ST Segment
- T Wave
- U Wave
- QRS Complex
- Osborn (J) Wave
Internal links can be added when the corresponding Appcardio ECG Academy pages are published.
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