QT Interval | ECG Anatomy Series

Conceptual Overview

The QT interval represents the total time for ventricular depolarization and repolarization - essentially the duration of ventricular systole from the start of ventricular contraction to complete relaxation. It begins at the onset of the QRS complex and ends when the T wave returns to the isoelectric baseline.

Understanding the QT interval is critical because:

Prolonged QT: Associated with increased risk of life-threatening ventricular arrhythmias, particularly Torsades de Pointes (polymorphic VT)
Shortened QT: Less common but associated with sudden cardiac death from atrial and ventricular fibrillation
Heart rate dependent: QT naturally shortens with faster heart rates and lengthens with slower rates - must be corrected (QTc)
Reversible causes: Electrolyte abnormalities and medications are common culprits that can be identified and treated

ECG waves, segments, and intervals showing QT interval — ECG components - the QT interval extends from the beginning of the QRS complex to the end of the T wave. Source: LITFL

Key concept: The QT interval is your window into ventricular repolarization. Abnormalities signal electrical instability and arrhythmogenic risk, often from correctible causes.

How to Measure the QT Interval

Measurement Technique

Accurate QT measurement requires careful technique:

Choose the right lead: Measure in lead II or V5-V6 (these typically have the most prominent T waves). Use the lead with the longest QT interval
Measure multiple beats: Assess several consecutive complexes and use the maximum (longest) interval
Define the start: Beginning of the QRS complex (onset of Q wave, or R wave if no Q is present)
Define the end: Use the maximum slope intercept method - where the steepest downslope of the T wave intersects the isoelectric baseline
Avoid the PR segment: Do not include the PR interval in your measurement

Dealing with U Waves

Large U waves (>1mm) fused to T wave: Include in the QT measurement
Small or separate U waves: Exclude from the measurement - measure only to the end of the T wave
When uncertain: Use the nadir (lowest point) between the T and U waves as the end of the T wave

QT interval measurement with U waves and maximum slope intercept method — QT interval measurement technique: Left/middle show U waves separate from T wave (exclude from measurement). Right shows large U wave fused to T wave (include in measurement). The maximum slope intercept method defines the end of the T wave. Source: LITFL

Practical tip: In atrial fibrillation or frequent ectopy, measure the QT in at least 3-5 beats and average them. Choose beats with similar preceding RR intervals when possible.

Corrected QT Interval (QTc)

Why Correction is Necessary

The QT interval is inversely proportional to heart rate:

Faster heart rates → shorter QT intervals
Slower heart rates → longer QT intervals
To assess for abnormal prolongation or shortening, we must correct for heart rate
QTc estimates what the QT interval would be at a standardized heart rate of 60 bpm

Correction Formulas

Multiple formulas exist to calculate QTc. The RR interval is measured in seconds (RR = 60 / heart rate).

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Formula	Equation	Best Use Case	Limitations
Bazett	QTc = QT / √RR	HR 60-100 bpm	Over-corrects at HR >100; under-corrects at HR <60
Fridericia	QTc = QT / ∛RR	HR <60 or >100 bpm	More accurate than Bazett at extreme heart rates
Framingham	QTc = QT + 0.154 (1 – RR)	Linear correction	Less commonly used clinically
Hodges	QTc = QT + 1.75 (HR – 60)	Linear correction	Uses heart rate directly (not RR interval)

Which formula to use?

Bazett formula: Most commonly used due to simplicity. Adequate for HR 60-100 bpm. Built into most ECG machines.
Fridericia formula: More accurate outside the 60-100 bpm range. Use when heart rate is very slow or very fast.
If HR = 60 bpm: No correction needed! The absolute QT = QTc.

Clinical utility: A study by Charbit et al found that automatic QTc using Bazett had 54% sensitivity for detecting QT prolongation, while Fridericia had 100% sensitivity. Consider using Fridericia in critical situations.

Remember: Modern ECG machines calculate QTc automatically, but always verify the measurement manually. Automated algorithms can be fooled by artifact, baseline wander, or unusual T-wave morphology.

Normal QTc Values & Interpretation

Reference Ranges

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Category	QTc Range	Clinical Significance
Normal (Men)	<440 ms	No increased arrhythmia risk from QT duration
Normal (Women)	<460 ms	Women have slightly longer baseline QTc than men
Borderline Prolonged	440-500 ms	Mild increased risk; evaluate for reversible causes
Prolonged (High Risk)	>500 ms	Significantly increased risk of Torsades de Pointes
Short QTc	<350 ms	Increased risk of AF, VF, and sudden cardiac death

Rule of Thumb

Quick bedside assessment: A normal QT interval should be less than half the preceding RR interval. If QT > 50% of RR, consider prolongation and calculate QTc formally.

Risk Stratification for Torsades de Pointes

QTc <440 ms: Low risk (baseline population risk)
QTc 440-500 ms: Mild increased risk - monitor closely, address reversible causes
QTc 500-550 ms: Moderate-high risk - consider telemetry, correct electrolytes, review medications
QTc >550 ms: Very high risk - continuous monitoring, aggressive electrolyte repletion, discontinue QT-prolonging drugs, consider cardiology consult

Clinical pearl: The absolute change in QTc matters as much as the final value. A sudden increase of >60ms from baseline is concerning even if the QTc remains <500ms.

Causes of Prolonged QTc (>440ms)

QT prolongation can result from a wide variety of causes. The mnemonic "ELECTROLYTES" captures many reversible causes:

Mnemonic: ELECTROLYTES

Electrolyte abnormalities (↓K+, ↓Mg2+, ↓Ca2+)
Long QT syndrome (congenital)
Elevated intracranial pressure
Cardiac (ischemia, myocarditis, cardiomyopathy)
Temperature (hypothermia)
ROSC (return of spontaneous circulation) post-arrest
Other drugs (see below)
Liver failure
Yield to medications (antiarrhythmics, psychotropics, antibiotics)
Toxins (organophosphates)
Endocrine (hypothyroid)
Starvation/anorexia

Electrolyte Abnormalities

Hypokalemia

The most common electrolyte cause of QT prolongation.

Mechanism: Reduced K+ slows repolarization, prolonging phase 3 of the action potential
ECG features: Apparent QTc prolongation (often due to T-U fusion), prominent U waves in precordial leads, ST depression, T wave flattening
Clinical significance: Risk increases dramatically when K+ <3.0 mEq/L

ECG showing hypokalemia with prolonged QTc and prominent U waves — Hypokalemia: Apparent QTc 500ms with prominent U waves in precordial leads. Patient's potassium was 1.9 mEq/L. Source: LITFL

Hypomagnesemia

Mechanism: Mg2+ deficiency impairs K+ channel function and prolongs repolarization
Often coexists: With hypokalemia (Mg2+ is required for K+ repletion)
Treatment: Correct Mg2+ before or alongside K+ replacement

Hypocalcemia

Mechanism: Low Ca2+ prolongs the plateau phase (phase 2) of the action potential
Unique feature: Prolongation is primarily in the ST segment, leaving the T wave relatively unchanged
Look for: Long, flat ST segment with normal or prolonged QT

Hypothermia

Mechanism: Cold slows all cardiac electrical activity
ECG features: Marked QTc prolongation, bradycardia, Osborn waves (J waves), shivering artifact, atrial arrhythmias
Severity: Prolongation worsens with decreasing temperature; QTc >600ms common in severe hypothermia

Myocardial Ischemia & Infarction

Mechanism: Ischemic myocardium has delayed and heterogeneous repolarization
Typical range: Modest QTc prolongation, usually 450-500ms
Clinical utility: Can help distinguish hyperacute STEMI from benign early repolarization (BER). Hyperacute MI typically has prolonged QTc; BER usually has normal QTc

ECG showing acute MI with prolonged QTc — Acute anteroseptal MI: QTc 495ms due to hyperacute MI. Myocardial ischemia produces modest QTc prolongation. Source: LITFL

Raised Intracranial Pressure

Mechanism: Autonomic surge from sudden ICP elevation causes "cerebral T waves"
Classic association: Subarachnoid hemorrhage
ECG features: Widespread, deep T wave inversions with markedly prolonged QTc (often >600ms)
Key point: These changes do NOT represent primary cardiac disease but neurogenic effect on the heart

ECG showing subarachnoid hemorrhage with cerebral T waves — Subarachnoid hemorrhage: QTc 630ms with widespread deep T wave inversion ("cerebral T waves") from raised intracranial pressure. Source: LITFL

Congenital Long QT Syndrome

Mechanism: Inherited channelopathies affecting cardiac ion channels (K+, Na+, Ca2+)
Multiple subtypes: LQTS 1-3 are most common (each with different triggers and T wave morphology)
Clinical significance: High risk of syncope, Torsades de Pointes, and sudden cardiac death
Triggers vary by type: Exercise (LQTS1), auditory stimuli (LQTS2), rest/sleep (LQTS3)
Treatment: Beta-blockers, lifestyle modifications, ICD in high-risk patients

Medications Causing QT Prolongation

Numerous medications prolong the QT interval. Common culprits include:

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Drug Class	Common Examples
Antiarrhythmics	Amiodarone, sotalol, dofetilide, ibutilide, quinidine, procainamide
Antipsychotics	Haloperidol, quetiapine, ziprasidone, chlorpromazine
Antidepressants	Citalopram, escitalopram, tricyclics (amitriptyline, nortriptyline)
Antibiotics	Fluoroquinolones (levofloxacin, moxifloxacin), macrolides (azithromycin, erythromycin)
Antifungals	Fluconazole, ketoconazole
Antiemetics	Ondansetron, droperidol
Opioids	Methadone (especially high doses)

Clinical pearl: Always review the medication list in patients with prolonged QTc. Multiple QT-prolonging drugs can have additive effects. Check interactions at CredibleMeds.org or QTdrugs.org.

Causes of Short QTc (<350ms)

Short QT syndrome is less common than prolonged QT but is equally dangerous, associated with increased risk of atrial fibrillation, ventricular fibrillation, and sudden cardiac death.

Hypercalcemia

Mechanism: Elevated Ca2+ shortens the plateau phase (phase 2) of the action potential
ECG features: Shortened ST segment (most prominent), short QTc, may see Osborn waves
Causes: Hyperparathyroidism, malignancy, vitamin D toxicity, immobilization

Congenital Short QT Syndrome (SQTS)

Mechanism: Autosomal dominant inherited disorder of potassium channels (gain of function mutations)
ECG features: Very short QTc (<300-350ms), tall peaked T waves, failure of QT to lengthen appropriately with slower heart rates
Clinical significance: High risk of paroxysmal atrial and ventricular fibrillation, sudden cardiac death at young age
Diagnostic clues: Family history of sudden death, lone AF in young adults, syncope

ECG showing congenital short QT syndrome with tall peaked T waves — Congenital short QT syndrome: Very short QTc (280ms) with tall, peaked T waves. Associated with increased risk of paroxysmal AF, VF, and sudden cardiac death. Source: LITFL

Digoxin Effect

Mechanism: Inhibition of Na+/K+ ATPase shortens repolarization
ECG features: Relative QT shortening, "reverse tick" ST depression (downward sloping ST in lateral leads), T wave flattening/inversion, increased arrhythmias
Note: Digoxin effect (therapeutic) is different from digoxin toxicity (life-threatening arrhythmias)

Other causes of short QTc: Hyperthermia, acidosis, hyperkalemia (early), increased sympathetic tone (catecholamines)

Drug-Induced QT Prolongation & Torsades Risk

The QT Nomogram

In the context of acute poisoning or drug overdose with QT-prolonging agents, the absolute QT interval (not QTc) better predicts Torsades de Pointes risk.

Developed by Chan et al (2007): A clinically validated tool for risk stratification in drug-induced QT prolongation
How to use: Plot the QT interval (ms) and heart rate (bpm) from the same ECG as a coordinate pair
Interpretation: Points that fall above the line indicate the patient is at risk of Torsades de Pointes
Clinical utility: More accurate than QTc alone in poisoning/overdose scenarios

Key distinction: For chronic drug therapy, use QTc. For acute poisoning, use the QT nomogram with absolute QT and heart rate.

Management of Drug-Induced QT Prolongation

Discontinue offending agent(s): Stop all QT-prolonging medications if possible
Correct electrolytes: Target K+ >4.0 mEq/L, Mg2+ >2.0 mg/dL
Continuous monitoring: Telemetry or ICU monitoring for high-risk patients
Avoid bradycardia: Slower heart rates worsen QT prolongation (consider pacing if symptomatic and bradycardic)
If Torsades develops: Immediate defibrillation if unstable; IV magnesium 2g bolus; overdrive pacing or isoproterenol

Magnesium for Torsades: IV magnesium sulfate 2g over 1-2 minutes is first-line therapy for Torsades de Pointes, even if serum Mg2+ is normal. May repeat dose. Mechanism: stabilizes cardiac membranes and reduces early afterdepolarizations.

Quick Hits – QT Interval Essentials

Definition: Time from Q wave start to T wave end - represents ventricular depolarization through repolarization
Normal QTc: <440ms (men), <460ms (women)
Prolonged QTc: >440ms (men) or >460ms (women) - risk of Torsades de Pointes increases dramatically >500ms
Short QTc: <350ms - increased risk of atrial and ventricular fibrillation
Rule of thumb: Normal QT should be less than half the preceding RR interval
Correction needed: QT varies with heart rate - must use corrected QT (QTc) for accurate interpretation
Key pearl: QTc >500ms = high risk for Torsades; always check electrolytes (K+, Mg2+, Ca2+) and medication list

Clinical Pearls

"Half the RR" rule: Quick bedside check - if QT is more than half the preceding RR interval, QTc is likely prolonged. This works best at normal heart rates (60-100 bpm).

Measure in the right lead: Always measure QT in lead II or V5-V6. These typically have the most prominent T waves and longest QT. Use whichever lead shows the longest interval.

Don't trust the machine blindly: Automated QTc calculations are frequently wrong. Always verify manually, especially in critical patients or when making treatment decisions.

Hypokalemia + QT-prolonging drug = danger: The combination of low K+ and a QT-prolonging medication creates synergistic risk. Correct K+ to >4.0 mEq/L in all patients on Class IA or III antiarrhythmics.

Trend matters more than single value: A QTc that was 420ms and is now 500ms is more concerning than a stable QTc of 480ms. Look for acute changes.

Women have longer QTc: Baseline QTc is ~10-20ms longer in women than men. Use sex-specific cutoffs (women <460ms, men <440ms).

Post-cardiac arrest QT: Prolonged QT is common after ROSC and often resolves over hours. However, avoid additional QT-prolonging agents in this vulnerable period.

Congenital LQTS red flags: Syncope during exercise, swimming, or emotional stress; family history of sudden death <40 years old; QTc >470ms in repeated ECGs. Consider genetics referral.

Hypocalcemia vs hypokalemia: Both prolong QT, but hypocalcemia primarily lengthens the ST segment (flat, prolonged ST with normal T), while hypokalemia creates prominent U waves that fuse with the T wave.

Cerebral T waves after SAH: Deep, symmetric T wave inversions with QT prolongation after subarachnoid hemorrhage do NOT indicate primary cardiac disease. They reflect autonomic surge from elevated ICP. Don't delay aneurysm treatment to "rule out MI."

References

Farkas, Josh MD. (2015). Table of Contents - EMCrit Project. EMCrit Project. https://emcrit.org/ibcc/toc/
Khan, M. G. (2007). Rapid ECG Interpretation. Humana.
Sigg, D. C., Iaizzo, P. A., Xiao, Y.-F., Bin He, & Springerlink (Online Service). (2010). Cardiac Electrophysiology Methods and Models. Springer Us.
Wang, K. (2012). Atlas of Electrocardiography. JP Medical Ltd.
ECG Library • LITFL • ECG Library Basics. (2018). Life in the Fast Lane • LITFL • Medical Blog. https://litfl.com/ecg-library/