ECG Basic – QRS Interval

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Appcardio ECG Academy · ECG Basics

QRS Interval: Duration, Width and Morphology

Learn how to measure QRS duration, distinguish narrow from wide complexes, identify supraventricular and ventricular activation patterns, and recognise important voltage and morphology clues on a 12-lead ECG.

Foundational measurementApprox. 9-minute readClinical interpretation

Learning objectives

01 · DEFINEDescribe the QRS complex and its relationship to ventricular depolarisation.

02 · MEASUREMeasure QRS duration accurately using ECG paper calibration.

03 · CLASSIFYDistinguish narrow, borderline, and wide QRS complexes.

04 · LOCALISEUse QRS width and atrial activity to frame the likely site of activation.

05 · RECOGNISEIdentify common causes of QRS widening and characteristic patterns.

06 · INTERPRETRecognise high voltage, low voltage, and electrical alternans without overcalling a diagnosis.

1. What does the QRS complex represent?

The QRS complex represents ventricular depolarisation: the electrical activation that precedes mechanical ventricular contraction. Its duration reflects how long the activation wavefront takes to spread through the ventricular myocardium.

In a normal heart, rapid conduction through the His–Purkinje system produces near-synchronous ventricular activation and a relatively narrow QRS. Delayed or abnormal activation—such as bundle branch block, ventricular pacing, pre-excitation, or a ventricular-origin beat—can widen or alter the complex.

Original schematic: QRS duration is measured from the earliest initial deflection to the latest return to the isoelectric line, considering all leads.

How to measure QRS duration

Confirm the ECG paper speed and voltage calibration. The usual settings are 25 mm/s and 10 mm/mV.
Identify the earliest onset of ventricular depolarisation—the first QRS deflection, whether a Q, R, or S wave.
Identify the latest point at which the QRS returns to the baseline before the ST segment.
Measure from onset to offset. When assessing the complete QRS duration, use the earliest onset and latest offset across the leads rather than relying on a single lead alone.

At standard paper speed (25 mm/s)

1 small box = 40 ms

One large box (5 small boxes) = 200 ms. At 50 mm/s, one small box represents 20 ms.

Interactive QRS duration estimator

Enter the measured horizontal width of the QRS complex in small ECG boxes. This converts box count into milliseconds; it does not interpret the ECG diagnosis.

QRS width (small boxes)

Paper speed

100 msCalculated duration · interpret in clinical context

2. QRS duration: narrow versus wide

QRS duration is a practical first discriminator in rhythm analysis. A narrow complex generally indicates that ventricular activation has travelled through the normal His–Purkinje system. A wide complex indicates delayed or altered ventricular activation, but does not by itself establish a ventricular origin.

Category	Duration	Practical interpretation
Narrow	<110 ms (commonly <100 ms in basic teaching)	Usually supraventricular activation with intact or near-normal intraventricular conduction.
Borderline / mildly prolonged	110–119 ms	May reflect conduction delay; assess morphology, patient context, and the measurement method.
Wide	≥120 ms	May be due to bundle branch block, ventricular activation, pre-excitation, pacing, metabolic or drug effects, or other intraventricular conduction delay.

Threshold clarification: The supplied LITFL lesson uses <100 ms for narrow complexes and describes >100 ms as broad/abnormal, while noting that ≥120 ms is required for complete bundle branch block or a ventricular rhythm. The AHA/ACCF/HRS statement recommends considering QRS duration >110 ms abnormal in adults, and uses ≥120 ms as a key duration criterion for complete RBBB/LBBB. These thresholds serve different teaching and diagnostic purposes; do not treat 100, 110, and 120 ms as interchangeable cut-offs.

Why a wide QRS is not synonymous with ventricular rhythm

A broad complex can arise from the ventricles, or from a supraventricular impulse that reaches the ventricles through an abnormal or delayed pathway. The latter is commonly called aberrant conduction.

Common causes of a wide QRS

Right or left bundle branch block.
Ventricular ectopic beats and ventricular tachycardia.
Pre-excitation through an accessory pathway, as in Wolff–Parkinson–White (WPW) pattern.
Ventricular pacing.
Hyperkalaemia and other major electrolyte or metabolic disturbances.
Sodium-channel-blocking drug toxicity, including tricyclic antidepressants.
Hypothermia and rate-related or intermittent aberrant conduction.

Schematic waveforms only; not diagnostic rhythm strips.

Narrow-complex activation

Narrow QRS rhythms are usually supraventricular. The impulse may originate in the sinoatrial node, atrial myocardium, or AV junction. P-wave appearance and its relationship to the QRS help refine the likely origin:

Sinus rhythm: a consistent sinus P wave precedes each QRS.
Atrial rhythm or flutter: abnormal P waves or organised flutter activity may be visible before or between QRS complexes.
Junctional rhythm or tachycardia: P waves may be absent, buried, or retrograde.

Broad-complex rhythm: ventricular or supraventricular with aberrancy?

Look for preceding atrial activity and the overall clinical context. Sinus or atrial rhythms with bundle branch block may show a P wave or flutter/fibrillatory activity preceding the broad QRS. However, a junctional impulse conducted with aberrancy may have no obvious preceding P wave and can resemble a ventricular complex.

Safety-critical principle: In a sustained regular wide-complex tachycardia, ventricular tachycardia must remain a major diagnostic consideration. QRS width or the apparent absence of P waves alone cannot reliably distinguish VT from supraventricular tachycardia with aberrancy. Use a structured wide-complex tachycardia assessment and the patient's clinical condition.

3. QRS naming and morphology

Capital letters describe relatively large deflections; lowercase letters describe small deflections. The sequence is named from left to right, following the order of deflections around the baseline.

Original simplified morphology examples. Real QRS complexes vary by lead and should be interpreted in a 12-lead context.

Q wave: the first negative deflection before any positive deflection.
R wave: the first positive deflection.
S wave: a negative deflection after an R wave.
QS complex: a completely negative complex with no positive deflection.
R′ (R-prime): a second positive deflection after an S wave.
Fragmented QRS: additional notching or fragmentation of the QRS complex; its significance depends on the clinical setting and lead distribution.

Pattern recognition in common conduction abnormalities

Pattern / cause	Typical QRS clue	Interpretive note
RBBB	rsR′/rSR′ pattern in V1–V2; broad or slurred terminal S waves in lateral leads.	Complete RBBB in adults requires QRS ≥120 ms plus appropriate morphology.
LBBB	Predominantly negative QRS in V1; broad, often notched R waves in I, aVL, V5–V6; absent normal lateral q waves.	Complete LBBB in adults requires QRS ≥120 ms plus appropriate morphology.
WPW pre-excitation	Short PR interval, slurred initial QRS upstroke (delta wave), often widened QRS.	Look for the complete pattern, not QRS width in isolation.
Ventricular pacing	Pacing spike may precede a broad QRS with a paced activation pattern.	Appearance depends on pacing site and configuration.
Hyperkalaemia	Progressive conduction slowing may produce QRS widening.	May coexist with peaked T waves and other ECG changes; ECG severity is variable.
Sodium-channel blocker toxicity	QRS widening; tricyclic toxicity may show a prominent terminal R wave in aVR.	Interpret with drug history, haemodynamics, and toxicology context.
Hypothermia	Bradycardia, prolonged intervals and possible Osborn (J) waves; artefact may occur with shivering.	QRS changes are part of a broader temperature-related ECG pattern.

Important spot diagnoses

Brugada ECG pattern: a characteristic right-precordial ST-segment pattern, often accompanied by an RBBB-like appearance. An RBBB-like QRS appearance alone is not diagnostic of Brugada syndrome.
WPW pattern: short PR interval with delta wave and often a wider QRS due to ventricular pre-excitation.
Tricyclic antidepressant toxicity: consider sodium-channel blockade when QRS widening occurs with a compatible exposure; a prominent terminal R in aVR is a recognised clue.

4. QRS voltage: high, low and alternating amplitude

High QRS voltage

Increased QRS amplitude can contribute to ECG criteria for left ventricular hypertrophy (LVH), but voltage alone does not establish anatomical hypertrophy. High voltage may also be seen in younger, slim, or athletic individuals without pathological LVH.

Sokolow–Lyon voltage criterion

S in V1 + tallest R in V5 or V6 > 35 mm

Measure amplitudes from the isoelectric baseline at standard calibration (10 mm/mV).

Voltage criteria have limited sensitivity and should be interpreted with other ECG findings and the clinical context. Echocardiography or other cardiac imaging is used when structural assessment is clinically required.

Low QRS voltage

The supplied reference defines low voltage when the peak-to-trough amplitude of all QRS complexes is:

Less than 5 mm in every limb lead; or
Less than 10 mm in every precordial lead.

Low voltage is a descriptive ECG finding, not a diagnosis. Potential explanations include pericardial effusion, obesity, emphysema, infiltrative or other myocardial disease, and technical factors such as incorrect gain or lead connection. Correlate with the clinical picture and verify calibration before interpretation.

Electrical alternans

Electrical alternans describes beat-to-beat variation in QRS amplitude or morphology. Marked alternation in the appropriate clinical setting may be associated with a large pericardial effusion and a swinging heart, but it is not specific and should prompt clinical assessment rather than be used as a stand-alone diagnosis.

Schematic illustration of alternating QRS amplitude; actual electrical alternans may also involve alternating morphology.

5. Practical interpretation checklist

1. Check calibrationConfirm paper speed and gain before measuring duration or voltage.

2. Measure globallyUse the earliest QRS onset and latest offset across leads when feasible.

3. Interpret the thresholdUse 110 ms as an adult abnormality threshold in the AHA statement; ≥120 ms is central to complete BBB criteria.

4. Do not equate wide with VTWide complexes have ventricular and supraventricular causes.

5. Inspect morphologyAssess RBBB/LBBB patterns, pre-excitation, pacing, and toxic-metabolic clues.

6. Interpret voltage cautiouslyHigh or low voltage is a finding; it needs clinical and structural correlation.

Common interpretation pitfalls

Measuring only one lead and missing an earlier onset or later offset elsewhere.
Calling every QRS wider than 100 ms a complete bundle branch block.
Assuming a wide-complex tachycardia is supraventricular because P waves appear to precede some complexes.
Diagnosing LVH from voltage alone without considering age, body habitus, other ECG criteria, and imaging.
Interpreting low voltage without checking gain, electrode placement, and technical quality.

Key takeaways

The QRS complex represents ventricular depolarisation; its duration reflects the time required for ventricular activation.
At 25 mm/s, each small box equals 40 ms; at 50 mm/s, each small box equals 20 ms.
Adult QRS duration above 110 ms is considered abnormal in the AHA/ACCF/HRS standardisation statement; complete RBBB or LBBB generally requires ≥120 ms plus characteristic morphology.
A wide QRS may reflect ventricular origin or supraventricular activation with aberrancy, pre-excitation, pacing, or metabolic/drug effects.
QRS morphology and voltage add diagnostic clues but must be interpreted with the full 12-lead ECG and clinical context.

References and further reading

1. Larkin J.QRS Interval. Life in the Fast Lane (LITFL) ECG Library Basics. Published August 1, 2020. Supplied PDF reference. Source article. The supplied LITFL resource states that it is distributed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International licence; review the licence and obtain permission where required before commercial reuse or adaptation.

2. Surawicz B, Childers R, Deal BJ, et al.AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: Part III: intraventricular conduction disturbances. J Am Coll Cardiol. 2009;53(11):976–981. doi:10.1016/j.jacc.2008.12.013. DOI.

3. Kligfield P, Gettes LS, Bailey JJ, et al.Recommendations for the standardization and interpretation of the electrocardiogram: Part I: the electrocardiogram and its technology. Circulation. 2007;115(10):1306–1324. doi:10.1161/CIRCULATIONAHA.106.180200. DOI.

4. Hancock EW, Deal BJ, Mirvis DM, et al.AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: Part V: electrocardiogram changes associated with cardiac chamber hypertrophy. J Am Coll Cardiol. 2009;53(11):992–1002. doi:10.1016/j.jacc.2008.12.015. DOI.

5. Sharma S, Drezner JA, Baggish A, et al.International criteria for electrocardiographic interpretation in athletes: consensus statement. International criteria for electrocardiographic interpretation in athletes: consensus statement. Br J Sports Med. 2017;51:704–731. doi:10.1136/bjsports-2016-097331. DOI.

Medical education disclaimer: This page is intended for educational purposes and does not replace clinical assessment, expert ECG interpretation, local protocols, or emergency management pathways. ECG findings must be interpreted in the context of symptoms, examination, previous tracings, medications, laboratory results, and haemodynamic status.