ECG criteria
- QRS duration: measure from the earliest onset to the latest offset using all available leads; in practice, the lead with the greatest measured duration is often chosen
- Normal duration: 0.06–0.10 s (60–100 ms); some guidelines allow up to 0.11 s as the upper limit of normal
- Wide QRS: ≥0.12 s (120 ms) — indicative of bundle branch block, pre-excitation, ventricular rhythm, or drug toxicity
- Amplitude: evaluated in mm (1 mm = 0.1 mV at standard calibration of 10 mm/mV)
- Morphology: presence and ratio of q, R, and S waves in each lead, direction of the main vector
- Precordial transition zone: usually between V3 and V4 (R=S)
- Intrinsicoid deflection time: from QRS onset to the peak of R, in V1 normal up to 0.035 s, in V6 up to 0.045–0.05 s
What it looks like on ECG
The QRS complex begins with the first deviation from the isoelectric line after the P wave (or from the end of the PR segment) and ends at the J point where the ST segment begins. It is usually described by the Q, R, and S components, but can be multiphasic and contain additional R′/S′ waves or notchings:
- Q — first negative deflection (not always present)
- R — first positive deflection
- S — negative deflection following R
Letters are written in uppercase if the wave is large (≥5 mm) and lowercase if small. Variants include: qR, QS, RS, rsR', qRs, etc.
Morphology changes predictably across the precordial leads: S predominates in V1–V2 (LV vector points away from the electrode), while R predominates in V5–V6. The transition from an S-dominant to an R-dominant complex is the transition zone, normally around V3–V4.
| Lead | Typical morphology |
|---|---|
| V1 | rS or QS (isolated QS in V1 is a possible normal variant) |
| V2 | rS with initial r (QS in V2 requires checking electrode placement and clinical context) |
| V3–V4 | transition zone, RS |
| V5–V6 | qR, tall R |
| I, II | qR or R |
| aVR | QS or rS |
QRS duration is measured in the lead where the complex appears widest (often V2–V3), from the beginning to the end of all its waves, including the smallest notches.
Mechanism
The QRS complex reflects the propagation of the depolarization wave through the ventricular myocardium. The impulse from the AV node travels through the bundle of His, its right and left branches (with left anterior and posterior fascicles), and then via Purkinje fibers to the working myocardium. First, the interventricular septum is activated from left to right (producing a small q wave in left leads and r in right leads), then the main mass of both ventricles, predominantly the LV as the more massive one (forming R in left leads and S in right leads), and lastly the basal regions and outflow tracts.
QRS duration depends on conduction velocity through the specialized conduction system: with normal conduction through both bundle branches, ventricular depolarization takes 0.06–0.10 s. Any delay (bundle branch block, aberrant conduction, ventricular ectopic focus, sodium channel-blocking drugs) slows impulse propagation through the myocardium instead of the rapid conduction system, widening the QRS.
Normal Variants
- A small septal q wave in I, aVL, V5–V6 is normal, reflecting septal depolarization
- Absence of q in V5–V6 in young individuals is a normal variant
- Isolated QS in V1 is a possible normal variant with a vertical heart position; QS simultaneously in V1–V2 or QS in V2 requires checking the correct placement of precordial electrodes and correlating with the rest of the ECG and clinical picture, as this pattern also occurs in prior anteroseptal myocardial infarction
- QRS duration of 0.10–0.11 s in some healthy individuals (borderline zone between normal and nonspecific conduction disturbance)
- In children and athletes, more prominent R-wave morphology in the right precordial leads can occur without pathology
Pathological changes
- QRS widening ≥0.12 s — right or left bundle branch block, nonspecific intraventricular conduction delay, pre-excitation (WPW, delta wave), hyperkalemia, class I antiarrhythmics and tricyclic antidepressant effect, ventricular rhythm (extrasystole, VT, idioventricular rhythm)
- Pathological Q wave — according to the Fourth Universal Definition of Myocardial Infarction criteria: Q duration ≥0.03 s and depth ≥0.1 mV (≥1 mm), or a QS complex, in two contiguous leads of a lead group (I/aVL; V1–V6; II/III/aVF); for V2–V3, special criteria apply — Q ≥0.02 s or a QS complex in V2 and V3. A pathological Q is a marker of prior myocardial infarction scar, but is not synonymous with it: a similar pattern can be caused by hypertrophic cardiomyopathy, bundle branch block, pre-excitation, pneumothorax, and other conditions, so Q must be evaluated only in conjunction with clinical findings and the rest of the ECG
- Low QRS voltage — obesity, emphysema, pericardial effusion, hypothyroidism
- High QRS voltage — ventricular hypertrophy (Sokolow–Lyon criteria, Cornell criteria)
- QRS notching — may be a normal variant or a marker of scar/fibrosis
- Shift of the transition zone — the lead where R=S may shift to the left (later, toward V5–V6) or to the right (earlier, toward V1–V2) in bundle branch blocks, ventricular hypertrophy, infarction, improper precordial electrode placement, or cardiac axis rotation. A transition zone shift per se is a nonspecific finding and is interpreted only alongside QRS morphology, complex duration, and clinical data
Clinical significance and management
QRS analysis is a key step in ECG interpretation following the assessment of rhythm and intervals. The physician must: 1) measure the duration using all leads to determine the earliest onset and latest offset; 2) evaluate morphology — a narrow complex indicates normal conduction or supraventricular origin of rhythm, while a wide complex requires differentiation between ventricular rhythm, SVT with aberrancy, pre-excitation, cardiac pacing, hyperkalemia, and drug toxicity; 3) review lead-specific morphology to diagnose bundle branch blocks, hypertrophy, and scarring; 4) correlate with clinical findings — sudden QRS widening in a patient with chest pain or hyperkalemia requires immediate action.
A wide QRS during tachycardia should be treated as ventricular tachycardia until proven otherwise, especially in a patient with a history of structural heart disease. In known or suspected severe hyperkalemia, any ECG changes, especially QRS widening, require immediate evaluation and protocol-driven treatment — typical sequence of changes: peaked T waves, followed by progressive interval prolongation and QRS widening as hyperkalemia worsens. A pathological Q wave is used in conjunction with clinical findings and ST-T dynamics to diagnose prior infarction.
Common interpretation errors
- Measuring QRS duration in only a single lead (e.g., II) without checking V2–V3, where the complex is often wider or may have an earlier onset/later offset
- Confusing a normal septal q wave with a pathological infarction Q wave without considering contiguous lead criteria, depth, and width
- Disregarding calibration when assessing amplitude (LVH/RVH voltage criteria depend on standard 10 mm/mV)
- Mistaking an artifact or baseline wander for QRS notching
- Forgetting that in bundle branch block, standard QRS criteria for infarction and hypertrophy do not apply without adjustments (e.g., Sgarbossa criteria in LBBB)
1. What QRS complex duration is considered the threshold for a "wide" complex requiring investigation of the cause?
Normal QRS duration is 0.06–0.10 s (up to 0.11 s according to some guidelines); values ≥0.12 s are considered a widened complex.
2. In which lead is the QS QRS morphology typically seen normally?
In aVR, the net ventricular depolarization vector is directed away from the electrode, so QS morphology without a prominent R wave is typical.
3. What does the QRS complex on an ECG reflect?
The QRS complex corresponds to the propagation of the depolarization wave through the ventricular myocardium via the His-Purkinje system and working myocardium.
Frequently asked questions
Why doesn't every QRS complex contain all three waves?
The presence of Q, R, and S waves depends on the direction of the net ventricular depolarization vector relative to a specific lead. For example, in aVR, the vector is directed in the opposite direction, which is why a QS complex without a prominent R wave is typical there.
What QRS duration is considered normal?
Normally, the QRS complex duration is 0.06–0.10 s (60–100 ms), with some guidelines allowing an upper limit of up to 0.11 s. Values ≥0.12 s are considered a widened complex, requiring a search for the cause (bundle branch block, pre-excitation, ventricular rhythm, drug toxicity).
How to differentiate a wide QRS caused by a bundle branch block from ventricular tachycardia?
During sinus rhythm, QRS morphology and consistency from cycle to cycle generally correspond to a known block. In wide QRS tachycardia, algorithms (Brugada criteria, Vereckei algorithm) are used, assessing AV dissociation, fusion, and capture beats—these features indicate ventricular tachycardia.
What is the QRS transition zone and why evaluate it?
The transition zone is the lead where the R and S wave amplitudes become equal (usually V3–V4). Shifting of the transition zone to the left or right is a non-specific sign that helps diagnose bundle branch blocks, ventricular hypertrophy, and incorrect precordial electrode placement only when evaluated alongside the rest of the ECG.
Is widening of the QRS complex dangerous?
Widening alone does not indicate prognosis without clinical context. Acute QRS widening in a patient with chest pain, hyperkalemia, or cardiotoxic drug ingestion requires urgent evaluation, whereas a chronic bundle branch block in a stable patient may be a long-standing finding without acute threat.
ECG Course
Interpretation from basics to myocardial infarction — learn to read any ECG using a systematic algorithm.
- Video lessons and theory for every topic
- Simulator case studies under every lesson
- Unlimited ECG simulator practice
- Study guide: "All ECGs in 25 minutes"
ECG Strip Simulator
ECG, radiology, histology, pathomorphology, pharmacology — thousands of flashcards with detailed explanations.
- Real ECG strips, not textbook drawings
- Instant answers and explanations
- Streaks and progress tracking in your dashboard
Related terms
More in the section «Basics: waves, intervals, axes»
Sources
- Goldberger's Clinical Electrocardiography, 9th ed.
- Hampton, The ECG Made Easy
- AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the Electrocardiogram, 2009
- Orlov V.N., Electrocardiography Guide
Educational material for medical students and physicians. Does not replace clinical guidelines and physical examination; the ECG must always be interpreted in conjunction with the clinical picture.