ECG criteria
- QRS width: assess whether the QRS is genuinely wide ($\ge$120 ms) or if it is a calibration artifact
- Regularity: irregular wide QRS — consider AF with aberrancy or pre-excitation
- AV dissociation: P waves are independent of QRS, beating at their own rhythm — a strong but not absolute sign of VT; capture and fusion beats are particularly specific, though their absence does not exclude VT
- Capture and fusion beats strongly support the diagnosis of VT and have very high specificity; their presence is practically diagnostic, but they should be evaluated in the context of the entire ECG
- QRS concordance in chest leads (all positive or all negative from V1 to V6) is a sign of VT; negative concordance is more specific than positive concordance
- Brugada criteria (evaluated sequentially, up to the first positive answer): 1) absence of an RS complex in all chest leads V1–V6 — VT; 2) RS interval >100 ms (from the onset of R to the nadir of S) in any chest lead — VT; 3) AV dissociation — VT; 4) morphological criteria for VT in V1/V2 and V6 (see the "ECG Appearance" section)
- Vereckei algorithm (aVR, evaluated sequentially, any positive criterion favors VT): initial R wave in aVR; initial r or q in aVR of >40 ms duration; notch on the initial downstroke of r or q in aVR; $v_i/v_t$ ratio $\le$1
- Comparison with baseline ECG: concordance of QRS morphology with a known bundle branch block in sinus rhythm points toward SVT with aberrancy
What it looks like on ECG
Wide QRS tachycardia ($\ge$120 ms) is a broad category that may represent ventricular tachycardia (VT) or supraventricular tachycardia (SVT) with aberrant conduction (bundle branch block, functional or organic) or with pre-excitation via an accessory pathway.
Brugada morphological criteria are strictly divided based on the QRS shape in V1 and do not overlap between types. For RBBB-type QRS (broad R or RS in V1): favoring VT are a monophasic R or qR complex in V1 (without the typical triphasic notched $rSR'$); in V6 — QS, QR, or R/S < 1. For LBBB-type QRS (broad S in V1): favoring VT are an initial R wave width in V1 >30 ms, an interval from QRS onset to the nadir of S in V1–V2 >60 ms, a notch/slurring on the downstroke of S in V1–V2 (Josephson's sign), and any Q wave in V6 (QR or QS).
Key landmarks by leads:
| Sign | Favors VT | Favors SVT with aberrancy |
|---|---|---|
| AV dissociation | characteristic, especially with capture/fusion beats | absent (P waves are coupled to QRS if visible) |
| V1–V6 concordance | complete negative concordance is a strong sign; complete positive concordance also increases the likelihood of VT, but is less specific and requires ruling out pre-excitation | absent |
| Morphology in RBBB pattern (V1) | monophasic R or qR in V1, R/S < 1 in V6 | typical RBBB (triphasic $rSR'$ in V1) |
| Morphology in LBBB pattern (V1–V2, V6) | initial R >30 ms, S nadir >60 ms from QRS onset, notch on S downstroke, any Q in V6 | typical bundle branch block configuration without these features |
| RS in chest leads | absent or RS >100 ms | RS <100 ms, typical appearance |
| QRS Axis | marked axis deviation, northwest axis | normal for bundle branch block |
In irregular wide QRS with rates exceeding 200 bpm and variable morphology, atrial fibrillation with WPW syndrome must be ruled out — in this condition, QRS width and shape vary from beat to beat.
Mechanism
Wide QRS in tachycardia arises from one of three mechanisms. First, the impulse originates in the ventricle (VT), and excitation spreads through the myocardium rather than the specialized conduction system, traveling more slowly and asynchronously for both ventricles — hence the width and unusual morphology. Second, a supraventricular impulse encounters a bundle branch block: organic, or functional rate-dependent aberrancy (rate-dependent bundle branch block with tachycardia), including Ashman phenomenon as a specific case (aberrancy in a beat terminating a short cycle that immediately follows a long cycle). In this case, one ventricle is depolarized with a delay via the interventricular septum. Third, a supraventricular impulse is conducted via an accessory pathway (antidromically in WPW), bypassing the AV node, which also produces a wide and abnormal QRS.
Causes
- Ventricular tachycardia: coronary artery disease and post-infarction scar, cardiomyopathies, channelopathies
- SVT with aberrancy: any supraventricular tachycardia (AVRT, AVNRT, atrial tachycardia, atrial flutter, or atrial fibrillation) with concomitant bundle branch block or rate-dependent aberrancy
- Antidromic tachycardia or AF in WPW syndrome with conduction over an accessory pathway
- Electrolyte disturbances and antiarrhythmic drugs that widen the QRS and complicate interpretation
Differential diagnosis
- Sinus tachycardia with baseline bundle branch block — compare with the patient's resting ECG; morphology matches
- Tachycardia in severe hyperkalemia — QRS is diffusely widened, T wave is tall and peaked, typical bundle branch block morphology is absent
- AF with pre-excitation (WPW) — irregular rhythm with variable QRS width and shape, rate may exceed 200 bpm
- Artifact or lead placement mimicking QRS widening — check all leads and repeat the ECG
Clinical significance and management
Any wide QRS tachycardia of unclear etiology in an adult should be managed as VT by default until proven otherwise — this protects against the fatal error of misdiagnosing true VT as SVT and treating it as a benign arrhythmia. The clinician should assess hemodynamics first: in unstable regular tachycardia with a pulse (hypotension, pulmonary edema, altered mental status, anginal pain), perform immediate synchronized cardioversion without delaying for differential diagnosis; in polymorphic VT, ventricular fibrillation, or pulseless arrest, deliver an unsynchronized shock/defibrillation according to resuscitation guidelines. In stable patients, record a 12-lead ECG, compare with baseline sinus rhythm ECG, apply the Brugada criteria and Vereckei algorithm, and evaluate the clinical history. Advanced age, coronary artery disease, prior myocardial infarction, and depressed left ventricular function significantly increase the probability of VT and are considered supporting features, but do not replace the ECG algorithm. Verapamil administration is contraindicated in wide QRS tachycardia of unknown etiology, as it may precipitate circulatory collapse in true VT. Adenosine may be considered as a diagnostic/therapeutic test only in stable regular monomorphic tachycardia without features of pre-excitation and must not delay electrical therapy; it is not used in irregular or polymorphic wide-complex tachycardia.
Common interpretation errors
- Relying solely on hemodynamic stability as a criterion for SVT — VT can be well-tolerated for prolonged periods without instability
- Ignoring the patient's prior ECG showing baseline bundle branch block, which would help quickly confirm aberrancy
- Administering verapamil "just in case" for wide QRS tachycardia of unclear origin
- Missing AV dissociation due to P waves being obscured by QRS or T waves
- Interpreting an irregular wide QRS as typical AF with aberrancy without ruling out AF with WPW
"A wide QRS without proven SVT is VT until proven otherwise."
1. Which feature is most specific for ventricular tachycardia in wide QRS tachycardia?
AV dissociation with capture and fusion beats indicates that the atria and ventricles are beating independently, which is characteristic of VT.
2. Which of the following is a criterion of the Vereckei algorithm for diagnosing VT?
The Brugada/Vereckei algorithm analyzes the initial part of the QRS complex in lead aVR; an initial r wave duration of more than 40 ms favors VT.
3. How should a physician manage a tachycardia with a wide QRS of unclear origin and stable hemodynamics?
By default, wide QRS tachycardia of unclear origin is treated as VT, because misdiagnosing it as SVT can be fatal.
Frequently asked questions
How to distinguish VT from SVT with aberration on ECG?
The main pillars are signs of AV dissociation, capture and fusion beats, complete QRS concordance in the precordial leads, and specific morphology in V1 and V6 according to the Brugada criteria and Vereckei algorithm. Comparison with a baseline sinus rhythm ECG in known bundle branch block often resolves the question faster than any formulas.
Is wide QRS tachycardia dangerous?
Yes, by default it should be considered a potentially life-threatening VT until proven to be SVT with aberration. Misdiagnosing VT as a benign arrhythmia and administering verapamil can lead to hemodynamic collapse.
Can the patient's age and medical history be used for diagnosis?
Yes, this is a significant supportive criterion: advanced age, coronary artery disease, prior myocardial infarction, and reduced left ventricular function substantially increase the likelihood of VT. However, these factors are considered as an adjunct to the ECG algorithm rather than a replacement—supraventricular tachycardia with aberration also occurs in such patients.
What to do if the type of tachycardia remains unclear?
In stable hemodynamics, tachycardia with an unclear wide QRS is interpreted and treated as VT. In case of instability, immediate cardioversion is indicated (synchronized for regular tachycardia with a pulse, unsynchronized shock for polymorphic VT or pulselessness) without delaying diagnosis.
How does the Brugada lead aVR algorithm differ from the Brugada criteria?
The Vereckei algorithm uses only 4 criteria, including the analysis of the initial part of QRS in lead aVR, and works faster at the bedside, whereas the Brugada criteria go through four consecutive steps assessing precordial leads and the RS interval.
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Related terms
More in the section "Criteria, Formulas, Algorithms"
Sources
- Goldberger's Clinical Electrocardiography, 9th Edition
- Surawicz, Knilans. Chou's Electrocardiography in Clinical Practice, 6th Edition
- Hampton. The ECG in Practice, 6th Edition
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.