Brugada criteria for VT

What it looks like on ECG

The algorithm is analyzed using 12 leads recorded during regular monomorphic wide QRS tachycardia.

Step 1 — concordance. Examine all precordial leads V1–V6: is there an RS-type complex (an R wave followed by an S) in at least one lead? If RS is absent in all leads (completely positive or completely negative QRS concordance in the precordial leads) — this is VT, no further checks are needed.

Step 2 — RS interval. If an RS complex is present in at least one precordial lead, measure the interval from the onset of the R wave to the deepest point (nadir) of the S wave in all precordial leads with an RS complex. At 25 mm/s, 1 mm = 0.04 s. If this distance is greater than 100 ms (2.5 mm) in at least one precordial lead — VT.

Step 3 — AV dissociation. Search for P waves that are unrelated to QRS complexes (different rate, independent atrial and ventricular rhythm). Dissociation sharply increases the probability of VT and is considered a diagnostic sign within the algorithm, but its absence does not exclude VT — 1:1 retrograde conduction to the ventricles may persist in VT. Signs that also favor VT include fusion beats and ventricular capture beats, although formally they are not part of the 4 main steps.

Step 4 — morphological criteria. Evaluate the QRS morphology in V1 (or V2) and V6 separately for the suspected RBBB pattern and the LBBB pattern; these are not a mandatory combination of features, but individual features within their respective morphology, each supporting VT. For RBBB-type morphology, signs favoring VT include a monophasic R or qR in V1/V2 or an R/S ratio <1 in V6. For LBBB-type morphology — an initial R wider than 30 ms, an interval from R onset to S nadir greater than 60 ms, notching on the downslope of S in V1/V2, or qR or QS in V6.

אם לא התקיים אף אחד מ-4 הקריטריונים — התוצאה מצביעה לטובת SVT עם הולכה אברנטית, אך אינה שוללת VT בוודאות מוחלטת.

Mechanism

In VT, the impulse originates in the ventricle and spreads through the myocardium slowly, bypassing the rapid His-Purkinje system, which is why the ventricles depolarize asynchronously and longer — hence the wide, atypical QRS and prolonged R-S interval. In SVT with aberration, the impulse arrives from above via the AV node and typically propagates through the existing, albeit partially blocked, bundle branch conduction system, which is why the QRS morphology more closely resembles a classic bundle branch block, and initial depolarization occurs faster. This is a trend, not an obligatory rule: in underlying conduction system disease, drug-induced conduction slowing, or concealed pre-excitation, the aberration morphology may deviate from the classic presentation; therefore, morphological criteria are not absolute, and a negative algorithmic result does not rule out VT. AV dissociation in VT reflects independent atrial and ventricular activation, whereas in SVT they are typically linked by retrograde or antegrade conduction.

Causes

The algorithm is applied in regular monomorphic wide QRS tachycardia of unclear origin, which may be caused by:

• monomorphic ventricular tachycardia (ischemic, scar-related, in cardiomyopathies)
• supraventricular tachycardia with baseline bundle branch block
• supraventricular tachycardia with rate-dependent (tachycardia-dependent) bundle branch block
• antidromic tachycardia in WPW syndrome
• tachycardia in patients taking QRS-widening drugs (sodium channel blockers)

Polymorphic VT, irregular wide QRS tachycardia (e.g., AF with pre-excitation), and hemodynamically unstable tachycardia are outside the scope of the algorithm — other approaches and emergency protocols are used for them.

Differential diagnosis

• SVT with aberration — distinguished by the preservation of classic RBBB/LBBB morphology, absence of AV dissociation, RS >100 ms, and concordance, while taking into account the limited specificity of criteria in baseline intraventricular conduction disturbances.
• Antidromic tachycardia in WPW — the Brugada algorithm often fails in such tachycardias because the QRS morphology does not match classic aberrations; when WPW is suspected, one should also rely on the Vereckei algorithm and the clinical context, keeping in mind that both algorithms can be unreliable in pre-excitation.
• Polymorphic or irregular wide QRS tachycardia — sequential evaluation of the RS interval, AV dissociation, and morphology in such tachycardia is not validated; it is managed according to algorithms for polymorphic VT/irregular tachycardia rather than Brugada.
• Artifact or motion interference mimicking a wide QRS — check for morphological stability in adjacent complexes and other leads.
• True narrow QRS tachycardia distorted by electrode placement — verify correct lead placement.

Clinical significance and management

Proper differentiation between VT and SVT with aberration directly determines management: VT requires alertness for hemodynamic instability and readiness for cardioversion or antiarrhythmic therapy. In unstable regular monomorphic tachycardia with a pulse, immediate synchronized cardioversion is performed. In unstable polymorphic VT or pulselessness — an unsynchronized shock (defibrillation) according to cardiac arrest protocols, without waiting for the Brugada algorithm to be completed. In a hemodynamically stable patient with regular monomorphic wide QRS tachycardia, when SVT is truly likely, vagal maneuvers or adenosine are acceptable in some cases; in irregular tachycardia, suspected pre-excitation, polymorphic tachycardia, or instability, they may be dangerous or ineffective. In case of diagnostic uncertainty in an adult patient with regular wide QRS tachycardia, the rule is to treat it as VT until proven otherwise, as this strategy is safer for the patient. The Brugada algorithm has high but not absolute sensitivity — false-positive and false-negative results have been reported, especially in WPW antidromic tachycardias and with conduction-slowing drugs. Therefore, it is used as one of the tools alongside the clinical picture (age, prior myocardial infarction, structural heart disease), medical history, and, if possible, comparison with the patient's baseline sinus rhythm ECG.

Common interpretation errors

• Starting evaluation not from the first step, but immediately looking for morphological criteria — skipping more reliable and earlier features (concordance, RS >100 ms).
• Confusing AV dissociation with rhythm irregularity — dissociation specifically requires independent atrial and ventricular rhythms.
• Measuring the RS interval in only a single arbitrary lead rather than all precordial leads with an RS complex, and missing a value >100 ms.
• Applying the algorithm to polymorphic, irregular tachycardia, or tachycardia with known pre-excitation (WPW), for which it is not intended.
• The negative result of all 4 steps is interpreted as a definitive diagnosis of SVT, forgetting that it only favors SVT and does not rule out VT with absolute reliability.

Frequently asked questions

Related terms

More in the section "Criteria, Formulas, Algorithms"

Entire section

Sources

• Surawicz B., Knilans T. Chou's Electrocardiography in Clinical Practice
• Hampton J. The ECG in Practice
• Brugada P. et al., original algorithm for differential diagnosis of wide QRS tachycardia (1991)
• Orlov V.N. Guide to Electrocardiography

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.