Clinical background
In regular wide complex tachycardia (QRS duration ≥120 ms, rate >100/min) the clinician faces an acute differential diagnosis: ventricular tachycardia (VT) versus supraventricular tachycardia (SVT) with aberrant conduction. The decision has immediate consequences for the choice of antiarrhythmic drug, the need for resuscitation and further investigation. VT accounts for up to 80% of cases [4], but haemodynamic tolerance overlaps heavily between the groups, and a stable patient may well have VT. The history (previous myocardial infarction, structural heart disease) has a positive predictive value for VT of over 95% [4], but is not sufficient on its own to exclude SVT.
The Brugada criteria were developed precisely because earlier ECG criteria had low specificity and were often absent altogether. The algorithm offers a sequential, stepwise approach in which each step is designed to have high specificity for VT, so that a positive step establishes the diagnosis immediately.
Applying the Brugada criteria
The algorithm is applied sequentially and stops at the first positive step:
If any RS complex is present, proceed:
If the RS interval is ≤100 ms in all leads, proceed:
If no AV dissociation is demonstrated, proceed:
A positive step diagnoses VT. If no step is positive, the rhythm is classified as SVT with aberrancy.
The variables in detail:
- Step 1: An RS complex is defined as a complex in which both an R wave and an S wave are present in the same precordial lead. Pure positive concordance (R in all of V1–V6) or pure negative concordance (QS in all of V1–V6) means the absence of an RS complex and is diagnostic of VT.
- Step 2: The RS interval is measured from the onset of the R wave to the nadir of the S wave in the precordial lead in which the interval is longest. An interval above 100 ms reflects slow initial ventricular depolarisation, which is typical of myocardial VT but not of SVT conducted through the His–Purkinje system [4].
- Step 3: AV dissociation means that atrial and ventricular activity are independent of each other. It may be demonstrated by irregular P waves unrelated to the QRS, capture beats (narrow, sinus-conducted QRS complexes among wide ones) or fusion beats. Specificity approaches 100%, but sensitivity is low (20–50% of all VT) [4].
- Step 4: The morphology criteria differ according to the bundle branch block-like pattern. In a right bundle branch block-like pattern (broad R in V1), VT-typical morphology is required in V1–V2 (monophasic R, qR, or RS with the R broader than the S, or a triphasic complex with the R taller than the R') and in V6 (R/S ratio <1 or QS). In a left bundle branch block-like pattern (broad S in V1), a broad R onset (>30–40 ms) in V1–V2 and a QS or QR complex in V6 are required.
Derivation cohort: Brugada et al. prospectively analysed 554 wide complex tachycardias (384 VT and 170 SVT) at a cardiology centre in Aalst, Belgium [1]. The gold standard was electrophysiological study. The sensitivity of the four steps taken together was 0.987 and the specificity 0.965 [1].
Interpretation in practice
The algorithm is binary: a positive step means VT, and if no step is triggered the rhythm is classified as SVT with aberrancy. There are no intermediate categories.
| Result | Interpretation | Clinical action |
|---|---|---|
| Any of steps 1–4 positive | VT | Treat as VT: amiodarone, procainamide or electrical cardioversion depending on haemodynamics. Avoid verapamil/diltiazem. |
| No step positive | SVT with aberrancy | Treat as SVT: vagal manoeuvres, adenosine, beta blocker or calcium channel blocker (if haemodynamically stable). |
A positive Step 1 or Step 2 is the easiest to assess and had the highest specificity in the derivation cohort. Step 3 requires careful searching for P waves, capture or fusion beats, and can be facilitated by the Lewis lead or by M-mode echocardiography [4]. Step 4 is the most complex and the one with the greatest inter-observer variability.
Validation and performance
In the original derivation cohort, performance was exceptionally high (sensitivity 98.7%, specificity 96.5%) [1]. External validations have, however, shown considerably poorer results, particularly with respect to specificity.
A systematic review and meta-analysis from 2023 included 11 studies of the Brugada algorithm, in total 3,422 patients with wide complex tachycardia in whom electrophysiological study was the gold standard [2]. Pooled sensitivity was 90.25% (95% CI 85.40–93.62) and pooled specificity 64.02% (95% CI 49.34–77.48). The area under the SROC curve was 0.94. The diagnostic odds ratio (DOR) was 16.48 (95% CI 6.25–43.48), which was lower than for both Vereckei-pre (DOR 60.70) and RWPT-II (DOR 27.00) [2]. Heterogeneity was high (I² 86–90% for sensitivity and specificity).
In a head-to-head comparison of five algorithms, Jastrzebski et al. retrospectively analysed 260 wide complex tachycardias (159 VT, 101 SVT) from 204 patients [3]. The Brugada algorithm had a sensitivity of 89.0%, a specificity of 59.2% and a diagnostic accuracy of 77.5%. None of the newer algorithms (Vereckei-aVR, Vereckei-pre, RWPT-II) was significantly more accurate than Brugada, but they differed in their sensitivity and specificity profiles [3].
The marked fall in specificity compared with the derivation cohort may be explained by several factors: patient selection (the derivation cohort came from an electrophysiological referral centre with a high proportion of VT), inter-observer variability particularly at Step 4, and the fact that external cohorts often include a higher proportion of SVT with aberrancy, which increases the number of false positives.
Limitations
The Brugada criteria are intended only for regular, monomorphic wide complex tachycardias. They must not be applied to irregular rhythms, above all not to atrial fibrillation with aberrancy, since the RS interval and morphology criteria cannot be assessed reliably at varying cycle length.
Pre-excited tachycardias (antidromic AVRT, atrial flutter with antegrade conduction over an accessory pathway) account for 1–5% of wide complex tachycardias [4] and are the algorithm's greatest pitfall. Because ventricular depolarisation occurs by myocardial conduction from an accessory pathway, pre-excited rhythms often meet the Brugada morphology criteria for VT and may be misclassified as VT. Positive precordial concordance, which triggers Step 1, can occur in pre-excited SVT over a left posterior accessory pathway [4]. The algorithm therefore cannot distinguish VT from pre-excited rhythms.
Pacing artefacts from modern pacemakers can be subtle on the surface ECG and mimic VT morphology. A pacemaker-mediated tachycardia may incorrectly satisfy the Brugada criteria [4].
Step 3 (AV dissociation) has low sensitivity (20–50%), since approximately 30% of all VT has 1:1 retrograde VA conduction [4]. The absence of demonstrable AV dissociation therefore does not exclude VT. Capture and fusion beats are specific but uncommon and require a slow VT with sinus activity able to capture the ventricles.
Step 4 is subjective and requires experience in morphological ECG interpretation. It is the step with the lowest inter-observer agreement and the one in which most misclassifications occur in external validations.
Drug-affected rhythms (class IA, IC, amiodarone) can widen the QRS and shift the RS interval, which may lead to a falsely positive Step 2 [4]. Hyperkalaemia can have similar effects.
References
- Brugada P, Brugada J, Mont L, Smeets J, Andries EW. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation. 1991;83(5):1649-59. PMID: 2022022
- Sun X, Teng Y, Mu S et al. Diagnostic accuracy of different ECG-based algorithms in wide QRS complex tachycardia: a systematic review and meta-analysis. BMJ Open. 2023;13(7):e069273. PMID: 37487685
- Jastrzebski M, Kukla P, Czarnecka D, Kawecka-Jaszcz K. Comparison of five electrocardiographic methods for differentiation of wide QRS-complex tachycardias. Europace. 2012;14(8):1165-71. PMID: 22333239
- Vereckei A. Current algorithms for the diagnosis of wide QRS complex tachycardias. Curr Cardiol Rev. 2014;10(3):262-76. PMID: 24827795