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Brugada Criteria (VT vs SVT)

Brugada Algorithm

Circulation 1991: Stepwise Diagnosis of WCT

Criterion 1 of 4

Absence of an RS complex in all precordial leads?

Examine V1–V6. If there are ONLY monophasic R, QS, or QR waves (positive or negative concordance), the diagnosis is VT.

Diagnostic Tips

Step 1 definition: Complexes like QR, QS, or monophasic R are not considered RS complexes.

Step 2 (RS > 100ms): Measure from the R deflection start to the S-wave nadir. 100ms = 2.5 small boxes.

Clinical Warning

Treatment for Wide Complex Tachycardia should prioritize ACLS protocols. In hemodynamically unstable patients, synchronize cardioversion immediately.

Guidelines & Evidence

Verified

Last Review: 2026-07-17

When to Use

When to Use the Brugada Algorithm

Primary Indication: Patients presenting with a regular wide-complex tachycardia (WCT) on 12-lead ECG with QRS duration ≥120 ms (0.12 seconds)
Differentiation Goal: Distinguish Ventricular Tachycardia (VT) from Supraventricular Tachycardia (SVT) with aberrant conduction (bundle branch block)
Clinical Context: Hemodynamically stable patients where a 12-lead ECG can be obtained before treatment
Epidemiologic Rationale: 80% of all wide-complex tachycardias are VT; in patients >50 years or with structural heart disease, >90% are VT
Secondary Use: Differential diagnosis of wide-complex tachycardia in emergency departments, intensive care units, and cardiology consultations

Do NOT Use If (Absolute Contraindication)

Patient is hemodynamically unstable. In the setting of instability (hypotension with systolic BP <90 mmHg, altered mental status, ischemic chest pain, acute heart failure, pulmonary edema, or cardiogenic shock), immediately proceed to synchronized DC cardioversion regardless of the rhythm mechanism. Do NOT delay treatment to apply diagnostic algorithms.

The Three Main Causes of Wide-Complex Tachycardia

CauseFrequencyElectrophysiologic MechanismECG Clues
Ventricular Tachycardia (VT)80% (90% if age >50 or structural disease)Re-entry, automaticity, or triggered activity originating in ventricular myocardium (outside His-Purkinje system). Cell-to-cell conduction is slow (myocyte-to-myocyte).AV dissociation, fusion/capture beats, extreme axis deviation, very wide QRS (>160 ms), precordial concordance, Brugada criteria positive.
SVT with Aberrant Conduction15%SVT (AVNRT, AVRT, atrial tachycardia, atrial flutter) conducted to ventricles with rate-related bundle branch block (phase 3 block) or pre-existing BBB.Typical RBBB or LBBB morphology, normal axis (except in RBBB where right axis is possible), RS interval <100 ms, Brugada criteria negative.
SVT with Accessory Pathway (Antidromic AVRT)3-5% (WPW syndrome)SVT where impulse travels anterograde down accessory pathway and retrograde up AV node. Entire ventricular activation is via accessory pathway (preexcited).Very wide QRS (>140 ms), delta wave visible (compare to sinus), mimics VT. Brugada algorithm often MISCLASSIFIES antidromic AVRT as VT (false positive). Rare, but consider in young patients with known WPW.

Clinical Warning: The 80/95 Rule

STATISTICAL REALITY: 80% of all wide-complex tachycardias are VT. In patients over 50 years of age or with known structural heart disease (prior MI, cardiomyopathy, heart failure), that figure exceeds 95%. CLINICAL IMPLICATION: When in doubt about the Brugada algorithm results, ALWAYS default to treating the rhythm as VT. Misdiagnosing VT as SVT can lead to administration of AV nodal blocking agents (adenosine, verapamil, diltiazem, beta-blockers) which are contraindicated in VT (may cause hemodynamic collapse, degeneration to VF, or death). The safer diagnostic error is to treat SVT as VT (with synchronized cardioversion or procainamide) rather than VT as SVT.

How it Works

Electrophysiologic Basis of the Algorithm

The Brugada algorithm exploits fundamental differences in ventricular activation between VT and SVT with aberrancy. In SVT with aberrant conduction, the impulse originates in the atria or AV node and depolarizes the ventricles via the normal His-Purkinje network—just with a bundle branch block. This results in relatively rapid ventricular activation (narrower QRS, shorter RS interval) and typical bundle branch block morphologies. In VT, the impulse originates in the ventricular myocardium and spreads cell-to-cell (myocyte-to-myocyte) outside the Purkinje system. This produces slower activation (wider QRS, longer RS interval), aberrant vectors (precordial concordance, extreme axis), and independent atrial and ventricular activity (AV dissociation).

Step 1: Absence of an RS Complex in ALL Precordial Leads (V1-V6)

CRITERION: Is there an RS complex in ANY precordial lead? • RS Complex DEFINITION: A biphasic complex with a clear R wave followed by a clear S wave (both positive and negative deflections). • NOT an RS complex: QR, QS, monophasic R, monophasic QS, rSR, or any complex without a clear R-to-S transition. If NO RS complex in ANY precordial lead → STOP → DIAGNOSE VT (100% specificity) If YES (RS complex present in at least one lead) → PROCEED to Step 2

Step 1 Explanation: Precordial Concordance

Absence of an RS complex means all precordial leads (V1-V6) show either entirely positive complexes (monophasic R waves = positive concordance) OR entirely negative complexes (monophasic QS waves = negative concordance). This indicates a uniform ventricular vector directed either entirely anteriorly (positive concordance) or entirely posteriorly (negative concordance). Such uniform vectors are virtually impossible with supraventricular rhythms because the normal His-Purkinje network would produce regional variations in activation (transition from V1 to V6). Positive concordance suggests a VT origin in the posterior wall (vector directed anteriorly). Negative concordance suggests an anterior wall origin (vector directed posteriorly).

Step 2: RS Interval > 100 ms in ANY Precordial Lead

CRITERION: In any precordial lead with an RS complex, measure the RS interval • RS Interval DEFINITION: Time from the onset of the R wave to the nadir (deepest point) of the S wave. • Measurement: Use calipers on ECG paper (25 mm/sec = 1 small box = 40 ms, 1 large box = 200 ms). If RS interval > 100 ms ( > 2.5 small boxes) in ANY lead → STOP → DIAGNOSE VT If RS interval ≤ 100 ms in ALL leads → PROCEED to Step 3

Step 2 Explanation: Sluggish Myocyte-to-Myocyte Conduction

The RS interval (sometimes called the intrinsic deflection or R-wave peak time) measures how long it takes for the depolarization wavefront to travel from the endocardium to the epicardium. In SVT with aberrancy, conduction occurs via the Purkinje fibers (fast conduction velocity: 2-4 m/s), resulting in an RS interval typically <60-80 ms. In VT, conduction is myocyte-to-myocyte (slow conduction velocity: 0.3-0.5 m/s), prolonging the RS interval to >100 ms. This criterion is independent of the overall QRS duration and works for both RBBB-like and LBBB-like morphologies. In the original Brugada study, an RS interval >100 ms was 100% specific for VT (no SVT had an RS interval >100 ms).

Step 3: Atrioventricular (AV) Dissociation

CRITERION: Is there evidence of AV dissociation? • AV Dissociation DEFINITION: Atria and ventricles beating independently at different rates. • Signs to look for: - P waves with a different rate than QRS complexes - P waves superimposed on QRS complexes (subtle notching, slurring) - Capture beats (narrow QRS complex that conducts normally from a sinus beat) - Fusion beats (hybrid QRS complex between a sinus beat and a ventricular beat) If AV dissociation is present → STOP → DIAGNOSE VT (100% specific) If AV dissociation is NOT present → PROCEED to Step 4

Step 3 Explanation: The Gold Standard Sign of VT

AV dissociation is the single most specific ECG finding for VT (100% specificity in the original Brugada study—no SVT with aberrancy had AV dissociation). However, it has poor sensitivity (only 20-40% of VTs show clear AV dissociation on surface ECG). The atria continue to be driven by the sinus node or an atrial focus, but the ventricles are driven by the VT focus independently. P waves may be visible in the T wave or QRS complex (causing notching). Capture beats occur when a sinus beat transiently captures the ventricles (normal conduction through the AV node and Purkinje system), producing a narrow QRS that is "early" (premature) compared to surrounding wide complexes. Fusion beats occur when a sinus beat and a VT beat simultaneously activate the ventricles, producing a hybrid QRS of intermediate width.

Step 4: Morphological Criteria for VT in Leads V1-V2 and V6

CRITERION: Do the QRS complexes in leads V1-V2 and V6 meet morphology criteria for VT? Two morphologies assessed based on the appearance in V1-V2: • RBBB-like morphology (dominant R wave in V1) → apply RBBB criteria • LBBB-like morphology (dominant S wave, no R wave in V1) → apply LBBB criteria If BOTH V1-V2 AND V6 morphology criteria suggest VT → DIAGNOSE VT If morphology criteria are NOT met for VT → DIAGNOSE SVT with aberrant conduction

Step 4A: Morphological Criteria for VT with RBBB-like Morphology (Dominant R in V1)

LeadVT Criteria (Indicates VT)SVT with Aberrancy PatternSpecificity
Lead V1 (or V2)• Monophasic R wave (tall, smooth) • qR complex (small Q wave, tall R wave) • Notched downslope to R wave where the LEFT rabbit ear is TALLER than the right rabbit ear (RSR with R > R')• Triphasic rSR (RSR') with the RIGHT rabbit ear taller (R' > R) – typical RBBB pattern94-98%
Lead V6• QS complex (no R wave, entirely negative) • qR complex (small Q wave, tall R wave) • R/S ratio < 1 (small R wave, deep S wave – only if left axis deviation also present)• Triphasic qRs or RS with R/S ratio >1 – typical RBBB pattern in V695-100%

Step 4B: Morphological Criteria for VT with LBBB-like Morphology (Dominant S in V1)

LeadVT Criteria (Indicates VT)SVT with Aberrancy PatternSpecificity
Lead V1 (or V2)• Initial R wave duration > 30-40 ms (width of the initial positive deflection) • Notching or slurring of the S wave (Josephson sign) • RS interval (R onset to S nadir) > 60-70 ms• Narrow initial R wave (<30 ms) • Sharp, smooth downslope of S wave • RS interval ≤ 60 ms – typical LBBB pattern96-100%
Lead V6• QS complex (no R wave, entirely negative) • qR complex (small Q wave, tall R wave) with delayed onset of R wave• Monophasic R wave (tall, smooth) – typical LBBB pattern98-100%

Step 4 Explanation: The Taller Left Rabbit Ear Sign (RBBB Morphology)

In lead V1, RBBB produces an rsR' (triphasic) pattern where the RIGHT rabbit ear (the second R wave, R') is taller than the left rabbit ear. This represents delayed depolarization of the right ventricle via the normal right bundle branch (but retrograde or slow). In VT with RBBB-like morphology, the entire ventricular activation is abnormal. The most specific sign of VT in this context is a notched downslope where the LEFT rabbit ear is taller (R > R'). This finding is virtually NEVER seen in SVT with aberrancy and should immediately trigger a VT diagnosis.

Step 4 Explanation: Josephson Sign (LBBB Morphology)

In lead V1 or V2 with LBBB-like QRS morphology, notching or slurring near the nadir (deepest point) of the S wave—called the Josephson sign—is highly specific for VT. This represents slow conduction through septal myocardium. A normal LBBB from aberrant conduction has a smooth, sharp S wave. Additionally, the initial R wave in V1-V2 is typically narrow (<30 ms) in SVT but >30-40 ms in VT. The RS interval (R onset to S nadir) is also prolonged (>60-70 ms) in VT compared to SVT (<60 ms).

Clinical Pearls

The Modified Brugada Algorithm: Adding Vereckei aVR

Some experts add the Vereckei aVR criterion as an "or" to Step 4. Vereckei (2008) proposed a 4-step algorithm using only lead aVR. The most useful sign: a dominant initial R wave in aVR (the QRS begins with an R wave) is highly specific for VT. This is because aVR looks at the heart from the right shoulder; a positive initial deflection implies the VT is originating in the left ventricle with a rightward/superior axis. This can help when precordial leads are ambiguous.

The RWPT (R Wave Peak Time) Criterion

A simpler alternative to the full Brugada algorithm is the "Ultrasimple Brugada" or RWPT criterion: Measure the time from the onset of the QRS to the peak of the R wave in leads V1-V2. An RWPT ≥50 ms in V1 or V2 suggests VT. This is easier to measure than the RS interval and has similar specificity (90-95%). Sensitive for VT but may be negative in fascicular VT (which has narrower QRS).

Limitations of the Brugada Algorithm (Known Pitfalls)

Idiopathic Ventricular Tachycardia (Outflow Tract VT, Fascicular VT): These VTs have narrower QRS (120-150 ms) and normal or near-normal axes. They mimic SVT with aberrancy and frequently misclassify as SVT (false negatives). Outflow tract VTs originate in the RVOT (RV outflow tract, often young, healthy patients, no structural disease) and have LBBB morphology with inferior axis (positive QRS in II, III, aVF). Fascicular VTs (left posterior fascicle, re-entry) have RBBB morphology with left axis and relatively narrow QRS (120-140 ms). Both are benign compared to scar-related VT but still require treatment (verapamil-sensitive for fascicular VT, adenosine-sensitive for some outflow tract VTs). The Brugada algorithm has lower sensitivity (~50-70%) for these "benign" VTs.
Antidromic AVRT (WPW Syndrome): This is the most important source of FALSE POSITIVE VT diagnoses (calling SVT "VT"). In antidromic AVRT, the impulse travels anterograde down the accessory pathway, preexciting the ventricles. The QRS is very wide (>140 ms, often >160 ms) and bizarre. It meets all 4 Brugada criteria for VT (absence of RS, long RS interval, possible AV dissociation? no, but morphology looks VT-like). Consider this in: (1) Young patients (<35 years), (2) Known WPW pattern on sinus ECG (delta wave, short PR), (3) Very fast rates >250 bpm, (4) History of paroxysmal palpitations since youth. If suspected, administer procainamide or ibutilide (NOT adenosine, which may precipitate VF in WPW).
Hyperkalemia and Sodium Channel Blocker Toxicity: Severe hyperkalemia (K >6.5-7.0 mEq/L) or tricyclic antidepressant (TCA) overdose can produce very wide QRS complexes (up to 200 ms) that meet Brugada criteria for VT. However, these patients will have sinus tachycardia (not re-entrant VT) on closer inspection; look for P waves (may be hidden). Treat the underlying electrolyte disturbance or overdose—do NOT cardiovert a hyperkalemic wide complex rhythm.
Bundle Branch Block Re-entry VT: This rare VT uses the bundle branches as part of the re-entry circuit. It produces an RBBB pattern that looks exactly like SVT with aberrancy. The Brugada algorithm may falsely classify it as SVT (false negative). Typically occurs in patients with dilated cardiomyopathy and His-Purkinje disease. Requires electrophysiology study for diagnosis.
Inability to Measure RS Interval: The algorithm fails when the RS interval cannot be reliably measured due to isoelectric baseline, artifact, or bizarre QRS morphology (e.g., monomorphic R or QS in all leads, some VTs have no RS complex anywhere). In the original study, 26% of VTs had no RS complex (Step 1 diagnosed them correctly). For ambiguous cases, rely on clinical context, history of MI, and default to "treat as VT."

Advanced Eponymous Signs

SignEponymDescriptionSensitivity for VTSpecificity for VT
Taller left rabbit ear (V1)Brugada sign (originally described)In RBBB morphology, notched R wave where the left peak is taller than the right peak (R > R' in V1). Opposite of typical RBBB.30-40%98-100%
Josephson signJosephson ME (1981)Notching or slurring near the nadir of the S wave in leads V1-V2 with LBBB morphology. Indicates slow septal conduction.40-50%96-98%
Capture beatsWellens HJJ (1978)Early narrow QRS complex in the midst of wide complexes indicating sinus beat captured the ventricle.5-10%100% (diagnostic of VT)
Fusion beats (Dressler beats)Dressler W (1960s)Hybrid QRS width (intermediate between narrow and wide) from simultaneous sinus and VT activation.10-15%100% (diagnostic of VT)
Northwest axis (Extreme right axis deviation)Wellens HJJ (1981)QRS positive in aVR and negative in leads I and aVF (+90° to +180° and -90° to -180°, axis from -90° to ±180°).20-30%95-98%

Performance Metrics (Original Brugada Study, 1991)

StepCriterionSensitivity (VT detection)Specificity (excluding SVT)Number of VTs diagnosed at this step
Step 1No RS complex in any precordial lead21% (83 of 384 VTs)100% (0 of 170 SVTs misclassified)83 VTs diagnosed
Step 2RS interval >100 ms in any lead45% (175 of 384 total VTs; 92 additional VTs from prior step)98% (3 of 170 SVTs misclassified as VT)92 additional VTs (total 175)
Step 3AV dissociation16% (62 of 384 total VTs; 62 additional VTs)100% (0 of 170 SVTs)62 additional VTs (total 237)
Step 4Morphology criteria (V1-V2 and V6)18% (142 of 384 total VTs; 142 additional VTs)96% (6 of 170 SVTs misclassified at final step)142 additional VTs (total 379/384 = 98.7%)
FinalCombined algorithm (all 4 steps)98.7% (379/384 VTs correctly classified)96.5% (164/170 SVTs correctly classified)5 VTs missed (fascicular VT), 6 SVTs misclassified (antidromic AVRT)

Next Steps

Management Algorithm Based on Brugada Results

Pearls: Medications to Use and Avoid in Wide-Complex Tachycardia

MedicationUse in WCTRationaleDosing (Stable VT/SVT)
Procainamide (Class Ia)FIRST LINE for stable VT – also effective for SVT with aberrancy, antidromic AVRT, preexcited atrial fibrillationSodium channel blocker; slows conduction velocity in myocardium and accessory pathways. Terminates 80% of stable monomorphic VT.20-50 mg/min IV push or infusion until VT terminates, hypotension (SBP <90), QRS widening >50%, or max 17 mg/kg. Maintenance: 1-4 mg/min (requires monitoring for QT prolongation, torsades).
Amiodarone (Class III)Effective second-line for stable VT – preferred in patients with structural heart disease (ischemic, cardiomyopathy, heart failure)Multiple ion channel effects (Na, K, Ca, beta blockade). Terminates 40-60% of stable VT. Does not worsen heart failure.150 mg IV over 10 minutes (may repeat x1 if no response). Then 1 mg/min infusion x6 hours, then 0.5 mg/min x18 hours. Total max 2.2 grams/day.
Lidocaine (Class Ib)Limited role – effective only for ischemic VT (acute MI, post-MI VT). Not effective for non-ischemic VT or SVT.Sodium channel blocker with preferential effect on ischemic tissue. Terminates <20% of non-ischemic monomorphic VT.1-1.5 mg/kg IV push (max 100mg). Repeat 0.5-0.75 mg/kg q5-10min to max 3 mg/kg. Maintenance: 1-4 mg/min.
AdenosineDiagnostic use only in stable patients – terminates AVNRT/AVRT (SVT). Does NOT terminate VT (except rare RVOT VT). Safe in VT (does not cause VF).Transient AV node block (5-10 seconds). If rhythm stops → SVT. If rhythm continues unchanged → VT.6 mg rapid IV push, followed by 20 mL saline flush. If no effect, 12 mg push. If still no effect, VT highly likely.
Verapamil / Diltiazem (CCB, Class IV)AVOID unless 100% certain rhythm is SVT with aberrancy. If given to VT, may cause severe hypotension, degeneration to VF, or asystole.Calcium channel blockers have negative inotropic and vasodilator effects. VT patients often have low cardiac output; CCBs can precipitate cardiovascular collapse.Do NOT give empirically. Only give if vagal maneuvers and adenosine terminated rhythm (confirming SVT).
Beta-blockers (Class II)AVOID in wide-complex tachycardia of uncertain origin. Safe only after confirmed SVT (AF, atrial flutter, AVNRT, AVRT).Negative inotrope and chronotrope. May worsen hypotension in VT. In VT, beta-blockade is safe only as long-term therapy after ICD placement (not acute termination).Do NOT give empirically. Esmolol 500 mcg/kg IV push is sometimes used for diagnostic testing (slows AV node, helps visualize P waves) but risk of hypotension.
Magnesium sulfateUse only for Torsades de Pointes (polymorphic VT with long QT) or suspected hypomagnesemia.Not effective for monomorphic VT or SVT with aberrancy. Magnesium is antiarrhythmic only in torsades.Torsades: 2-4 grams IV push over 1-2 min. Followed by 3-6 grams infusion over 12-24 hours.

Emergency Department Documentation Checklist

Time of presentation and ECG acquisition – Critical for determining duration of arrhythmia (ischemia risk increases with prolonged VT).
Hemodynamic status – Stable vs unstable (SBP, mental status, chest pain, heart failure signs).
Brugada algorithm steps documented – "Step 1: RS complex present in V4 (Yes), Step 2: RS interval 80 ms (<100 ms), Step 3: AV dissociation absent, Step 4: Morphology criteria met for VT (RBBB pattern, taller left rabbit ear in V1, qR in V6). Conclusion: VT."
Prior ECGs (if available) – Compare to prior baseline (preexisting BBB, prior MI, prior VT, WPW pattern).
Structural heart disease history – Prior MI, cardiomyopathy, heart failure, valvular disease, cardiac surgery, family history of SCD (HCM, ARVD, Brugada syndrome, LQTS).
Medications – Antiarrhythmics (may confound), QT-prolonging drugs, digoxin toxicity, TCAs, cocaine / methamphetamine.
Electrolytes – K, Mg, Ca, Phos (hyperkalemia can mimic VT).
Treatment administered – Procainamide dose and timing, cardioversion energy and synchronization (or not).
Response to treatment – Termination of tachycardia, conversion to sinus rhythm, precipitation of VF/asystole/complications.
Disposition – Admit to ICU/CCU (all VT patients require admission). If SVT with aberrancy and episode terminated, may discharge with outpatient cardiology referral (if low risk: no structural disease, normal ECHO, young patient).

The Evidence

Original Derivation and Validation Study (1991)

A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex

Brugada P et al. • Circulation. 1991;83(5):1649-1659. doi: 10.1161/01.CIR.83.5.1649

View Source

Prior Criteria (Wellens et al, 1978), referenced in Brugada

The value of the electrocardiogram in the differential diagnosis of a tachycardia with a widened QRS complex

Wellens HJJ et al. • American Journal of Medicine. 1978;64(1):27-33. doi: 10.1016/0002-9343(78)90176-6

LBBB Morphology Criteria (Kindwall et al, 1988)

Electrocardiographic criteria for ventricular tachycardia in wide complex left bundle branch block morphology tachycardias

Kindwall KE et al. • American Journal of Cardiology. 1988;61(15):1279-1283. doi: 10.1016/0002-9149(88)91168-3

Modern Validation (LITFL, ECGbook.com)

VT versus SVT: Brugada Algorithm

Burns E et al. • LITFL: Life in the Fast Lane (Medical Education Blog). 2024;Published October 8, 2024. Available from: https://litfl.com/brugada-algorithm-vt-vs-svt/

View Source
Brugada Algorithm (VT vs. Aberrant SVT) - ECG

Medmastery / ECGbook.com • ECGbook.com (Medical Education Platform). 2024;Comprehensive review with example ECGs (wide complex tachycardia, RBBB/LBBB patterns, AV dissociation)

View Source

Vereckei aVR Algorithm (2008)

Application of a new algorithm in the differential diagnosis of wide QRS complex tachycardia

Vereckei A et al. • European Heart Journal. 2008;28(5):589-600. doi: 10.1093/eurheartj/ehm373

Origins & History

Pedro Brugada and Josep Brugada (1991)

The Brugada brothers (Pedro, Josep, and Ramon) are renowned Belgian and Spanish cardiologists. Pedro Brugada (born 1952, Barcelona) and Josep Brugada (born 1958) were working at the Cardiovascular Center, OLV Hospital in Aalst, Belgium, and the University of Limburg in Maastricht, the Netherlands, when they developed the algorithm in 1990-1991. They noted that existing criteria (Wellens, 1978; Kindwall, 1988) had poor specificity and were frequently discordant, leading to diagnostic errors. They hypothesized that the intrinsic deflection (RS interval) would be prolonged in VT regardless of QRS morphology. Their 1991 Circulation paper validated the algorithm prospectively in 554 patients with electrophysiologically proven arrhythmias. The algorithm was named after them, though separately they are also known for describing Brugada syndrome (a genetic arrhythmia syndrome characterized by ST elevation in V1-V3 and sudden cardiac death, first described in 1992—one year after the algorithm was published).

Key Contributors and Timeline

YearContributor(s)InstitutionContribution
1978Wellens HJJ, Bar FWHM, Lie KIUniversity of Limburg, Maastricht, NetherlandsFirst systematic criteria for VT vs SVT: AV dissociation, QRS >140 ms, left axis, morphology in V1/V6
1981Josephson MEHospital of the University of Pennsylvania, PhiladelphiaDescribed 'Josephson sign' (notched S wave in LBBB VT)
1988Kindwall KE, Josephson MEUniversity of PennsylvaniaSpecific criteria for LBBB morphology VT (R wave >30 ms, RS interval >60 ms)
1991Brugada P, Brugada J, Mont L, Smeets J, Andries EWOLV Hospital, Aalst, Belgium / University of Limburg, MaastrichtOriginal publication of the 4-step Brugada algorithm (Circulation). Sensitivity 98.7%, specificity 96.5%, n=554. Became standard of care for WCT differential diagnosis.
2008Vereckei A, Duray G, Szénási G, Altemose GT, Miller JMSemmelweis University, Budapest, HungarySimplified aVR algorithm as alternative to Brugada (4 steps, lead aVR only).
2017ACC/AHA/HRS Guideline for Management of Ventricular ArrhythmiasAmerican College of Cardiology / Heart Rhythm SocietyEndorses Brugada algorithm for differential diagnosis of wide QRS tachycardia (Class IIa, Level B-NR)
2024LITFL, ECGbook.com (modern education)Medical Education PlatformsContinued dissemination of algorithm with updated clinical pearls, pitfalls, and example ECGs.

Legacy and Current Guidelines

The Brugada algorithm remains the most widely taught and clinically used approach to wide-complex tachycardia differential diagnosis more than 30 years after its publication. No subsequent algorithm (Vereckei, Pava, or others) has consistently outperformed it in head-to-head comparisons. The algorithm is included in all major emergency medicine, cardiology, and critical care textbooks and is recommended by the ACC/AHA/HRS guidelines (2017). Its primary limitations—poor sensitivity for fascicular VT and poor specificity for antidromic AVRT—are well described, and clinicians are taught to recognize these exceptions. The "default to VT when uncertain" rule, based on the algorithm's 80% VT prevalence data, has likely prevented thousands of deaths from inappropriate verapamil administration. Pedro Brugada passed away in 2022; his legacy includes both the Brugada algorithm and Brugada syndrome.

Last Comprehensive Review: 2026-07-17

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