Diagnostic criteria of broad QRS complex tachycardia: decades of evolution
Authors, Journal, Affiliations, Type, DOI
- Becker S.N. Alzand, Harry J.G.M. Crijns
- Europace (2011) 13, 465–472
- Department of Cardiology, Maastricht University Medical Center, The Netherlands
- Review article
- DOI: 10.1093/europace/euq430
Overview
This review traces the 45-year evolution of ECG criteria for differentiating ventricular tachycardia (VT) from supraventricular tachycardia (SVT) with aberrant conduction in broad QRS complex tachycardia (BCT). VT accounts for ~80% of all BCTs and carries the least favourable prognosis; misdiagnosis and treatment with agents such as verapamil or adenosine can cause severe haemodynamic deterioration and precipitate ventricular fibrillation. The review covers classical criteria (Sandler–Marriott 1965, Wellens 1978), the Brugada 4-step algorithm (1991), and the Vereckei aVR algorithm (2007/2008), with detailed discussion of limitations including BCT during antiarrhythmic drug treatment, bundle branch reentry tachycardia, fascicular VT, and pre-excited SVT. The authors conclude that combining three clinical criteria (any morphological criterion + AV dissociation + history of myocardial disease) achieves >95% PPV for VT, with procainamide as the preferred drug when diagnosis is uncertain.
Keywords
Broad QRS complex tachycardia, ventricular tachycardia, supraventricular tachycardia, AV dissociation, ECG algorithms, Brugada algorithm, Vereckei algorithm
Key Takeaways
History and Physical Examination
- VT is the most common cause of BCT, accounting for ~80% of all cases
- Clinical history alone carries very high PPV for VT:
- Prior myocardial infarction: PPV 98%
- Congestive heart failure: PPV 100%
- Recent angina pectoris: PPV 100%
- Age >35 years: sensitivity 92%
- Haemodynamic status (syncope, blood pressure, clinical status) is NOT helpful in determining tachycardia mechanism
- VT typically does not respond to carotid sinus massage (CSM); reentrant SVT usually slows/terminates with CSM
- Cyclic-AMP-related VT that terminates with CSM has been reported (exception)
Atrioventricular Dissociation
- AV dissociation is one of the most useful practical criteria for VT diagnosis
- However, retrograde ventriculo-atrial (VA) conduction (1:1, 2:1, or Wenckebach) occurs in up to 50% of VTs — AV dissociation therefore absent in half of VT cases
- IV adenosine (not completely safe) may assist diagnosis by establishing complete VA block and revealing AV dissociation when VA conduction is present
Clinical detection of AV dissociation:
- Stroke volume/BP fluctuations with variable intensity of the first heart sound
- Canon A waves (simultaneous atrial + ventricular contraction) strongly suggest VT
- Frog sign (neck pulsation every beat) is seen in AVNRT, NOT in VT (even with retrograde VA conduction) — mechanistic difference: during AVNRT, retrograde P occurs early in systole when the AV ring is positioned backward toward atria; during VT with retrograde conduction, the retrograde P occurs later when the AV ring has moved toward the apex, enlarging atria and minimizing venous backflow
ECG detection of AV dissociation:
- Best detected in the lead where P-wave is most prominent (often inferior leads)
- QRS variability may indicate AV dissociation (ventricular filling variation)
- Lewis lead technique: Modify lead I by placing right arm electrode at right 2nd ICS (adjacent to sternum) and left arm electrode at right 4th ICS (adjacent to sternum); calibrate at 1 mV = 20 mm — enhances P-wave detection during BCT
Echocardiographic detection:
- AV dissociation detectable by M-mode, mitral valve movement, flow Doppler, or tissue Doppler
Classical ECG Criteria
Sandler & Marriott (1965):
- 92% of VEBs with RBBB pattern have monophasic or biphasic pattern in lead V1
- Triphasic pattern (rsR', rSR', RsR') in V1 found in only 6% of VEBs → triphasic favours aberrancy
- Precordial concordance (all leads upright or all inverted) almost diagnostic for ventricular origin
- Positive concordance: may also occur in antidromic tachycardia using left posterior or left lateral AP
- Negative concordance: nearly always VT (one case report exception: pectus excavatum + SVT with LBBB)
Marriott (1971):
- "Rabbit ears" sign for double-peaked R-wave in lead V1:
- "Good rabbit" (taller right peak) = typical for RBBB aberrancy
- "Bad rabbit" (taller left peak) = suggests ventricular origin
Swanick et al. (1972):
Criteria favouring ventricular origin for right VEB vs SVT with LBBB:
- S-wave depth in V4 > S in V1
- Wide r-wave ≥0.03 s in lead V1
- Negative QRS polarity in lead I
Wellens classical criteria (1978):
- First to use His-bundle recording to determine tachycardia origin
- Formed the basis of all subsequent morphological algorithms
- QR pattern in leads other than aVR or QS pattern in V5–V6 during VT: present in 89% with old MI, constantly absent in idiopathic VT (Coumel et al.)
The Brugada Algorithm (1991)
Analysed 554 BCTs; sensitivity 0.987, specificity 0.965:
Four sequential steps (applicable regardless of RBBB or LBBB morphology):
- Is there an RS complex in ANY precordial lead? If NO → diagnose VT
- Is the RS interval >100 ms in any precordial lead? If YES → diagnose VT
- Is AV dissociation present? If YES → diagnose VT
- Morphological criteria for VT in V1 and V6? If BOTH positive → VT; otherwise → SVT with aberrant conduction
The Vereckei aVR Algorithm (2007 and 2008)
Vereckei 2007 (287 patients; lead aVR + 12-lead):
Criteria for VT:
- Presence of AV dissociation
- Presence of an initial R-wave in lead aVR
- Vi/Vt ≤1 (initial 40 ms voltage / terminal 40 ms voltage)
Vereckei 2008 simplified — lead aVR only (313 patients):
Four criteria for VT in aVR (same accuracy as 2007 algorithm):
- Presence of an initial R-wave
- Width of initial r- or q-wave >40 ms
- Notching on the initial downstroke of a predominantly negative QRS complex
- Vi/Vt ≤1
Griffith Criteria (1991)
Multivariate analysis, 102 patients, 15 clinical + 11 ECG variables:
Independent predictors of VT:
- History of previous MI
- Lead aVF: predominantly negative deflection (especially with Q-wave in RBBB pattern); QS or qR in aVF in LBBB pattern highly suggestive of VT; Rs complex in aVF specific for SVT
- RBBB pattern: monophasic or biphasic V1 suggests VT; triphasic RSR'/rSR' configuration suggests SVT
- Axis change >40° between sinus rhythm and tachycardia
Predictive score: 0 criteria = almost certainly SVT; 1 = probably SVT; 2 = probably VT; 3–4 = almost certainly VT (accuracy 93%; 95% with independent P-wave activity + VEB morphology matching tachycardia)
Alberca Specificity Analysis (1997)
Of 12 morphological criteria, only 5 achieved >90% specificity (232 patients with SR + fixed intraventricular conduction delay):
- Rsr' or Rr' in V1 with RBBB morphology → specificity 98%
- QS, QR, or R pattern in V6 with RBBB morphology → specificity 98%
- Any Q in V6 with LBBB morphology → specificity 92%
- Concordant pattern in all precordial leads → specificity 100%
- Absence of RS complex in all precordial leads (especially useful for LBBB) → specificity 91%
Limitations of Morphological Criteria
BCT during antiarrhythmic drug treatment:
- Class Ic agents (flecainide, propafenone): Proarrhythmia (monomorphic VT) AND bizarre aberrant conduction mimicking VT; QRS 180–240 ms with bizarre RBBB + right or northwest axis, or atypical LBBB + left axis; mechanism: use-dependent conduction delay greater in ventricular myocardium than His-Purkinje → exaggerated asynchrony → bizarre BBB
- Class III agents (dofetilide — pure IKr blocker): Atypical aberrant conduction and sequential bilateral BBB mimicking multiple monomorphic VTs; mechanism: class III AADs prolong Purkinje refractory period >> ventricular myocardium; differential effects within Purkinje system (L/R, distal/proximal, posterior/anterior fascicle) cause bizarre QRS; cycle-length-dependent refractory period changes cause sequential bilateral block; misdiagnosis enhanced by atypically long coupling intervals and relatively long BCT cycle lengths
Bundle branch reentry tachycardia:
- Uncommon VT in patients with acquired heart disease + significant conduction system impairment
- Surface ECG in SR: intraventricular conduction defects ± PR prolongation
- VT QRS: typical BBB pattern (usually LBBB), may be identical to SR morphology
- Key distinguishing feature: rapid intrinsicoid deflection in right precordial leads (initial ventricular activation via specific conduction system — contrast to myocardial VT origin)
- Interfascicular tachycardia: usually RBBB morphology; axis depends on reentrant circuit direction (anterograde left anterior + retrograde left posterior fascicle → right axis deviation; reversed → left axis deviation)
Fascicular ventricular tachycardia:
- Relatively narrow QRS VT; typically in young patients without structural heart disease
- Three subtypes: (1) left posterior fascicle origin → RBBB + superior axis (most common); (2) left anterior fascicle origin → RBBB + right-axis deviation; (3) upper septal fascicle → narrow QRS + normal axis (rare)
- QRS duration: 100–140 ms
- RS duration in precordial leads <80 ms → below Brugada threshold of >100 ms → Brugada algorithm misclassifies as SVT
- RS duration contrast: fascicular VT <80 ms vs structural heart disease VT generally >100 ms
- Capture beats and fusion beats may be present (supports VT diagnosis)
- Bifascicular VT (alternating anterior/posterior focus): seen in digitalis intoxication or Andersen–Tawil syndrome
Pre-excited SVT:
- No morphological differentiation is theoretically possible between VT and SVT with AV conduction over an accessory pathway
- Steurer et al. (1994): 149 VT, 113 with prior MI, 118 pre-excited SVT — 3 ECG criteria for VT:
- Predominantly negative QRS in leads V4–V6
- QR complex in one or more of V2–V6
- AV relation ≠ 1:1 (more QRS complexes than P-waves)
- Sensitivity 75%, specificity 100%
ECG artefact:
- Knight et al.: artefact mimicking BCT misdiagnosed as VT by 94% of internists, 58% of cardiologists, 38% of electrophysiologists
Authors' Conclusion / Practical Approach
To achieve >95% PPV for VT, combine three criteria:
- Any morphological criterion (from Brugada, Vereckei, classical criteria)
- AV dissociation (detected clinically, by ECG, or echocardiographically)
- History of myocardial disease (MI, cardiomyopathy, congenital heart disease, previous surgery)
If diagnosis still uncertain AND typical BBB morphology absent → diagnose VT by default
Drug of choice when uncertain: procainamide (prolongs myocardial refractory period, AP refractory period, and retrograde fast AV nodal pathway — avoids potentially harmful drugs such as verapamil and adenosine in possible VT)
Limitations of the Document
- 2011 review; predates the Basel algorithm (2022), PROCAMIO trial (2015), and other contemporary tools
- Narrative review — no systematic methods or PRISMA framework; selection of included studies is at authors' discretion
- Brugada and Vereckei algorithm sensitivities/specificities cited from original papers, which used tertiary EP laboratory cohorts with high VT prevalence (~75–80%); performance in community or non-EP settings is lower
- Fascicular VT and pre-excited SVT sections are relatively brief given the diagnostic complexity of these entities
- Vi/Vt measurement (Vereckei algorithm) is technically demanding and not well-standardised
Key Concepts Mentioned
- concepts/Wide-Complex-Tachycardia — central topic; historical evolution of BCT diagnostic criteria
- concepts/ECG-Conduction-Disturbances — bundle branch block patterns; aberrant conduction vs VT
- concepts/Drug-Induced-Arrhythmia — class Ic and class III AAD-induced BCT mimicking VT
- concepts/Bidirectional-Ventricular-Tachycardia — Andersen–Tawil syndrome mention in fascicular VT context
Key Entities Mentioned
- entities/Brugada-Syndrome — note: Brugada P is author of 1991 BCT algorithm; distinct from Brugada syndrome
- entities/Flecainide — class Ic proarrhythmia; SVT mimicking VT during treatment
- entities/Dofetilide — class III IKr blocker; sequential bilateral BBB mechanism
Wiki Pages Updated
wiki/sources/svt-vt-europace-2011.md(created)wiki/concepts/Wide-Complex-Tachycardia.md(updated — historical criteria, limitations, clinical exam, AV dissociation detection, fascicular VT, bundle branch reentry, AAD-induced BCT)wiki/sourceindex.md(updated)wiki/wikiindex.md(updated)