ECG criteria
- Three or more wide QRS complexes in a row, HR >100 bpm (usually 100–250 bpm)
- A QRS width of ≥120 ms defines wide-complex tachycardia, but does not confirm VT on its own. Thresholds of ≥140 ms for RBBB-like morphology and ≥160 ms for LBBB-like morphology are auxiliary features of specific algorithms rather than universal criteria (fascicular and some septal VTs may have a QRS <120 ms)
- For typical monomorphic VT, the rhythm is usually regular with nearly equal RR intervals; in polymorphic VT, including torsades de pointes, RR intervals and QRS morphology can vary significantly—regularity alone neither rules out nor confirms VT
- AV dissociation: P waves are independent of QRS complexes and visible separately (best seen in leads II, V1, and long rhythm strips); a frequent but not mandatory sign—retrograde VA conduction and 1:1 conduction are possible
- Fusion and capture beats confirm the ventricular origin
- Complete QRS concordance in chest leads V1–V6 (all positive or all negative) supports the diagnosis of VT; negative concordance is particularly specific for VT, whereas positive concordance is less specific (found, in particular, in antidromic AV reentrant tachycardia) and must be evaluated alongside other features
- Brugada criteria and Vereckei algorithm: step-by-step evaluation of QRS morphology in regular monomorphic wide-complex tachycardia (not applicable to polymorphic tachycardia)
- Morphology identical across all complexes—monomorphic VT, or varying—polymorphic VT
What it looks like on ECG
The tracing shows a series of predominantly wide QRS complexes (≥120 ms), usually at a rate of 150–200 bpm; capture beats and fusion beats may be present, meaning narrow or relatively narrow complexes can appear among the wide ones. An extreme QRS axis ("northwest axis" or indeterminate axis), usually between −90° and ±180°, may be present; it supports the diagnosis of VT but is not proof in itself.
Key findings specifically for diagnosing VT rather than SVT with aberrancy:
| Sign | What to look for | Where to look |
|---|---|---|
| AV dissociation | P waves follow their own rhythm and are not related to QRS complexes (a frequent but not mandatory sign) | II, V1, long rhythm strip |
| Ventricular capture beats | A narrow "normal" complex among the wide ones | any lead |
| Fusion beats | Intermediate QRS morphology | chest leads |
| Concordance | All QRS complexes in leads V1–V6 point in the same direction (up or down); negative concordance is more specific | V1–V6 |
| Brugada/Vereckei criteria | Absence of an RS complex in chest leads, RS interval >100 ms, initial R wave in aVR, Vi/Vt ratio, and other step-by-step features | chest leads, aVR |
The Brugada and Vereckei algorithms were designed for regular monomorphic wide-complex tachycardia; they are not intended for polymorphic VT. In monomorphic VT, all complexes have the same shape—usually reflecting a stable activation pathway, most commonly via a re-entry mechanism (often around a scar), though the mechanism cannot be definitively established from a single ECG. In polymorphic VT, the QRS morphology changes from beat to beat—this type of VT is more dangerous and frequently degenerates into ventricular fibrillation. Torsades de pointes is a distinct subtype of polymorphic VT characterized by a gradual change in QRS amplitude and polarity around the isoelectric line, typically in the setting of a prolonged QT interval.
Mechanism
VT arises through three main mechanisms: re-entry within the ventricle (most commonly around a post-infarction scar—the most frequent cause of monomorphic VT), abnormal automaticity of an ectopic ventricular focus, and triggered activity due to early or delayed afterdepolarizations (characteristic of torsades de pointes in long QT syndrome). In most VTs, excitation spreads via a pathway uncharacteristic of sinus rhythm and activates the ventricles less synchronously, resulting in a wide QRS complex. Certain forms of VT (fascicular, some reentrant forms) utilize the Purkinje fibers and may present with a relatively narrow QRS. AV dissociation is frequently observed because the atria continue to be driven by the sinus node independently of the ventricles, but it is not mandatory—retrograde atrial activation and ventriculoatrial conduction, including 1:1 conduction, can occur.
Causes
- Coronary artery disease, post-infarction scar (the most common cause of sustained monomorphic VT)
- Acute myocardial infarction
- Dilated and hypertrophic cardiomyopathies
- Arrhythmogenic right ventricular cardiomyopathy
- Cardiac sarcoidosis, myocarditis
- Long QT syndrome, Brugada syndrome, catecholaminergic polymorphic VT (channelopathies with a structurally normal heart)
- Electrolyte disturbances (hypokalemia, hypomagnesemia)
- Cardiotoxicity from drugs and poisons that prolong the QT interval
- Idiopathic right ventricular outflow tract (RVOT) VT, fascicular VT—in patients without structural heart disease
Differential diagnosis
- Supraventricular tachycardia with aberrant conduction or underlying bundle branch block—differentiated by AV dissociation, capture and fusion beats, Brugada criteria, and the Vereckei algorithm (applicable to regular monomorphic tachycardia); when in doubt, wide-complex tachycardia should be managed as VT until proven otherwise
- Antidromic tachycardia in WPW syndrome—also presents with a wide QRS, but conduction occurs via an accessory pathway; history of pre-excitation and delta waves on baseline ECG are helpful
- Ventricular flutter—an extremely rapid ventricular tachyarrhythmia, typically around 250–300 bpm or higher (the exact rate threshold is approximate), presenting as a continuous sinusoidal wave without discernible QRS complexes and ST-T segments—this is the definitive diagnostic feature
- Ventricular fibrillation—completely irregular, chaotic waves without discernible complexes
- Accelerated idioventricular rhythm—similar wide-complex morphology, but the rate is typically 40–100 bpm (sometimes up to 110), often with a gradual onset and offset and variable AV dissociation; rate alone does not reliably distinguish it from slow VT, and clinical context is mandatory
Clinical significance and management
VT is a potentially life-threatening rhythm: sustained VT (lasting longer than 30 seconds or associated with hemodynamic instability) can degenerate into ventricular fibrillation and cardiac arrest. For the clinician, key ECG tasks include determining QRS width and regularity, searching for signs of AV dissociation, and assessing the patient's hemodynamic stability in real time (which dictates management, rather than the ECG appearance alone). Any wide-complex tachycardia in a patient with coronary artery disease or structural heart disease is treated as VT until proven otherwise—this reduces the risk of mismanaging it as SVT.
For unstable regular monomorphic VT with a palpable pulse, immediate synchronized cardioversion is indicated. For polymorphic VT, synchronization is often impossible or unreliable, so immediate unsynchronized defibrillation is indicated in the presence of instability. Pulseless VT (of any morphology) constitutes cardiac arrest, requiring immediate unsynchronized defibrillation and CPR according to resuscitation guidelines. Stable sustained monomorphic VT is managed with antiarrhythmic drugs, and in cases of recurrent episodes, catheter ablation and implantable cardioverter-defibrillator (ICD) placement are considered according to indications.
Polymorphic VT and torsades de pointes are managed differently: in the presence of instability or absence of a pulse, immediate unsynchronized defibrillation is performed regardless of the cause; for torsades de pointes in the setting of a prolonged QT interval, additional interventions include intravenous magnesium, correction of potassium and magnesium levels, elimination of rhythm pauses, discontinuation of QT-prolonging drugs, and temporary overdrive pacing in appropriate cases. This differs from the management of polymorphic VT with a normal QT interval, where magnesium therapy is not the primary treatment.
Common interpretation errors
- Assuming wide-complex tachycardia is SVT with aberrancy "by default"—in adults with heart disease, it is statistically more likely to be VT
- Missing AV dissociation because P waves are poorly visible—one must search for them in leads II and V1, using a long rhythm strip or Lewis lead if necessary; the absence of visible dissociation does not rule out VT
- Confusing QRS concordance with simply high-amplitude waves in the chest leads
- Ignoring the medical history (prior myocardial infarction, cardiomyopathy)—it dramatically increases the probability of VT
- Applying the Brugada and Vereckei criteria (designed for monomorphic wide-complex tachycardias) to polymorphic VT
- Ordering synchronized cardioversion for unstable polymorphic VT instead of immediate defibrillation—synchronization often fails with irregular and changing complexes and dangerously delays the shock
1. Which feature is most specific for ventricular tachycardia in differential diagnosis with SVT with aberrancy?
AV dissociation, capture beats, and fusion beats indicate independent ventricular and atrial activity, which is specifically characteristic of VT.
2. What minimum QRS width is typically used as a criterion for a wide complex when VT is suspected?
A QRS complex is considered wide when its duration is 120 ms or more; this threshold value defines wide-complex tachycardia, although the width alone does not confirm VT.
3. What management is indicated for unstable polymorphic ventricular tachycardia?
In polymorphic VT, shock synchronization is often impossible or unreliable; therefore, in the presence of instability, an immediate unsynchronized shock is indicated.
Frequently asked questions
How to distinguish VT from SVT with aberrant conduction?
Look for AV dissociation, fusion beats, and ventricular capture beats—these are signs of VT. The Brugada and Vereckei algorithms (for regular monomorphic tachycardia) as well as QRS concordance in the chest leads are helpful. When in doubt, wide QRS tachycardia in an adult patient with heart disease is treated as VT.
Is ventricular tachycardia dangerous?
Yes, sustained VT can degenerate into ventricular fibrillation and lead to cardiac arrest, especially the polymorphic form. For unstable regular monomorphic VT with a pulse, immediate synchronized cardioversion is indicated; for unstable polymorphic VT or pulseless VT, immediate unsynchronized defibrillation is indicated.
How does monomorphic VT differ from polymorphic VT?
In monomorphic VT, all QRS complexes have the same morphology, which usually reflects a stable activation pathway (most commonly a re-entry mechanism, often around a scar). In polymorphic VT, QRS morphology and RR intervals vary from complex to complex, the prognosis is worse, and the risk of progression to ventricular fibrillation is higher.
Is VT always accompanied by a wide QRS?
Practically always, because excitation typically spreads via a pathway uncharacteristic of sinus rhythm. The exception is fascicular and certain septal VTs, where early involvement of the Purkinje fibers may result in a QRS that is only slightly widened or even <120 ms.
What are capture and fusion beats in VT?
A ventricular capture beat is a narrow, normal complex that occurs when a sinus impulse fortuitously manages to conduct through the AV node and activate the ventricles before the arrival of the next ventricular impulse. A fusion complex has an intermediate QRS morphology when sinus and ventricular activation overlap. Both signs confirm the diagnosis of VT.
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Related terms
More in the section "Ventricular Arrhythmias"
Sources
- Goldberger A. "Clinical Electrocardiography" (current edition)
- Surawicz B., Knilans T. «Chou's Electrocardiography in Clinical Practice»
- Hampton J. «The ECG Made Easy»
- ESC Guidelines for the management of ventricular arrhythmias and the prevention of sudden cardiac death
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.