ECG criteria
- A rhythm of ventricular complexes with a rate usually $\ge$100 bpm (most commonly 100–250 bpm), regular or nearly regular; VT typically presents as a wide-complex tachycardia with QRS $\ge$120 ms, but a narrow QRS does not rule out VT — especially with fascicular or septal origin
- QRS morphology is identical across all complexes in each lead (monomorphism) — unlike polymorphic VT
- AV dissociation: P waves march independently of QRS complexes without a fixed relationship (look for " marching" P waves in II, V1); a strong but not mandatory sign — 1:1 retrograde conduction or hidden P waves are possible
- Fusion beats and capture beats — proof of VT in the presence of intact AV conduction
- QRS concordance in the chest leads (all complexes in V1–V6 directed upward or all downward); negative concordance is particularly specific for VT, while positive concordance is occasionally seen in SVT as well
- Frontal plane axis deviation into the "northwest" quadrant (from -90° to ±180°) is characteristic of VT
- Brugada algorithm (absence of RS complexes in chest leads, RS interval >100 ms from the onset of R to the nadir of S, AV dissociation, morphological criteria in V1–V2 and V6) and Vereckei algorithm (a separate sequence assessing aVR and initial/terminal QRS velocity) shift the diagnosis toward VT in wide-complex tachycardia; a QRS width >140 ms with an RBBB-like morphology or >160 ms with an LBBB-like morphology is an auxiliary rather than an independent sign
- Absence of typical RBBB or LBBB morphology seen in standard bundle branch blocks (atypical QRS morphology)
What it looks like on ECG
The ECG shows a tachycardia of ventricular complexes where each complex in a given lead repeats the shape of the previous one — hence "mono"-morphic. The QRS is usually wide ($\ge$120 ms), although in fascicular or septal VT it can be relatively narrow. The rate is typically 100–250 bpm, with a regular or slightly irregular rhythm.
Key features differentiating VT from supraventricular tachycardia with aberrancy (relevant in wide-complex tachycardia):
| Sign | What to look for |
|---|---|
| AV dissociation | P waves arise independently of QRS complexes; a strong but not mandatory sign — 1:1 retrograde VA association is possible |
| Fusion beats | Intermediate QRS morphology between sinus and ventricular beats |
| Ventricular capture beats | A single complex with the morphology of a conducted supraventricular impulse; may not be narrow in the presence of pre-existing bundle branch block or delayed conduction |
| Chest lead concordance | All QRS complexes in V1–V6 are unidirectional (upward or downward); negative concordance is especially specific |
| QRS Axis | Northwest axis deviation (extremely rare in SVT with aberrancy) |
QRS morphology in V1 and V6 is analyzed using two separate algorithms. Brugada algorithm: absence of an RS complex in the chest leads, an RS interval from the onset of the R wave to the nadir of S greater than 100 ms in any chest lead with an RS complex, AV dissociation, and morphological criteria in V1–V2 and V6. The Vereckei algorithm is a separate sequence of criteria that includes analyzing the initial R wave in aVR and the initial-to-terminal QRS velocity ratio. An auxiliary morphological sign in RBBB-like VT is a notched (slurred) terminal portion of the descending S-wave limb in V1–V2, known as the Josephson sign; it does not replace the formal steps of the Brugada and Vereckei algorithms.
Evaluation of the ST segment and T wave during wide tachycardia is unreliable: secondary repolarization abnormalities at high rates and aberrant ventricular activation distort standard ischemic criteria, and ST-T waves are not always simply discordant to the QRS. This is not a reason to delay ACS evaluation until rhythm restoration — clinical presentation, ECG dynamics, cardiac troponins, and indications for emergency coronary angiography should be assessed in parallel with tachycardia termination; a repeat ECG for targeted ST-T assessment is obtained after sinus rhythm is restored.
Mechanism
Monomorphic VT is caused either by reentry around a fixed anatomical substrate (most commonly a post-myocardial infarction scar or scar cardiomyopathy zone) or by an abnormal automaticity/triggered activity focus within a localized area of the ventricular myocardium. Because the impulse always follows the same pathway or originates from a single point, the ventricular depolarization vector remains constant from beat to beat — hence the stable QRS morphology. The ventricles activate independently of the atria: sinus P waves may continue at their own rate, unrelated to the QRS complexes (AV dissociation). Retrograde conduction is also possible — 1:1 ventriculoatrial conduction via the AV node, in which case AV dissociation is absent. Occasionally, a sinus impulse succeeds in conducting anterograde through the AV node, producing a ventricular capture beat or fusion complex.
Causes
- Prior myocardial infarction with a scar zone (most common cause)
- Coronary artery disease, acute myocardial ischemia
- Dilated and hypertrophic cardiomyopathy
- Arrhythmogenic right ventricular cardiomyopathy
- Cardiac sarcoidosis, myocarditis with scar formation
- Idiopathic VT from the right or left ventricular outflow tract (without structural heart disease)
- Fascicular VT in young patients without organic heart disease (QRS may be relatively narrow)
- Congenital heart disease post-surgical correction (suture scar)
- Electrolyte abnormalities and proarrhythmic drug effects (less common as an isolated cause of the monomorphic form)
Differential diagnosis
- Supraventricular tachycardia with aberrant conduction — differentiated by AV dissociation (if present), fusion and capture beats, chest lead concordance, and northwest axis; when in doubt, use the Brugada or Vereckei algorithms for VT
- SVT with pre-existing bundle branch block — compare QRS morphology during tachycardia with a baseline sinus rhythm ECG (if available): identity points toward SVT
- Antidromic tachycardia in WPW syndrome — wide QRS due to accessory pathway conduction, but morphology usually does not match typical bundle branch block
- Polymorphic ventricular tachycardia — QRS morphology changes from beat to beat, whereas in monomorphic VT it is stable
- Atrial flutter with accessory pathway conduction or aberrancy — regular wide-complex rhythm, but careful analysis reveals atrial flutter activity at a characteristic rate
Clinical significance and management
Monomorphic VT may present with stable hemodynamics or rapidly lead to instability, syncope, or cardiac arrest — up to degeneration into ventricular fibrillation. Any wide-complex tachycardia should be treated as ventricular in origin until proven otherwise.
For unstable monomorphic VT with a pulse (hypotension, pulmonary edema, anginal pain, altered mental status) — immediate synchronized electrical cardioversion; in the absence of a pulse — defibrillation and cardiac arrest protocol. For stable hemodynamics — 12-lead ECG recording, evaluation using VT criteria, pharmacological termination with antiarrhythmics per stable wide tachycardia management algorithms, and preparation for electrical cardioversion if pharmacological therapy fails.
Post-termination — echocardiography and evaluation for structural heart disease; coronary angiography if ACS/myocardial ischemia is suspected or other clinical indications exist, rather than automatically due to a history of CAD. Subsequently, assess indications for implantable cardioverter-defibrillator (ICD) placement per current ventricular arrhythmia guidelines, and consider catheter ablation for recurrent monomorphic VT with a known substrate.
Common interpretation errors
- Treating any wide tachycardia as "SVT with aberrancy" without applying VT criteria is a dangerous mistake that can cost a patient's life
- Ruling out a diagnosis of VT solely because QRS <120 ms — a narrow QRS is possible in fascicular and septal VT
- Ignoring P waves when searching for AV dissociation — they must be specifically looked for in leads II and V1; they may be hidden within the QRS complex or T wave. The absence of obvious dissociation does not rule out VT
- Confusing monomorphic and polymorphic VT due to baseline wander or artifacts — multiple consecutive complexes must be analyzed
- Applying Brugada criteria without accounting for class IC antiarrhythmic drugs or severe hyperkalemia, which distort QRS morphology
- Dismissing a VT diagnosis simply because the patient is hemodynamically stable — stability does not rule out a ventricular origin of the rhythm
1. Which sign is most specific for ventricular tachycardia when analyzing a wide QRS rhythm?
AV dissociation, capture beats, and fusion beats prove independent ventricular activity and are considered highly specific signs of VT, although not mandatory—1:1 retrograde VA conduction is possible.
2. How does monomorphic VT differ from polymorphic VT on an ECG?
The defining feature of monomorphic VT is identical QRS morphology from complex to complex in each lead.
3. What is the physician's tactic for monomorphic VT with hemodynamic instability and a maintained pulse (hypotension, pulmonary edema)?
For unstable VT with a maintained pulse, immediate synchronized cardioversion is indicated; defibrillation is used in the absence of a pulse.
Frequently asked questions
How to distinguish monomorphic VT from SVT with aberrant conduction?
They look for AV dissociation, fusion and capture beats, QRS concordance in the precordial leads, and northwest axis deviation—these signs indicate a ventricular origin. When in doubt, the Brugada algorithm or Vereckei algorithm is used.
Is monomorphic ventricular tachycardia dangerous?
Yes, it can be accompanied by hemodynamic instability, syncope, and progression to ventricular fibrillation. The degree of danger depends on the rate, duration of the episode, and the presence of structural heart disease.
How does monomorphic VT differ from polymorphic VT?
In the monomorphic form, the QRS retains the same morphology in each lead throughout the tachycardia, whereas in the polymorphic form, the morphology, amplitude, and/or QRS axis change from complex to complex. The mechanism of polymorphic VT is specified separately: it does not boil down to an "unstable focus."
Can VT have a narrow QRS?
Yes. Although most monomorphic VTs yield a QRS ≥120 ms, fascicular and some septal idiopathic VTs may have a relatively narrow QRS. The threshold of ≥120 ms is a criterion for wide-complex tachycardia, not an absolute condition for the diagnosis of VT; therefore, a narrow QRS does not exclude a ventricular origin of the rhythm.
What to do with a wide QRS complex tachycardia if it is unclear whether it is VT or SVT?
By default, the rhythm is treated as ventricular tachycardia until proven otherwise, and managed according to the wide QRS tachycardia algorithm: in case of instability with a maintained pulse — immediate synchronized cardioversion; in the absence of a pulse — defibrillation; in case of stability — application of VT criteria and preparation for pharmacological or electrical termination.
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Related terms
More in the section "Ventricular Arrhythmias"
Sources
- Hampton J.R. The ECG in Practice
- Surawicz B., Knilans T.K. Chou's Electrocardiography in Clinical Practice
- Orlov V.N. Guide to Electrocardiography
- ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death, 2022
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.