Ventricular tachycardia


Ventricular tachycardia (VT) refers to any rhythm faster than 100 beats/min with three or more beats in a row, arising distal to the bundle of His, which usually present with wide QRS complexes (>120 ms).

VT may occur in patients with and without structural heart disease or inherited arrhythmogenic syndromes.

This distinction is important in determining  the patient’s prognosis:

  • Patients with VT in the setting of a structural heart disease carry increased risk of sudden cardiac death
  • Patients with VT in the absence of heart disease generally have a very good prognosis

Symptoms of VT can vary greatly and depend on multiple factors such as heart rate, duration, presence of underlying heart disease and others.

It may be asymptomatic, especially in case of short episodes, but potential symptoms include palpitations, lightheadedness, syncope, chest pain and anxiety.

It can also lead to hemodynamic collapse, degeneration to ventricular fibrillation and sudden cardiac death.


Three main mechanisms are responsible for triggering and sustaining VTs:

  • Reentry
    - It is currently thought to be the most common mechanism, typical situation involves creation of a reentry circuit related to a scarred myocardium as a result of myocardial infarction
    - For reentry to occur, certain conditions must be met that are related to the following:
        a) the presence of a unidirectional block within a conducting pathway
        b) critical timing
        c) the length of the effective refractory period of the normal tissue
  • Triggered activity
    - Occurs as a result of early or delayed afterdepolarizations and typically induces Torsades des Pointes 
  • Abnormal automaticity
    - The rhythm is generated in a region of a ventricular myocardium

Picture 1 Reentry model 

Cardiovascular physiology concepts.


VTs can be divided by multiple criteria:

  • by duration:
    - non-sustained VT = 3 to more consecutive PVC and a VT lasting up to 30s
    - sustained VT = VT lasting more than 30s
  • by clinical presentation, which determines acute management:
    - hemodynamically stable - can be managed pharmacologically first
    - hemodynamically unstable - requires prompt termination with DC cardioversion
    - incessant - continuously running VT, which terminates spontaneously or after cardioversion
    - arrhythmical storm - three or more episodes of VT within 24 hours that require intervention
  • by presence of different morphologies:
    - monomorphic VT = all beats have similar appearance as they have the same origin
    - polymorphic VT = different morphologies are present originating from different sites
  • by the mechanism of origin
    - reentry - more often in structural heart disease (prognostically malignant or potentially malignant); they can usually be triggered by programmed ventricular pacing; they can be interrupted by cardioversion or antitachycardia pacing
    - focal - more often idiopathic (prognostically benign); the mechanism is abnormal automaticity, triggered activity, or microreentry; they often occur as repetitive runs of VT; they cannot usually be triggered by programmed stimulation, but rather catecholamines or exercise; sometimes they are incessant and difficult to suppress by cardioversion or antiarrhythmics
  • by morphology of the complexes
    - this is determined by the origin of the VT and enables localisation of the origin of a VT by a 12 lead ECG 
  • specific types of VT such as Torsades des Pointes, bidirectional VT 
  • ventricular fibrillation and ventricular flutter can also be classified as VTs, but are considered separately

ECG characteristics

  • it is important to distinguish VT from other arrhythmias, usually other wide complex tachycardias 
  • heart rate is >100/min
  • wide QRS complexes with LBBB or RBBB morphology are present, as well as atypical morphology can be present
  • tachycardias with very wide complexes are usually of ventricular origin
  • AV dissociation (atrial activation, usually from the sinus node, is independent from ventricular activation, which is originating from the AV junction, His-Purkinje system, or ventricles)
  • capture beats (the sinoatrial node transiently 'captures' the ventricles, in the midst of AV dissociation, to produce a QRS complex of normal duration)
  • fusion beats (supraventricular and a ventricular impulse coincide to produce a hybrid complex)
  • morphologic criteria which are considered in algorithms for VT diagnosis such as Brugada or Vereckei criteria

Picture 2 Signs of ventricular tachycardia



  • Several algorithms have been proposed to differentiate between a SVT conducted with aberrancy and a VT
  • Presented are two if the frequently used - Brugada criteria/algorithm and Vereckei criteria/algorithm

Brugada algorithm as well as Vereckei criteria are stepwise algorithms:

  • In each step a criteria for VT must be assessed and only after ruling out each of the criteria/going through all of the steps a diagnosis of SVT can be made.
  • In practice, applying Brugada criteria may be difficult for inexperienced doctors as in step 3, morphology criteria must be assessed. The original overall accuracy was reported to be 98%, although subsequent analysis found the accuracy to be lower at approximately 80%.
  • Vereckei criteria use only one lead to differentiate VT and SVT - aVR. It uses morphologic criteria in a stepwise approach. The most difficult step in this algorithm is the last one as well as voltage change in time must be assessed.

Picture 3 Brugada criteria

Picture 4 Vereckei criteria (lead aVR)

Picture 5 Overview of all useful information about how to differentiate between VT and SVT.

FASCICULAR VENTRICULAR TACHYCARDIA - please see more information about this tachycardia in it´s own chapter - Fascicular ventricular tachycardia.

OUTFLOW TRACT VENTRICULAR TACHYCARDIA - please see more information about this tachycardia in it´s own chapter - Outflow tract tachycardia.


  • Acute management depends on the clinical presentation
    - Hemodynamically unstable patients with monomorphic VT require prompt synchronised DC    cardioversion
    - Hemodynamically unstable patients with polymorphic VT require prompt defibrillation
  • Treatment of hemodynamically stable patients is more complex and depends on the type of VT and underlying heart disease (if present)
  • Options include pharmacotherapy, catheter ablation or ICD implantation
  • Patients who present with resuscitated cardiac arrest are generally candidates for secondary prevention with ICD implantation

ECG 1 Monomorphic ventricular tachycardia 182/min in a patient with ischemic cardiomyopathy - RF ablation performed in commissure between right and left coronary cusps, and also in right coronary cusp.

ECG 2 Monomorphic ventricular tachycardia 151/min in a patient with ischemic cardiomyopathy. Extensive RF ablation was performed in anterior and apical parts of the left ventricle. 

ECG 3 Ventricular tachycardia - see clear AV dissociation (e.g. lead I).

The Einthoven triangle is your best friend !

Concordance in precordial leads:

When all QRS complexes in the precordial leads are either upright or negative (positive or negative concordance, respectively), VT is strongly suggested. Negative concordance is virtually diagnostic of VT generated from the anteroapical left ventricle. Positive concordance is strongly suggestive of VT generated from the posterobasal left ventricle but may occur with a posterior bypass tract.

Wellens, H. Ventricular Tachycardia: Diagnosis of Broad QRS Complex Tachycardia. Heart (British Cardiac Society). 86. 579-85. 10.1136/heart.86.5.579.

VT origin and QRS width 

An origin close to the interventricular septum results in more simultaneous right and left ventricular activation and therefore a more narrow QRS complex. In contrast a VT origin in the laterál ventricular wall results in sequential ventricular activation and a wider QRS complex.

Of course other factors also play a role in the QRS width during VT, such as scar tissue (after myocardial infarction), ventricular hypertrophy, and muscular disarray (as in hypertrophic cardiomyopathy).

QRS width of more than 0.14 seconds in right RBBB tachycardias and 0.16 seconds during LBBB argues for a VT.

Wellens, H. Ventricular Tachycardia: Diagnosis of Broad QRS Complex Tachycardia. Heart (British Cardiac Society). 86. 579-85. 10.1136/heart.86.5.579.

QRS axis in the frontal plane

VT origin in the apical part of the ventricle has a superior axis (to the left of −30). An inferior axis is present when the VT has an origin in the basal area of the ventricle. On the contrary, presence of an inferior axis in LBBB shaped QRS tachycardia argues for a VT arising in the outflow tract of the right ventricle.

Wellens, H. Ventricular Tachycardia: Diagnosis of Broad QRS Complex Tachycardia. Heart (British Cardiac Society). 86. 579-85. 10.1136/heart.86.5.579.

Transition zone

Late precordial transition zone suggest an RVOT origin of VT, whereas an early precordial transition zone characterizes LVOT origin.


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  8. Cardiovascular physiology concepts.
  9. Anestesia.TK.