Ventricular tachycardia

Last updated: September 28, 2023

Summarytoggle arrow icon

Ventricular tachycardia (VT) is a potentially life-threatening arrhythmia originating in the cardiac ventricles. VT usually results from underlying cardiac diseases, such as myocardial infarction or cardiomyopathy, but it can also be idiopathic or caused by drugs and electrolyte imbalances. Clinical manifestations range from palpitations and syncope to cardiogenic shock and sudden cardiac death (SCD). The characteristic ECG findings of VT are wide QRS complexes (> 120 ms), tachycardia (≥ 100/minute), and signs of AV dissociation. In the acute setting, management of VT may require immediate cardioversion, defibrillation, or administration of antiarrhythmic drugs. Most patients who develop symptomatic, recurrent VT require long-term therapy involving antiarrhythmic medication, automated implantable cardioverter-defibrillator (AICD) insertion, or catheter ablation of the arrhythmogenic focus. Torsades de pointes (TdP) is a type of polymorphic VT occurring in patients with a prolonged QT interval. Intravenous magnesium sulfate and correction of the underlying etiology of prolonged QTc are important aspects of TdP management.

Ventricular fibrillation is a type of ventricular tachyarrhythmia but is covered in a separate article (see “Ventricular fibrillation”).

Definitiontoggle arrow icon

Reference: [3]

Etiologytoggle arrow icon

Cardiac causes [3][4]

Ischemic heart disease is the most common cause of ventricular tachycardia. [3]

Extracardiac causes [4]

Drug-induced toxicity and electrolyte abnormalities are the most common extracardiac causes of ventricular tachycardia.

Pathophysiologytoggle arrow icon


VT can result from an alteration in myocardial automaticity, electrical conduction, or ventricular repolarization secondary to several factors (see “Etiology” for details).


  • Asynchronous atrial and ventricular beats and rapid ventricular rhythm → ↓ blood flow into the ventricle during diastole cardiac output
  • Consequent hemodynamic compromise → symptoms of syncope, MI, angina

Reference [3]

Clinical featurestoggle arrow icon

If sustained VT is suspected, immediately obtain an ECG to confirm the diagnosis and initiate treatment as it can rapidly progress to ventricular fibrillation and cause sudden cardiac death.

Reference: [3]

Initial management of sustained VTtoggle arrow icon

See “Approach to tachycardia” for details on the initial management of undifferentiated tachycardia.

All patients [3][11]

Attach defibrillator pads to unstable patients and use a cardioverter-defibrillator or bedside monitor to obtain a rhythm strip for rapid assessment.

Hemodynamically unstable patients [3][11]

Pulseless VT and ventricular fibrillation are managed similarly with CPR and defibrillation.

Hemodynamically stable patients [3][11]

See also “Management of stable wide-complex tachycardia” (WCT) for an algorithm to diagnose and treat undifferentiated WCTs.

A WCT may occur as a result of either VT or SVT with aberrancy. The Brugada criteria can help differentiate between the two.

Antiarrhythmics may precipitate acute hypotension and/or rhythm deterioration to TdP or ventricular fibrillation; be prepared to provide immediate defibrillation or hemodynamic support as required.

Avoid procainamide and sotalol in patients with QT prolongation on their baseline ECG, as this may precipitate TdP. [3]

Further management

  • Once stabilized, evaluate for an underlying cause (see “Diagnostics”).
  • Consider long-term management (see “Treatment”).
  • Disposition [13]

Diagnosticstoggle arrow icon


Obtain an ECG in all patients with suspected VT (ongoing or resolved). A narrow-complex tachycardia on ECG or rhythm strip excludes VT.

If the patient becomes unstable at any time, presume a diagnosis of VT and proceed directly to treatment. Do not delay initial management of VT for detailed diagnostics.

ECG findings of VT [3]

  • Rate: ≥ 100/minute, (most commonly 150–200/minute) [13]
  • Rhythm: typically regular [14]
  • QRS complexes
    • Duration: >120 ms; or > 3 small squares on the ECG (known as wide QRS complex)
    • Can be monomorphic VT or polymorphic VT
    • QRS morphology consistent with VT: The presence of any of the following is highly suggestive of VT. [13]
      • RBBB pattern
        • V6: R:S ratio < 1 (amplitude), QS wave (i.e., no R wave), or QR wave (i.e., no S wave)
        • V1: monophasic R wave, QR wave (i.e., no S wave), or RS wave (i.e., no Q wave)
      • LBBB pattern
        • V1 or V2: R wave duration > 0.03 seconds, S wave notched or slurred, or duration of Q wave to the lowest point of S wave > 0.07 seconds
        • V6: QR wave (i.e., no S wave) or QS wave (i.e., no R wave)
      • No RS complex in all precordial leads
      • RS duration > 100 ms in any precordial lead
    • QRS morphology reflects pathways of de- and repolarization and can indicate the origin of VT. [15]
  • Signs of AV dissociation [16]
    • Dissociated P waves
      • No relationship between P waves and QRS complexes
      • Indicates that atrial and ventricular contractions are occurring independently
    • Fusion complexes
      • Mixed QRS morphology containing components of a ventricular complex and a normal sinus QRS complex
      • Caused by an atrial impulse transmitted to the ventricles colliding with the ventricular impulse
    • Capture beats (seen occasionally)

3 consecutive wide QRS complexes at a frequency ≥ 100/minute and signs of AV dissociation confirm a diagnosis of VT. [16]

In wide-complex tachycardia (WCT), signs of AV dissociation help distinguish between VT (AV dissociation present) from SVT with aberrancy (AV dissociation absent). See “Brugada criteria” for further information.

Baseline ECG

Always obtain a 12-lead ECG following VT termination and patient stabilization to look for clues to help identify the underlying etiology.

Investigating the underlying cause

Laboratory studies [3]

Imaging [3]

  • Indications: all patients with confirmed VT to assess LVEF and evaluate for structural cardiac defects [17]
  • Modalities
  • Findings: Variable; may include valvular defects, regional wall motion abnormalities, ↓ LVEF, and evidence of myocardial infiltration, scarring, or inflammation.

A bedside TTE may help identify regional wall motion abnormalities indicative of acute (or prior) myocardial infarction.

Further assessment of suspected arrhythmia [3][17]

Differential diagnosestoggle arrow icon

VT vs. SVT with aberrancy [13][20][21]
Features Favors VT Favors SVT with aberrancy
Clinical Typical age
  • ≥ 50 years
  • ≤ 35 years
Physical examination
Response to vagal maneuvers
  • None
ECG Fusion complexes
  • Yes
  • No
Signs of AV dissociation
  • Yes
QRS complex
  • Duration typically < 0.14 seconds
  • QRS morphology consistent with SVT
  • Normal
Baseline ECG findings

If uncertainty persists, assume a diagnosis of VT and treat accordingly.

The differential diagnoses listed here are not exhaustive.

Treatmenttoggle arrow icon

Approach [3][11]

Long-term management of patients with VT

Pharmacological therapy (antiarrhythmics) is often used alongside device therapy (e.g., AICD) to minimize symptoms, risk of recurrence, and risk of sudden cardiac death. Ablation of the arrhythmogenic foci is potentially curative.

Pharmacological therapy [3][17]

Medications to minimize VT recurrence [3][17]
Drug class Indications Medications
Safe in known heart disease β-blockers
  • Recurrent VT: Consider in combination with a β-blocker.
Caution in known heart disease


(class III antiarrhythmic)

Class Ic antiarrhythmics
Calcium channel blockers

AICD for VT [3]

Ablation [3][23]

  • Overview
    • Potential curative treatment for VT
    • Most patients do not subsequently require an AICD or further antiarrhythmic therapy. [24][25]
    • Following an EP study, the arrhythmogenic focus is ablated.
  • Indications
    • Recurrent VT despite optimal therapy
    • Antiarrhythmics are not tolerated
    • Patient preference
  • Options

Subtypes and variantstoggle arrow icon

Torsades de pointes (TdP) [3][8]

Electrical storm [30][31]

Aggressively treat electrical storm as it has high morbidity and mortality.

ARVC-associated VT [3][12]

Young adults with arrhythmogenic right ventricular cardiomyopathy (ARVC) can present with life-threatening VT.

Urgently refer patients with suspected ARVC to cardiology for confirmation of diagnosis and definitive treatment as it can cause sudden cardiac death.

VT in patients with AICDs [13][30]

Multiple appropriate shocks

Lack of appropriate shocks

Inappropriate shocks

Complicationstoggle arrow icon

We list the most important complications. The selection is not exhaustive.

Acute management checklist for sustained VTtoggle arrow icon

Referencestoggle arrow icon

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