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, (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 tachycardia: ≥ 3 consecutive ventricular complexes (wide QRS complex) at a frequency of ≥ 100/minute
- Classification by duration
- Classification by morphology
- Monomorphic VT: QRS morphology similar in all beats, indicating a single arrhythmogenic focus
- Polymorphic VT: QRS morphology varies in each beat, indicating multiple arrhythmogenic foci
- Premature ventricular complex : ≤ 3 consecutive ventricular complexes often followed by a complete compensatory pause
Cardiac causes 
- Cardiac scars: secondary to myocardial infarction or cardiac surgery
- Myocardial ischemia: secondary to angina
- Inflammatory causes: myocarditis, endocarditis, or rheumatic heart disease
- Idiopathic: areas of increased automaticity in a structurally normal heart
- Nonischemic cardiomyopathy (CM)
Inherited arrhythmia syndromes (channelopathies)
- A group of genetic syndromes caused by mutations in genes that encode cardiac ion channels resulting in a predisposition for arrhythmias 
- Can lead to sudden cardiac death if uncontrolled
- Examples: Congenital long QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia (CPVT)
Extracardiac causes 
- Certain drugs ; 
Monomorphic VT (similar QRS complexes)
- Increased automaticity
- Reentry circuit
- Polymorphic VT (dissimilar QRS complexes): abnormal ventricular repolarization (e.g., due to , drug toxicity, electrolyte abnormalities)
- 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
- Often asymptomatic, especially in NSVT
- Cardiovascular features
- Symptoms may be unprovoked or exacerbated by physical and/or emotional triggers (e.g., exercise, anger). 
See “tachycardia.” for details on the initial management of undifferentiated
All patients 
- Urgently consult cardiology.
- Bring a defibrillator pads to the patient. to the bedside and attach the
- Assess for hemodynamic stability and .
Hemodynamically unstable patients 
- Pulseless VT: Commence CPR while preparing to defibrillate and administer shock as soon as possible(see “ACLS” for details).
- VT with pulse: See “ ” for details.
- Refractory VT: Consider infusion of amiodarone or beta blockers (see “Electrical storm”).
- Deterioration to ventricular fibrillation: Defibrillation and CPR (managed the same as pulseless VT)
Hemodynamically stable patients 
- Confirm the underlying rhythm
- Differentiate VT from if unclear (see “Diagnostics” for an approach).
- If the diagnosis remains uncertain, treat as VT (∼ 80% of WCT is caused by VT).
- Regular monomorphic WCT of unclear origin: Consider adenosine as a diagnostic and therapeutic measure for possible underlying SVT, unless an is suspected. 
- First-line treatment of VT: pharmacological cardioversion with antiarrhythmics
- Refractory VT: electrical cardioversion
A WCT may occur as a result of either VT or . The can help differentiate between the two.
- Once stabilized, evaluate for an underlying cause (see “Diagnostics”).
- Consider long-term management (see “Treatment”).
- Disposition 
- High risk of recurrence or electrical storm: Admit to critical care unit.
- Resolved sustained VT: Admit most patients to hospital for observation and further investigations.
- Nonsustained VT: Admission for workup and risk stratification is typically required for all new cases of nonsustained VT; Discuss disposition of patients with known nonsustained VT with a specialist.
Ongoing stable undifferentiated WCT (on presenting rhythm strip or 12-lead ECG)
- High likelihood of VT (e.g., high clinical suspicion and clearly apparent ): Presume VT diagnosis and begin prior to detailed diagnostics.
- Uncertain likelihood of VT: Distinguish between VT and if the patient remains stable.
- Resolved confirmed VT (i.e., spontaneous resolution or successful cardioversion)
- Resolved tachyarrhythmia of unclear origin: Consult cardiology for specialized studies, e.g., stress ECG, ambulatory ECG monitoring, EP study
If the patient becomes unstable at any time, presume a diagnosis of VT and proceed directly to treatment. Do not delay for detailed diagnostics.
ECG findings of VT 
- Rate: ≥ 100/minute, (most commonly 150–200/minute) 
- Rhythm: typically regular 
- 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. 
- RBBB 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
- RS duration > 100 ms in any
- QRS morphology reflects pathways of de- and repolarization and can indicate the origin of VT. 
Signs of AV dissociation 
- Dissociated P waves
- Fusion complexes
- Capture beats (seen occasionally)
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.
- May be normal
- Features of the underlying cause may be seen, such as:
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
- All patients: BMP and serum magnesium levels
- Further studies: to evaluate for the underlying cause
- Indications: all patients with confirmed VT to assess LVEF and evaluate for structural cardiac defects 
- Findings: Variable; may include valvular defects, regional wall motion abnormalities, ↓ LVEF, and evidence of myocardial infiltration, scarring, or inflammation.
Further assessment of suspected arrhythmia 
- Exercise stress test: Consider if there is suspicion for VT provoked by stress/exertion (e.g., CPVT)
Ambulatory ECG monitoring (Holter monitor or cardiac event recorder)
- Evaluation of suspected intermittent VT
- Assessment of response to antiarrhythmic treatment in confirmed VT
- Coronary angiography
- Can be used to provoke a VT or map ectopic foci, and can be combined with catheter ablation as a treatment
- Undifferentiated tachycardia: See “ .”
- Wide-complex tachycardia: : Usually caused by VT, but can be due to supraventricular tachycardia with aberrancy in ∼ 20% of cases. 
|VT vs. SVT with aberrancy |
|Features||Favors VT||Favors SVT with aberrancy|
|Clinical||Typical age|| || |
|Physical examination|| |
|Response to vagal maneuvers|| |
|ECG|| || |
| || |
|QRS complex|| || |
|Axis|| || |
If uncertainty persists, assume a diagnosis of VT and treat accordingly.
The differential diagnoses listed here are not exhaustive.
- Ongoing or sustained VT: Stabilize with pharmacological or electrical cardioversion (see “Initial management of VT”).
Nonsustained VT or resolved sustained VT
- Treat reversible causes if identified.
- Correct any electrolyte imbalances
- Stop .
- Consider digoxin immune fab (fragment antigen-binding) for digoxin toxicity.
- Treat underlying myocardial ischemia if present (see “Treatment of acute coronary syndrome” for details).
- No identifiable reversible cause or recurrent VT
- Treat reversible causes if identified.
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 
- β-blockers are typically used as first-line therapy because they reduce the risk of sudden cardiac death.
- Other medications (e.g., class Ic antiarrhythmics or class III antiarrhythmics) may be combined with β-blockers if symptoms persist.
|Medications to minimize VT recurrence |
|Safe in known heart disease||β-blockers|
|Caution in known heart disease|
|Class Ic antiarrhythmics|
|Calcium channel blockers|
AICD for VT 
- Used to terminate episodes of VT in order to prevent sudden cardiac death.
- Typically combined with pharmacological therapy
- May be used for primary or secondary VT prevention
: all of the following criteria are met 
- Expected survival > 1 year
- Recurrent VT despite treatment of reversible causes
- One or more of the following:
- Recurrent VT despite optimal therapy
- Antiarrhythmics are not tolerated
- Patient preference
Subtypes and variants
Torsades de pointes (TdP) 
- Definition: a type of polymorphic VT occurring in patients with a prolonged QT interval
- Clinical features: similar to
- Laboratory and imaging studies: same as for VT (see “Diagnostics”)
- Characteristic ECG findings include: 
- Hemodynamically unstable patients: Defibrillation plus CPR.
- Hemodynamically stable patients: Administer IV magnesium sulfate . 
- Identify and treat the underlying
- Restrict or withdraw . 
- Maintain electrolyte balance.
- Chronic hypoxia (e.g. COPD): Supplement O2.
- Hypothyroidism: screen with serum TSH and treat with L-thyroxine replacement as needed 
- TdP refractory to magnesium sulfate: Consider overdrive pacing with pacemaker or isoproterenol infusion. 
Long-term management 
- Consult cardiology.
- Consider β-blockers to minimize the risk of sudden cardiac death (see “Long-term pharmacotherapy in VT” for details).
- Persistent prolonged QT interval despite β-blocker therapy: Consider insertion (with pharmacotherapy) or left cardiac sympathetic denervation.
- Congenital LQTS: See “Treatment” in “Long QT syndrome.”
- Complications: can progress to life-threatening ventricular fibrillation 
Electrical storm 
- Definition: ≥ 3 episodes of sustained VT, V-fib, or appropriate shocks delivered by an AICD within a 24-hour period
- Follow ACLS.
- Treat reversible causes, e.g., correction of electrolyte imbalances, for , , for , for patients with and fever.
- Consider IV antiarrhythmic infusions under specialist guidance for pharmacological cardioversion. 
- Consult cardiology for definitive treatment.
Aggressively treat morbidity and mortality. as it has high
-associated VT 
Young adults with arrhythmogenic right ventricular cardiomyopathy (ARVC) can present with life-threatening VT.
- Suggestive baseline ECG: may show RBBB,
- Pharmacological cardioversion (preferred agents) 
- Further management: Cardiology consult to consider EP study, beta blockers, and AICD placement (See “ ” for details).
Urgently refer patients with suspected to cardiology for confirmation of diagnosis and definitive treatment as it can cause .
VT in patients with AICDs 
Multiple appropriate shocks
- AICD may be present between shocks delivered by
- ECG shows VT
- Treat as and consider if is ineffective.
Lack of appropriate shocks
- AICD are typically present without shocks delivered by
- ECG shows VT
- Begin .
- Urgently consult cardiology for
- See “ ” for further information.
- Perform ABCDE survey, checking for signs of hemodynamic instability.
- Attach defibrillator pads and cardiac monitor.
- Obtain 12-lead ECG or rhythm strip.
- Establish IV access.
- Urgently consult cardiology.
- Pulseless patients: Perform CPR and defibrillation.
- Unstable patients: Presume VT diagnosis and perform electrical cardioversion or defibrillation under based on VT morphology.
- ACLS, start antiarrhythmic infusion (e.g., amiodarone, beta blockers), and admit to critical care unit. : Follow
- Stable patients: Treat based on likelihood of ECG findings, e.g., .
, using clinical evaluation and
- VT likely: Attempt pharmacological cardioversion (e.g., with amiodarone, procainamide, or sotalol) first; electrical cardioversion if unsuccessful.
- Torsades de pointes: Administer IV magnesium sulfate.
- SVT with aberrancy likely: Treatment depends on underlying rhythm and likelihood of underlying accessory pathway (see “ ” and “Management of stable WCT”).
- Unclear diagnosis: Treat as VT.
- Repeat ECG once VT terminated.
- Evaluate and treat underlying causes once stable (see “Etiology”)
- Admit to hospital for further investigations and observation.