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Clinical Subject Page

Ventricular Tachycardia (VT)

ICD-10

I47.20

Specialty

Cardiology

Onset

Acute

Reviewed

June 2026

On This Page

Overview

Ventricular tachycardia (VT) is a rapid heart rhythm that originates in the ventricles (the lower chambers of the heart). It is a potentially life-threatening arrhythmia that can reduce the heart’s ability to pump blood effectively and may progress to ventricular fibrillation or sudden cardiac death if not treated promptly.

Etiology & Risk Factors

Etiology

Structural Heart Disease

  • Previous myocardial infarction (most common cause of sustained monomorphic Ventricular Tachycardia VT )

  • Ischemic heart disease

  • Heart failure

  • Dilated cardiomyopathy

  • Hypertrophic cardiomyopathy

  • Arrhythmogenic right ventricular cardiomyopathy (ARVC)

  • Myocarditis

  • Cardiac sarcoidosis

Acute Cardiac Causes

  • Acute myocardial ischemia or infarction

  • Acute heart failure

  • Myocarditis

Electrolyte & Metabolic Causes

  • Hypokalemia

  • Hypomagnesemia

  • Severe hypoxemia

  • Acidosis

Drugs & Toxins

  • QT-prolonging drugs

  • Antiarrhythmic drugs

  • Digoxin toxicity

  • Stimulants

Inherited Electrical Disorders

  • Long QT syndrome

  • Brugada syndrome

  • Catecholaminergic polymorphic Ventricular Tachycardia VT (CPVT)

Risk Factors For Ventricular Tachycardia (VT)

        • Previous MI

        • Reduced left ventricular ejection fraction

        • Heart failure

        • Structural heart disease

        • Previous ventricular arrhythmia

        • Electrolyte abnormalities

        • QT prolongation

        • Family history of sudden cardiac death

Pathophysiology

      • Ventricular Tachycardia (VT) results from abnormal myocardial automaticity, electrical conduction, or ventricular repolarization.
      • Monomorphic VT
        • Caused by:
          • Reentry circuit around myocardial scar tissue (most common)
          • Increased automaticity (e.g., idiopathic VT)
        • Produces wide QRS complexes (≥120 ms).
      • Polymorphic VT
        • Caused by abnormal ventricular repolarization, such as:
          • Long QT syndrome
          • Drug toxicity
          • Electrolyte abnormalities
      • Rapid ventricular rhythm causes poor ventricular filling during diastole → decreased cardiac output → hemodynamic compromise.

      Simple Flow

      Abnormal ventricular electrical activity → Rapid ventricular contractions → Reduced ventricular filling → ↓ Cardiac output → Hypotension, syncope, shock

Clinical Presentation

Common Symptoms

  • Palpitations

  • Chest pain or chest pressure

  • Shortness of breath (dyspnea)

  • Dizziness

  • Syncope (fainting)

Signs

    • Regular tachycardia (HR ≥100/min)

    • Hypotension

    • Cardiogenic shock

    • Loss of consciousness

    • Cardiac arrest (severe cases)

Ventricular Tachycardia (VT)​ overview
Ventricular Tachycardia (VT)​ overview

History Taking

  • “Do you feel your heart racing or pounding?”
  • “Did the palpitations start suddenly?”
  • “Have you had chest pain or chest pressure?”
  • “Are you feeling short of breath?”
  • “Have you felt dizzy or lightheaded?”
  • “Have you fainted or nearly fainted?”
  • “Did the symptoms start during exercise or emotional stress?”
  • “Do you have a history of a heart attack, heart failure, or cardiomyopathy?”
  • “Are you taking any medications that can affect the heart rhythm?”
  • “Have you ever been told you have low potassium, low magnesium, or a long QT interval?”

Types of Ventricular Tachycardia (VT)

Ventricular Tachycardia · Types & Classification

VT = ≥3 consecutive ventricular beats at rate >100 bpm with wide QRS (≥120 ms) Any sustained VT is a medical emergency. Haemodynamic status determines immediate management — DC cardioversion if unstable. All VT requires investigation for underlying structural heart disease.
By Duration
Non-sustained VT (NSVT) — <30 seconds, terminates spontaneously
Often asymptomatic; may cause palpitations. Prognostic significance depends on underlying heart disease.
Sustained VT — ≥30 seconds or requiring termination due to haemodynamic compromise
High risk of degeneration to VF. Requires urgent management and investigation.
By QRS Morphology
Monomorphic VT — identical QRS complexes beat to beat
Fixed re-entrant circuit; usually from scar tissue (post-MI). Most common type.
Polymorphic VT — varying QRS morphology beat to beat
Multiple changing circuits; higher risk of VF. Includes Torsades de Pointes. Often ischaemic or channelopathy-related.
By Haemodynamic Status
Haemodynamically stable — BP maintained, conscious, no shock
Chemical cardioversion possible: amiodarone, lidocaine, procainamide.
Haemodynamically unstable — hypotension, syncope, chest pain, altered consciousness
Immediate synchronised DC cardioversion. No time for pharmacology.
Pulseless VT — treat as VF
CPR + unsynchronised defibrillation immediately. ACLS protocol.
By Pattern / Behaviour
Incessant VT — continuous, occupying >50% of time; difficult to terminate
VT storm — ≥3 separate episodes within 24h requiring intervention
Medical emergency; IV amiodarone, sedation, catheter ablation, IABP.
Bundle branch re-entrant VT — macro-reentry using the His-Purkinje system; LBBB morphology
Monomorphic VT
Polymorphic VT
Torsades de Pointes
ECG appearance
Uniform, identical QRS complexes; fixed morphology throughout episode
Continuously changing QRS morphology; no two beats identical
Twisting of QRS axis around isoelectric line — "torsades de pointes" (French: twisting of the points)
Rate
100–250 bpm; typically regular
100–300 bpm; irregular
200–250 bpm; irregular; characteristically self-terminating but recurrent
Mechanism
Fixed re-entrant circuit — usually around scar tissue (post-MI, cardiomyopathy). May also be triggered activity or automaticity.
Multiple changing re-entrant wavelets; often triggered by acute ischaemia, catecholamines, or electrolyte disturbance
Early afterdepolarisations (EADs) in setting of prolonged QT — triggered activity. Pause-dependent initiation.
Underlying cause
Post-MI scar, dilated CM, HCM, ARVC, sarcoidosis, Chagas disease
Acute MI / ischaemia, catecholaminergic VT (CPVT), Brugada syndrome, electrolyte disturbance
Long QT syndrome (congenital or acquired), drugs (antiarrhythmics, antibiotics, antipsychotics), hypokalaemia, hypomagnesaemia
QT interval before episode
Normal QT interval
Normal or shortened QT (Brugada / short QT syndrome)
Prolonged QTc — defining feature. QTc >500 ms = high risk. "Short-long-short" initiating sequence.
Acute treatment
Stable: Amiodarone IV Lidocaine
Unstable: Synchronised DC cardioversion
Treat cause (ischaemia, electrolytes)
Amiodarone IV
Unstable / pulseless: Defibrillation
IV Magnesium sulphate 2g over 10 min (first line)
Correct QT-prolonging drugs & electrolytes
Avoid class Ia/III antiarrhythmics — worsen QT
Long-term management
ICD — first line for sustained VT with structural heart disease
Catheter ablation if recurrent or ICD shocks
β-blockers for underlying CM
Treat underlying cause; ICD if high risk of VF; ablation for CPVT trigger foci; quinidine for Brugada
Congenital LQTS: β-blockers (nadolol) + ICD if high risk
Acquired: remove offending drug; correct electrolytes; pacing if bradycardia-dependent
Treatment overview — acute & long-term
Acute — unstable VT
Pulseless VT: CPR + unsynchronised defibrillation (200J biphasic) — treat as VF
Unstable with pulse: Synchronised DC cardioversion (100–200J)
Amiodarone 300mg IV bolus post-shock if recurrent
Correct reversible causes: electrolytes, ischaemia, hypoxia
Acute — stable VT
Amiodarone IV 150mg over 10 min then infusion — first line
Lidocaine IV 1–1.5 mg/kg — especially post-MI VT
Procainamide IV — effective but limited availability
Torsades: IV Magnesium 2g; overdrive pacing; isoproterenol
Fascicular VT: Verapamil IV
Long-term prevention
ICD — first-line for sustained VT with structural heart disease (EF <35%)
Catheter ablation — recurrent monomorphic VT; ICD storm; idiopathic VT (RVOT, fascicular)
β-blockers — reduce VT burden; mandatory post-MI and in HF
Amiodarone oral — adjunct to ICD; reduces shocks
Treat underlying cause: revascularisation, optimise HF therapy

Investigations

1. 12-Lead ECG – First-line Investigation

  • Confirms VT

  • Findings:

    • Wide QRS complex (>120 ms)

    • Heart rate ≥100/min (usually 150–200/min)

    • Regular rhythm (usually)

    • AV dissociation

    • Fusion beats or capture beats

2. Laboratory Tests

  • BMP (electrolytes and renal function)

  • Serum magnesium

  • Troponin (if myocardial ischemia is suspected)

  • BNP/NT-proBNP

  • Toxicology screen

  • Drug levels (e.g., digoxin, lithium)

  • Genetic testing (if inherited arrhythmia is suspected)

3. Imaging

  • Transthoracic echocardiography (TTE) – first-line imaging

  • Cardiac MRI (myocardial scar or infiltrative disease)

  • Cardiac CT (if MRI is contraindicated)

4. Additional Tests

      • Holter monitor/Event recorder (intermittent VT)

      • Exercise stress test (exercise-induced VT)

      • Coronary angiography (suspected myocardial infarction or coronary artery disease)

      • Electrophysiology (EP) study (to identify the arrhythmia mechanism and before catheter ablation)

Diagnosis

Diagnostic Approach

  • Obtain a 12-lead ECG in all patients with suspected VT.

  • If the patient is unstable, presume VT and treat immediately—do not delay treatment for further investigations.

  • After stabilization, investigate the underlying cause with laboratory tests and cardiac imaging.

Diagnostic ECG Findings

  • ≥3 consecutive wide QRS complexes (>120 ms)

  • Heart rate ≥100/min (commonly 150–200/min)

  • Usually regular rhythm

  • AV dissociation

  • Fusion beats or capture beats

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Management of Ventricular Tachycardia (VT)

1. Initial Management

  • Assess hemodynamic stability.

  • Ongoing or sustained Ventricular Tachycardia (VT) :

    • Stabilize with electrical cardioversion or antiarrhythmic medication.

  • After stabilization, evaluate and treat the underlying cause.

2. Treat Reversible Causes

  • Correct electrolyte abnormalities (e.g., potassium and magnesium).

  • Stop QT-prolonging drugs.

  • Treat myocardial ischemia if present.

  • Treat drug toxicity (e.g., digoxin toxicity).

3. Long-Term Management

  • β-blockers – first-line therapy to reduce the risk of sudden cardiac death.

  • Amiodarone (often combined with a β-blocker for recurrent VT).

  • Consider other antiarrhythmic drugs when appropriate.

4. Device Therapy

  • Implantable cardioverter-defibrillator (AICD/ICD)

    • Prevents sudden cardiac death.

    • Used in patients with recurrent VT or those at high risk.

5. Catheter Ablation

  • Potentially curative treatment.

  • Indicated for:

    • Recurrent VT despite optimal therapy.

    • Intolerance to antiarrhythmic drugs.

    • Patient preference.

Complications

      • Progression to ventricular fibrillation (VF)
      • Sudden cardiac death
      • Arrhythmia-induced cardiomyopathy

Prognosis

  • Generally good with appropriate treatment.
  • Catheter ablation has better success and lower recurrence than in atrial fibrillation.
  • Many patients respond well to rhythm control, but atrial flutter frequently progresses to atrial fibrillation, so long-term follow-up is important.
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Key Points / Clinical Pearls

  • Ventricular Tachycardia (VT) is a life-threatening arrhythmia that originates in the ventricles.
  • ECG hallmark: Wide QRS complex (>120 ms) with a heart rate ≥100/min.
  • Sustained VT is a medical emergency.
  • Most common cause: Myocardial infarction (MI) and structural heart disease.
  • Symptoms: Palpitations, chest pain, dyspnea, dizziness, and syncope.
  • Diagnosis: 12-lead ECG.
  • Unstable Ventricular Tachycardia (VT):  Immediate synchronized cardioversion (or defibrillation if pulseless).
  • Treat reversible causes: Correct electrolyte abnormalities, stop QT-prolonging drugs, and treat myocardial ischemia.
  • Long-term treatment: β-blockers, ICD (AICD), and catheter ablation when indicated.
  • Major complications: Ventricular fibrillation and sudden cardiac death.