Ventricular Tachycardia

Ventricular tachycardia is any heart rhythm faster than 100 beats/min, with 3 or more irregular beats in a row, arising distal to the bundle of His. Ventricular tachycardia is the most common form of wide-complex tachycardia, and it is associated with a high mortality rate. Ventricular tachycardia is often caused by myocardial ischemia, structural disease, congenital conditions, or electrolyte derangement. Individuals may present with chest pain, dyspnea, palpitations, syncope, and hemodynamic instability. Diagnosis is based on characteristic ECG findings of wide-complex QRS, fusion, and capture beats. Management may require antiarrhythmic medications or electrical cardioversion to avoid complications such as heart failure, multiorgan failure, and cardiac arrest.

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Epidemiology and Etiology


  • Half of cardiac mortality in the United States is caused by ventricular tachycardia.
  • Incidence ↑ with age
  • More common in men
  • Torsades de pointes more common in women


  • Heart disease:
    • Coronary artery disease (most common), especially with prior MI
    • Atherosclerosis
    • Smoking
    • Diabetes mellitus
  • Structural disease:
    • Congestive heart failure
    • Cardiomyopathy
    • Myocarditis
  • Congenital disorders:
    • Long-QT syndrome
    • Wolff-Parkinson-White syndrome
  • Electrolyte derangement:
    • Hypokalemia
    • Hypomagnesemia
    • Hypocalcemia
  • QT-prolonging agents:
    • Antibiotics
    • Macrolides
    • Fluoroquinolones
    • Antiarrhythmics
    • Amiodarone
    • Quinidine
    • Digitalis toxicity
    • 1st-generation antipsychotic agent such as haloperidol
    • Tricyclic antidepressants
  • Idiopathic: right ventricular outflow tract (RVOT) tachycardia


  • Ventricular tachycardia is due to abnormal ectopic contractions in the ventricle:
    • Benign ventricular tachycardia 
      • Ectopic signal is regular and stationary.
      • Cardiac output is maintained.
    • Life-threatening ventricular tachycardia: if ectopic signal has a variable location or rate
  • Myocardial scar formation → slows conduction of cardiac electrical impulses
    • Usually from ischemic damage
    • Unexcitable scar tissue is surrounded by hyperirritable myocardial cells:
      • Electrical impulses slow as they pass through the scar.
      • Rest of the ventricle has time to repolarize.
    • Remaining ventricular tissue depolarizes again as the impulse exits the scar (known as reentry).
    • Ventricular contractions are rapid and out of sync with the atria:
      • If tolerated, the arrhythmia may cause cardiomyopathy over time.
      • If not tolerated, acute decompensation, including cardiac arrest, may occur.
  • Medications and genetic disorders that result in a prolonged or delayed repolarization may result in early afterdepolarizations and torsades de pointes.
  • Monomorphic ventricular tachycardia is caused primarily by abnormal reentry circuits, leading to ↑ automaticity.
  • Polymorphic ventricular tachycardia is caused primarily by abnormal ventricular repolarization:
    • Electrolyte abnormalities
    • Long-QT syndrome

Clinical Presentation

Family history

  • Premature sudden death (< 40 years old)
  • Long-QT syndrome
  • Short-QT syndrome
  • Brugada syndrome
  • Arrhythmogenic right ventricular dysplasia
  • Catecholaminergic polymorphic ventricular tachycardia
  • Hypertrophic cardiomyopathy


  • May be asymptomatic
  • Chest pain
  • Hypotension 
  • Syncope
  • Fatigue
  • Confusion
  • Palpitations
  • Dizziness
  • Dyspnea
  • Sudden death


  • Hypotension
  • Tachypnea
  • Signs of diminished perfusion:
    • Diminished level of consciousness
    • Pallor
    • Diaphoresis
    • ↑ Jugular venous pressure
    • S1 may vary in intensity.


Diagnosis is by ECG or cardiac monitoring.

There are 2 primary types of ventricular tachycardia:

  1. Monomorphic:
    • Wide QRS complexes (often > 200 msec)
    • Uniform QRS morphology
  2. Polymorphic:
    • Wide QRS complexes (> 120 msec)
    • Torsades de pointes: beat-to-beat axis deviation of the QRS complexes around the baseline
Ventricular tachycardia

Rhythm strip of ventricular tachycardia showing a regular, wide complex rhythm with a rate over 100/min
This is a shockable rhythm.

Image: “Lead II rhythm ventricular tachycardia Vtach VT” by Glenlarson. License: Public Domain
Torsades de pointes

Example of an ECG tracing showing beat-to-beat axis deviation of the QRS complexes around the baseline in torsades de pointes

Image: “Torsade de pointes” by Panthro. License: Public Domain


Management of ventricular tachycardia is based on whether a pulse is present and, if it is, whether the individual is hemodynamically stable.

Management of ventricular tachycardia

Management of ventricular tachycardia

Image by Lecturio.

For pulseless ventricular tachycardia

Follow the adult cardiac arrest algorithm.

  • CPR to help maintain blood flow through the body
  • Defibrillation:
    • Delivery of an electrical shock to the heart
    • Can use manual defibrillator or automated external defibrillator (AED)
  • Consider the addition of antiarrhythmics, if needed:
    • Amiodarone
    • Lidocaine
  • IV/intraosseous access 
  • Advanced airway
Ventricular fibrillation/pulseless ventricular tachycardia management algorithm

Ventricular fibrillation/pulseless ventricular tachycardia management algorithm

Image by Lecturio.

For ventricular tachycardia with a pulse

  • If hemodynamically unstable:
    • 1st-line treatment of unstable individuals is synchronized direct-current cardioversion.
    • Usually starts at 100 J
  • If hemodynamically stable:
    • Sustained monomorphic ventricular tachycardia without signs of end-organ damage should receive medication-induced cardioversion with:
      • Procainamide
      • Amiodarone
      • Sotalol
      • Lidocaine
    • Polymorphic ventricular tachycardia should be treated with:
      • IV magnesium sulfate
      • Isoproterenol
      • Pacing
      • Antiarrhythmic agent that will not prolong the QT interval (procainamide and amiodarone are contraindicated)
      • Synchronized cardioversion if medical therapy is unsuccessful at 50–200 J monophasic.
      • Correction of electrolyte abnormalities
  • If left ventricular dysfunction is present, cardioversion should be undertaken with amiodarone or lidocaine.
  • If ventricular tachycardia is the result of digitalis toxicity, manage with antidigitalis antibody and electrocardiovert to achieve normal sinus rhythm.
  • Most effective long-term therapy for ↓ mortality is an implantable cardioverter-defibrillator (ICD).

Evaluating for underlying causes

  • Cardiac enzymes: ↑ after MI
  • Coronary angiography to evaluate myocardial ischemia
  • Electrolytes
    • Hypokalemia
    • Hypomagnesemia
    • Hypocalcemia
  • Urine drug screen for medications or stimulants that may affect heart rate
  • Echocardiography if structural cause is suspected
  • Holter monitor can be used to detect intermittent ventricular tachycardia not detected by regular ECG.

Differential Diagnosis

  • Hypokalemia: plasma potassium concentration < 3.5 mEq/L. Hypokalemia can be due to renal losses, GI losses, transcellular shifts, or poor dietary intake. Hypokalemia is usually asymptomatic if minor; however, it can lead to cardiac arrhythmias, muscle weakness, rhabdomyolysis, paralysis, and respiratory failure. Diagnosis is by history and lab testing. Management is by correcting the potassium deficit and treating the underlying cause.
  • Coronary artery disease: inadequate supply of blood to the myocardium, typically caused by atherosclerosis. The myocardium becomes ischemic when oxygen supply does not meet oxygen demand. Diagnosis is based on history and ECG findings, cardiac stress tests, or heart catheterization. Management is primarily based on reducing oxygen demand of the heart and increasing the delivery of oxygen.
  • Myocardial infarction: ischemia of an area of myocardial tissue due to insufficient blood flow and oxygenation. The clinical presentation of MI is with chest pain. Diagnosis is by history, ECG changes, increases in cardiac enzymes, and evidence of wall-motion abnormalities. Management is with thrombolytic therapy rather than percutaneous intervention. All individuals receive nitrates, pain control, aspirin, anticoagulation, and beta-blockers.
  • Long-QT syndrome: disorder of the heart’s electrical activity. Long-QT syndrome affects the repolarization of the heart after a heartbeat and may be congenital or acquired. The syndrome is typically characterized by a prolongation of the QT interval on the ECG and by the occurrence of syncope or cardiac arrest.
  • Ventricular fibrillation: type of ventricular tachyarrhythmia (> 300/min) often preceded by V-fib. In this arrhythmia, the ventricle beats rapidly and sporadically. The ventricular contraction is uncoordinated, leading to a decrease in cardiac output and immediate hemodynamic collapse. Ventricular fibrillation is most commonly caused by underlying ischemic heart disease. 
  • Cardiac arrest: sudden complete cessation of cardiac output with hemodynamic collapse. Individuals with cardiac arrest present in a pulseless, unresponsive, and apneic state. Rhythms associated with cardiac arrest are V-fib/tachycardia, asystole, or pulseless electrical activity. Management of cardiac arrest starts with BLS outside the hospital and advanced cardiac life support (ACLS) when in the hospital.


  1. Kashou, A. H., Noseworthy, P. A., DeSimone, C. V., Deshmukh, A. J., Asirvatham, S. J., May, A. M. (2020). Wide complex tachycardia differentiation: A reappraisal of the state‐of‐the‐art. Journal of the American Heart Association, 9(11).
  2. Al-Khatib et. Al., (2018). 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Journal of the American College of Cardiology 72(14).
  3. Link et. Al., (2010). Part 6: Electrical Therapies: Automated External DEFIBRILLATORS, Defibrillation, CARDIOVERSION, and Pacing * 2010 American Heart Association guidelines for cardiopulmonary resuscitation and Emergency CARDIOVASCULAR CARE. Circulation 122(18 Suppl 3). 
  4. (1997). A comparison of antiarrhythmic-drug therapy with implantable defibrillators in patients resuscitated from near-fatal ventricular arrhythmias. New England Journal of Medicine 337:1576–1584. 
  5. Compton, S. (2017). Ventricular tachycardia treatment & management. Emedicine. Retrieved August 6, 2021, from

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