Ventricular tachycardia
| Ventricular tachycardia | |
| Lead II: rhythm, ventricular tachycardia |
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Differentiating Ventricular Tachycardia from other Disorders |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief:Sara Zand, M.D.[2] Cafer Zorkun, M.D., Ph.D. [3], Avirup Guha, M.B.B.S.[4] Nehal Eid, M.D.[5]
Synonyms and keywords: V tach; tachycardia - ventricular; VT
Ventricular tachycardia (VT) is a cardiac arrhythmia of three or more consecutive complexes originating in the ventricles at a rate greater than 100 beats per minute.[1] VT is a potentially life-threatening arrhythmia that may cause hemodynamic compromise, syncope, or degenerate into ventricular fibrillation and sudden cardiac death.
Ventricular tachycardia is one of the most clinically significant cardiac arrhythmias. It arises from abnormal electrical activity within the ventricular myocardium and is usually manifested as a tachyarrhythmia with a wide QRS complex (≥120 ms) on electrocardiography.[2] Management requires assessment of the risk of sudden cardiac death, evaluation for underlying heart disease, and consideration of the risks and benefits of available treatments.[2]
VT is classified based on duration, morphology, and clinical context:
| Classification | Definition |
|---|---|
| Sustained VT | VT lasting >30 seconds or requiring termination due to hemodynamic compromise in 30 seconds[1] |
| Nonsustained VT (NSVT) | ≥3 beats of VT, terminating spontaneously in 30 seconds[1] |
| Monomorphic VT | Stable single QRS morphology from beat to beat; typically due to a fixed substrate such as myocardial scar[1] |
| Polymorphic VT | Changing or multiform QRS morphology from beat to beat; suggests acute myocardial ischemia, channelopathy, or metabolic derangement[1] |
| Bidirectional VT | Beat-to-beat alternation in the QRS frontal plane axis; often associated with digitalis toxicity or catecholaminergic polymorphic ventricular tachycardia[1] |
| Torsades de pointes | Polymorphic VT occurring in the setting of a prolonged QT interval, characterized by waxing and waning QRS amplitude[1] |
| Electrical storm | ≥3 episodes of sustained VT or ventricular fibrillation within 24 hours[3] |
| Idiopathic VT | Monomorphic VT occurring in the absence of structural heart disease; often due to an automatic focus in a characteristic location (e.g., right ventricular outflow tract)[1] |
The mechanisms of VT vary depending on the presence or absence of structural heart disease:
Structural Heart Disease
In the presence of structural heart disease, VT is typically monomorphic and usually due to a reentrant mechanism resulting from the formation of an abnormal electrical circuit in the myocardium.[2] Myocardial scars from previous myocardial infarction or surgical procedures create regions of discontinuous electrical propagation, which results in reentry.[2] Additional pathophysiological factors contributing to arrhythmogenesis include activation of the autonomic nervous system, stretching of the cardiac chambers, molecular changes associated with hypertrophy, and heart failure.[2]
Any disease process that predisposes to myocardial scar may cause reentrant VT, including dilated cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy (ARVC), hypertrophic cardiomyopathy, cardiac sarcoidosis, Chagas disease, and surgically repaired congenital heart disease.[4] Unlike post-MI scar, which has a predilection for the subendocardium, scar in nonischemic disease states may occur in midmyocardial and epicardial locations.[4]
Focal VT originating from the Purkinje system in the setting of acute ischemia has been attributed to triggered activity and delayed afterdepolarizations.[4]
Structurally Normal Heart
In the absence of structural heart disease, monomorphic VT (idiopathic VT) is often due to an automatic focus along the pulmonic, aortic, mitral, or tricuspid valve annulus, or less often, reentry in or near the fascicles of the left bundle branch.[3] The risk of sudden cardiac death in these patients is generally low.[2]
Polymorphic VT and ventricular fibrillation occurring in the absence of structural heart disease are rare and may be due to a cardiac channelopathy (e.g., long QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia), medication-induced QT prolongation, or may be idiopathic.[1]
The causes of VT can be broadly categorized as follows:
| Category | Examples |
|---|---|
| Ischemic heart disease | Acute coronary syndrome, prior myocardial infarction with scar-related reentry |
| Nonischemic cardiomyopathy | Dilated cardiomyopathy, hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy |
| Infiltrative/inflammatory | Cardiac sarcoidosis, cardiac amyloidosis, myocarditis, Chagas disease |
| Channelopathies | Long QT syndrome, short QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia |
| Congenital/surgical | Repaired tetralogy of Fallot, other surgically repaired congenital heart disease |
| Idiopathic | Right ventricular outflow tract VT, fascicular VT (left posterior or anterior) |
| Drug-induced | Digitalis toxicity, QT-prolonging medications, sympathomimetic agents |
| Metabolic/electrolyte | Hypokalemia, hypomagnesemia, hypoxia, acidosis |
Patients with structural heart disease are at increased risk for sustained VT and ventricular fibrillation. The risk and predictors of VT depend on the type, severity, and duration of structural heart disease, increasing with the severity of ventricular dysfunction and the presence of symptomatic heart failure.[1] Approximately one third of patients with an implantable cardioverter-defibrillator (ICD) will have episodes of VT and receive an ICD shock within 3 years after implantation.[5] Worldwide, approximately 4 million people die from sudden cardiac death every year, caused in more than half of cases by ischemic cardiomyopathy.[6]
Diagnosis
History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | EKG Examples | Chest X Ray | Echocardiography | Cardiac MRI | Coronary Angiography
Treatment
Medical Therapy | Electrical Cardioversion | Ablation | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies
Case Studies
Related Chapters
- Tachycardia
- Ventricular fibrillation
- Supraventricular tachycardia
- Pulseless ventricular tachycardia
- Catecholaminergic polymorphic ventricular tachycardia
- Right ventricular outflow tract ventricular tachycardia
- Polymorphic ventricular tachycardia
- ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 Al-Khatib SM, Stevenson WG, Ackerman MJ, Bryant WJ, Callans DJ, Curtis AB, Deal BJ, Dickfeld T, Field ME, Fonarow GC, Gillis AM, Granger CB, Hammill SC, Hlatky MA, Joglar JA, Kay GN, Matlock DD, Myerburg RJ, Page RL (2018). "2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death". J Am Coll Cardiol. 72 (14): e91–e220. doi:10.1016/j.jacc.2017.10.054. PMID 29097296.
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 Shivkumar K (2019). "Catheter Ablation of Ventricular Arrhythmias". N Engl J Med. 380 (16): 1555–1564. doi:10.1056/NEJMra1615244. PMID 30935556.
- ↑ 3.0 3.1 John RM, Tedrow UB, Koplan BA, Albert CM, Epstein LM, Sweeney MO, Miller AL, Michaud GF, Stevenson WG (2012). "Ventricular arrhythmias and sudden cardiac death". Lancet. 380 (9852): 1520–9. doi:10.1016/S0140-6736(12)61413-5. PMID 23101719.
- ↑ 4.0 4.1 4.2 Dukkipati SR, Koruth JS, Choudry S, Miller MA, Whang W, Reddy VY (2017). "Catheter Ablation of Ventricular Tachycardia in Structural Heart Disease: Indications, Strategies, and Outcomes-Part II". J Am Coll Cardiol. 70 (23): 2924–2941. doi:10.1016/j.jacc.2017.10.030. PMID 29216988.
- ↑ Sapp JL, Tang A, Parkash R, Stevenson WG, Healey JS, Gula LJ, Nair GM, Essebag V, Rivard L, Roux JF, Nery PB, Sarrazin JF, Amit G, Raymond JM, Deyell MW, Lane C, Sacher F, de Chillou C, Kuriachan V, AbdelWahab A, Nault I, Dyrda K, Wilton S, Jolly U, Kanagasundram A, Wells GA (2025). "Catheter Ablation or Antiarrhythmic Drugs for Ventricular Tachycardia". N Engl J Med. 392 (8): 737–747. doi:10.1056/NEJMoa2409501. PMID 39555820 Check
|pmid=value (help). Vancouver style error: initials (help) - ↑ Kahle AK, Jungen C, Alken FA, Heeger CH, Tilz RR, Kuck KH, Ouyang F, Schäffer B, Willems S (2022). "Management of Ventricular Tachycardia in Patients With Ischaemic Cardiomyopathy: Contemporary Armamentarium". Europace. 24 (4): 538–551. doi:10.1093/europace/euab274. PMID 34967892 Check
|pmid=value (help).