Empty
1. Knuuti J, Wijns W, Saraste A, Capodanno D, Barbato E, Funck-Brentano C, et al. 2019 ESC Guidelines for the diagnosis and management of chronic coronary syndromes. Eur Heart J. 2020;41(3):407-477.
PMID: 31504439
DOI: https://doi.org/10.1093/eurheartj/ehz425
2. Fihn SD, Gardin JM, Abrams J, Berra K, Blankenship JC, Dallas AP, et al. 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS guideline for the diagnosis and management of patients with stable ischemic heart disease. J Am Coll Cardiol. 2012;60(24):e44-e164.
PMID: 23182125
DOI: https://doi.org/10.1016/j.jacc.2012.07.013
3. Khan MA, Hashim MJ, Mustafa H, Baniyas MY, Al Suwaidi SKBM, AlKatheeri R, et al. Global epidemiology of ischemic heart disease: Results from the Global Burden of Disease Study. Cureus. 2020;12(7):e9349.
PMID: 32742886
DOI: 10.7759/cureus.9349
4. Ibanez B, James S, Agewall S, Antunes MJ, Bucciarelli-Ducci C, Bueno H, et al. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J. 2018;39(2):119-177.
PMID: 28886621
DOI: https://doi.org/10.1093/eurheartj/ehx393
5. Amsterdam EA, Wenger NK, Brindis RG, Casey DE Jr, Ganiats TG, Holmes DR Jr, et al. 2014 AHA/ACC guideline for the management of patients with non–ST-elevation acute coronary syndromes. J Am Coll Cardiol. 2014;64(24):e139-e228.
PMID: 25260716
DOI: https://doi.org/10.1016/j.jacc.2014.09.017
Background
I) Definition
Ventricular tachycardia (VT) is a life-threatening arrhythmia characterized by a rapid heart rhythm (typically >100 bpm) originating from the ventricles. It results in wide QRS complexes (≥120 ms) and can be either sustained or nonsustained. VT is commonly associated with structural heart disease and may degenerate into ventricular fibrillation (VF), leading to sudden cardiac death if not promptly managed.
II) Classification/Types
By Duration:
- Nonsustained VT (NSVT): ≥3 consecutive ventricular beats lasting <30 seconds and self-terminating
- Sustained VT: Lasts ≥30 seconds or requires intervention due to hemodynamic instability
By Morphology:
- Monomorphic VT: Uniform QRS complexes; common in scar-related reentry (e.g., post-MI)
- Polymorphic VT: Varying QRS morphologies; includes torsades de pointes
- Bidirectional VT: Alternating QRS axis; seen in digoxin toxicity or CPVT
By Context:
- Ischemic VT: Associated with prior myocardial infarction
- Idiopathic VT: Occurs in structurally normal hearts (e.g., outflow tract VT)
- Inherited VT syndromes: Long QT syndrome, Brugada syndrome, CPVT
Pathophysiology
VT results from abnormal ventricular automaticity, triggered activity, or most commonly, reentrant circuits within diseased myocardium. Scar tissue from prior infarction or cardiomyopathy can create electrical heterogeneity that sustains a reentrant loop, especially in monomorphic VT. Polymorphic VT may arise from prolonged repolarization (e.g., torsades de pointes due to QT prolongation).
Epidemiology
- More common in males and older adults
- Strongly associated with structural heart disease (ischemic heart disease, cardiomyopathies)
- Major cause of sudden cardiac death
- Nonsustained VT may be found incidentally on Holter monitoring
- Sustained VT more often presents symptomatically or with hemodynamic
Etiology
I) Causes
- Myocardial infarction (especially with scar formation)
- Nonischemic cardiomyopathy
- Electrolyte abnormalities (hypokalemia, hypomagnesemia)
- Drug toxicity (e.g., digoxin, antiarrhythmics, QT-prolonging drugs)
- Inherited arrhythmia syndromes (e.g., Long QT, Brugada, CPVT)
- Valvular heart disease
- Idiopathic VT (e.g., RV outflow tract VT)
II) Risk Factors
- Prior MI or structural heart disease
- Left ventricular dysfunction (low EF)
- History of heart failure
- Use of QT-prolonging medications
- Genetic predisposition (family history of sudden cardiac death)
Clinical Presentation
I) History (Symptoms)
- Palpitations (sudden and rapid)
- Lightheadedness, presyncope, or syncope
- Chest discomfort or pressure
- Dyspnea
- Fatigue
- Sudden cardiac arrest (if VT progresses to VF)
II) Physical Exam (Signs)
- Rapid, wide-complex tachycardia (100–250 bpm)
- Hypotension, diaphoresis, or signs of shock (in unstable VT)
- Cannon A waves (AV dissociation)
- Variable S1 heart sounds
- Possible signs of underlying heart disease (murmurs, displaced apex)
Differential Diagnosis (DDx)
- Supraventricular tachycardia with aberrant conduction (SVT with bundle branch block)
- Antidromic AVRT (e.g., WPW)
- Torsades de pointes
- Accelerated idioventricular rhythm (AIVR)
- Atrial fibrillation with pre-excitation
- Sinus tachycardia with wide QRS (e.g., due to hyperkalemia)
Diagnostic Tests
Initial Work-Up
- ECG (during episode): Wide QRS complex (>120 ms), AV dissociation, fusion/capture beats suggest VT
- ECG (baseline): Evidence of previous MI, bundle branch block, or QT prolongation
- Cardiac biomarkers: Rule out ongoing ischemia or infarction
- Electrolytes: Assess for hypokalemia/hypomagnesemia
- Echocardiography: Evaluate for structural abnormalities
- Holter or event monitor: For intermittent or nonsustained VT
- Cardiac MRI: To assess scar, infiltrative disease
- Electrophysiology Study (EPS): For risk stratification or ablation planning
- Genetic testing: If inherited arrhythmia suspected
Treatment
I) Initial Approach
Hemodynamically unstable (pulseless or hypotensive):
- Immediate synchronized cardioversion (or defibrillation if pulseless VT/VF)
Hemodynamically stable:
- IV antiarrhythmics (e.g., amiodarone, procainamide, lidocaine)
- Correct underlying triggers (electrolytes, ischemia, toxins)
II) Medications
Drug Class | Examples | Notes |
Antiarrhythmics | Amiodarone, Procainamide, Lidocaine | First-line for acute termination in stable VT |
Beta-blockers | Metoprolol, Carvedilol | Reduce sympathetic drive; prevent recurrence |
ACE inhibitors/ARBs | Lisinopril, Losartan | Improve LV function; long-term mortality benefit |
Diuretics | Furosemide | For symptomatic heart failure |
Sotalol/Flecainide | (in select cases) | Avoid in structural heart disease |
Device Therapy:
- Implantable Cardioverter-Defibrillator (ICD): First-line for secondary prevention or high-risk patients
- Catheter Ablation: Considered in recurrent monomorphic VT or ICD storms
- Revascularization: For ischemic VT with ongoing myocardial ischemia
Consults/Referrals
- Cardiology: Essential for evaluation and medication management
- Electrophysiology: For ablation and ICD placement
- Emergency Medicine: For acute VT or cardiac arrest
- Primary Care/Internal Medicine: Ongoing management and comorbidities
- Genetics: In suspected inherited arrhythmia syndromes
Patient Education, Screening, Vaccines
Education
- Recognize warning signs of VT or ICD shocks
- Adherence to medications and follow-up
- Avoid QT-prolonging drugs
- Maintain normal potassium and magnesium levels
- Emergency response training for family (e.g., CPR)
Screening/Prevention
- Routine ECGs and Holter monitoring in cardiomyopathy
- Genetic screening for inherited syndromes if family history
- Screen for reversible causes: ischemia, drugs, electrolytes
Vaccinations
- Influenza and pneumococcal vaccines in patients with heart failure or ICDs
- No specific vaccine required for VT itself
Follow-Up
Short-Term
- Monitor ECG for recurrence
- Titrate antiarrhythmic medications
- Address reversible contributors (electrolytes, ischemia)
Long-Term
- Regular ICD checks if placed
- Surveillance imaging (e.g., echocardiography)
- Risk factor modification (HTN, diabetes, smoking)
- Cardiac rehabilitation in ischemic heart disease
Prognosis
- Nonsustained VT: Often benign in structurally normal hearts
- Sustained VT with structural disease: High recurrence risk; ICD reduces mortality
- Idiopathic VT: Good prognosis with ablation or medications
- Polymorphic VT (torsades): Can be fatal if unrecognized or untreated
- ICD: Dramatically reduces risk of sudden cardiac death
