What is Ventricular Tachycardia (VT), how is it diagnosed and what are the treatment options?

What is Ventricular Tachycardia (VT)?

Ventricular tachycardia is defined as three or more consecutive ventricular complexes occurring at a rate greater than 100 beats per minute, originating from the ventricles rather than the normal conduction system. 1

Classification

• Sustained VT lasts longer than 30 seconds or requires termination due to hemodynamic compromise in less than 30 seconds 1
• Nonsustained VT terminates spontaneously in less than 30 seconds 1
• Monomorphic VT shows a consistent QRS morphology, typically associated with structural heart disease and myocardial scarring 2
• Polymorphic VT displays continually changing QRS morphology, often associated with acute myocardial ischemia, channelopathies, or ventricular hypertrophy 2

Mechanisms

The three primary mechanisms underlying VT are:

• Reentry is the most common mechanism in structural heart disease, particularly in post-myocardial infarction scars, requiring anatomical or functional conduction block, slow conduction pathway, and unidirectional block 1
• Triggered activity is common in outflow tract VT (especially right ventricular outflow tract), resulting from delayed afterdepolarizations dependent on intracellular calcium overload and cyclic adenosine monophosphate elevation 2, 1
• Abnormal automaticity occurs when ventricular tissue spontaneously depolarizes at accelerated rates 1

How to Diagnose VT

Electrocardiographic Features

When evaluating wide-complex tachycardia, presume it is VT if the diagnosis is unclear—this is the safest approach. 3

Key Diagnostic Criteria on 12-Lead ECG:

• QRS duration >120 ms (though in infants may be <90 ms but clearly different from sinus complex) 2
• AV dissociation (ventricular rate faster than atrial rate) is diagnostic of VT 2
• Fusion complexes (merging of supraventricular and ventricular impulses) confirm VT 2, 1
• Concordance of precordial QRS complexes (all positive or all negative) suggests VT or pre-excitation 2, 1

Distinguishing VT from Supraventricular Tachycardia with Aberrancy:

The Brugada criteria and Vereckei algorithm (examining lead aVR) can help differentiate VT from SVT with aberrant conduction 2. However, a 12-lead ECG should be recorded for all patients with sustained VT who present hemodynamically stable 2, 3.

Clinical Assessment

Hemodynamic stability is the critical first determination:

• Unstable VT presents with hypotension, altered mental status, loss of consciousness, chest pain, or acute heart failure 2
• Stable VT allows the patient to maintain adequate perfusion despite the arrhythmia 3

Additional Diagnostic Workup

• Measure QT interval carefully during sinus rhythm to exclude long QT syndrome 2
• Echocardiography to assess ventricular function and identify structural heart disease 2
• 24-hour Holter monitoring for complex ventricular arrhythmias 2
• Electrophysiological testing can confirm diagnosis and mechanism when ECG is inconclusive 1

Treatment of VT

Immediate Management Based on Hemodynamic Status

Unstable VT (Hemodynamically Compromised)

Direct current cardioversion is recommended immediately for patients presenting with sustained VT and hemodynamic instability (Class I recommendation). 2

• Provide immediate sedation before cardioversion if the patient is hypotensive but conscious 2
• Use unsynchronized cardioversion for polymorphic VT if the patient is unstable 3

Stable Monomorphic VT

Direct current synchronized cardioversion with appropriate sedation is the first-line treatment for stable sustained monomorphic VT. 3

If medical management is chosen instead:

• Intravenous procainamide (Class IIa) is most efficacious for patients without severe heart failure or acute myocardial infarction 2, 3, 4

  • Dose: Maximum 10 mg/kg at 50-100 mg/min IV over 10-20 minutes with continuous blood pressure and ECG monitoring 4

• Intravenous amiodarone (Class IIa) for patients with heart failure or suspected ischemia 2, 3

  • Loading: 150 mg over 10 minutes, then 1 mg/min for 6 hours, then 0.5 mg/min maintenance 5
  • Recommended starting dose is approximately 1000 mg over first 24 hours 5

• Intravenous lidocaine is only moderately effective 2

Critical Caution:

Calcium channel blockers (verapamil, diltiazem) should NOT be used to terminate wide-QRS-complex tachycardia of unknown origin, especially in patients with myocardial dysfunction. 3 The exception is LV fascicular VT (RBBB morphology with left axis deviation), where IV verapamil or beta-blockers may be appropriate 2, 3.

Stable Polymorphic VT

• Direct current cardioversion (unsynchronized if unstable) 3
• IV beta-blockers are useful, especially if ischemia is suspected 3
• IV amiodarone loading is useful in the absence of long QT syndrome 3
• If torsades de pointes with acquired long QT: immediately discontinue the offending drug (Class I) 2

Long-Term Management

Catheter Ablation

Urgent catheter ablation is recommended in patients with scar-related heart disease presenting with incessant VT or electrical storm (Class I recommendation). 2

• Catheter ablation is recommended for patients with ischemic heart disease and recurrent ICD shocks due to sustained VT (Class I) 2, 3
• Catheter ablation should be considered after a first episode of sustained VT in patients with ischemic heart disease and an ICD (Class IIa) 2
• Catheter ablation is useful (Class I) in patients with structurally normal hearts with symptomatic, drug-refractory VT arising from RV or LV outflow tracts 2

Ablation techniques include activation mapping, substrate ablation using three-dimensional electro-anatomical mapping, and epicardial approaches when needed (particularly in dilated cardiomyopathy or ARVC) 2.

Implantable Cardioverter-Defibrillator (ICD)

ICD therapy is indicated for documented syncopal ventricular tachycardia or fibrillation without correctable causes, and for patients with depressed cardiac function at high risk for sudden death. 2

• ICD implantation is effective for termination of sustained VT in patients with normal or near-normal ventricular function and no structural heart disease who are receiving chronic optimal medical therapy (Class IIa) 2
• Left ventricular ejection fraction is the primary stratification tool for identifying candidates for prophylactic ICD 6

Pharmacological Therapy

For long-term suppression in appropriate candidates:

• Beta-blockers and/or calcium channel blockers for outflow tract VT in structurally normal hearts 2
• Amiodarone (Class 3 agent) for VT with mild cardiac dysfunction, given its low pro-arrhythmic risk 2
• Drug therapy is generally less preferred than ablation or ICD in high-risk patients 2

Special Populations

Idiopathic VT (Structurally Normal Hearts)

• Right ventricular outflow tract (RVOT) VT typically presents with left bundle-branch, inferior-axis morphology 2, 1
• Often exercise-induced, adenosine-sensitive, and facilitated by catecholamines 2, 1
• Symptoms tend to be mild and syncope is rare 2
• Catheter ablation is first-line curative therapy for symptomatic, drug-refractory cases 2