Causes of Ventricular Tachycardia with Wide Complex
The primary causes of ventricular tachycardia with wide complex include coronary artery disease, cardiomyopathy, electrolyte abnormalities, medication adverse effects, and congenital heart disorders. 1
Pathophysiologic Causes
Ventricular tachycardia (VT) originates from myocardium or conduction tissue below the atrioventricular node, presenting with QRS complexes wider than 120 ms and rates typically exceeding 120 beats/min. Major causes include:
Structural Heart Disease
- Coronary artery disease/myocardial infarction - Most common cause, particularly with myocardial scarring 1, 2
- Cardiomyopathy (dilated, hypertrophic, arrhythmogenic right ventricular)
- Myocarditis
- Valvular heart disease (especially with ventricular dilation)
- Congenital heart disease
- Cardiac tumors
Electrolyte and Metabolic Disturbances
- Hypokalemia
- Hypomagnesemia
- Hypocalcemia
- Acidosis
Medication-Related Causes
- Antiarrhythmic drug toxicity (particularly Class IA agents like procainamide)
- QT-prolonging medications (leading to torsades de pointes)
- Tricyclic antidepressants
- Digitalis toxicity
Other Causes
- Catecholaminergic states (stress, exercise, pheochromocytoma)
- Long QT syndrome (congenital or acquired)
- Brugada syndrome
- Idiopathic VT (no structural heart disease)
- Trauma (myocardial contusion)
- Central nervous system injury
Differential Diagnosis of Wide Complex Tachycardia
When evaluating wide complex tachycardia, it's crucial to distinguish between:
- Ventricular tachycardia - Primary ventricular origin
- Supraventricular tachycardia with aberrancy - Including:
- SVT with bundle branch block
- SVT with AV conduction over accessory pathway
- Metabolic/toxic causes of wide QRS complexes 3
ECG Features Suggesting VT
The American College of Cardiology guidelines highlight several ECG features that strongly suggest VT 4, 5:
- AV dissociation (visible in only about 30% of VT cases)
- QRS width >0.14 seconds with RBBB pattern or >0.16 seconds with LBBB pattern
- RS interval >100 ms in any precordial lead
- Negative concordance in precordial leads
- Presence of fusion or capture beats
- QR complexes (seen in ~40% of post-MI VT)
Clinical Context
A history of previous myocardial infarction strongly suggests VT in patients presenting with wide QRS tachycardia 4. The presence of structural heart disease significantly increases the likelihood that a wide complex tachycardia is ventricular in origin rather than supraventricular with aberrancy.
Management Considerations
For hemodynamically unstable patients with wide complex tachycardia, immediate synchronized cardioversion is the first-line treatment (Class I, LOE B) 5. For stable patients, IV procainamide, amiodarone, or sotalol may be considered, with specific agent selection based on the patient's cardiac function and underlying cause 4, 5.
Pitfalls to Avoid
- Never administer calcium channel blockers (verapamil, diltiazem) for wide QRS tachycardia of unknown origin due to risk of catastrophic hemodynamic collapse if the rhythm is VT 5
- Avoid beta-blockers as first-line treatment for undiagnosed wide QRS tachycardia 5
- When in doubt about the diagnosis of wide complex tachycardia, always treat as VT 4, 6
Understanding the underlying cause of ventricular tachycardia is essential for both acute management and long-term treatment planning to reduce morbidity and mortality.