ventricular tachycardia

Ventricular tachycardia arises from abnormal automaticity, triggered activity, or reentry within ventricular myocardium, most commonly in the setting of structural heart disease (post-MI scar, cardiomyopathy) or channelopathies (e.g., long QT syndrome, Brugada syndrome). On ECG, VT shows a wide QRS complex (>120 ms) tachycardia; distinguishing it from supraventricular tachycardia with aberrancy is critical and relies on features such as AV dissociation, fusion/capture beats, extreme axis deviation, and concordance of QRS complexes across precordial leads (Brugada criteria).

Clinically, VT can present with palpitations, presyncope, syncope, or sudden cardiac death, particularly if hemodynamically unstable or if it degenerates into ventricular fibrillation. Sustained VT lasts >30 seconds or causes hemodynamic compromise; nonsustained VT terminates spontaneously within 30 seconds.

Management depends on stability: unstable VT (hypotension, altered mental status, ischemic chest pain, or heart failure) requires immediate synchronized cardioversion; pulseless VT is treated like ventricular fibrillation with defibrillation and ACLS protocols. Stable monomorphic VT can be treated with antiarrhythmics such as amiodarone, procainamide, or lidocaine. Polymorphic VT associated with QT prolongation (torsades de pointes) is treated with IV magnesium sulfate, correction of electrolytes, and removal of offending QT-prolonging drugs.

Long-term management includes treating underlying structural heart disease, beta-blockers, and implantable cardioverter-defibrillator (ICD) placement in patients with recurrent VT, reduced ejection fraction, or high risk of sudden cardiac death. Catheter ablation may be considered for recurrent monomorphic VT refractory to medical therapy.