Ventricular tachycardia recognition: wide-complex tachycardia approach
Ventricular tachycardia (VT) originates below the bundle of His — in the ventricular myocardium rather than the conduction system. Because activation bypasses the normal His-Purkinje network, conduction is slow and the QRS is wide (≥120 ms). The default assumption for wide-complex tachycardia must be VT, not SVT with aberrancy, because the consequence of treating VT as SVT can be hemodynamic collapse.
The Brugada four-step algorithm: (1) Absence of RS complex in all precordial leads — if true, diagnose VT (100% specific). (2) RS interval >100 ms in any precordial lead — if true, diagnose VT. (3) AV dissociation — P waves marching through QRS at a different rate — diagnose VT (pathognomonic). (4) Morphologic criteria in V1 and V6: RBBB morphology with monophasic R or qR in V1 (instead of triphasic rSR') and QS or rS in V6 (instead of upright Rs) — diagnose VT.
Capture beats and fusion beats are pathognomonic for VT. A capture beat is a narrow complex occurring during VT when a sinus impulse transiently conducts through the AV node — proves AV dissociation. A fusion beat is a hybrid complex with intermediate morphology from simultaneous sinus and ventricular activation.
Monomorphic vs polymorphic VT: clinical significance
Monomorphic VT has a consistent, regular QRS morphology beat-to-beat — all complexes look the same. It typically originates from a fixed scar-based reentry circuit, most commonly from prior MI. Rate is usually 120–250 bpm. Monomorphic VT is the most common sustained VT morphology and is the target of catheter ablation in patients with recurrent VT storms.
Polymorphic VT has continuously changing QRS morphology — no two consecutive complexes look alike. It often reflects dynamic ischemia, electrolyte instability, or drug toxicity. Torsades de pointes is a specific polymorphic VT with a characteristic twisting of the QRS axis around the isoelectric line in the context of a prolonged QT interval. It requires different management than monomorphic VT.
Ventricular fibrillation (VF) produces chaotic electrical activity with no organized QRS complexes. Unlike VT, which may be associated with a pulse, VF is always pulseless and requires immediate defibrillation. The ACLS algorithm for pulseless VT and VF is identical: CPR + defibrillation + epinephrine + amiodarone or lidocaine.
Stable vs unstable VT: treatment decisions
Hemodynamic stability, not rhythm alone, determines the immediate treatment pathway for VT with a pulse. Unstable VT (hypotension <90 mmHg systolic, altered consciousness, pulmonary edema, or chest pain with ischemic ECG changes) requires immediate synchronized cardioversion regardless of heart rate.
Stable VT (maintained blood pressure, alert, no angina) can be triaged to pharmacologic therapy: IV amiodarone 150 mg over 10 minutes is first-line for stable VT in most clinical protocols. IV lidocaine 1–1.5 mg/kg IV bolus is an alternative, particularly with concurrent ischemia. IV procainamide is preferred in electrophysiology protocols and for pre-excited tachycardias. All pharmacologic therapy should be undertaken with cardioversion immediately available — hemodynamics can deteriorate rapidly.