A 52-year-old man with a history of anterior wall MI presents with recurrent syncope. ECG shows monomorphic ventricular tachycardia (VT) with a rate of 160 bpm. Which single feature best distinguishes this arrhythmia from polymorphic VT (Torsades de Pointes)?

## Distinguishing Monomorphic VT from Polymorphic VT ### Key Morphologic Difference **Key Point:** Monomorphic VT is defined by a **single, uniform QRS morphology and axis** that remains constant throughout the entire run of tachycardia. In contrast, polymorphic VT (including Torsades de Pointes) shows **beat-to-beat variation in QRS morphology and axis**. ### Clinical and Electrophysiologic Comparison | Feature | Monomorphic VT | Polymorphic VT / Torsades | |---------|---|---| | **QRS Morphology** | Uniform, identical beats | Variable, changing beat-to-beat | | **QRS Axis** | Fixed axis | Rotating / twisting axis | | **Baseline QT** | Usually normal | Prolonged (Long QT syndrome, drugs, electrolyte abnormality) | | **Mechanism** | Re-entry (scar-related) | Early afterdepolarization (EAD) / triggered activity | | **Underlying Substrate** | Prior MI, scar | Repolarization abnormality | | **Rate** | 140–250 bpm, stable | 200–300 bpm, often faster | ### Why Morphology is the Discriminator **High-Yield:** The **single best discriminating feature is uniform QRS morphology and fixed axis** in monomorphic VT. This is the defining electrocardiographic criterion and is immediately apparent on a 12-lead ECG or rhythm strip. Polymorphic VT, by definition, lacks this uniformity — the QRS changes from beat to beat. **Clinical Pearl:** In a post-MI patient (like this case), monomorphic VT arises from a fixed re-entrant circuit in scar tissue, producing identical electrical activation each cycle. Polymorphic VT arises from a repolarization disorder (prolonged QT, hypokalemia, hypomagnesemia, or drug-induced) and shows variable morphology because the site of impulse origin or the pathway changes dynamically. ### Mechanism Distinction **Key Point:** Although monomorphic VT is typically **re-entrant** and polymorphic VT is typically **triggered (EAD-mediated)**, mechanism alone is not visible on the surface ECG — morphology is. ### Management Implication - **Monomorphic VT:** ICD, beta-blockers, sotalol, amiodarone; consider ablation if incessant. - **Polymorphic VT / Torsades:** Correct QT prolongation, electrolyte repletion (K^+^, Mg^2+^), beta-blockers, avoid QT-prolonging drugs. [cite:Harrison 21e Ch 235]