Ventricular Tachycardia

Three or more wide, bizarre QRS complexes in a row at 150–250 bpm — the rhythm that forces you to decide in seconds whether to defibrillate or medicate.

Ventricular tachycardia (VT) originates below the bundle of His, producing wide QRS complexes (≥0.12 seconds) at a rate of 150–250 bpm. It is classified by duration and morphology. Sustained VT lasts ≥30 seconds or causes hemodynamic collapse before that mark. Nonsustained VT is three or more consecutive PVCs lasting <30 seconds that self-terminates. Monomorphic VT shows uniform QRS shape, suggesting a single irritable focus — often from scar tissue post-MI. Polymorphic VT (including torsades de pointes) shows varying QRS morphology and is frequently linked to prolonged QT intervals. The critical nursing decision tree hinges on whether the patient has a pulse. Pulseless VT is treated identically to ventricular fibrillation — immediate defibrillation per ACLS. VT with a pulse but hemodynamic instability (hypotension, altered consciousness, chest pain) calls for synchronized cardioversion. Stable VT with a pulse is treated pharmacologically, most commonly with IV amiodarone. You must continuously assess level of consciousness because stable VT can deteriorate to pulseless VT or V-fib within seconds.

Key Distinctions

Don't confuse VT with SVT with aberrant conduction — VT has wide QRS complexes and AV dissociation; SVT with aberrancy usually has identifiable P waves or responds to vagal maneuvers. Pulseless VT uses defibrillation (unsynchronized), while VT with a pulse and instability uses synchronized cardioversion — mixing these up is a common NCLEX trap. Torsades de pointes is a polymorphic VT treated with IV magnesium, not standard amiodarone.

Clinical Pearl

Wide and fast, check the pulse fast. No pulse = defibrillate. Pulse + unstable = synchronized cardioversion. Pulse + stable = amiodarone.