The answer is B. Intravenous magnesium sulfate
Intravenous magnesium sulfate is first-line for torsades de pointes in a patient who still has a pulse, and it works even when the serum magnesium is normal. Magnesium suppresses the early afterdepolarizations that trigger the rhythm rather than correcting a measured deficiency, which is why it is given empirically. The usual approach is 2 g IV over several minutes, repeated and then infused as needed. Alongside it, do the other three things this stem is begging for: stop every offending drug, replace potassium aggressively into the high-normal range (4.5 to 5 mEq/L), and correct any other electrolyte deficit.
The mechanism explains the treatment. A long QT means prolonged repolarization, which lets an early afterdepolarization reach threshold during phase 3; that triggered beat lands on the vulnerable T wave — the classic R-on-T phenomenon — and launches a reentrant polymorphic rhythm. Everything in this stem stacks one QT insult on another. Three separate QT-prolonging drugs are on board, and the lists worth memorizing are the antiarrhythmics (class IA such as quinidine and procainamide, class III such as sotalol and dofetilide), the antipsychotics (haloperidol, ziprasidone), the macrolides and fluoroquinolones, methadone, and the antiemetics. Layered on top are the electrolyte derangements that prolong QT: hypokalemia, hypomagnesemia, and hypocalcemia. Congenital long QT syndromes (Romano-Ward, and Jervell and Lange-Nielsen with congenital deafness) do the same thing genetically, and bradycardia or heart block lengthens QT by pause dependence.
Know the escalation ladder, because the right answer changes with the patient’s pulse and blood pressure. If magnesium fails or the episodes are pause-dependent and recurrent, raise the heart rate to shorten the QT: overdrive pacing at roughly 90 to 110 beats per minute, or isoproterenol as a bridge — though isoproterenol is avoided in congenital long QT, where it can paradoxically lengthen the interval. If the patient becomes hemodynamically unstable, cardiovert; if pulseless, defibrillate. Torsades is one of the few settings where an unsynchronized shock is used for a rhythm with organized complexes, because the constantly shifting polymorphic QRS gives the synchronizer nothing reliable to track.
Sorting the distractors: intravenous amiodarone is the trap, and it is the single most common wrong answer on this question — it is the reflex drug for wide-complex ventricular tachycardia, but it is a class III agent that prolongs the QT, which is the very abnormality driving this rhythm; intravenous procainamide fails for the same reason through a different class, since class IA agents also prolong repolarization, and the pairing of these two options is the point — the whole antiarrhythmic reflex is wrong here; synchronized cardioversion is the correct answer for a patient who is unstable, but this patient has a pulse, is stable between episodes, and her runs are terminating on their own, so shocking her is both unnecessary and technically unreliable in a polymorphic rhythm; and adenosine is a diagnostic and therapeutic agent for regular narrow-complex supraventricular tachycardia with no role in polymorphic VT.
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