The correct answer is drug-induced QT prolongation. What is the observation? The observation is repetitive polymorphic VT with a long-short initiation sequence in the setting of QT interval prolongation with abnormal STT waves. Again, lots of non-specific and specific changes in the electrocardiogram. Given the history and use of methadone, drug-induced long QT syndrome is most likely. Prior to polymorphic VT, the patient's not tachycardic, so perhaps not cocaine-related. TTE revealed, in fact, what was mild, relatively mild LVH, and the hypokalemia is also mild, making choices A through C, go back to those, ischemia, decreased repolarizing reserve, and hypokalemia induced by hydrochlorothiazide a bit less likely. A pre-existing mutation KCNH2 cannot be ruled out, but off methadone, her QT interval was dramatically shorter. This is the QT on her baseline electrocardiogram with profound QT interval prolongation, and the QT wave abnormalities consistent with drug-induced long QT syndrome. Off methadone, T waves are not normal, but in fact, the QT interval is a lot shorter. Again, most consistent with drug-induced, in this case, methadone-induced QT interval prolongation, and polymorphic VT as a result of drug-induced QT interval prolongation.

methadone

QT prolongation

ventricular tachycardia

electrocardiogram

long QT syndrome