HRS Board Review 2025 New Courses (Reviewers Copy)-Workshop 1_Tomaselli_2025

Video Transcription

Next question is another case. 51-year-old woman presents with syncope. She has no premonitory symptoms, but has a history of hypertension and substance use disorder.  Her medications currently are hydrochlorothiazide 25 milligrams daily, nifedipine XL 60 milligrams daily, and methadone 100 milligrams daily.  Her labs are remarkable for a magnesium of 2.3 milligrams per deciliter and a potassium of 3.3 milliequivalents per liter. Trans thoracic echo is performed and  revealed left ventricular hypertrophy, and a normal left ventricular ejection fraction of 65 percent. Now, shortly after admission, the following ECG in figure 7-1 is observed.  We'll give you a little time to look at this.  Which of the following is most likely responsible for this arrhythmia? Schemia induced by cocaine use, decreased repolarizing reserve due to left ventricular hypertrophy,  hypokalemia induced by hydrochlorothiazide, drug-induced QT prolongation, and hypokalemia in the setting of a KCNH2 or HERG mutation.  I'll give you some time to consider the responses here and show you the ECG again.

Video Summary

A 51-year-old woman with a history of hypertension and substance use disorder presents with syncope. Her medications include hydrochlorothiazide, nifedipine, and methadone. Labs show low potassium (3.3 mEq/L) and normal magnesium levels. An echocardiogram reveals left ventricular hypertrophy and normal ejection fraction. After admission, an ECG is taken. The potential causes for her arrhythmia are evaluated: ischemia from cocaine use, decreased repolarization due to ventricular hypertrophy, hypokalemia from hydrochlorothiazide, drug-induced QT prolongation, or hypokalemia with a genetic mutation.

Keywords

syncope

hypokalemia

ventricular hypertrophy

arrhythmia

QT prolongation