LAUSR

A 25-year-old woman was admitted after a witnessed syncopal event at home. She reported feeling fatigued in the days before the event. She denied any palpitations, chest pain, seizure aura, or other symptoms immediately preceding syncope. Medical history was notable for fibromyalgia, pseudoseizure, and scoliosis. Prescribed medications included pregabalin, oxycodone, and lamotrigine, although the patient reported that she had self-discontinued all of these medications in the past month. There was no family history of arrhythmias, sudden cardiac death, or any metabolic disorders. On arrival to the emergency department, the patient was conscious. Blood pressure was 50/40 mm Hg. Physical examination was unremarkable with the exception of intranuclear ophthalmoplegia and depressed affect. Laboratory tests revealed an increase in serum creatinine (1.6 mg/dL, n=0.5–1.4), normal serum sodium (141 meq/L, n=135–148), normal serum potassium (4.8 meq/L, n=3.5–5.1), normal serum magnesium (2.2 mg/dL, n=1.6–2.4), and normal serum calcium (9.0 mg/dL, n=8.4–10.5). The results of thyroid testing and troponin were normal. Standard urine toxicology screen was negative. ECG on arrival demonstrated a wide QRS complex, alternating between left bundle-branch block and right bundle-branch block morphology, with rate 80 bpm (Figure 1A and 1B). Telemetry intermittently showed a clear sinus rhythm with prolonged PR and QRS intervals. Baseline ECG 1 year ago had demonstrated normal sinus rhythm with no QT prolongation or other abnormalities. She was started on dopamine infusion at 18 μg/kg/min and transferred to our institution. What is the likely etiology of the patient’s wide QRS rhythm and how should it be managed? Please turn the page to read the diagnosis. Anum S. Minhas, MD Steven P. Schulman, MD