LAUSR

To the Editor: A 72-year-old African American woman presented to her primary care physician complaining of cough symptoms. She was subsequently diagnosed with acute bronchitis and prescribed clarithromycin and prednisone. The next day after taking prednisone, she claimed that she began to feel dizzy and lightheaded. These symptoms persisted and worsened for an additional day, leading the patient to request emergency medical services. When emergency personnel arrived, she was found to have a blood glucose level too high to register on the Accu-Chek (Roche, Indianapolis, IN), bradycardia with a heart rate (HR) in the 40 seconds, and hypotension (60/40 mm Hg). She was administered a 500-mL bolus of normal saline and 0.5 mg of atropine and transported to the hospital [Figure 1—electrocardiogram (ECG) on admission]. On arrival, she was found to have a blood glucose level of 688 mg/dL, serum creatinine of 2.11 mg/dL (baseline ;1 mg/dL), lactic acid of 6.2 mmol/L, and subsequently administered a dopamine drip. Her medical history was significant for heart failure preserved ejection fraction 60%–65%, coronary artery disease, hypertension, diabetes, and hyperlipidemia. Home medications included losartan 100 mg daily, nifedipine XL 60 mg daily, metoprolol 25 mg twice a day, paroxetine 20 mg daily, atorvastatin 20 mg, and insulin lispro protamine/insulin lispro (75/25) 40 units every morning and 60 units every evening. She reported no recent changes in her medication use other than the recent addition of clarithromycin 500 mg twice a day and prednisone 20 mg 4 times a day for acute bronchitis. After arrival, she was transferred to the intensive care unit where she went into a bradycardic arrest (HR in the low 30 seconds), followed by pulseless electrical activity. Cardiopulmonary resuscitation was performed for 3 minutes using epinephrine and atropine, and return of spontaneous circulation was achieved with rebound sinus tachycardia (Figure 2 ECG during arrest). In addition, she was intubated secondary to her acidotic state from hypoperfusion. Her ECG showed a junctional rhythm identified as junctional bradycardia with an HR of 40 and T wave inversions in the lateral leads. Electrophysiology was consulted, and she was maintained on dopamine at 10 mg/kg/ min to keep blood pressure and HR within normal limits. To determine the etiology of pulseless electrical activity, a sepsis workup was performed, and it was unremarkable. Blood cultures remained negative for the duration of the admission. Hypovolemic shock could have been a potential cause; however, the patient needed pressor support to maintain hemodynamic parameters after fluid resuscitation. An echocardiogram revealed normal ventricular wall motion with heart failure preserved ejection fraction 60%–65% (unchanged from previous echocardiogram 4 months before). Because no other causes were determined and