A 50 Year-Old Homeless Man With Symptomatic Palpitations

Abstract

The patient is a 50-year old man with Hepatitis C, HIV, and pneumonia who recently became homeless and presented with 3 days of worsening palpitations and shortness of breath. Initially the palpitations were sporadic; however, they had become more frequent over the three days prior to admission. He had a corresponding increase in shortness of breath along with significant decreases in his exercise tolerance. He presented to the Emergency Department (ED) when he could no long perform his usual activities of daily living. In the ED, patient was found to have a narrow complex tachycardia with a rate of 234 beats per minute (bpm) (Figure 1).His past history is significant for HIV diagnosed in 1979 with a recent CD4 Count of 16. The patient was not on HAART medication due to noncompliance resulting from financial issues. He also has a history of Hepatitis C secondary to remote intravenous drug abuse. He had pneumonia approximately three weeks prior to admission, which was incompletely treated with antibiotics. The patient also noted a 30-pack year history of tobacco use.In the ED, the patient was given large volumes of normal saline followed by 3 sequential doses of adenosine, all of which failed to terminate his tachycardia. He was then started on an esmolol infusion with resultant hypotension to a systolic blood pressure (SBP) of 80mmHg. The esmolol infusion was subsequently stopped and patient received diltiazem. Following the diltiazem infusion, the patient still had no decrease in his rapid heart rate. A cardiology consultation was requested and procainamide was recommended for chemical cardioversion; however, the patient's blood pressure had deteriorated to SBP of 70mmHg with a heart rate of 240 bpm and the patient was urgently electrically cardioverted. Sinus rhythm was restored at a rate of 110 bpm and the SBP improved to 130 mmHg. He was then referred to the Electrophysiology (EP) service in order to evaluate for a more durable and definitive management of his supraventricular tachycardia (SVT). An EP study was performed and revealed an atrioventricular accessory pathway on the left lateral mitral annulus that was responsible for his SVT. The accessory pathway was successfully ablated as evidenced by intracardiac electrograms and by a lack of initiation of supraventricular tachycardia following isoproteronol administration after ablation (Figure 2).