Electrocardiogram of a man with a single-chamber cardioverter/defibrillator.

A 70-year-old man with diabetes mellitus, systemic arterial hypertension, and over 7 years of intermittent congestive symptoms due to a nonischemic dilated cardiomyopathy, with a left ventricular ejection fraction of 20%, as well as chronic kidney disease, with a current serum creatinine of 4.24 mg/dL, had an implantable cardioverter/defi brillator/ pacemaker lead placed through the left subclavian vein into the right ventricle 21⁄2 years before presentation. During his most recent admission for worsening congestive symptoms, the serum B-type natriuretic peptide level was 3845 pg/mL, up from a 12-month low of 253 pg/mL 4 months earlier. An electrocardiogram recorded on admission is shown in the Figure. Th e atrial rhythm was sinus bradycardia at a rate of 52 beats per minute. Th ere was fi rst-degree atrioventricular block, and an electronic ventricular pacemaker sensed and captured normally in the VVI mode at a rate of 60 beats per min. Th e P waves were broad (0.16 seconds) and notched (0.09 seconds between the two upright peaks in lead II), fi ndings typical of left atrial enlargement (1, 2). Th ere was a nonspecifi c intraventricular conduction defect with a QRS duration of 0.13 seconds. Th e paced QRS complexes had a duration of 0.20 seconds and resembled left bundle branch block, consistent with the device’s pacing the right ventricle. Th e third paced complex was a fusion complex with the electronic pacemaker contributing little or nothing to the QRS morphology, i.e., a so-called pseudofusion complex. As kidney failure worsens, the ability to eliminate salt and water is impaired, and the relative contributions of the failing kidneys and of the failing heart to the patient’s congestive