Abstract

Information about a real patient is presented in stages (boldface type) to expert clinicians (Drs. Neal K. Lakdawala and Jacob P. Laubach) who respond to the information, sharing his or her reasoning with the reader (regular type). A discussion by the authors follows. A 63-year-old man with previous combat-related Agent Orange exposure and no healthcare contact for 40 years presented to his primary care physician with dyspnea on exertion, orthopnea, and bilateral lower extremity edema. Electrocardiography reportedly showed sinus rhythm, and transthoracic echocardiography demonstrated moderate left ventricular hypertrophy with normal systolic function. New onset heart failure with preserved ejection fraction, attributed to hypertensive heart disease, was diagnosed, and he was begun on diuretics with an initial modest improvement in his symptoms. He presented to our hospital 1 month later with worsening heart failure symptoms and inadequate outpatient response to escalating doses of oral furosemide. The patient reported dyspnea with minimal activity, severe orthopnea, nightly paroxysmal nocturnal dyspnea, and worsening lower extremity edema. There was a history of abdominal distension, although he found that his arms were thinner and his eyes appeared more sunken-in. On examination he was cachectic with a pulse of 85 beats per minute, blood pressure of 82/70 mm Hg, and respiratory rate of 28 breaths per minute with labored breathing. His skin was cool to touch. A diminished single first heart sound, persistently split second sound with a prominent pulmonary component, and S3 gallop were present. Jugular venous pressure was estimated at 18 cm H 2 O. The remainder of the examination was notable for dullness to percussion at the lung bases, ascites, tender hepatomegaly, and marked bilateral lower extremity pitting edema. ECG revealed sinus rhythm with low voltages in the limb leads and no criteria …

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