This patient should be admitted to the hospital and given intravenous furosemide. His presentation is characteristic for heart failure with preserved ejection fraction (HFpEF). He has volume overload manifested by increasing abdominal girth, increased exertional dyspnea, and progressive orthopnea. His left ventricular ejection fraction is normal, but he has mild left ventricular hypertrophy and a long history of hypertension. Additionally, he has a markedly elevated B-type natriuretic peptide level. The etiology of his acute exacerbation into heart failure is most likely acute atrial fibrillation, but because he is already on diltiazem and has a normal heart rate, he may have been in atrial fibrillation for some time and not noticed it.

In contrast to patients with a reduced ejection fraction, no drugs have been shown to reduce mortality rates in patients with HFpEF. Instead, guidelines emphasize controlling blood pressure and volume. Patients with HFpEF are often volume sensitive, and careful use of diuretics to maintain euvolemia is important. This patient is not already taking a diuretic, and starting with a low dose of furosemide is a reasonable approach. If the patient were already on an oral diuretic, giving at least the equivalent dose intravenously would be suggested. Patients with HFpEF should be encouraged to monitor their weight closely, as small differences in volume can quickly cause volume overload and subsequent hospital admissions.

β-Blocker therapy is relatively contraindicated in this patient with acute decompensated heart failure as it may exacerbate his heart failure. Once his heart failure is successfully treated with diuretics, this patient may benefit from β-blocker therapy to help manage his heart rate and blood pressure, but this should be avoided in the setting of acute volume overload, whenever possible.

Despite the fact that the patient is currently in atrial fibrillation, cardioversion at this point is incorrect. Because he is hemodynamically stable with good rate control, there is no indication for immediate cardioversion. In addition, because it is unclear how long he has been in atrial fibrillation, cardioversion without a transesophageal echocardiogram to rule out thrombus or initiation of prophylactic anticoagulation would place the patient at risk for embolization at the time of the procedure.

Several small trials have suggested that aldosterone antagonists may improve diastolic function in patients with HFpEF. However, a recent trial comparing spironolactone with placebo showed a reduction in heart failure hospitalizations but no difference in mortality rates or all-cause hospitalizations in patients with HFpEF, and spironolactone was associated with significant increases in serum creatinine and potassium levels. Given this minimal benefit but substantial increase in risk of adverse effects, the addition of spironolactone for his current symptoms is not appropriate in this patient with HFpEF.