The most appropriate additional treatment for this patient is nitroprusside. After several days of diuresis, this patient has a normal right atrial pressure (0-5 mm Hg) and pulmonary capillary wedge pressure above normal but within the acceptable range for patients with heart failure (<18 mm Hg) to provide optimal ventricular filling. These hemodynamic parameters suggest that the cardiac output is very low and is the major explanation for the patient's heart failure symptoms. Acute heart failure is typically marked by a combination of volume overload (manifested by an increased pulmonary capillary wedge pressure, usually ≥18 mm Hg) and reduced cardiac output. Part of the reason for reduced cardiac output is a very high systemic vascular resistance, as the systemic circulation increases afterload to maintain blood pressure in the setting of low stroke volume. With correction of the volume overload state, the next step in therapy is to reduce afterload with nitroprusside.

Nitroprusside is an intravenously administered vasodilator that lowers systemic vascular resistance and, therefore, increases cardiac output. This therapy should be used only in the setting of invasive monitoring, including a right heart catheter and possibly an arterial line to closely measure systemic pressure. Counterintuitive to what would be expected, the blood pressure usually rises with nitroprusside because of the improved cardiac performance. Nitroprusside is associated with possible rebound vasoconstriction following discontinuation and potential toxicity due to its metabolism to cyanide with longer term use; therefore, therapy is generally limited to no more than 24 to 48 hours in most patients. Patients with cardiogenic shock may also be treated with an inotropic agent such as dobutamine.

Changing to continuous intravenous furosemide is not indicated because the patient has normal filling pressures manifested by the pulmonary capillary wedge pressure of 16 mm Hg and right atrial pressure of 4 mm Hg. More aggressive diuresis will not impact the principal problem, which is low cardiac output and a high systemic vascular resistance. Studies have evaluated the efficacy of continuous versus intermittent boluses of intravenous diuretics in patients hospitalized with acute heart failure. There was no difference demonstrated in patients' symptoms, kidney function, or length of stay between the two strategies. High- versus low-dose diuretics also have been evaluated. Patients taking high dosages exhibited a trend toward more diuresis and slight worsening of kidney function. Diuresis should be performed using whatever strategy is necessary to remove the fluid.

Dopamine was recently compared with nesiritide and placebo in patients with acute heart failure and mild kidney dysfunction. No benefit was demonstrated with either dopamine or nesiritide compared with placebo for either urine output or protection of kidney function. In general, the results of studies evaluating the use of inotropic therapy for the treatment of patients hospitalized with acute heart failure have been negative. For the routine care of patients hospitalized with heart failure, dopamine, dobutamine, and milrinone have not been shown to be helpful and may be associated with adverse outcomes.

Esmolol is an intravenous β-blocker. Like all β-blockers, it has some negative inotropic activity, and use of this drug might worsen the patient's hemodynamic status, not improve it.