Using typical historical, physical examination and key diagnostic test features, a clinical profile of ADHF is defined. An assessment of initial severity is determined, based primarily upon level of respiratory distress and evidence of hypoperfusion. Further risk stratification is then derived after the initial work-up is completed which includes tests that demonstrate important prognostic information such as serum sodium, renal function, troponin, BNP, and the initial systolic blood pressure [22–25]. For the purposes of this chapter’s focus on OU care, sections pertaining to the potentially life-threatening complications of respiratory failure or cardiogenic shock will not be discussed.

Figure 15.2 provides further management strategies in patients with ADHF who have a predominance of symptoms due to pulmonary congestion [26]. This algorithm divides patients into two clinical groups based upon the initial presenting blood pressure. Patients who are initially hypertensive may benefit more from aggressive vasodilator therapy and a modest dose of diuretics, while those who are initially normotensive are often substantially volume overloaded and require more aggressive diuretic therapy. Both groups may be candidates to undergo protocolized care and OU monitoring. In the OU, responses to treatment and achieving therapeutic targets determine disposition, whether to be discharged to home or admitted for inpatient care.

Another algorithm with more patient-specific treatment recommendations for management of ADHF in the OU is described in Fig. 15.3 [27]. In this strategy, treatment of ADHF is generally based on the presence or absence of volume overload and an assessment of the patient’s cardiac output. On the left side of Fig. 15.3 [A, C, D, E, F], treatment recommendations are given for patients with ADHF experiencing signs and symptoms of volume overload, manifested by pulmonary congestion [27]. One of the limitations of this algorithm is grouping all patients with pulmonary congestion together, regardless of the etiology. There is no consideration of the patient’s blood pressure or whether systolic or diastolic dysfunction is present. Nonetheless, it is quite helpful with general management principles. The right side of the algorithm provides treatment recommendations for patients with low cardiac output, and since most OUs exclude these patients, little discussion of this component of the algorithm is warranted.

Volume overload is divided into mild and moderate-severe groups; patients with mild volume overload (Fig. 15.3 [C]) are treated with intravenous diuretic therapy, typically loop diuretics [D]. Dosages in patients previously taking diuretics are guided by the total home daily dose, given as an intravenous bolus. Therapy for patients not taking oral diuretics at home is based upon renal function, and clinicians should exercise caution with diuretic therapy in such patients to avoid further renal injury. Success of diuretic therapy is driven by urine output goals, and recommendations for repeat diuretic dosing are described in the algorithm [27]. Again, caution should be exercised with extremely high doses of loop diuretics; prerenal azotemia and electrolyte abnormalities are common and should be recognized and treated quickly. A management strategy for electrolyte disturbances in this setting is included in the accompanying standing orders (Fig. 15.4) [27].

The authors recognize that patients with more severe pulmonary congestion, which typically include those with severe hypertension and resultant acute pulmonary edema, are likely to have an inadequate response to intravenous diuretic therapy alone. In these patients, the initial pharmacologic regimen should be more aggressive and include both an intravenous diuretic and a parenteral vasodilator (Fig. 15.3 [F]) if the blood pressure allows [27]. Intravenous nitroglycerin or nesiritide may be used to produce a more rapid response and more effectively relieve the signs and symptoms of congestion in these patients. No specific recommendations are provided as to which vasodilator should be used. Of note, the suggested starting dose of nitroglycerin (5–10 mcg/min) described in Fig. 15.3 [F] should be considerably higher [27].